Oncowikia Blog

MicroCHIPS,, Implanted Remote-Controlled Drug Delivery

2012-02-18T03:53:00.000-08:00

Seven osteoporosis patients in Denmark, as a part of a clinical trial, received their daily doses of medicine without having to visit the doctor nor having to administer it themselves. Via a remote controlled device implanted in their body, their physician administered treatment remotely while the patients were at home.
These abdominal implants that the women received were made by MicroCHIPS, a Waltham, Massachusetts based company. The device, during this clinical trial, over a period of four months, delivered 20 daily doses of teriparatide, a hormone treatment that improves bone formation and reduces the risk of fracture. The trial, proved that the remote injections worked just as well as in-person injections.
The research is published in the February 15 issue of Science Translational Medicine. It was also presented at the annual American Association for the Advancement of Science meeting, which is being held in Vancouver, B.C.

MicroCHIPS Press release;

MicroCHIPS Announces Clinical Results for First Successful Human Trial
Of Implantable, Wireless Microchip Drug Delivery Device

Study Validates Microchip Approach to Multi-Year Drug Delivery Without Injections
Novel Technology Supports Improved Patient Outcomes and Remote Medicine

Editors Note: Digital Images/Video of MicroCHIPS device available.

WALTHAM, Mass – February 16, 2012 – MicroCHIPS, Inc., a developer of implantable drug delivery devices and biosensors, announces today the results of the first successful human clinical trial with an implantable, wirelessly controlled and programmable microchip-based drug delivery device. The MicroCHIPS study was published in today’s online edition of the journal Science Translational Medicine.

"These data validate the microchip approach to multi-year drug delivery without the need for frequent injections, which can improve the management of many chronic diseases like osteoporosis where adherence to therapy is a significant problem," said study lead author Robert Farra, MicroCHIPS President and Chief Operating Officer. "We look forward to making further progress to advance our first device toward regulatory approvals, as well as developing a range of products for use in important disease areas such as osteoporosis, cardiovascular disease, multiple sclerosis, cancer, and chronic pain."

In the trial, post menopausal women diagnosed with osteoporosis received daily doses of the marketed osteoporosis drug teriparatide through microchip delivery rather than daily injection. The drug released from the implanted microchip demonstrated similar measures of safety and therapeutic levels in blood to what is observed from standard, recommended multiple subcutaneous injections of teriparatide.

In the study, seven osteoporotic postmenopausal patients between the ages of 65 and 70 received the microchip-based implant. The primary objective of the clinical trial was to assess the pharmacokinetics (PK) of the released drug teriparatide from the implanted devices. Safety measures included evaluation of the biological response to the implant and monitoring indicators of toxicity. Secondary objectives were to assess the bioactivity of the drug and to evaluate the reliability and reproducibility of releasing the drug from the device.

The device and drug combination were found to be biocompatible with no adverse immune reaction. The resulting PK profiles from the implant were comparable to and had less variation than the PK profiles of multiple, recommended subcutaneous injections of teriparatide. The study also demonstrated that the programmable implant was able to deliver the drug at scheduled intervals. Drug delivery and evaluation in patients occurred over a one month period and provided proof-of-concept measures of drug release and device durability that support implantable device viability for 12 months or more.

The microchip device was implanted and explanted using local anesthetic. Patient surveys found that the microchip device was well-tolerated, and patients indicated that they would repeat the implant procedure. "Each procedure lasted less than 30 minutes," said treating surgeon Pia Georg Jensen, MD. "The patients were able to walk out of the facility and go home unescorted."

To assess efficacy and improvement in bone fracture risk, the study measured biological markers of bone formation (P1NP), and bone resorption (CTX). In the study, changes in serum calcium, P1NP, and CTX resulting from drug implant therapy were found to be qualitatively and quantitatively similar to those reported in previous studies during daily subcutaneous injections of teriparatide.

"A microchip that continues to deliver teriparatide with this or similar consistency and efficiency over 12 to 24 months could improve bone mass, density, architecture, and strength," said study co-author Robert Neer, Founder & Director of the Massachusetts General Hospital Bone Density Center and Associate Professor of Medicine at Harvard Medical School.

Implantable medical devices such as pacemakers and pain pumps perform important functions to help patients return to a healthier state and to manage their disease. The design of a next-generation microchip drug delivery device is the only approach to an implantable device that can be wirelessly programmed to release drugs inside the body without percutaneous connections in or on the patient. An implantable microchip device also provides real-time dose schedule tracking, and as part of a network, physicians can remotely adjust treatment schedules as necessary.

"This trial demonstrates how drug can be delivered through an implantable device that can be monitored and controlled remotely, providing new opportunities to improve treatment for patients and to realize the potential of telemedicine," said study co-author Robert Langer, ScD, Institute Professor at the David H. Koch Institute for Integrative Cancer Research at MIT, and cofounder of MicroCHIPS, Inc. "The convergence of drug delivery and electronic technologies gives physicians a real-time connection to their patient’s health, and patients are freed from the daily reminder, or burden, of disease by eliminating the need for regular injections."

MicroCHIPS is currently developing new designs of its microchip-based implant to include as many as 400 doses per device providing daily dosing for one year or multi-year therapy for less frequent dosing regimens. Components of the original microchip technology, such as the array of micro reservoirs used to contain drug and the first microchip opening mechanism, were developed at the Massachusetts Institute of Technology and licensed to MicroCHIPS.

The study with the implantable microchip in osteoporosis patients was funded and managed by MicroCHIPS. In addition to osteoporosis, the company is advancing applications for the microchip device for other therapeutic applications in proprietary programs and through strategic partnerships. The company plans to file for regulatory approval for its first microchip device in 2014.

About MicroCHIPS
http://www.mchips.com/
MicroCHIPS, Inc. is enabling remote medicine through its electronic, wirelessly controlled implanted devices. These implants are designed to improve the health of millions of people with critical conditions that require careful monitoring and therapy. The microchip-based implants can sense vital biochemical changes, deliver potent drug therapies and wirelessly communicate status to networked patients and clinicians. The technologies use microreservoir arrays to hermetically store and protect pharmaceuticals or sensors for extended periods of time. The microchip is controlled by microprocessors, wireless communications or sensor feedback loops for precise, dynamic control of drug delivery or sensing. MicroCHIPS has a deep portfolio of intellectual property including more than 85 issued or pending patents with coverage in the US, Europe, the Far East and throughout the world. MircoCHIPS is funded by leading venture capital firms Flybridge Capital Partners, InterWest, Intersouth Partners, Medtronic and Polaris Venture Partners.

# # #

For more information, contact:

Barbara Yates
barbara@theyatesnetwork.com
(781) 258-6153

Human Papilloma Virus (HPV) Responsible For Rising Oropharyngeal Cancer In The USA?

2011-10-04T09:38:00.000-07:00

HPV which is responsible for cervical cancer now appear to be responsible for throat cancer. A Research team tested tumor samples from 271 patients with throat cancer diagnosed from 1984 to 2004. The Human papilloma virus was found in only 16% of the samples that were from the 1980s and increased to 72% of the samples collected during 2000s.

The researchers estimated that over all, throat cancers caused by the virus have increased to 2.6 per 100,000 people in 2004 from 0.8 cases per 100,000 people in 1988. If the trend continues, by 2020 the virus will be causing more throat cancer than cervical cancer, the study concluded.

There are two vaccines Gardasil and Cervarix, targetting HPV Type 16 and other strains of the HPV but they are only for girls, to protect them from cervical cancer. Now doctors say it might be a good idea to administer the vaccines to boys as well.

See th editorial doi: 10.1200/JCO.2011.37.8893; listen to the podcast by Dr Gillison at www.jco.org/podcast

New Companion Diagnostic for Non-Small Cell Lung Cancer From LabCorp.

2011-10-03T15:56:00.000-07:00

October 03, 2011 05:08 PM Eastern Daylight Time

BURLINGTON, N.C.-Laboratory Corporation of America^®Holdings (LabCorp^®) (NYSE: LH) announced today the nationwide availability of a new FDA-approved companion diagnostic for lung cancer patients.

The drug XALKORI^®, available from Pfizer, and Abbott Molecular’s Vysis ALK Break Apart FISH Probe companion diagnostic test were simultaneously approved by the FDA on August 26, 2011 for use in patients with advanced ALK-positive non-small cell lung cancer (NSCLC). The Vysis ALK Break Apart FISH Probe test detects all ALK gene rearrangements and is the only available diagnostic assay that has been clinically validated to predict response to the targeted therapy XALKORI. An estimated 6,500-11,000 individual will develop advanced ALK-positive NSCLC in the United States in 2011.

“2011 has been an important year for personalized medicine,” indicated Dr. Mark Brecher, LabCorp's Chief Medical Officer. “The recent approval of XALKORI for NSCLC and its companion test demonstrates how laboratory diagnostics will play an even larger role in cancer care, assisting physicians in administering the treatments best suited to the disease.”

Approximately 3% to 5% of NSCLC tumors are characterized by genetic rearrangements in a gene called ALK. The ALK gene encodes a key cell signaling protein, and when altered by a rearrangement that combines ALK with other gene sequences, the pathway becomes constitutively active and drives cell proliferation and uncontrolled growth. The drug XALKORI inhibits the mutant ALK protein, and thereby diminishes the ability of the cancer cells to grow and divide. There is limited efficacy data in patients that lack the ALK rearrangement and a clinically validated companion diagnostic is essential for identifying which patients will benefit from therapy. The new FDA-approved Vysis ALK Break Apart FISH Probe Kit for XALKORI detects a specific rearrangement in the ALK gene using a technique called fluorescence in-situ hybridization (FISH). The Vysis ALK Break Apart FISH Probe Kit has been optimized only for identifying and quantifying rearrangements of the ALK gene from formalin-fixed, paraffin-embedded human NSCLC tissue specimens.

LabCorp’s Center for Molecular Biology and Pathology (CMBP), was instrumental in the studies supporting the approval of this new companion diagnostic. CMBP collaborated with Abbott Molecular in the analytical validation of the ALK companion diagnostic. LabCorp’s Esoterix Clinical Trials Services provided testing for tumor samples in these studies that supported FDA approval.

The Vysis ALK Break Apart FISH Probe test is now available for patient testing nation-wide through LabCorp.

About LabCorp^®

Laboratory Corporation of America^® Holdings, an S&P 500 company, is a pioneer in commercializing new diagnostic technologies and the first in its industry to embrace genomic testing. With annual revenues of $5.0 billion in 2010, over 31,000 employees worldwide, and more than 220,000 clients, LabCorp offers a broad test menu ranging from routine blood analyses to reproductive genetics to DNA sequencing. LabCorp furthers its scientific expertise and innovative clinical testing technology with its Centers of Excellence: The Center for Molecular Biology and Pathology, National Genetics Institute, ViroMed Laboratories, Inc., The Center for Esoteric Testing, Litholink Corporation, Genzyme Genetics^SM*, DIANON Systems, Inc., US LABS, Monogram Biosciences, Inc., and Esoterix and its Colorado Coagulation, Endocrine Sciences, and Cytometry Associates laboratories. LabCorp conducts clinical trials testing through its Esoterix Clinical Trials Services division. LabCorp clients include physicians, government agencies, managed care organizations, hospitals, clinical labs, and pharmaceutical companies. To learn more about our organization, visit our Web site at: www.labcorp.com.

*Genzyme Genetics and its logo are trademarks of Genzyme Corporation and used by Esoterix Genetic Laboratories, LLC, a wholly-owned subsidiary of LabCorp, under license. Esoterix Genetic Laboratories and LabCorp are operated independently from Genzyme Corporation.

XALKORI is a trademark of Pfizer.

This press release contains forward-looking statements. Each of the forward-looking statements is subject to change based on various important factors, including without limitation, competitive actions in the marketplace and adverse actions of governmental and other third-party payors. Actual results could differ materially from those suggested by these forward-looking statements. Further information on potential factors that could affect LabCorp’s financial results is included in the Company’s Form 10-K for the year ended December 31, 2010, and subsequent SEC filings.

LabCorp^®
Investor/Media Contact:
Stephen Anderson, 336-436-5274
Company Information: www.labcorp.com

Two doses of the Cervarix vaccine for human papilloma virus (HPV) is as effective as multiple dozes.

2011-09-12T12:14:00.000-07:00

Two doses of the vaccine Cervarix targeting human papilloma virus (HPV) were discovered to be as effective as the current standard three-dose regimen after four years of follow-up, according to researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, and their colleagues. The results of the study, based on data from a community-based clinical trial of Cervarix in Costa Rica, appeared online Sept.9, 2011, in the Journal of the National Cancer Institute.

Worldwide, approximately 500,000 new cases of cervical cancer are diagnosed every year, and about 250,000 women die from the disease. An overwhelming majority of these new cases and deaths occur in low-resource countries. Virtually all cases of cervical cancer are caused by persistent infection with HPV. Cervarix is one of two vaccines approved by the U.S. Food and Drug Administration for the prevention of cervical cancer caused by HPV types 16 and 18, which together account for 70 percent of all cervical cancer cases. The vaccine is intended to be administered in three doses given over the course of six months. To date, investigators have observed up to eight years of protection from persistent HPV infection with the vaccine. Studies are ongoing to determine the maximum length of protection.

Overcoming Cetuximab Resistance In Cancer Treatment Possible With ERBB2 inhibitors.

2011-09-08T12:28:00.000-07:00

Kimio Yonesaka, MD, PhD, formerly of Dana-Farber and now at Kinki University School of Medicine, in Osaka, Japan, together with other scientists including Pasi Jänne, MD, PhD, of Dana-Farber , have discovered a pair of backup circuits in cancer cells that enable the cells to bypass the effect of a widely used cancer drug cetuximab, an antibody that interferes with cancer cell growth by blocking a structure known as the epidermal growth factor receptor (EGFR).
Their research found out that interfering the said backup circuits ERBB2 with targeted therapies may heighten or restore the cetuximab’s potency. The paper covering the study is published in the Sept. 7 issue of Science Translational Medicine.
"ERBB2 activates a critical signaling pathway that is not normally blocked by cetuximab, and in this way subverts cetuximab’s function, Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug."" says Jänne, the study's co-senior author with Kazuhiko Nakagawa, MD, PhD, of Kinki University.
"We hope the findings of our study will inspire the development of clinical trials aimed at overcoming cetuximab resistance, We've identified biomarkers that can be used to select cetuximab-resistant patients who may benefit from a combination of cetuximab and ERBB2 inhibitors."" Yonesaka remarks.

Abstract from Science Translational Medicine.

Cetuximab, an antibody directed against the epidermal growth factor receptor, is an effective clinical therapy for patients with colorectal, head and neck, and non–small cell lung cancer, particularly for those with KRAS and BRAF wild-type cancers. Treatment in all patients is limited eventually by the development of acquired resistance, but little is known about the underlying mechanism. Here, we show that activation of ERBB2 signaling in cell lines, either through ERBB2 amplification or through heregulin up-regulation, leads to persistent extracellular signal–regulated kinase 1/2 signaling and consequently to cetuximab resistance. Inhibition of ERBB2 or disruption of ERBB2/ERBB3 heterodimerization restores cetuximab sensitivity in vitro and in vivo. A subset of colorectal cancer patients who exhibit either de novo or acquired resistance to cetuximab-based therapy has ERBB2 amplification or high levels of circulating heregulin. Collectively, these findings identify two distinct resistance mechanisms, both of which promote aberrant ERBB2 signaling, that mediate cetuximab resistance. Moreover, these results suggest that ERBB2 inhibitors, in combination with cetuximab, represent a rational therapeutic strategy that should be assessed in patients with cetuximab-resistant cancers.

Dana-Farber Press Release;

September 07, 2011 Scientists at Dana-Farber Cancer Institute and colleagues overseas have discovered a pair of backup circuits in cancer cells that enable the cells to dodge the effect of a widely used cancer drug. Jamming those circuits with targeted therapies may heighten or restore the drug’s potency, according to a study published in the Sept. 7 issue of Science Translational Medicine.
The research focused on the drug cetuximab, an antibody that interferes with cancer cell growth by blocking a structure known as the epidermal growth factor receptor (EGFR). Cetuximab is effective in many patients with colorectal cancer or squamous cell cancer of the head and neck, but the benefits rarely last longer than a year, and some patients receive no benefit from the drug.

Until now, scientists haven't known why cancers that initially respond to cetuximab become resistant to it, or how to overcome such resistance.

In the new study, researchers led by Pasi Jänne, MD, PhD, of Dana-Farber and Kimio Yonesaka, MD, PhD, formerly of Dana-Farber and now at Kinki University School of Medicine, in Osaka, Japan, found that in some cetuximab-resistant cancer cells, a protein known as ERBB2 was actively sending "grow" signals, circumventing the "stop growing" signals triggered by cetuximab. The researchers discovered that ERBB2's activity sprang from an oversupply of the protein’s parent gene, Her2/neu, or by a related protein, ERBB3, when prompted by high levels of the protein heregulin. In both cases, the new growth messages are unaffected by cetuximab.

"ERBB2 activates a critical signaling pathway that is not normally blocked by cetuximab, and in this way subverts cetuximab’s function," says Jänne, the study's co-senior author with Kazuhiko Nakagawa, MD, PhD, of Kinki University. "Because ERBB2 isn’t affected by cetuximab, this is an easy way for cancers to become resistant to the drug."

The findings suggest that combining cetuximab with ERBB2-inhibiting drugs could be an effective therapy for cancers that are cetuximab-resistant from the start or for those that become resistant over time, the study authors say. Several such inhibitors have already been approved, while others are undergoing clinical study.

"We hope the findings of our study will inspire the development of clinical trials aimed at overcoming cetuximab resistance," Yonesaka remarks. "We've identified biomarkers that can be used to select cetuximab-resistant patients who may benefit from a combination of cetuximab and ERBB2 inhibitors."

Jänne estimates that up to 40 percent of colorectal cancers are cetuximab-resistant when first diagnosed. He notes that although the ERBB2 pathway may be responsible for many cases of cetuximab resistance, there are undoubtedly other pathways, yet to be discovered, that play a similar role. Further research is needed to confirm ERBB2's role in cetuximab resistance and to develop strategies for testing ERBB2 inhibitors and cetuximab in clinical trials.

Funding for the study was provided by grants from the National Institutes of Health, the American Cancer Society, the William Randolph Hearst Foundation, and the Hazel and Samuel Bellin research fund.

Co-authors of the paper include Kreshnik Zejnullahu, Dalia Ercan, Andrew Rogers, Juliet Philips, MS, Jason Sun, Takafumi Okabe, MD, PhD, Jeffrey Swanson, MD, and Ramesh Shivdasani, MD, PhD, Dana-Farber; Isamu Okamoto, MD, PhD, Taroh Satoh, MD, Masayuki Takeda, MD, PhD, Yasuhito Fujisaka, MD, Toshio Shimizu, MD, PhD, Osamu Maenishi, Hiroyuki Itoh, MD, Kiyotaka Okuno, MD, Minoru Takada, MD, Masahiro Fukuoka, MD, and Kazuto Nishio, MD, PhD, Kinki University, Osaka, Japan; Federico Cappuzzo, MD, Massimo Roncalli, MD, and Annarita Destro, PhD, Instituto Clinico Humanitas, Rozzano, Italy; John Souglakos, MD, PhD, University of Crete, Heraklion, Greece; Yonggon Cho, and Marileila Varella-Garcia, University of Colorado Cancer Center, Denver; Koichi Taira, MD, and Koji Takeda, MD, Osaka City General Hospital, Japan; and Eugene Lifshits and Jeffrey Engelman, MD, PhD, Massachusetts General Hospital.

cetuximab (From NCI Drug Dictionary)
A recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR) with antineoplastic activity. Cetuximab binds to the extracellular domain of the EGFR, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition in signal transduction and anti-proliferative effects. This agent may inhibit EGFR-dependent primary tumor growth and metastasis. EGFR is overexpressed on the cell surfaces of various solid tumors. Check for or using this agent. ()

Synonyms:		Anti-EGFR Monoclonal Antibody Anti-Epidermal Growth Factor Receptor Monoclonal Antibody C225 monoclonal antibody Chimeric Anti-EGFR Monoclonal Antibody Chimeric Monoclonal Antibody C225 Immunoglobulin G1, anti-(human epidermal growth factor receptor) (human-mouse monoclonal C225 gamma1-chain), disulfide with human-mouse monoclonal C225 kappa-chain, dimer monoclonal antibody C225

US brand name:		Erbitux

Abbreviations:		Chimeric MoAb C225 MOAB C225

Code names:		C225 IMC-C225

P53 Gene Mutations Found To Play Major Role In Early Cancer

2011-08-24T05:59:00.000-07:00

Mutations to a gene called p53 have been linked to half of all cancers, leading to tumor growth and the spread of cancerous cells.

Now, a Cornell-led study identifies for the first time the mechanisms by which p53 controls cell movement and invasion into other areas of the body.

Using cultures of ovarian surface epithelium cells, where ovarian cancer originates, the researchers found that when they inactivated the p53 gene, the cells began to move and invade the underlying gelatinous protein mixture used in the lab that resembles an extracellular tissue environment.

"People thought that cell motility and invasion were part of later stages of cancer, but we show that this characteristic can be found in cells at the very beginning of cancer formation," said Chang-Il Hwang, lead author of the paper recently published in the Proceedings of the National Academy of Sciences and a graduate student in the lab of Cornell biomedical sciences professor and senior author Alexander Nikitin.

Under normal circumstances, p53 regulates the expression of a receptor protein called MET. But when p53 mutates, MET overexpresses, leading to cell movement and invasive growth. The researchers found two distinct pathways by which p53 regulates and suppresses MET.

"One of the next steps is to study ways to inhibit MET," said Hwang. "Our findings support the idea that suppression of MET could be a particularly reasonable and effective approach to controlling cancer carrying p53 mutations. We hope our findings can be generalized into other types of cancer as well."

In tests, the researchers found the p53 and MET network were consistent in both lung and colon cancer.

Mutations of p53 take many forms, with the most common mutation affecting one of the pathways that regulates MET but not the other pathway. By understanding how different p53 mutations affect each of the two pathways, researchers may one day develop individualized cancer therapies by suppressing MET, said Hwang.

"Different p53 mutations may affect the cancer from different angles," he added.

The study was funded by the National Institutes of Health, the Marsha Rivkin Center for Ovarian Cancer, Cornell's College of Veterinary Medicine and the Ovarian Cancer Research Fund.

Cornell

FDA Rejection Of Exelbine For Treating Non-small Cell Lung Cancer Affects ADVENTRX Pharmaceuticals Share Prices

2011-08-10T08:24:00.000-07:00

ADVENTRX Pharmaceuticals Inc. (Amex:ANX) Fell hard due to the new about FDA Rejection of New Drug Application For Lung Cancer Treatment; Shares Drop -1.48 (57.87%) @ 11:18AM EDT.

ADVENTRX Pharmaceuticals Inc. will hold a conference call and a webcast;

Conference Call and Webcast
ADVENTRX will hold a conference call on Wednesday, August 10, 2011 beginning at 8:30 a.m. Eastern time to review the developments discussed in this news release and answer questions. Individuals interested in listening to the conference call may do so by dialing (800) 860-2442 for domestic callers, (412) 858-4600 for international callers and requesting the ADVENTRX Pharmaceuticals Update Call, or, from the webcast on the investor relations section of the Company's Web site at www.adventrx.com. A telephone replay will be available for five days approximately one hour after the conclusion of the call by dialing (877) 344-7529 for domestic callers, or (412) 317-0088 for international callers, and entering conference number 10003222. The webcast will be available on the Company's Web site for 30 days following the completion of the call.

Press Release;

SAN DIEGO, Aug. 9, 2011 /PRNewswire/ -- ADVENTRX Pharmaceuticals, Inc. (NYSE Amex: ANX) announced today that it received a complete response letter from the U.S. Food and Drug Administration (FDA) regarding the Company's New Drug Application (NDA) for Exelbine (vinorelbine injectable emulsion) for the treatment of non-small cell lung cancer.

The FDA determined that it could not approve the Exelbine NDA in its present form. In particular, the complete response letter noted that, based on inspections at clinical sites, the authenticity of the drug products used in the pivotal bioequivalence trial (Study 530-01) could not be verified, which placed the results of the trial into question. The letter stated that the bioequivalence trial will need to be repeated to address this deficiency.

In addition, the FDA requested information regarding product quality, or CMC matters. All CMC information requests in the complete response letter were the subject of FDA inquiries from earlier in the review cycle, and the Company had submitted responses to each request prior to receipt of the complete response letter.

"We are disappointed with the FDA's determination and, next week, plan to request a type A meeting to discuss its response. Following that meeting, we will be in a better position to comment on the future of our Exelbine program. However, we believe the authenticity of the drug products used in the pivotal study is verifiable and plan to discuss FDA's concerns in this regard. We also will inquire whether FDA has comments to our previously submitted responses," said Brian M. Culley, Chief Executive Officer of ADVENTRX.

"In the meantime, our resources and focus are on ANX-188 and ANX-514, which we believe are the long-term value drivers for our company. Our cash and equivalents of $40.7 million at July 31, plus cost savings from delaying or potentially discontinuing the Exelbine program, will provide us the capital to continue to advance both of these programs," Mr. Culley added.

The Company believes that FDA's concern over drug product authenticity stems from the procedures used to select testing and reserve samples in Study 530-01 and the availability of testing and reserve samples for inspection. The Company believes the procedures used to select testing and reserve samples in Study 530-01 were adequate to verify the authenticity of the drug products. Of note, Exelbine and the reference product come in different package presentations, require different preparation procedures and have different physical characteristics. Based on the different characteristics between the study drugs, the Company believes it is unlikely that study sites would confuse the two study drugs or fail to recognize which drug was being administered to a patient.

Brain Tumor, Scientists Find Cause Of The Tumors, Gene Mutations.

2011-08-05T10:07:00.000-07:00

Scientists from Johns Hopkins University and Duke University have completed a comprehensive map of genetic mutations occurring in the second-most common form of brain cancer, oligodendroglioma. The papers were published the August 4 ahead-of-print issue of the journal Science.
These findings were only possible due to the advancement of science and technology.

"The team used whole genome sequencing technology so that no genes would be excluded, and we found to our surprise that one gene, on chromosome 19, was mutated in six out of the seven initial tumor specimens we sequenced,A mutation frequency of 85 percent is very high." said Hai Yan, MD, PhD, Duke associate professor of pathology and co-corresponding author of the study.

Press release by John Hopkins (the Press release by Duke University is here);

Release Date: 08/04/2011

--Findings reveal cause of the tumors

Johns Hopkins Kimmel Cancer Center scientists have completed a comprehensive map of genetic mutations occurring in the second-most common form of brain cancer, oligodendroglioma. The findings, reported in the Aug. 4 issue of Science, also appear to reveal the biological cause of the tumors, they say.

To create the map, the scientists sequenced protein-coding genes in seven oligodendroglioma tissue samples, and focused attention on recurring mutations in two genes not previously associated with these tumors – CIC and FUBP1. The investigators say that CIC and FUBP1 are known to regulate cell-signaling processes, and CIC mutations have been rarely linked to sarcoma, breast and prostate cancers.

More mutations in the two genes were found in an additional 27 oligodendroglioma samples. In all, two-thirds of the samples studied had CIC and FUBP1 mutations.

“Whenever we find genes mutated in a majority of tumors, it is likely that the pathway regulated by that gene is critical for the development and biology of the tumor,” says Nickolas Papadopoulos, Ph.D., associate professor of oncology at the Johns Hopkins Kimmel Cancer Center.

In brain cancer, the Johns Hopkins investigators say CIC and FUBP1 mutations may be the “missing link” in what scientists describe as a “two-hit” theory of cancer development. The theory is based on the fact that each cell in the human body has two copies of 23 chromosomes containing thousands of protein-producing genes. If a gene on one chromosome is damaged or deleted, the other copy makes up for the loss of protein. But if the second copy fails as well, the cell cannot make the proper protein and may become cancerous.

In oligodendrogliomas, the “first hit” has long been known to occur in regions of chromosome 1 and 19, which fuse together resulting in a loss of many genes on both chromosomes. Up to 70 percent of oligodendroglioma patients have these DNA fusions, and most of them respond better to chemotherapy and radiation than those who lack the deletions in the chromosomes. For more than a decade, researchers have been looking for evidence of a “second hit” in specific mutated genes that allow oligodendrogliomas to develop.

In the current study, the Johns Hopkins investigators found mutations in the remaining copies of the CIC and FUBP1 genes on chromosomes 1 and 19, suggesting that these mutations represent the second hit needed to create cancer.

“Thanks to the Human Genome Project and advances in cancer genome sequencing, a single study can now resolve decade-old questions and reveal the genetics of this brain cancer,” says Kenneth Kinzler, Ph.D., professor and co-director of the Ludwig Center at Johns Hopkins. “Knowing the genetic roadmap of a cancer is the key to attacking it.”

Oligodendrogliomas account for up to 20 percent of brain cancers and more commonly occur in younger people aged 30 to 45. The cancer forms most often in the frontal lobe of the brain in cells that coat neurons. Median survival of 10 years is considered far better than other brain cancers. Oligodendrogliomas are treated initially with surgery, followed by chemotherapy and radiation.

The research team says its next step will be to test whether patients with CIC and FUBP1 mutations have the same favorable prognosis as those who have the chromosome 1 and 19 fusion, says Chetan Bettegowda, M.D., Ph.D., chief resident in the Department of Neurosurgery at Johns Hopkins.

“We can focus now on when these mutations develop during tumor formation, whether they can guide prognosis, and how they might form targets for therapy,” says Bettegowda.

Bettegowda says the gene map uncovered mutations in other genes, such as PIK3CA, which have been well-studied in cancer. It is possible, he says, that oligodendroglioma patients with mutations in PIK3CA or other genes could be enrolled in current clinical trials using experimental therapies that target these mutations.

Funding for the research was provided by the Virginia and D.K. Ludwig Fund for Cancer Research, the Pediatric Brain Tumor Foundation, the Duke Comprehensive Cancer Center Core, the Burroughs Wellcome Fund, the James S. McDonnell Foundation, state funding from Sao Paulo (FAPESP), the National Cancer Institute and National Institutes of Health.

Contributors to the research include Nishant Agrawal, Yuchen Jiao, Mark Sausen, Laura D. Wood, Ralph H. Hruban, Fausto J. Rodriguez, Daniel P. Cahill, Gregory Riggins, Victor Velculescu and Bert Vogelstein of Johns Hopkins; Roger McLendon, Darell Bigner and Hai Yan of Duke University; and Sueli Mieko Oba-Shinjo and Suely Kazue Nagahashi Marie of the University of Sao Paulo, Brazil.

Under agreements between the Johns Hopkins University, Genzyme, Exact Sciences, Inostics, Qiagen, Invitrogen and Personal Genome Diagnostics, Papadopoulos, Vogelstein, Kinzler and Velculescu are entitled to a share of the royalties received by the university on sales of products related to genes and technologies described in this manuscript. Papadopoulos, Vogelstein, Kinzler, and Velculescu are co-founders of Inostics and Personal Genome Diagnostics, are members of their Scientific Advisory Boards, and own Inostics and Personal Genome Diagnostics stock, which is subject to certain restrictions under Johns Hopkins University policy.

Stand Up To Cancer, Where Your Money Goes!

2011-08-01T13:01:00.000-07:00

Stand Up To Cancer PI3K Pathway scientists explain their ongoing progress and look towards the future.

If you ever wondered where all the money you donated to Stand Up To Cancer go. Please watch the above video. And if you have not donated yet or want to learn more about Stand Up To Cancer PI3K Pathway, follow the link below.

"Rarely do you see responses with investigational drugs in phase one but with these compounds some very dramatic responses are being seen." - Dr. Lewis C. Cantley SU2C PI3K Dream Team Leader
SU2C, Stand Up To Cancer

Sarilumab Succeeds In Treating Rheumatoid Arthritis But Fails In Addressing Ankylosing Spondylitis in Phase 2b Trial

2011-07-13T08:31:00.000-07:00

Sanofi (EURONEXT: SAN and NYSE: SNY) and Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) announced the outcome from Phase 2b trials in rheumatoid arthritis (RA) and ankylosing spondylitis (AS) with sarilumab (REGN88/SAR153191), a novel, high-affinity, subcutaneously administered, fully-human antibody targeting the interleukin-6 receptor (IL-6R).
Sarilumab Succeeded in treating Rheumatoid Arthritis but failed in addressing Ankylosing Spondylitis, a long-term disease that causes inflammation of the joints between the spinal bones, and the joints between the spine and pelvis in Phase 2b Trial.

"Following these encouraging Phase 2b results in rheumatoid arthritis, the companies are currently discussing the dose(s) of sarilumab to advance into the Phase 3 portion of the MOBILITY trial," said Elias Zerhouni, President, Global Research & Development, Sanofi.

Further details about the MOBILITY trial are available at http://clinicaltrials.gov/ct2/results?term=SAR+153191+mobility.

Press release;

PARIS and TARRYTOWN, N.Y., July 12, 2011 /PRNewswire/ -- Sanofi (EURONEXT: SAN and NYSE: SNY) and Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) today announced results from Phase 2b trials in rheumatoid arthritis (RA) and ankylosing spondylitis (AS) with sarilumab (REGN88/SAR153191), a novel, high-affinity, subcutaneously administered, fully-human antibody targeting the interleukin-6 receptor (IL-6R).
The Phase 2b MOBILITY trial in rheumatoid arthritis demonstrated that patients treated with sarilumab in combination with a standard RA treatment, methotrexate (MTX), achieved a significant and clinically meaningful improvement in signs and symptoms of moderate-to-severe RA compared to patients treated with MTX alone. The MOBILITY study is a 306-patient, dose-ranging, multi-national, randomized, multi-arm, double-blind, placebo-controlled study, that compared five different dose regimens of sarilumab in combination with MTX to placebo plus MTX. The primary endpoint of the study was the proportion of patients achieving at least a 20% improvement in RA symptoms (ACR20) after 12 weeks.
In the MOBILITY trial, there was a dose response observed in patients receiving sarilumab in combination with MTX. An ACR20 response after 12 weeks was seen in 49.0% of patients receiving the lowest sarilumab dose regimen and 72.0% of patients receiving the highest dose regimen compared to 46.2% of patients receiving placebo and MTX (p=0.02, corrected for multiplicity, for the highest sarilumab dose regimen). The most common adverse events (>5%) reported more frequently in active treatment arms included infections (non-serious), neutropenia, and liver function test abnormalities. The types and frequencies of adverse events were consistent with those previously reported with IL-6 inhibition. The incidence of serious adverse events among the five sarilumab treatment groups and placebo group were comparable.
Sarilumab also demonstrated significant benefit compared to placebo in secondary endpoints, including ACR 50, ACR 70, and DAS 28 scores, additional measures of clinical activity used in RA trials.
"Following these encouraging Phase 2b results in rheumatoid arthritis, the companies are currently discussing the dose(s) of sarilumab to advance into the Phase 3 portion of the MOBILITY trial," said Elias Zerhouni, President, Global Research & Development, Sanofi.
"The MOBILITY results provide evidence that IL-6R blockade with sarilumab represents a promising new anti-inflammatory investigational therapy for reducing RA disease symptoms. We are very pleased that the first of our novel VelocImmune^®derived antibodies is poised to enter Phase 3 development," said George D. Yancopoulos, M.D., Ph.D., Chief Scientific Officer of Regeneron and President of Regeneron Research Laboratories.
In the Phase 2b ALIGN trial in ankylosing spondylitis (AS), sarilumab did not demonstrate significant and clinically meaningful improvements in signs and symptoms of active AS compared to placebo in patients who had inadequate response to NSAIDs. Sarilumab was generally well tolerated. The most common adverse events reported more frequently in active treatment arms included infections and neutropenia.
Full data of both Phase 2b trials will be submitted for presentation at an upcoming scientific conference.
About Sarilumab
Sarilumab (REGN88/ SAR153191) is the first fully human monoclonal antibody directed against the alpha subunit of the IL-6 receptor complex (IL-6R alpha). Sarilumab is a high affinity, sub-cutaneously delivered, specific inhibitor of IL-6 signaling. It blocks the binding of IL-6 to its receptor and interrupts the resultant cytokine-mediated inflammatory signaling cascade. Sarilumab was developed using Regeneron VelocImmune^® antibody technology.
About the MOBILITY Trial
The MOBILITY trial is a randomized, double-blind, placebo-controlled, multicenter, two-part, dose ranging and confirmatory study with an operationally seamless design, evaluating efficacy and safety of sarilumab on top of MTX in patients with active RA who are inadequate responders to MTX therapy. The primary objective of part A of the dose ranging MOBILITY trial was to demonstrate that sarilumab on top of MTX is effective in reducing the signs and symptoms of RA at 12 weeks. The five doses tested were 100 milligrams (mg) and 150 mg every week and 100 mg, 150 mg and 200 mg every other week. The primary objective of part B of the MOBILITY trial will be to demonstrate that sarilumab on top of MTX is effective in reducing the signs and symptoms of RA at 24 weeks. Further details about the MOBILITY trial are available at http://clinicaltrials.gov/ct2/results?term=SAR+153191+mobility.
About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease affecting approximately 0.5%–1% of the global adult population. Abnormal immune response causes an inflamed, thickened synovium, the membrane that lines the joint. As synovitis expands, the inflammatory process can damage the bone and cartilage of the joint and the surrounding tissues. RA-related inflammation can involve the heart and the lung. In 10% of patients with RA the liver is affected. Complications of RA include anemia and leucopenia. At times RA can be very painful and affect a person's ability to carry out everyday tasks. Most people with RA experience periods when their symptoms worsen (flares or active disease) separated by periods in which the symptoms improve. Studies suggest that blockade of IL-6 signaling, one of several key cytokines involved in the inflammatory processes related to RA, may reduce inflammation of the joints, prevent long-term damage and relieve certain systemic effects of RA such as decreased hemoglobin, fatigue and osteoporosis.
About the ALIGN Trial
The 300-patient ALIGN trial is a randomized, double-blind, placebo-controlled, dose ranging study to evaluate the efficacy and safety of sarilumab in patients with AS who had an inadequate response to NSAIDs. The primary outcome measure of the trial was the percentage of patients who achieved a 20% improvement in AS International Working Group Criteria for improvement (ASAS20) at 12 weeks. The secondary endpoints included ASAS40 response, partial remission, and changes in disease activity, safety and tolerability. In the ALIGN trial, the same dose regimens were tested as in part A of the MOBILITY trial. Further details about the ALIGN trial can be found at http://clinicaltrials.gov/ct2/results?term=SAR153191+align.
About Sanofi
Sanofi, a global and diversified healthcare leader, discovers, develops and distributes therapeutic solutions focused on patients' needs. Sanofi has core strengths in the field of healthcare with seven growth platforms: diabetes solutions, human vaccines, innovative drugs, rare diseases, consumer healthcare, emerging markets and animal health. Sanofi is listed inParis (EURONEXT: SAN) and in New York (NYSE: SNY).
About Regeneron Pharmaceuticals, Inc.
Regeneron is a fully integrated biopharmaceutical company that discovers, develops, and commercializes medicines for the treatment of serious medical conditions. In addition to ARCALYST^® (rilonacept) Injection for Subcutaneous Use, its first commercialized product, Regeneron has therapeutic candidates in Phase III clinical trials for the potential treatment of gout, diseases of the eye (wet age-related macular degeneration, central retinal vein occlusion, and diabetic macular edema), and certain cancers. Additional therapeutic candidates developed from proprietary Regeneron technologies for creating fully human monoclonal antibodies are in earlier stage development programs in rheumatoid arthritis and other inflammatory conditions, pain, cholesterol reduction, allergic and immune conditions, and cancer. Additional information about Regeneron and recent news releases are available on Regeneron's web site at www.regeneron.com.
Sanofi Forward Looking Statements
This press release contains forward-looking statements as defined in the Private Securities Litigation Reform Act of 1995, as amended. Forward-looking statements are statements that are not historical facts. These statements include projections and estimates and their underlying assumptions, statements regarding plans, objectives, intentions and expectations with respect to future financial results, events, operations, services, product development and potential, and statements regarding future performance. Forward-looking statements are generally identified by the words "expects", "anticipates", "believes", "intends", "estimates", "plans" and similar expressions. Although Sanofi's management believes that the expectations reflected in such forward-looking statements are reasonable, investors are cautioned that forward-looking information and statements are subject to various risks and uncertainties, many of which are difficult to predict and generally beyond the control of Sanofi, that could cause actual results and developments to differ materially from those expressed in, or implied or projected by, the forward-looking information and statements. These risks and uncertainties include among other things, the uncertainties inherent in research and development, future clinical data and analysis, including post marketing, decisions by regulatory authorities, such as the FDA or the EMA, regarding whether and when to approve any drug, device or biological application that may be filed for any such product candidates as well as their decisions regarding labeling and other matters that could affect the availability or commercial potential of such products candidates, the absence of guarantee that the products candidates if approved will be commercially successful, the future approval and commercial success of therapeutic alternatives, the Group's ability to benefit from external growth opportunities as well as those discussed or identified in the public filings with the SEC and the AMF made by Sanofi, including those listed under "Risk Factors" and "Cautionary Statement Regarding Forward-Looking Statements" in Sanofi's annual report on Form 20-F for the year ended December 31, 2010. Other than as required by applicable law, Sanofi does not undertake any obligation to update or revise any forward-looking information or statements.
Regeneron Forward-Looking Statements
This news release includes forward-looking statements that involve risks and uncertainties relating to future events and the future financial performance of Regeneron, and actual events or results may differ materially from these forward-looking statements. These statements concern, and these risks and uncertainties include, among others, the nature, timing, and possible success and therapeutic applications of Regeneron's product candidates and research and clinical programs now underway or planned, the likelihood and timing of possible regulatory approval and commercial launch of Regeneron's late-stage product candidates, determinations by regulatory and administrative governmental authorities which may delay or restrict Regeneron's ability to continue to develop or commercialize Regeneron's product and drug candidates, competing drugs that may be superior to Regeneron's product and drug candidates, uncertainty of market acceptance of Regeneron's product and drug candidates, unanticipated expenses, the availability and cost of capital, the costs of developing, producing, and selling products, the potential for any license or collaboration agreement, including Regeneron's agreements with the Sanofi Group and Bayer HealthCare, to be canceled or terminated without any product success, and risks associated with third party intellectual property and pending or future litigation relating thereto. A more complete description of these and other material risks can be found in Regeneron's filings with the United States Securities and Exchange Commission, including its Form 10-K for the year ended December 31, 2010 and Form 10-Q for the quarter ended March 31, 2011. Regeneron does not undertake any obligation to update publicly any forward-looking statement, whether as a result of new information, future events, or otherwise, unless required by law.
Contacts

Sanofi:

Global Product Communications
Corporate Media Relations

Ingrid Gorg-Armbrecht
Marisol Peron

Tel: +33 (0) 1 53 77 46 25
Tel: +33 (0) 1 53 77 45 02

Mobile: + 33(0) 6 38 10 50 87
Mobile: +33 (0) 6 08 18 94 78

E-mail:ingrid.goerg-armbrecht@sanofi.com
E-mail: marisol.peron@sanofi.com

Regeneron:

Investor Relations
Media Relations

Michael Aberman, M.D.
Peter Dworkin

Tel: 1 (914) 345-7799
Tel: 1 (914) 345-7640

michael.aberman@regeneron.com
peter.dworkin@regeneron.com

SOURCE Regeneron Pharmaceuticals, Inc.

Asbestos, You And Cancer Risk

2011-07-08T08:45:00.000-07:00

Asbestos is the name of a group of minerals with long, thin fibers. It was once used widely as insulation. It also occurs in the environment. Asbestos fibers are so small you can't see them. Disturbing asbestos can cause fibers to float in the air. When this happens, they are easy to inhale. You breathe out most fibers, but some become lodged in the lungs. Over time, they can build up in the lungs, causing scarring and inflammation. This can eventually affect breathing and lead to disease, such as

Asbestosis, or scarring of the lungs that makes it hard to breathe
Mesothelioma, a rare cancer that affects the lining of the lungs or abdomen
Lung cancer
Lung diseases associated with asbestos usually develop over many years. Smoking cigarettes increases the risk.

Exposure to asbestos may increase the risk of asbestosis, other nonmalignant lung and pleural disorders, lung cancer, mesothelioma, and other cancers.
Smokers who are also exposed to asbestos have a greatly increased risk of lung cancer.
Individuals who have been exposed (or suspect they have been exposed) to asbestos on the job, through the environment, or at home through a family contact should inform their physician and report any symptoms.
Government agencies can provide additional information on asbestos exposure.
Learn more at National Cancer Institute in Spanish

Why You Should Get Screened for Prostate Cancer

2011-06-16T07:56:00.000-07:00

Prostate cancer screening means looking for cancer before it causes symptoms. This helps to find cancer at an early stage when it may be easier to treat.

Tests that are commonly used to screen for prostate cancer are—

Digital rectal exam (DRE): A doctor or nurse will insert a gloved, lubricated finger into the rectum to feel the prostate. This allows the examiner to estimate the size of the prostate and feel for any lumps or other abnormalities.
Prostate specific antigen test (PSA): The PSA test is a blood test that measures the level of PSA in the blood. PSA is a substance made by the prostate. The levels of PSA in the blood can be higher in men who have prostate cancer. The PSA level may also be elevated in other conditions that affect the prostate.

As a rule, the higher the PSA level in the blood, the more likely a prostate problem is present. But many factors, such as age and race, can affect PSA levels. Some prostate glands produce more PSA than others. PSA levels also can be affected by—

Certain medical procedures.
Certain medications.
An enlarged prostate.
A prostate infection.

Because many factors can affect PSA levels, your doctor is the best person to interpret your PSA test results.

Should I Get Screened for Prostate Cancer?

Not all medical experts agree that screening for prostate cancer will save lives. Currently, there is not enough evidence to decide if the potential benefits of prostate cancer screening outweigh the potential risks.

Potential benefits of prostate cancer screening include—

Screening can detect cancers early.
Treatment for prostate cancer may be more effective when it is found early.

Potential risks of prostate cancer screening include—

False positive test results (indicating that you have prostate cancer when in fact you do not) that lead to further tests and can cause anxiety.
Treatment of some prostate cancers that may have never affected a man's health even if left untreated.
Treatment may lead to serious side effects such as impotence (inability to keep an erection) and incontinence (inability to control the flow of urine, resulting in leakage).

CDC and other federal agencies follow the prostate cancer screening guidelines set forth by the U.S. Preventive Services Task Force, which state that there is insufficient evidence to recommend for or against routine screening for prostate cancer using PSA or DRE.

CDC Prostate Cancer information center.

Transforms Cancer Care with Cisco Telepresence, A Webinar.

2011-06-08T06:09:00.000-07:00

You have an oppertunity to join a live, immersive one-hour seminar,on how telepresence can transform the treatment of cancer patients. It will be held on June 23 1:00 PM EST. In the this Webinar Michael Young, Director of Telemedicine at the University of North Carolina Lineberger Comprehensive Cancer Center, will be discussing how Cisco TelePresence is helping to transform the treatment of cancer patients and cancer care.

Learn first-hand how oncologists are using Cisco TelePresence to:

•Review patient cases with top specialists irrespective of
distance or location
•Accelerate discussions about treatment options and facilitate
timely recommendations
•Enable immersive, high-quality consultations

If your organization is looking for a better way to enable clinician collaboration beyond your hospital’s four walls, or you want to learn how oncologists employ video conferencing together with data sharing, this is one session you don’t want to miss. You can register at Cisco by following the link below.
Registration

Eli Lilly's ALMTA Reaches Primary Endpoint In Phase III Study (PARAMOUNT) In Keeping Lung Cancer Alive.

2011-06-06T08:22:00.000-07:00

Eli Lilly and company has reached a decisive endpoint in the Phase III ALIMTA study, PARAMOUNT. The study evaluated ALIMTA® (pemetrexed for injection) in the continuation maintenance setting to determine the progression free survival, or the time a patient alive without worsening of the non-small cell lung cancer (NSCLC), a specific type of lung cancer.

"PARAMOUNT demonstrated that an ALIMTA continuation maintenance regimen—single-agent ALIMTA following ALIMTA plus cisplatin induction therapy—can improve progression-free survival in patients with the most common form of lung cancer," said Allen S. Melemed, M.D., M.B.A., ALIMTA medical product development leader at Lilly Oncology. "This finding continues to validate the use of ALIMTA maintenance treatment for certain patients living with this devastating disease."

Here is the Eli Lily Press Release;

Pivotal Phase III ALIMTA study met primary endpoint

INDIANAPOLIS, June 5, 2011 /PRNewswire/ -- Eli Lilly and Company (NYSE: LLY) announced today that PARAMOUNT, its Phase III study evaluating ALIMTA® (pemetrexed for injection) in the continuation maintenance setting, met its primary endpoint of progression-free survival, or the time a patient is alive without their disease worsening, for patients with a specific type of lung cancer called advanced nonsquamous non-small cell lung cancer (NSCLC).
"Continuation maintenance" treatment is when one of the same medicines used in first-line treatment setting is continued as maintenance therapy in an effort to control the cancer.
Results from the study will be presented on Sunday, June 5 at 11:30 a.m. CDT during the Lung Cancer Oral Abstract Session (Abstract #CRA7510) at the 47th Annual Meeting of the American Society of Clinical Oncology (ASCO) in Chicago, Ill. Lilly will present overall survival results from PARAMOUNT at a medical meeting in the future.
PARAMOUNT is the second study to evaluate the use of ALIMTA as a maintenance therapy in patients with advanced nonsquamous NSCLC, and the first study to evaluate the use of continuation maintenance with ALIMTA(1) following first-line ALIMTA plus cisplatin therapy.
Results of this multicenter, double-blind trial demonstrated the median progression-free survival measured from randomization (after first-line treatment) was 3.9 months on the ALIMTA arm as compared to 2.6 months on the placebo arm with a hazard ratio of 0.64. Said another way, the study showed that ALIMTA continuation maintenance arm resulted in a 36 percent improvement of survival without disease worsening over the placebo arm. The maintenance disease control rate, or the percentage of patients achieving either a response or stable disease first measured at 6 weeks post-randomization was 71.8 percent (2.8%/69.0%) on the ALIMTA arm and 59.6 percent (0.6%/59.0%) on the placebo arm.
"PARAMOUNT demonstrated that an ALIMTA continuation maintenance regimen—single-agent ALIMTA following ALIMTA plus cisplatin induction therapy—can improve progression-free survival in patients with the most common form of lung cancer," said Allen S. Melemed, M.D., M.B.A., ALIMTA medical product development leader at Lilly Oncology. "This finding continues to validate the use of ALIMTA maintenance treatment for certain patients living with this devastating disease."
A total of 939 patients with advanced nonsquamous NSCLC were enrolled in the study and received ALIMTA (500 mg/m2 on day one of a 21-day cycle) in combination with cisplatin (75 mg/m2) induction therapy. Patients whose disease had not progressed during the ALIMTA+cisplatin induction and had a performance status of 0-1 (n=439) were randomized to receive ALIMTA maintenance (500 mg/m2 on day one of a 21-day cycle) plus best supportive care (n=359) or placebo plus best supportive care (n=180) until disease progression. All patients received vitamin B12, folic acid and dexamethasone.
Overall, the most serious (grade 3/4) drug-related adverse events (AEs) were higher for those treated with ALIMTA continuation maintenance versus placebo (9.2% vs. 0.6% laboratory and 8.9% vs. 4.4% non-laboratory). The most commonly reported drug-related AEs observed on the ALIMTA arm versus placebo were anemia (4.2% vs. 0.6%), fatigue (4.5% vs. 0.6%), and neutropenia (3.6% vs. 0%). There was one potentially drug-related death on each arm. Discontinuations due to AEs were 5.3 percent with ALIMTA and 3.3 percent with placebo.
The study was conducted in patients with advanced nonsquamous NSCLC because past studies have shown that advanced NSCLC patients with a nonsquamous histology (those with adenocarcinoma, large cell carcinoma, or other subtypes) experienced improved efficacy over the relative comparator arm in the trial (an increase in progression-free survival, as well as overall survival), when treated with an ALIMTA regimen.(1,2) Patients with advanced NSCLC with squamous cell histology were not included in the PARAMOUNT study as ALIMTA has not shown to be effective in this patient population relative to the comparators in these previous trials.
About Non-Small Cell Lung Cancer (NSCLC)
Globally, lung cancer is the most common form of cancer and the biggest killer, causing 1.3 million cancer deaths annually.(3) About 85 — 90 percent of all lung cancers are NSCLC.(4) The liver, bones and brain are potential targets if the cancerous cells enter the bloodstream.
NSCLC comprises a group of histologies or tumor types differentiated by cellular structure. Nonsquamous histology includes adenocarcinoma and large cell carcinoma, which account for more than half of all NSCLC diagnoses(5), as well histologies classified as "other."

Eli Lily

Pfizer's Sutent Approved By FDA For Treating Rare Type Of Pancreatic Cancer

2011-05-20T16:32:00.000-07:00

The U.S. Food and Drug Administration today approved Sutent (sunitinib) to treat patients with progressive neuroendocrine cancerous tumors located in the pancreas that cannot be removed by surgery or that have spread to other parts of the body (metastatic).

Neuroendocrine tumors found in the pancreas are slow-growing and rare. It is estimated that there are fewer than 1,000 new cases in the United States each year.

This is the second new approval by the FDA to treat patients with this disease; on May 5, the agency approved Afinitor (everolimus).

“FDA believes it is important to provide cancer patients with as many treatment options as possible,” said Richard Pazdur, M.D., director of the Office of Oncology Drug Products in the FDA’s Center for Drug Evaluation and Research. “The agency is committed to working with companies to bring innovative new therapies to the market and encourages companies to continue exploring additional uses for approved products.”

The safety and effectiveness of Sutent was established in a single study of 171 patients with metastatic (late-stage) or locally advanced (disease that could not be removed with surgery) disease who received Sutent or a placebo (sugar pill). The study was designed to measure the length of time a patient lived before their disease spread or worsened (progression-free survival).

Results from the study demonstrate that Sutent provided benefit to patients by prolonging the median length of time they lived without the cancer spreading or worsening to 10.2 months compared to 5.4 months for patients who received placebo.

In patients treated with Sutent for neuroendocrine pancreatic tumors, the most commonly reported side effects included diarrhea, nausea, vomiting, fatigue, anorexia, high blood pressure, energy loss (asthenia), stomach (abdominal) pain, changes in hair color, inflammation of the mouth (stomatitis), and a decrease in infection-fighting white blood cells (neutropenia).

Sutent is also FDA-approved to treat patients with late-stage kidney cancer (metastatic renal cell carcinoma) and to treat patients with GIST (gastrointestinal stromal tumor), a rare cancer of the stomach, bowel, or esophagus.

Sutent is marketed by New York City-based Pfizer.

Zytiga (abiraterone acetate) Approved For Treating Late-stage Prostate Cancer

2011-05-20T13:13:00.000-07:00

The U.S. Food and Drug Administration today approved Zytiga (abiraterone acetate) in combination with prednisone (a steroid) to treat patients with late-stage (metastatic) castration-resistant prostate cancer who have received prior docetaxel (chemotherapy).

In prostate cancer, the male sex hormone testosterone stimulates prostate tumors to grow. Drugs or surgery are used to reduce testosterone production or to block testosterone’s effects. However, sometimes prostate cancer can continue to grow even when testosterone levels are low. Men with these cancers are said to have castration-resistant prostate cancer.

Zytiga is a pill that targets a protein called cytochrome P450 17A1 (CYP17A1) which plays an important role in the production of testosterone. The drug works by decreasing the production of this hormone that would stimulate cancer cells to continue growing.

The application was reviewed under the FDA’s priority review program, which provides for an expedited six-month review for drugs that may offer major advances in treatment, or provide a treatment when no adequate therapy exists. Zytiga is being approved ahead of the product’s June 20, 2011 regulatory goal date.

“Zytiga prolonged the lives of men with late-stage prostate cancer who had received prior treatments and had few available therapeutic options,” said Richard Pazdur, M.D., director of the Office of Oncology Drug Products in the FDA’s Center for Drug Evaluation and Research.

Zytiga’s safety and effectiveness were established in a clinical study of 1,195 patients with late-stage castration-resistant prostate cancer who had received prior treatment with docetaxel chemotherapy. Patients received either Zytiga once daily in combination with prednisone two times a day or a placebo (sugar pill) twice daily in combination with prednisone.

The study was designed to measure overall survival, the length of time from when the treatment started until a patient's death. Patients who received the Zytiga and prednisone combination had a median overall survival of 14.8 months compared to 10.9 months for patients receiving the placebo and prednisone combination.

The most commonly reported side effects in patients receiving Zytiga included joint swelling or discomfort, low levels of potassium in the blood, fluid retention (usually of the legs and feet), muscle discomfort, hot flashes, diarrhea, urinary tract infection, cough, high blood pressure, heartbeat disorders, urinary frequency, increased nighttime urination, upset stomach or indigestion and upper respiratory tract infection.

Zytiga is marketed by Horsham, Pa.-based Centocor Ortho Biotech, Inc.

The press release could be found here.

Digoxin (Lanoxin) A Heart Drug Might Aid Fighting Prostate Cancer

2011-05-20T13:02:00.000-07:00

According to a recent study which was published in the journal Cancer Discovery suggests that digoxin (Lanoxin), a drug has long been used to treat heart failure and heart rhythm abnormalities, might help patients with prostate cancer.
The study conducted by Johns Hopkins in a two-part study to explore and locate current drugs on the market for other deceases and conditions could treat prostate cancer. The researchers screened 38 non-chemotherapy drugs to see if they had any effect on cancer. The research found out that Digoxin reduced the growth of prostate cancer cells in the laboratory by 50%

Identification of novel indications for commonly prescribed drugs could accelerate translation of therapies. We investigated whether any clinically used drugs might be useful in treating prostate cancer by coupling an efficient, high-throughput laboratory-based screen and a large prospective cohort study. In stage one, we conducted an in vitro prostate cancer cell cytotoxicity screen of 3,187 compounds. Digoxin emerged as the leading candidate, given its potency in inhibiting proliferation in vitro (the concentration of the drug at which proliferation was inhibited by 50%: mean of 163 nM) and its common use. In stage two, we evaluated the association between the leading candidate drug from stage one and prostate cancer risk in 47,884 men followed up from 1986 through 2006. Regular digoxin users [vs nonusers: relative risk (RR) = 0.76; 95% confidence interval (CI), 0.61–0.95], especially users for ≥10 years (RR = 0.54; 95% CI, 0.37–0.79; P trend < 0.001), had a lower prostate cancer risk. Digoxin was highly potent in inhibiting prostate cancer cell growth in vitro, and its use was associated with a 25% lower prostate cancer risk.

The second part of the study, conducted from 1986 - 2006, they examined the impact of digoxin use in 47,884 men between the ages of 40 and 75 who participated. fter 20 years, some 5,000 cases of prostate cancer had been reported. The digoxin users had a 25% lower risk of prostate cancer than nonusers, and the risk was lower still among men who had used the drug for 10 years or longer.
You can read the complete article over at the Journal Cancer Discovery Research paper.

The anti-inflammatory drug celecoxib (Celebrex) Triggers Liver Cancer Cell Death By Forcing Cancer Cells To Commit Suicide!

2011-05-16T10:57:00.000-07:00

COLUMBUS, Ohio – The anti-inflammatory drug celecoxib, known by the brand name Celebrex, triggers liver cancer cell death by reacting with a protein in a way that makes those cells commit suicide, according to a new study.

Researchers also found that the combination of celecoxib with each of two chemotherapy drugs killed more liver cancer cells in culture, making those combinations more effective than either drug on its own.

"Each chemotherapy drug alone will reduce the growth of cancer cells, but when each single drug is combined with Celebrex, a greater growth suppression effect was observed," said Jiayuh Lin, senior author of the study and an associate professor of pediatrics at Ohio State University. "For clinicians, this research suggests the possibility of a new therapeutic strategy."

Celecoxib has this effect by acting on STAT3, a gene inside liver cancer cells that, when activated, allows those cancer cells to resist the effects of chemotherapy drugs. The researchers determined that the celecoxib molecule binds to STAT3 on so-called "hot spots," effectively blocking its ability to function.

Powerful computing techniques were employed before the researchers ever considered celecoxib as a potential treatment for cancer. Celebrex is a nonsteroidal anti-inflammatory drug, or NSAID, and a Cox-2 inhibitor, meaning it helps control inflammation by inhibiting an enzyme known as cyclooxygenase-2. It is most commonly prescribed to treat the pain of arthritis.

Chenglong Li, an assistant professor of medicinal chemistry and pharmacognosy at Ohio State, has developed computer simulations to identify optimal drug fragment combinations that attach simultaneously to proteins in ways that block the proteins' functions. By searching a database of existing federally approved drugs, he found that celecoxib was structurally similar to a template molecule that he had determined would most effectively bind to STAT3 and inhibit its function.

"Normally, STAT3 is persistently activated in cancer cells. If you have a good molecule that sticks to STAT3, it will prevent its activation," Li said. And when STAT3 is inhibited, cellular survival pathways are blocked that cause the cancer cell to chop itself up and die.

The research appears online and is scheduled for later print publication in the journal Cancer Prevention Research.

The biological portion of the study further defined the role of a pro-inflammatory protein in liver cancer's development. The protein, called interleukin-6, or IL-6, is a cytokine, a chemical messenger that causes inflammation, which can have both beneficial and damaging effects in the body. Previous research by other scientists has shown that high levels of IL-6 in the blood are associated with hepatocellular carcinoma, the most common type of liver cancer.

Lin and colleagues determined that IL-6 initiates a chemical reaction called phosphorylation of STAT3. That reaction activates STAT3 inside liver cancer cells, where STAT3 in turn activates at least three other known genes that allow the cells to resist the effects of chemotherapy.

The scientists treated five different types of hepatocellular carcinoma cells with two different doses of celecoxib for two hours, and followed by giving them IL-6 for 30 minutes. The pre-treatment with the lower dose of celecoxib inhibited IL-6's ability to start the reaction that activates STAT3. The higher dose blocked STAT3 altogether.

The researchers then treated a line of liver cancer cells with celecoxib in combination with two chemotherapy drugs: doxorubicin, which is used to treat breast, ovarian, gastric, thyroid and several other cancers, and sorafenib, which is the only chemotherapy medication approved by the Food and Drug Administration for liver cancer treatment. Its brand name is Nexavar.

With both drugs, the addition of celecoxib treatment reduced the number of viable liver cancer cells by anywhere from approximately 50 percent to more than 90 percent, depending on the doses. The combination of celecoxib and sorafenib also significantly limited the cancer cells' ability to form colonies, a key element of tumor growth and survival after the drug treatment.

"Because liver cancer has a very low five-year survival rate, it is most likely that even sorafenib alone may not be effective to cure the cancer," said Lin, also an investigator in Ohio State's Comprehensive Cancer Center and the Center for Childhood Cancer at Nationwide Children's Hospital. "We hope that using both drugs together could be more effective. Both celecoxib and sorafenib are already approved by the FDA, so we think this combined treatment should be able to be used in the clinic pretty quickly."

The fifth most common cancer in humans, liver cancer remains one of the most difficult to successfully treat. Patients' overall five-year survival rate is about 10 percent, according to the American Cancer Society.

These experiments were conducted in cell cultures. Further testing would be needed to determine celecoxib's effectiveness in human cancers, Lin noted.

And the powerful computational work led by Li, also an investigator in Ohio State's Comprehensive Cancer Center, is likely to lead to the development of new molecules with even more precise structural relationships with the proteins they are designed to block.

Li's method is called Multiple Ligand Simultaneous Docking. In this work, he used computer simulations to identify "hot spots" on the STAT3 protein – tiny pockets to which molecules could most successfully attach to inhibit the protein's activity. He then searched through drug banks containing more than 7,500 existing and experimental medications to find the most suitable molecular fragments that could be pieced together to produce a new molecule shaped in such a way that it would fit into those pockets.

After designing a template molecule that would most effectively bind to STAT3, he compared that template to the 1,400 federally approved drugs already on the market.

"Celecoxib is almost identical to the molecule template. It attaches to STAT3 in three places. We can optimize celecoxib, and that is expected to come soon. But applying our technique to find those pieces and determining that they come from an existing drug makes the discovery process much faster," said Li, a key co-author of the paper and frequent research collaborator with Lin.

Li has termed this approach as in silico (computer-driven) drug repositioning or repurposing.

The discovery that celecoxib can bind to STAT3 also appears to apply to other cancers. Both Lin and Li were key authors on a recent paper that suggested that celecoxib's ability to block STAT3's function might also make it effective as a treatment for rhabdomyosarcoma, the most common soft tissue cancer in children and adolescents. This research was published in the April 15 issue of the journal Biochemical and Biophysical Research Communications.

Contact: Jiayuh Lin
lin.674@osu.edu
614-722-5086
Ohio State University

Co-authors of the liver cancer and rhabdomyosarcoma studies include Yan Liu, Aiguo Liu and Suzanne Reed of the Center for Childhood Cancer at Nationwide Children's Hospital (Aiguo Liu is also affiliated with Tongji Hospital at Huazhong University of Science and Technology in Wuhan, China); and Huameng Li of Ohio State's Division of Medicinal Chemistry and Pharmacognosy and the Biophysics Graduate Program.

This work was supported by grants from the National Institutes of Health and the Department of Defense Congressionally Directed Medical Research Programs.

Contact: Jiayuh Lin, (614) 722-5086; lin.674@osu.edu or Chenglong Li, (614) 247-8786; cli@pharmacy.ohio-state.edu

Written by Emily Caldwell, (614) 292-8310; caldwell.151@osu.edu

Cyber Seminar On Modeling Impact On Cancer Intervention and Surveillance From NCI's CISNET

2011-05-16T10:09:00.000-07:00

CISNET is a NCI-sponsored consortium investigating using statistical modeling to improve the understanding of cancer control interventions in prevention, screening, and treatment and their effects on population trends in incidence and mortality.
The models from CISNET could be used in wide variety of needs. They could range from, gaining support for establishment of policies, guidelines, evidence-based cancer control interventions and guide public health research and priorities.
These models could also used to project future trends, and to find the optimal cancer control strategies. CISNET modelers are looking to engage with cancer control planners on local and regional questions amenable to modeling.
So as a part of this engagement, the cyber-seminar for this month will include a panel of the leaders from the five CISNET Coordinating Centers, each with a focus on a specific cancer site (Breast, Colorectal, Esophageal, Lung and Prostate), as well as programmatic leaders from the NCI and CDC.

NCI’s Dr. Eric (Rocky) Feuer, CISNET Director, will provide an overview of the CISNET Consortium.. CISNET modelers will then discuss how modeling tools and data can be used by cancer control practitioners and planners to drive evidence-based interventions and provide current examples of modeling applications. During the cyber-seminar, CDC ‘s Dr. Laura Seeff, will also announce a new exciting joint NCI-CDC opportunity for comprehensive cancer control practitioners to work with CISNET researchers in addressing public health problems relevant to their communities through modeling.
Some examples of questions that you could answer using modeling include:
- What is your region’s anticipated need for colonoscopy and if that need was met how would it impact mortality?
- What is the comparative effectiveness of traditional mammogram vs. digital mammogram in your region?
- What would be the impact on lung cancer incidence given specific interventions?
Interested callers will be invited to follow up with the CISNET consortium members to outline possible questions for collaboration (proposal submission form available on Research to Reality).

You can register for the cyber-seminar here.
More information about CISNET

Afinitor (Everolimus) Approved By FDA To Treat Rare Type Of Pancreatic Cancer

2011-05-09T18:15:00.000-07:00

FDA approves new treatment for rare type of pancreatic cancer

On Thursday, the U.S. Food and Drug Administration approved Afinitor (everolimus) to treat patients with progressive neuroendocrine tumors located in the pancreas (PNET) that cannot be removed by surgery or that have spread to other parts of the body (metastatic).

Neuroendocrine tumors found in the pancreas are slow-growing and rare. It is estimated that there are fewer than 1,000 new cases in the United States each year.

“Patients with this cancer have few effective treatment options,” said Richard Pazdur, M.D., director of the Office of Oncology Drug Products in the FDA’s Center for Drug Evaluation and Research. “Afinitor has demonstrated the ability to slow the growth and spread of neuroendocrine tumors of the pancreas.”

The safety and effectiveness of Afinitor was established a clinical trial in 410 patients with metastatic (late-stage) or locally advanced (disease that could not be removed with surgery) disease. Patients in the study were selected to receive Afinitor or placebo (sugar pill). The trial was designed to measure the length of time a patient lived before their disease spread or worsened (progression-free survival).

In patients treated with Afinitor, the median length of time they lived without the cancer spreading or worsening was 11 months compared with 4.6 months in patients who received placebo. Patients who received placebo were able to receive Afinitor if their disease worsened.

In patients treated with Afinitor for neuroendocrine pancreatic tumors, the most commonly reported side effects included inflammation of the mouth (stomatitis), rash, diarrhea, fatigue, swelling (edema), stomach (abdominal) pain, nausea, fever, and headache.

Afinitor is also approved to treat patients with kidney cancer (advanced renal cell carcinoma) after they fail treatment with Sutent (sunitinib) or Nexavar (sorafenib); and patients with subependymal giant cell astrocytoma (a type of brain cancer) associated with tuberous sclerosis (a disease that causes tumors in various parts of the body), who cannot be treated by surgery.

Afinitor has another trade name, Zortress, and is approved to treat certain adult patients to prevent organ rejection after a kidney transplant. Zortress has a different safety profile in these patients.

Afinitor is marketed by East Hanover, N.J.-based Novartis.

For more information:

FDA: Office of Oncology Drug Products

FDA: Approved Drugs: Questions and Answers

NCI: Pancreatic Cancer

More Accurate Biomarkers Need To Be Developed For Detecting Early Ovarian Cancer

2011-03-09T04:52:00.000-08:00

A long-awaited assessment of potential biomarkers for detecting early ovarian cancer shows that blood levels of the CA-125 protein remain the best predictor of the disease. But if there is to be any hope that screening will reduce deaths from this disease, then more accurate markers would have to be developed, researchers concluded in the March Cancer Prevention Research.

None of the 28 potential serum markers tested in the study out performed CA-125. But for screening, the researchers noted, doctors would need a test that could detect a signal from tumors more than 6 months before diagnosis; CA-125 had its strongest signal within 6 months of diagnosis.

Although the results may seem disappointing, the findings can inform future efforts to detect the disease early, the study authors wrote. This idea was echoed by several biomarker experts who were not involved in the work but who stressed the importance of the findings.

“This is a landmark study,” said Dr. Mark H. Greene of NCI’s Division of Cancer Epidemiology and Genetics, who co-authored an accompanying editorial. “For the first time, we have a rigorous analysis of years of ovarian cancer biomarker research to determine whether these markers represent an improvement over where the field began, with CA-125.”

The results, he continued, show that a new approach is needed to find an effective screening strategy for ovarian cancer. (Preliminary results from the study were presented in 2009.)

NCI Cancer Bulletin

RANKL, A Key Factor In Breast Cancer Metastasis.

2011-02-16T11:32:00.000-08:00

When doctors discover high concentrations of regulatory T cells in the tumors of breast cancer patients, the prognosis is often grim, though why exactly has long been unclear.
Now new research at the University of California, San Diego School of Medicine suggests these regulatory T cells, whose job is to help mediate the body’s immune response, produce a protein that appears to hasten and intensify the spread of breast cancer to distant organs and, in doing so, dramatically increase the risk of death.
The findings are reported in the Feb. 16 advance online edition of the journal Nature.
The researchers found that mice with breast cancer were more likely to develop metastatic lung cancer due to elevated levels of RANKL, an inflammatory protein normally involved in bone remodeling. Regulatory T cells were found to be the primary source of RANKL in these tumors. However, the same increase in metastasis was seen when synthetic RANKL was injected directly into tumors, suggesting that RANKL was the key to the ability of regulatory T cells to promote the spread of breast cancer. The scientists also determined that interfering with the ability of RANKL to interact with cancer cells seemed to block tumor progression, and may represent a potential target for drug therapy.

“What is exciting about this study is that now that we understand an increase in RANKL translates to an increase in metastasis, we can get to work on figuring out ways to stop or slow the production of RANKL in breast cancer patients,” said Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at UCSD's Laboratory of Gene Regulation and Signal Transduction and Moores Cancer Center.

RANKL is a well-known factor in a variety of degenerative bone diseases, including rheumatoid arthritis and bone metastasis. In June 2010, the Food and Drug Administration approved the first RANKL-inhibiting drug for use in postmenopausal women at risk for osteoporosis.

“When we were able to control the RANKL production in the mice, we were able to slow or stop the spread of the cancer,” Karin said. “The next logical step is to turn to drugs that block RANKL production to see how they might affect the spread of breast cancer.”

Other breast cancer studies have linked RANKL to early stages in the development of synthetic progestin-driven breast tumors. According to the Women’s Health Initiative and the Million Women Study, hormone replacement therapy and contraceptives with progestin significantly increase the risk of developing breast cancer. The findings from these studies and the new UCSD research suggest that drugs that block RANKL may be effective in preventing both the early stages of breast cancer and the advanced progression of the disease.
Collaborators on the study are first authors Wei Tan and Weizhou Zhang, Amy Strasner and Sergei Grivennikov, UCSD Laboratory of Gene Regulation and Signal Transduction; Jin Q. Cheng, Department of Molecular Oncology, H. Lee Moffitt Cancer Center, Tampa, Fla.; and Robert M. Hoffman, AntiCancer Inc, San Diego.
The research was supported by the National Institutes of Health, Susan G. Komen Breast Cancer Foundation and Crohn’s and Colitis Foundation of America.
The journal Nature.

Coronary Artery Disease (CAD) Global Clinical Trials Review, Q1, 2011

2011-02-11T06:37:00.000-08:00

This report provides in-depth information and data relating to the clinical trials on Coronary Artery Disease. It includes an overview of the trial numbers and their recruitment status as per the site of trial development throughout the world, focusing on the status of participation by the developing nations. It offers coverage of disease clinical trials by their phase, trial status, prominence of the sponsors and also provides information pertaining to the number of trials for the key drugs for treating Coronary Artery Disease).

DUBLIN--(BUSINESS WIRE)--Research and Markets (http://www.researchandmarkets.com/research/b90ca9/coronary_artery_di) has announced the addition of GlobalData's new report "Coronary Artery Disease (CAD) Global Clinical Trials Review, Q1, 2011" to their offering.

The clinical trial report, "Coronary Artery Disease (CAD) Global Clinical Trials Review, Q1, 2011" provides data on the Coronary Artery Disease clinical trial scenario. This report provides in-depth information and data relating to the clinical trials on Coronary Artery Disease. It includes an overview of the trial numbers and their recruitment status as per the site of trial development throughout the world, focusing on the status of participation by the developing nations.

It offers coverage of disease clinical trials by their phase, trial status, prominence of the sponsors and also provides information pertaining to the number of trials for the key drugs for treating Coronary Artery Disease).

This report is built using data and information sourced from proprietary databases, primary and secondary research and in-house analysis by Our team of industry experts.

Scope

* Data on the number of clinical trials conducted in North America, South And Central America, Europe, Middle-East and Africa and Asia-pacific and top five national contributions in each, along with the clinical trial scenario in BRIC nations

* Clinical trial (complete and in progress) data by phase, trial status and trial success rate
* Review of key discontinued trials (suspended, withdrawn and terminated)
* Overview of the enrollment pattern by phase for the past decade
* Number of clinical trials segmented by key drugs
* Clinical trial overview of top 20 companies, which include Pfizer Inc., AstraZeneca PLC, Eli Lilly and Company, and so on.
* Clinical trial overview of top 20 Universities / Institutes / Hospitals including National Cancer Institute, Cancer Research UK, Cancer Research Institute , and others

Reasons to buy:

* Understand the dynamics of a particular indication as a whole
* Examine the performance of the trials in terms of their status, recruitment, success rates and others
* Obtain discontinued trial information for trials across the globe
* Understand the commercial landscape of the major Universities / Institutes / Hospitals or Companies

To view the reports full table of contents and for more information visit http://www.researchandmarkets.com/research/b90ca9/coronary_artery_di

In Their Own Words, Translating Clinical Care For Callers To Cancer Information Service :NCI

2011-02-10T07:53:00.000-08:00

NCI’s Cancer Information Service (CIS), a resource which handles approximately 100,000 calls, e-mails, and live chat sessions annually, where more than 70 information specialists, who are trained and monitored by experienced oncology nurses, tackle these requests for help and information, often engaging in lengthy discussions about treatment options with someone who has just been diagnosed with cancer, or with the spouse of a cancer patient who’s having a hard time taking care of their loved one and needs some help or guidance on what to do or where to turn.
“My background in oncology and as a bedside nurse really helps to bring some of the clinical aspects of cancer care to the information specialists, who often don’t have that intimate level of knowledge,” said Randy Jacobs, an oncology nurse educator with the CIS.

Read more at NCI’s Cancer Information Service: Providing Information and Assistance Nationwide

February Fourth Is World Cancer Day!

2011-02-04T12:08:00.000-08:00

On February 4, 2011, we are joining many many people and organizations from around the world in supporting World Cancer Day to promote ways to reduce the burden of cancer. The World Health Organization estimates that 84 million people will die of cancer between 2005 and 2015 without intervention. Cancer is the second leading cause of death in the United States, exceeded only by heart disease; it kills more than half a million Americans every year.
Please To help fight the global cancer epidemic, the Union for International Cancer Control (UICC) is urging individuals to take action and support the World Cancer Declaration - at www.worldcancerday.org/signdeclaration

Millions of cancer cases are preventable - lifestyle factors key to saving lives

Latest cancer preventability data released to mark World Cancer Day

GENEVA, Switzerland, 04 February 2011 – On World Cancer Day, new independent evidence confirms that the increasing global trend of unhealthy and sedentary lifestyles is responsible for putting millions at an unnecessarily high risk of cancer.

New estimates released today by the World Cancer Research Fund (WCRF) global network suggest that across a range of countries, making lifestyle changes including maintaining a healthy weight, eating a healthy diet and taking regular physical activity can reduce the risk of common cancers by up to a third.i

These findings are further supported by the World Health Organization’s (WHO) new Global Recommendations on Physical Activity for Health.ii This landmark report reinforces that regular physical activity has the potential to prevent many diseases such as breast and colon cancers, cardiovascular diseases and diabetes. The report addresses three age groups (5-17 years old, 18-64 years old, and 65 years old and above) and provides concrete recommendations for levels of physical activity needed for health;Error: Reference source not found these recommendations are especially helpful for low- and middle-income countries, where few national guidelines for physical activity exist.
"Physical activity is recommended for people of all ages as a means to reduce risks for certain types of cancers and other non-communicable diseases," says Dr Tim Armstrong, from WHO's Department of Chronic Diseases and Health Promotion. "In order to improve their health and prevent several diseases, adults should do at least 150 minutes moderate physical activity throughout the week. This can be achieved by simply walking 30 minutes five times per week or by cycling to work daily".
There is also consistent evidence that other healthy living initiatives are vital in reducing the risk of cancer including stopping tobacco use, avoiding exposure to passive smoke, avoiding excessive sun exposure and protecting against cancer-causing infections. And to help fight the global cancer epidemic, the Union for International Cancer Control (UICC) is urging individuals to take action and support the World Cancer Declaration - at www.worldcancerday.org/signdeclaration
Signing the Declaration will help UICC in its effort to motivate global leaders to set realistic and achievable directives for preventing cancer during the United Nations Summit for Non-Communicable Diseases in September 2011. There has only been one UN General Assembly special session focused on health since 1947; the announcement of the 2011 summit is an unprecedented step in the battle against cancer.

Dr Eduardo Cazap, President of UICC summarised, “Support World Cancer Day by signing the World Cancer Declaration and help us achieve the goal of one million supporters for a Cancer Free World. With individuals, governments and policy makers of the world working together, we have the ability to ease the global burden of cancer now and for future generations.”
Background information

About cancer
Cancer is a leading cause of death around the world and its incidence continues to rise. Each year 12.7 million people discover they have cancer and 7.6 million people die from the disease.
Evidence shows that 30-40% all cancers deaths can be prevented,i and one-third can be cured through early diagnosis and treatment.

There are about 200 known types of cancer.ii As with most illnesses cancer is multifactorial which means that there is no single cause for any one type of cancer. However, certain largely controllable or avoidable lifestyle and environmental factors are also known to be causes of cancer. For more information on health living initiatives please visit: www.worldcancerday.org/prevention

About UICC
The Union for International Cancer Control (UICC) is the leading international non-governmental organisation dedicated to the global prevention and control of cancer. UICC’s mission is to eliminate cancer as a life-threatening disease for future generations. Founded in 1933, UICC unites 400 member organisations, specialised and engaged in cancer control, in more than 120 countries across the world. UICC is non-profit, non-political and non-sectarian. Its headquarters are in Geneva, Switzerland. For more information please visit www.uicc.org or join our join us on Facebook: www.facebook.com/pages/Cancer-Free-World/134386073255136

About the World Cancer Declaration
The World Cancer Declaration is a tool to help bring the growing cancer crisis to the attention of government leaders and health policymakers in order to significantly reduce the global cancer burden by 2020. It represents a consensus between government officials, public health experts and cancer advocates from around the world who are committed to eliminate cancer as a life-threatening disease
for future generations.

The Declaration outlines 11 targets to be achieved by 2020 including: significant drops in global tobacco consumption, obesity and alcohol intake, universal vaccination programmes for hepatitis B and human papilloma virus (HPV) to prevent liver and cervical cancer, universal availability of effective pain medication and dispelling myths and misconceptions about cancer. As the custodian of the Declaration, UICC encourages priority actions to achieve the Declaration’s targets locally and nationally and promotes a comprehensive response across the globe. For more information please visit – www.uicc.org/declaration

About the UN high level meeting on non-communicable diseases
In May 2010, the United Nations General Assembly unanimously passed a resolution on the prevention and control of non-communicable diseases (NCDs), calling for a UN Summit on NCDs to be held on the 19-20 September 2011 in New York. The Summit will address the prevention and control of cancer, cardiovascular disease, chronic respiratory disease and diabetes, which together account for 60% (35 million) of global deaths. The largest burden - 80% (28 million) - occurs in low- and middle- income countries, making NCDs a major risk to global development and economic growth. For more information on the NCD summit visit: www.ncdalliance.org

For more information, please contact:
UICC Press Relations
Leah Peyton
Email: leah.peyton@toniclc.com
Tel: 0044 207 798 9923 / 0044 7788 191 434

Contacts

Sanofi:
Global Product Communications	Corporate Media Relations
Ingrid Gorg-Armbrecht	Marisol Peron
Tel: +33 (0) 1 53 77 46 25	Tel: +33 (0) 1 53 77 45 02
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E-mail:ingrid.goerg-armbrecht@sanofi.com	E-mail: marisol.peron@sanofi.com

Regeneron:
Investor Relations	Media Relations
Michael Aberman, M.D.	Peter Dworkin
Tel: 1 (914) 345-7799	Tel: 1 (914) 345-7640
michael.aberman@regeneron.com	peter.dworkin@regeneron.com