Oncology Market Trends

Cancer Research Blog Carnival #14 — Sciencebase Science Blog

2008-10-06T07:01:00.000-07:00

Image via WikipediaWell, this morning I had a nice surprise after finding that some posts in my science and cancer blog made the Cancer Research Blog Carnival this weekend, thanks to the host David Bradley and ScienceBase.

You can read more about this great Carnival concept on his blog about the online event.

Everyone knows someone who has had cancer, so it's nice to learn what research is going on via the blogosphere. Who knows, one day we may find a cure for this terrible disease.

Picture of the Day

2008-09-21T14:50:00.001-07:00

From Trazy's Flickr Photostream - you can see it here. He does some awesome macro shots of various biology related subjects.

This one is a "monster" culture cell - a huge mutant with two nuclei and one centrosome. A normal cell can be seen at the lower right.

9/11 'in memoriam'

2008-09-11T06:52:00.000-07:00

Like many who lost friends and acquaintances on 9/11 seven years ago, today will be spent in quiet reflection.

Normal blogging service will resume tomorrow.

Are colon cancer patients getting enough follow up care?

2008-09-09T05:58:00.000-07:00

About 150,000 Americans are expected to be diagnosed with colorectal cancer this year. Survival after five years varies from 90 percent for cancer that hasn't spread to 10 percent for advanced cases.

According to the results released this week by the journal Cancer, many colon cancer patients aren't getting the screenings recommended after surgery to make sure the disease hasn't returned.

The study found that only 40 percent of the 4,426 older patients in the study got all the doctor visits, blood tests and the colonoscopy advised in the three years after cancer surgery.

A federal database of cancer cases and Medicare records for patients was used to see if the guidelines were being followed. They focused on those 66 and older with less advanced cancer who had surgery that could cure them.

Patients were tracked for three years, beginning six months after surgery. When the study began in 2000, the minimum guidelines called for at least two doctor visits a year, twice yearly blood tests for two years and a colonoscopy within three years. A colonoscopy is now recommended in the first year.

Nearly all patients made the doctor visits and almost three-quarters got a colonoscopy, but many didn't get the blood tests that can signal a return of the deadly colon cancer.

Overall, 60 percent of the patients didn't meet the guidelines. Of those who did, more than half actually got advanced medical scans like CT scans and PET scans that are not recommended for routine screening. The scans could have been done because of signs or symptoms of a recurrence, but the researchers said they suspect they were done for routine follow-up.

There was less screening among older age groups, African-Americans and those with other health problems.

It is unclear whether the doctors simply didn't offer the tests or patients failed to get them was clear. The authors suggested that perhaps the follow-up care was being provided by doctors who aren't specialists and unfamiliar with the guidelines. Whether the providers and insurers have a role is also unknown.

One is also left to wonder how well screening and follow up is performed for other big cancers such as breast, lung and prostate carcinomas. There is no doubt that detecting cancer and recurrence early will improve overall survival and reduce the financial burden of the disease for all concerned.

Eeek, I've been tagged! Now what?

2008-09-02T05:23:00.000-07:00

I got tagged by my friend Sarah Arrow this morning. She's a lovely Essex lass who is the salt of the earth and would do anything for her friends. You can find her on Twitter or her excellent courier blog. Being tagged is a game bloggers play where they have to write six random things about their self, and tag six other people. It's a great way to spread the word about other people's blogs.

Ok, here goes on six random little known things about me:

1. I've had every bone in my body x-rayed, courtesy of a wild childhood getting into all manner of scrapes.

2. I'm allergic to animal fur and tend to stay away from furry pets.

3. Curry is my favourite food.

4. I don't mind rain.

5. I am hopeless at music and anything arty.

6. Science was my favourite subject at school.

The rules, borrowed from Sarah's blog are …

1. Link to the person who tagged you.
2. Post the rules on the blog.
3. Write six random things about yourself.
4. Tag six people at the end of your post.
5. Let each person know they have been tagged.
6. Let the tagger know when your entry is up.

Right then, who to Tag...

Chet Thaker

Irina Ponomareva

Linda Mattacks

Ann Godridge

Deepak

Paulo Nuin

Cancer: the privacy vs. honesty argument

2008-07-28T04:21:00.000-07:00

There has been a lot of hype and noise surrounding Steve Jobs' appearance at the WWDC conference and not just because of the new iPhone launch either. His gaunt appearance started a furore amongst the tech analysts and journalists as to how his health was, it was material they claimed.

Thus the setting was established for a interesting battle over someone's privacy and control versus the media herd wanting 'honesty'. Yet, Jobs has been very honest up front - his surgery for early stage pancreatic cancer is well known, no more need be said it's a private matter after that.

Image by Getty Images via Daylife

The same journalists who praise research and information about stocks should practice what they preach and check out pancreatic cancer, it's all in the public domain. Fifteen minutes spent researching and reading about the topic would tell them all they need to know, without the rather distasteful and rather slimey hounding that is going on at present. Perhaps it's laziness, but sometimes I'm surprised that people who claim to be experts in one area cannot be bothered to research another in the public domain. It makes you wonder what their motives are, especially in the middle of a new product launch for the 3G iPhone.

Take another recent example, Prof Randy Pausch, who sadly died this week from pancreatic cancer. Late last year he gave an inspirational lecture at Carnegie Mellon University but made it clear up front what he wanted to talk about and what was off limits, ie his cancer and his family. His boundaries, like Jobs, on privacy were clear just as the initial medical condition was in both situations. After that, it's nobody's business, you can make your own judgements and act accordingly.

This issue is not about control or honesty, it's about money and greed for the investors. A little bit of research goes a long way, even the analysts will tell a novice investor that, so it cuts both ways.

We also have to remember that the media prey on negative news and 'noise' to generate interest and readership. You don't see much cheerful or good news do you? It's negative and fearful. Good news doesn't sell. Sadly.

Ethnicity and breast cancer - does it matter?

2008-07-25T13:22:00.000-07:00

Breast cancer research needs to evaluate whether a person's ethnicity influences their response to treatment and its outcome, according to researchers at Imperial College London and published in The Lancet online.

Emerging evidence suggests that particular drugs may benefit people from one ethnic group more than others, because of differences in their genetic makeup. Most key trials looking at treatments for breast cancer have been carried out in predominantly caucasian populations in Europe, North America and Australasia.

Other populations might not respond to a drug in the same way as the Caucasian populations in these trials. The researchers suggested that clinical trials should record participants' ethnicity and analyse whether there are differences in how patients from particular ethnic groups respond to a particular therapy.

One example is a drug called Herceptin (trastuzumab), which is commonly used to treat people with breast cancer that is HER-2 positive. Most studies of trastuzumab have not reported the ethnicity of participants. A recent study showed that people with a particular genotype responded better than others to treatment with this drug. The genotype in question is more common in some ethnic groups than in others, so it could be argued that an individual's ethnicity could be a key factor in determining which treatments are most likely to benefit them.

Another research group at the University of Miami, Fl has been looking at whether breast tissue samples from different ethnicities include groups of differentially expressed genes. Gene expression in breast tissue from African-American women differs
from that in Caucasian and Hispanic women, just as gene expression in Hispanic women differs from both African-American and Caucasian women.

In their latest study, Baumbach et al. are focusing on women with “triple-negative” breast cancer. These women are negative for the genes for estrogen receptor (ER), progesterone receptor (PR) and HER2/neu, an epidermal growth factor receptor. This combination is associated with a particularly poor prognosis.

Thee results showed surprising differences in normal tissues; some of the differences were specific to African-Americans and were not found in Hispanics or Caucasians. They tended to have a basal-like phenotype and to have an aggressive form of breast cancer before the age of 50. The research also showed that in considering BRCA1 and BRCA2, while they had a lower incidence of deleterious germline mutations but a higher number of missense mutations. They are now doing real time PCR analyses to see if the biggest differences can be validated and proteomic research will follow in the future, making this a large and very important long term study that may influence treatment paradigms in the future.

Does diet affect your risk of developing prostate cancer?

2008-07-20T07:47:00.000-07:00

It is scientific fact that Japan has a lower incidence of prostate cancer unless the Japanese men move to western societies and eat a different diet.

This short but compelling video explains what factors may increase the risk of developing prostate cancer:

Video

Are you as informed as you should be?

Promising new tool for monitoring lung cancer

2008-07-14T04:37:00.000-07:00

A non-surgical technique that may help doctors monitor how well non-small cell lung cancer patients are responding to treatment is currently being tested. Using a device known as a CTC-chip to analyze circulating tumour cells from patient's blood samples, it was possible to identify whether patients had genetic mutations that would make them less likely to respond to certain therapies.

The research, published in the New England Journal of Medicine, is still in the early stages. However, if future studies confirm it works, the technique could offer lung cancer patients a non-invasive, safe way to monitor their disease and find out which treatments will work. Currently, in order to get that type of information, patients would have to undergo dangerous, invasive procedures to sample tissues and cells.

The current findings will need to be replicated in larger studies before the chip is used widely, since only 27 patients participated in the pilot study.

The CTC-chip opens up a whole new field of studying tumors in real time. When the device is ready for larger clinical trials, it should provide new ways of measuring treatment response, defining prognostic and predictive measures, and studying the biology of blood-borne metastasis, which is the primary method by which cancer spreads and becomes lethal.

Blood samples from 27 patients, 23 of whom had a cell-surface protein mutation known as the epidermal growth factor receptor (EGFR) mutation were tested. Using the CTC-chip, the researchers were able to identify the mutation from the circulating blood tumour cells 92% of the time.

It was also noticed the chip could detect changes over time. Research has shown that tumours with the EGFR mutation are more likely to respond to a class of drugs known as tyrosine kinase inhibitors, or TKIs; Tarceva (erlotinib) and Iressa (gefitinib) are 2 TKIs used to treat lung cancer. However, the patient's tumours eventually come back. Using the CTC-chip, the researchers found out why; it appears that the tumour cell's genetic makeup evolved over the course of treatment.

Biopsy samples taken at the time of diagnosis can never tell us about changes emerging during therapy or genotypic differences that may occur in different sites of the original tumour, but the CTC-chip offers the promise of noninvasive continuous monitoring.

This information could one day help doctors see when a patient was becoming resistant to treatment so that new therapies could be tried earlier. However, there is still work to do to make this technique more efficient on the larger scale outside of the clinical trial setting.

More on the cancer vaccine front

2008-07-07T20:07:00.000-07:00

Hot off the press with the negative news surrounding Gardasil and its paralysis side effects, comes the news that another cancer vaccine, Oncophage (Antigenics), failed to demonstrate sufficient efficacy in renal cell cancer in a phase III trial.

The data was published in The Lancet online.

The accompanying editorial, from James Yang, a respected physician from the NCI, criticised the company for its over enthusiastic and misleading press releases, noting that:

"The credibility of the field of cancer immunotherapy is weakened when some investigators, and particularly vaccine companies, cannot accept the results of randomized trials."

Will infusing granulocytes cure human cancer?

2008-07-02T08:16:00.001-07:00

Scientists at Wake Forest University Baptist Medical Center are about to begin a trial to determine whether a new cancer treatment will be as effective at eradicating cancer in humans as it has proven to be in mice.

The treatment will involve transfusing specific white blood cells, called granulocytes into patients with advanced forms of cancer. A similar treatment using white blood cells from cancer-resistant mice has previously been highly successful, curing 100 percent of lab mice afflicted with advanced malignancies.

Granulocyte - image via WikipediaThe study is being announced on June 28 at the Understanding Aging conference in Los Angeles. It will involve treating cancer patients with white blood cells from healthy young people whose immune systems produce cells with high levels of cancer-fighting activity.

The basis of the study was the discovery of a cancer-resistant mouse and their subsequent finding that white blood cells from that mouse and its offspring cured advanced cancers in ordinary laboratory mice. They have since identified similar cancer-killing activity in the white blood cells of some healthy humans.

Human cancer-fighting cells from healthy donors have been tested against human cervical, prostate and breast cancer cells in the laboratory, with good results. The scientists say the anti-tumor response primarily involves granulocytes of the innate immune system, a system known for fighting off infections.

Granulocytes are the most abundant type of white blood cells and can account for as much as 60 percent of total circulating white blood cells in healthy humans. Donors can give granulocytes specifically without losing other components of blood through a process called apheresis that separates granulocytes and returns other blood components back to donors.

In a small study of human volunteers, it was found that cancer-killing activity in the granulocytes was highest in people under age 50. This activity can be lowered by factors such as winter or emotional stress. They said the key to the success for the new therapy is to transfuse sufficient granulocytes from healthy donors while their cancer-killing activities are at their peak level.

For the upcoming study, 500 local potential donors who are 50 years old or younger and in good health are being recruited to have their blood tested. Of those, 100 volunteers with high cancer-killing activity will be asked to donate white blood cells for the study. Cell recipients will include 22 cancer patients who have solid tumours that either didn't respond originally, or no longer respond, to conventional therapies.

The goal of the phase II study is to determine whether patients can tolerate a sufficient amount of transfused granulocytes for the treatment. Participants will be monitored on a regular basis, and after three months scientists will evaluate whether the treatment results in clear clinical benefits for the patients. If this phase of the study is successful, the study will be expanded to determine if the treatment is best suited to certain types of cancer.

PTLD may help predict lymphatic spread of localized prostate cancer

2008-06-24T05:00:00.000-07:00

A recent study published in The Prostate showed that analysing peritumoural lymphatic vessel density (PTLD) in prostate biopsy cores could help to predict the lymphatic spread of clinically localized prostate cancer.

Researchers examined positive biopsy cores from 99 patients who underwent radical prostatectomy, immunostaining them with a monoclonal antibody against lymphatic endothelium. It was found that peritumoural lymphatic vessels were present in at least one positive biopsy core in 90.9 percent of cases, while intratumoral lymphatic vessels were seen in just 23.2 percent of cases.

Positive biopsy core rates were significantly associated with average and maximal PTLD and the presence of intratumoral lymphatic vessels.

This approach may become a useful technique for predicting early spread of the disease and suggests that patients with high PTLD in biopsy specimens should be carefully monitored after surgery.

Hatch Kennedy Bill To Help Millions Suffering From Traumatic Brain Injury

2008-05-28T11:58:00.000-07:00

Sen. Edward Kennedy's battle with a malignant brain tumour (glioblastoma multiforme) is likely to put a dramatic personal stamp on a health care cause he first championed nearly 40 years ago: The nation's war on cancer.

Kennedy had already begun work on an overhaul of the 1971 National Cancer Act when his tumour was diagnosed, and advocates hope the fact that Kennedy has fallen victim to this disease will generate public support and lend new urgency to the need to update the bill. The 76-year-old Kennedy has been a prominent and passionate advocate of cancer research and other health care issues throughout his long tenure in the Senate.

His name has become virtually synonymous with the push for universal health care coverage. He was a leader in enacting several landmark bills, including the Americans with Disabilities Act of 1990, the State Children's Health Insurance Program and the Kennedy-Kassebaum bill protecting workers from losing health insurance when they switch jobs, or from being denied coverage due to pre-existing conditions. He's been instrumental in promoting biomedical research, AIDS research and treatment, a national bone marrow donor registry and anti-tobacco bills.

Kennedy has been working closely with Republican Sen. Kay Bailey Hutchison of Texas and plans to file the legislation in the coming weeks. As one of the Senate's shrewdest legislators and dealmakers, Kennedy is known for joining forces with Republicans to win passage of major bills.

The bill Kennedy plans to put forth seeks to improve the coordination of cancer research, prevention and treatment while giving more money to the National Cancer Institute and other public research agencies.

Congress is on a Memorial Day recess, and it is unclear when Kennedy, chairman of the Senate Health, Education, Labor and Pensions Committee, will be back on Capitol Hill. He returned to his family's Hyannis Port, Mass. compound last week after being released from Massachusetts General Hospital in Boston.

Kennedy emerged as a leader in winning passage of the National Cancer Act after he became chairman of the Senate's health subcommittee in 1971. At the time, there was wide concern about cancer as the nation's second leading cause of death.

His family has been touched by cancer over the years; two of his children, Kara and Edward Kennedy Jr., are cancer survivors. Edward Kennedy Jr. lost a leg to bone cancer in 1973 at age 12, and Kara was diagnosed with lung cancer five years ago. Both were given a 15 percent chance of survival, but are cancer-free now. The senator threw himself into their care, finding the best medical advice and treatment options for them.

A few weeks ago, Kennedy and Hutchison teamed up with seven-time Tour de France winner and cancer survivor Lance Armstrong at a Senate hearing and a news conference calling on Congress and the country to step up the fight against cancer. The events were aimed at building support for the bill. Kennedy mentioned how his children overcame the disease. When Kennedy's diagnosis was revealed, Armstrong said renewing the fight against cancer would be a good way to honour the senator.

References:

Hatch-Kennedy Bill

Cancer drug sales may rise to $80 billion by 2011

2008-05-15T10:10:00.000-07:00

The global market for cancer drugs will grow twice as fast as that for all other pharmaceuticals as the developing world spends more on health care. It could reach $80 billion by 2012, according to IMS Health, which tracks prescription drug sales.

IMS noted that expensive new treatments, coupled with an increasing number of patients on chemotherapy in major markets and evidence that more people in emerging markets are gaining access to modern targeted therapies will contribute to sales of cancer drugs growing at a compound rate of 12 to 15 percent.

In 2008, sales of oncology products will exceed $48 billion, contributing nearly 17 percent of global pharmaceutical sales growth this year, led by Genentech's breast cancer drug Herceptin, Novartis' leukemia drug Gleevec and other blockbusters, according to IMS.

The cancer market may see double-digit sales growth, fueled by increased use of targeted therapeutic agents introduced over the past 10 years, along with first-time innovations coming to the market and chronic treatment for growing numbers of patients. China, Brazil, Russia and other emerging countries are also becoming bigger customers for pharmaceuticals as they invest more in treating and diagnosing cancer.

IMS expects growth to be fueled by the introduction of 25 to 30 new chemical entities between 2008 and 2012, as expensive new biotechnology drugs and the increasing use of combination therapies contribute to the exploding cost of treatment.

Data from clinical studies of many of the newest cancer drugs will be presented and discussed at the nation's largest oncology meeting later this month in Chicago. Much of the data will be unveiled on Thursday ahead of the American Society of Clinical Oncology meeting.

There are several factors that could moderate growth over the next five years. They include financial constraints of payers, slowing growth of some current blockbuster therapies and patent expirations of four cancer drugs with annual sales exceeding $1 billion, including Eli Lilly's Gemzar and Taxotere from Sanofi-Aventis.

Are ESA's safe enough for cancer patients?

2008-05-11T05:04:00.000-07:00

Earlier this year the FDA held a fourth session with the Oncologic Drugs Advisory Committee (ODAC) to review erythropoietin stimulating agents (ESA's). In 1993, ESA's were approved to reduce the number of red blood cells transfusions in cancer patients who have chemotherapy induced anemia. There is no doubt that the drugs do reduce the number of transfusions. They are also believed to alleviate symptoms such as fatigue and improve quality of life associated with the anemia, although the FDA has said that these remain 'unproven'.

The biggest challenge facing ODAC and the FDA though, is deciding whether ESA's very benefit in anemia is also a negative in terms of increased mortality and/or tumour progression. Eight controlled clinical trials suggest that there is evidence of increased risk of mortality and tumour progression in patients who have head & neck cancer, breast cancer, non-small cell lung cancer (NSCLC) and cervical cancer. According to the FDA, the new studies are either much larger than the original ones used to establish safety of the ESA's or have a different underlying histology.

In addition, the FDA claims that there is insufficient data to rule out mortality, shorter time to progression or lower loco-regional control in cancer other than NSCLC. As a result, FDA have asked ODAC to consider the following options:

- Remove the indication to treat anemia caused by cancer chemotherapy
- Restrict the indication to only patients who will not be cured by treatment intervention and contraindicate in adjuvant therapy
- Restrict use to specific cancer sub-types where safety has been adequately assessed (only NSCLC)
- Contraindicate use where harmful effected have been demonstrated (breast and head & neck cancers)
- Mandate risk management strategies

What is clear is that ESA's do offer a valuable clinical benefit in chemotherapy-induced anemia when used appropriately to avoid transfusions. The question is really one of risk-benefit because the very mechanism by which they work might also induce negative consequences.

It will be interesting to see what happens; The ESA market is worth several billion a year and sales are likely dropping with the repeated FDA discussions about risk benefit and safety.

Poniard report encouraging data in several cancers

2008-05-06T16:01:00.000-07:00

The results of the Phase I trials with picoplatin, a new generation platinum, in prostate and colorectal cancer were presented earlier this year. Encouraging bioavailability data has also been presented from the ongoing Phase I trial of oral picoplatin.

The final phase II efficacy results in SCLC confirmed previously announced interim results showing a survival benefit in patients with recurrent SCLC who failed prior platinum-containing first-line chemotherapy or who progressed within six months of first-line therapy. The median overall survival in the picoplatin Phase II trial was 27 weeks for refractory and resistant small cell lung cancer patients, a population for which there is no approved therapy in the US.

The pivotal Phase III SPEAR trial in small cell lung cancer continues to enroll patients and patient enrollment in the Phase II trial in metastatic colorectal cancer has now completed.

Poniard's Chief Medical Officer stated that:

"Picoplatin, to date, has demonstrated good tolerability, with no severe neuropathies when combined with 5-fluorouracil and leucovorin in the FOLPI regimen. In our Phase 2 trial, we are performing a head-to-head comparison of the efficacy and safety of picoplatin with oxaliplatin. We will be presenting preliminary Phase 2 data and updated Phase 1 data at the 2008 American Society of Clinical Oncology (ASCO) Annual Meeting."

2008-05-05T07:58:00.000-07:00

In 2005, the importance of KRAS mutations in the development of resistance to treatment with gefitinib (Iressa) and erlotinib (Tarceva) in non-small cell lung cancer (NSCLC) were first reported by Pao and colleagues.

The same year, another study (Moroni et al., ) assessed the relationship between epidermal growth factor receptor (EGFR) gene copy number, and KRAS and BRAF mutations as biomarkers of response to EGFR-targeted monoclonal antibodies for metastatic colorectal cancer.

The study found that in patients treated with cetuximab (Erbitux) or panitumumab (Vectibix), a correlation existed between clinical response and tumour EGFR copy number, and that KRAS or BRAF mutations occur mainly in patients with metastatic colorectal cancer resistant to treatment with these drugs.

Subsequent studies confirmed the association of KRAS mutations and resistance with such compelling evidence that led to the approval of panitumumab in Europe for the treatment of KRAS wild-type only metastatic colorectal cancer. As for EGFR copy number, later studies also confirmed an association with clinical outcome.

In a recent article, Moroni et al., conceded that the new challenge in metastatic colorectal cancer is that EGFR FISH pattern is often not homogeneous and has variable ratios, which makes the scoring of EGFR signals and defining the EGFR pattern by FISH difficult. Standardisation of methods is, therefore, needed to reach better reproducibility and optimum sensitivity.

As the authors explained, "From a clinical point of view, we can risk treating a non-responsive patient, but we cannot risk not treating a potentially responsive one."

Do vitamin D receptors influence the risk of breast cancer?

2008-05-03T06:17:00.000-07:00

Certain vitamin D receptor (VDR) gene polymorphisms could affect the risk of breast cancer, as well as the estrogen receptor status of tumours in postmenopausal women, according to findings from a German study.

In Breast Cancer Research, Dr. Jenny Chang-Claude of the German Cancer Research Center, Heidelberg and colleagues note that VDR polymorphisms may influence cancer risk by altering the potentially anti-carcinogenic effects of vitamin D. Epidemiological studies have, however, previously yielded inconsistent results.

The researchers conducted a study of 1408 women with breast cancer and 2612 age-matched controls. They found no differences in serum 25-hydroxyvitamin D by VDR genotype. Overall, there was no association between the four individual polymorphisms analyzed and the risk of breast cancer.

What was interesting was that the Taql polymorphism was associated with the estrogen receptor status of tumours. Specifically, for t allele carriers compared to noncarriers among the breast cancer cases, the odds ratio was 1.18 for estrogen receptor-positive tumors and 0.88 for estrogen receptor-negative tumors.

Further analysis showed that the haplotype FtCA, which contains the Taql t allele, was associated with a significantly greater cancer risk (odds ratio, 1.43) than was FTCG, the most frequent haplotype.

It was concluded that the results support the potential effects of VDR polymorphisms on postmenopausal breast cancer risk. Future epidemiological studies assessing the association of vitamin D and breast cancer risk should therefore take the receptor status of the tumour and other gene variants of oestrogen metabolism into account.

Cancer research: blocking a gene may block cancer growth

2008-05-01T09:47:00.000-07:00

Activating a cancer suppressor gene called nutlin-3a can block cancer cell division, according to researchers at the National Cancer Institute (NCI), part of the National Institutes of Health.

Nutlin-3a activates the p53 gene, leading to cellular senescence, a process by which cells lose their ability to grow and divide. An opportunity for new genetic mutations occurs each time a cell divides, therefore limiting the number of cell divisions in a cancer cell inhibits tumour progression. This study is published in the May 1, 2008, issue of Cancer Research.

Eradicating stem cells in breast cancer

2008-04-30T05:36:00.000-07:00

Results from a small clinical trial of 45 patients with locally advanced breast cancer suggests that the novel agent lapatinib (Tykerb, GlaxoSmithKline) has an effect on tumour-causing breast cancer stem cells. Lapatinib is approved to treat breast cancer that has metastasized and contains the protein marker called HER-2 in the US, but not the EU.

Chemotherapy can remove breast cancer tumours, but it often fails to root out the stem cells that can revive the cancer.

Comparing the challenge to eradicating stubborn weeds from a garden, the researchers at Baylor in Houston, Texas, said chemotherapy often fails because it leaves behind many of the stem cells that lead to recurrence.

Think of it this way: it's not enough to kill the dandelion blossom and stalk that appear above ground; you have to kill the root beneath the soil as well. The finding underscores the need to develop a treatment that can target stem cells in addition to the tumour itself. It appears that these cells, by their nature, are often resistant to the effects of anti-cancer drugs.

A cocktail of chemotherapy, together with the drug lapatinib, appears to kill both the tumour and the stem cells (6th European Breast Cancer Conference (EBCC): Abstract 204).

The Baylor researchers took biopsies from tumours of the patients with, and without, the HER-2 marker before and after different treatments. In the group of people whose tumours did not carry the HER-2 marker, the 31 patients received conventional chemotherapy. While the number of tumors significantly decreased, the proportion of cancer stem cells was greater than before the treatment.

The other group were given lapatinib and two common breast cancer chemotherapy drugs. That group saw a dramatic drop in tumour cells, and the percentage of cancer stem cells remained unchanged or even dropped slightly, but the tumour shrank dramatically. In contrast to treatment with conventional chemotherapy, the relative proportion of stem cells did not go up. The stem cells were, therefore, killed off with the same frequency as the bulk of the tumour.

This is the first time this has been demonstrated and offers an insight to developing new treatment strategies for fighting cancer in the future.

Source: Journal of Nat Cancer Institute

Genetic mutations and lung cancer - new developments in oncology

2008-04-29T07:08:00.000-07:00

New results on genetic techniques that are helping doctors diagnose and treat lung cancer were released today at the 1st European Lung Cancer Conference jointly organized by the European Society for Medical Oncology (ESMO) and the International Association for the Study of Lung Cancer (IASLC) in Geneva, Switzerland.

In one report (Abstract No. 81O; 25th April), Israeli researchers from Rosetta Genomics, a biotechnology company developing microRNA-based technologies for diagnostic and therapeutic applications, described a test that may help make crucial distinctions between types of lung cancer. They demonstrated that the method can accurately distinguish between squamous and non-squamous forms of non-small-cell lung cancer, based on the levels of different microRNA molecules found in tissue samples.

MicroRNAs are short RNA molecules that regulate many cancer-related processes. Recently, the launch of new targeted therapies for non-squamous, non-small-cell lung cancer underlines the importance of accurate, objective diagnosis has taken center stage. The ability of physicians to accurately differentiate squamous from non-squamous NSCLC may be used as important treatment guide. For example, some treatments for non-squamous non-small-cell lung cancer can be deadly or ineffective in patients with the squamous form of the disease. Researchers expect the test to be approved for use during 2008.

In another report (Abstract No. 106PD; 25th April), Italian researchers showed that genetic analysis can help identify patients who are at high risk of relapse after surgery to remove lung cancer. The 3 gene signature may allow oncologists to classify patients with stage I non-small-cell lung cancer who underwent curative surgical resection in high or low risk molecular category, beyond conventional predictors and decide which appropriate treatments they should receive.

The test includes the gene LCK, which is an important marker of immune cell anticancer activity, DUSP-6 which regulates a signaling pathway involved in cancer spread, and ERCC1, which is thought to be a significant prognostic and therapeutic biomarker in non-small-cell lung cancer. These findings mean that we can potentially improve not only the prognostic stratification of patients, but also the choice of the more appropriate adjuvant drug after surgery, i.e. which patients will benefit most.

Source: ESMO

Magnets in cancer treatments - a new oncology tool or a bad idea?

2008-04-29T06:20:00.000-07:00

Biopsy results can be ambiguous: sometimes they can be negative simply because there are too few malignant cells in the sample to be detected - not because all trace of disease has gone. Researchers from the University of New Mexico and the company Senior Scientific, both in Albuquerque, have devised a solution that harnesses the power of magnetic attraction.

The idea is to use magnetic iron oxide nanoparticles encased in a biocompatible material. These in turn can be coated with antibodies that bind to chemicals found only in cancerous cells. When injected into the body, thousands of the particles stick to cancer cells, turning them into miniature magnets. The cells can then be drawn towards magnets encased in the tip of a biopsy needle (Source: Physics in Medicine and Biology, vol 52, p 4009).

A mathematical model of the system confirmed that significant numbers of cancer cells, laden with nanoparticles, could be attracted to a needle within two or three minutes. In the lab, the researchers showed that a magnetised needle could attract leukemia cells surrounded by nanoparticles and suspended in blood or other synthetic materials designed to mimic bodily fluids. Nanoparticles have been used before to destroy diseased cells, but this was the first time they actually retrieved cells.

More recently, researchers have been wondering if cancer treatments be enhanced by something as simple as a magnet. A promising way to tackle some diseases is to deliver cells with modified genes to diseased tissue. Getting enough of the modified cells to the affected area can be tricky.

Claire Lewis and colleagues from the University of Sheffield inserted magnetic nanoparticles, as well as cancer-fighting genes, into monocytes, the white blood cells commonly used in gene therapy, and injected them into mice with tumours. A magnet placed above the tumour caused the cancer-fighting monocytes to congregate there (Source: Gene Therapy, DOI: 10.1038/gt.2008.57).

Metatasis in cancer - a new treatment strategy?

2008-04-28T10:13:00.000-07:00

Metastasis is the spread of a tumour to different parts of the body and is a major driver of mortality in patients with advanced cancer.

Increasingly, researchers are discovering biomarkers that may predict early metastasis. For example, the chemokine receptors CCR7 and CXCR4 have been shownto play an important role in cancer metastasis. By studying the differential expression of CCR7 and CXCR4, alongwith the biomarker HER2-neu, is possible to evaluate whether thesebiomarkers could predict axillary lymph node metastasis in breastcancer.

As more biomarkers are identified in different cancer types, improved knowledge of this complex process may provide a platform for the development of molecularly targeted therapeutics aimed at either the tumor cell or its interaction with the host microenvironment.