Positives About Negative

Does Angelina Jolie's Story Help or Hurt?

2013-05-15T13:53:00.001-05:00

I've been traveling and have had little time to post about—or even process—Angelina Jolie's opinion piece, “My Medical Choice,” in the NY Times.

I am not sure I have anything to add to the discussion, but I have had so many people ask me about it that I felt I should respond. I am doing so in a highly equivocal way, as I have mixed emotions on the piece. (The more I learn about breast cancer and its treatment, the fuzzier my opinions. Things used to be clearer when I knew less.)

I do think Jolie does an exceptional job explaining her specific case, providing great details for those who are unsure what might be ahead of them. She certainly makes it real and true—and doesn't glamorize it. This is a hard decision and the treatment is hard on your body. She makes that clear—and good for her for taking the risk of going public with a decision that some might trivialize, with insensitive and uninformed comments.

I do worry, though, about how we approach celebrity information. Too often we want to do what they do, be who they are. It concerns me, then, that women who do not have the risk factors Jolie faced—she had an 87 percent risk of breast cancer—might also think they need a double mastectomy. This could be much more aggressive treatment than makes sense for them—more aggressive than might be good for them. In fact, there has been an increase in the number of double mastectomies in recent years, sometimes in cases of DCIS.

I hope we keep the risks—of cancer as well as of the effects of it treatment— in perspective. It is a fine line—I want us to be informed, proactive, and in control. But I do not want us unnecessarily fearful. I think Jolie helps us with the former but also puts us at risk of the latter.

As I said, the more I learn, the less I truly understand.

My Mom and the Golden Shoes

2013-05-11T18:32:00.003-05:00

I just bought a pair of shoes in a color that reminds me of rocks in a mountain stream. The manufacturer calls it “pewter,” but I think it looks more gold. It shimmers and takes on the hue of whatever I wear. As I tried them on in the store, I loved them immediately. They are excellent shoes, made even more so because they are dead ringers for my favorite pair from more than 50 years ago.

I was in the eighth grade when my mom worked as a sales clerk at Sweetbriar’s dress shop in Pueblo, Colorado. It was a pretty fancy place for Pueblo in the early 1960s, with central air and a sunken dressing room area surrounded by mirrors. One Christmas, Mom brought me home a special outfit from the store. The dress had a velvet top and a full brown chiffon bottom with taffeta underneath. With it came the dark gold shoes, with black lace anklets.

Now, very few little girls had dark gold shoes and black lace anklets, I have to tell you. That was one classy fashion statement.

I was a tall, skinny kid without a lot of grace. (After dance class once, one of the nuns asked me how I could be so graceful on the dance floor and so clumsy everywhere else. Yes, she did.) But in the outfit Mom brought home, I was Grace Kelly.

I wore in on Christmas, feeling like my own sort of ornament, and I did not want to ever take it off, because I knew I had nowhere else special enough to wear it.

So it hung in the closet for a few months and then I could stand it no more. I decided I should wear it to school on one of the days we got to wear something other than our navy blue serge uniforms. Mom said it might be a little too fancy, but I insisted and she ultimately gave in. Drama was involved.

That's how, one warm March day, I trotted down Spruce Street in velvet, chiffon, taffeta, gold shoes, and black lace anklets, headed to a normal day of eighth grade. I was a sight, I just knew it. OK, I am now sure of it.

I was by far the fanciest little girl at St. Francis Xavier School that day. Maybe that year. I did not know what “overdressed” meant and certainly would not have thought that I was capable of it. I just thought I was pretty doggone special.

The nuns kindly commented on my pretty dress and reminded me that I should be a little careful on the playground. (Was I trying to play baseball? Perhaps. I honestly don't remember, but I would not put that past me.) The other kids just sort of shrugged it off, as far as I know. I don't remember anybody teasing me for wearing dance recital duds on a plain old Friday.

Were we kinder back then, or was I just oblivious? I am pretty sure the second is true, and I hope the first is as well. Maybe, though, they just saw how happy I was and left me alone.

And now, as I look at my new shoes, I miss my mom, like I have missed her since she died 20 years ago. She was a great mom. Like all of us, though, she often focused on what she didn't do, what she wished she could have given me. She wanted to splurge on these kinds of gifts all the time and was sad that her extravagance was so unusual. We didn't have much money, so this dress and shoes were an unexpected treat for me. But that is why they are such an important memory.

And when I remember my Christmas outfit, I don't wish I’d had more like it. Instead, I treasure that one warm memory and, as I do, I think of the love that came with those clothes. I know Mom sacrificed something else, no doubt for herself, to buy it for me. Her main focus at that moment of time was making me happy.

That was my mom. Loving, generous, and dear, but worried that she was just not doing enough.

If I could talk to her, I would tell her that love was always more than enough. And always will be.

That she'll be with me whenever I wear my new shoes.

And when I don't.

2013-05-09T21:07:00.001-05:00

I've been fiddling with the paint brushes and am about 75 percent finished with this. I am not sure when—and if—it will be at 100 percent, but at least I no longer feel like throwing it away. Creating is good for my soul, even when the result isn't what I expect. As with many things, it is all about the journey.

Rudeness, Social Media, and Cancer

2013-05-08T16:10:00.001-05:00

Mary says Robin Roberts is “more concerned about her 'star ness' than her health.” When Kathy and Michele object, calling Mary “rude,” Mary responds. “If she wasn't a celebrity, you wouldn't care, admit it. She wouldn't care about me. So, I just treat them as regular folk. Can't be PC all the time. I work in the real world.”

That was the discussion one morning last week on wxyz.com.

Mary sounds like a royal pain in the asterisk. And she naturally has to share it because we share every blasted thing because we can in our 24/7 wired world.

Roberts had posted on Facebook that she had to stay home from her job as cohost of Good Morning America due to an infection that could be related to treatment for myelodysplastic syndrome brought on by chemotherapy treatment for breast cancer.

So WXYZ.com ran the story, encouraging comments, which, in the way of comments went their own way from unnatural coziness to unnatural nastiness.

Mary says she lives in some “real world” somewhere. But in what world is it OK to be rude to people who are sick? (Or, for that matter, who aren’t sick?) Robin did not ask for this media scrutiny and, I suspect, wishes it would go away. Imagine people following your prognosis and posting/printing/tweeting it over and over and over? You’re trying to beat the beast of cancer while also fighting constant reports about your fight—many of which are inaccurate and most of which are invasive. That seems at least one fight too many.

And Robin didn't ask for strangers like me to blog about her using her first name as though we were buddies. Hey, Robin, whazzup?

But, Robin’s "star-ness aside" (that's not a word, Mary), what’s with being rude? Mary appears pretty unapologetic— she used her full name, after all. Does that signal the fact that she thinks it is just fine to be so critical of a fellow human being fighting a deadly disease? Worse, does she think she is somehow right? That because she thinks it, it is therefore good and worth sharing?

That seems to be a mentality right now. We think it therefore we say it. I wish this tendency would go away—this sharing of our deepest misunderstandings and darkest thoughts. But it is truly sad that it has infected the cancer world, which already has enough infections to fight.

• Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.

• Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

A Calming Labyrinth

2013-05-07T21:54:00.002-05:00

All spiritual traditions have some form of meditative repetition. Catholics have the rosary, others have prayer beads. Eastern religions have mantras.

The labyrinth is one of the oldest of these forms. As you follow a labyrinth, you focus only on the action at hand—where you walk, how you turn, making your way step by step in a well-patterned maze. The goal is not so much to get through as to lose yourself in the process, to think of nothing but the moment.

I have tried a lot of different forms of meditation, but this is the one that works best for me—it gives my mind something to do while I try to rest it. What I gain is a reprieve from the many daily worries that weigh on my spirit.

If you have a local labyrinth, I encourage you to try it. It will not solve your problems, but it can help ease your mind for a while. The one pictured above is at the Paleakula Gardens Peace Sanctuary on the island of Hawaii.

HMGA1 Turns TNBC Cells Back to More Normal and Slows Their Growth

2013-05-04T11:21:00.003-05:00

From a News Release from the Johns Hopkins University School of Medicine

Researchers at Johns Hopkins have identified a gene that, when repressed in tumor cells, puts a halt to cell growth and a range of processes needed for tumors to enlarge and spread to distant sites. The researchers hope that this so-called “master regulator” gene may be the key to developing a new treatment for tumors resistant to current drugs.

“This master regulator is normally turned off in adult cells, but it is very active during embryonic development and in all highly aggressive tumors studied to date,” says Linda Resar, M.D., an associate professor of medicine, oncology and pediatrics, and affiliate in the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. “Our work shows for the first time that switching this gene off in aggressive cancer cells dramatically changes their appearance and behavior.” A description of the experiments appears in the May 2 issue of the journal PLOS ONE.

Resar has been investigating genes in the master regulator’s family, known as high mobility groupor HMG genes, for two decades. In addition to their role in cancer, these genes are essential for giving stem cells their special powers, and that’s no coincidence, she says. “Many investigators consider cancer cells to be the evil twin of stem cells, because like stem cells, cancer cells must acquire special properties to enable the tumor to grow and metastasize or spread to different sites,” she explains.

In a previous study, she and her team devised techniques to block the HMGA1 gene in stem cells in order to study its role in those cells. In their prior work, they discovered that HMGA1 is essential for reprogramming adult cells, like blood or skin cells, into stem cells that share most, if not all, properties of embryonic stem cells.

In the newly reported study, the Resar team applied the same techniques to several strains of human breast cancer cells in the laboratory, including the so-called triple negative cells — those that lack hormone receptors or HER2 gene amplification. The Resar team blocked HMGA1 expression in breast cancer cells and followed their appearance and growth patterns.

"Remarkably, within a few days of blocking HMGA1 expression, they appeared rounder and much more like normal breast cells growing in culture,” says Resar. The team also found that the cells with suppressed HMGA1 grow very slowly and fail to migrate or invade new territory like their HMGA1-expressing cousins.

The team next implanted tumor cells into mice to see how the cells would behave. The tumors withHMGA1 grew and spread to other areas, such as the lungs, while those with blocked HMGA1 did not grow well in the breast tissue or spread to distant sites.

“From previous work, we know that HMGA1 turns on many different genes needed during very early development, but it’s normally turned off by the time we’re born,” says postdoctoral fellow Sandeep Shah, Ph.D., who led the study. “Flipping that master regulator back on seems to be necessary for a cancer to become highly aggressive, and now we’ve seen that flipping HMGA1 off again can reverse that aggressive behavior.”

The next step, Resar says, is to try to develop a therapy based on that principle. The team is working with other researchers at Johns Hopkins to see whether HMGA1-blocking molecules could be delivered to tumors inside nanoparticles. Another possible approach, she says, would be to block not HMGA1 itself, but one of the pathways or processes that it affects.

• Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.

• Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

To the NY Times: TNBC is not automatically aggressive and is seldom lethal.

2013-04-30T12:43:00.004-05:00

I sent this to the NewYork Times Magazine today, in response to Peggy Orenstein's "Our Feel-Good War on Breast Cancer," published last Sunday, April 28. 2013).

Women with triple-negative breast cancer throughout the country groaned when they saw Peggy Orenstein’s blithe mischaracterization of this type of breast cancer. She uses the typical shorthand terms “aggressive” and “lethal” to define TNBC, a complex set of diseases that, in many cases, are no more aggressive than other forms of breast cancer. And TNBC is seldom lethal. Non-metastatic TNBC has an impressive survival rate—as high as 87 percent in some studies. And Her2-positive can be more aggressive than TNBC, as can some forms of hormone-positive breast cancer.

Likewise, triple-negative is not synonymous with basal-like. There is a strong association between the two, but not all TNBC tumors are basal-like and not all basal-like tumors are triple-negative.

All breast cancers can be aggressive and all can be lethal, but no one type is automatically both. Writers who use such fearful language ignore the psychological impact of their words on women who are already terrified and confused. The fact is that the great majority of women with TNBC survive and go on to live long, meaningful lives.

Words matter, as do facts.

EGFR treatments again effective against some types of TNBC

2013-04-27T12:04:00.000-05:00

We’re getting closer. For several years, researchers have said that triple-negative breast cancer is not one disease, but many, with numerous studies focusing on the genetic similarities that create subsets of TNBC. And drug combinations work better that single agents, according to a new article in Genetic Engineering and Biotechnology News (April 26, 2013).

According to researchers, nearly half of all TNBC cells express the epidermal growth factor receptor (EGFR). Current clinical trials are testing anti-EGFR drugs that may target these types of TNBC. Two such antibodies—two EGFR antibodies (panitumumab and mAb111)—show promise.

BUT, I have to warn that the first sentence of the article will make all TNBC patients shudder:

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer that does not currently have any targeted therapeutics available.

Here’s my reaction to that comment.

• TNBC can be more aggressive than other forms, but it is not always aggressive and the great majority of women with TNBC survive beautifully.

• We need to differentiate between metastatic and non-metastatic TNBC. Non-metastatic TNBC does have therapeutics—chemo often works better for it than for other forms of breast cancer. Metastatic TNBC does not have targeted therapies yet—but let’s hope this research makes a difference there.

•••••

• Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.

• Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Combo stops late-stage TNBC in mice

2013-04-20T19:14:00.002-05:00

Researchers in Australia have successfully tested a drug combination to fight late-stage triple-negative breast cancer in mice—with a 100 percent success rate. The treatment trial—at Queensland Institute of Medical Research— demonstrates that targeting radiation to an overload of proteins (known as EGFR) together with a dramatically reduced dose of chemotherapy is effective in stopping both the cancer growth and its recurrence.

“It’s when breast cancer reoccurs, or spreads, that most fatalities are reported,” Professor Kum Khanna, from QIMR’s Signal Transduction Laboratory. “This is early stage research, and there’s a long way to go, but it’s the first time we’ve seen a therapy that stops the recurrence and treats the spread of these triple-negative breast cancers.” .

Researchers hope that the process can successful go through stage 1, 2, and 3 clinical trials within ten years.

Ten years!!!!!!!!! Hurry, folks. We're waiting.

Read the news release here.

Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.

Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Protein Inhibits Growth of TNBC Tumors

2013-04-20T15:46:00.003-05:00

A monoclonal antibody targeting a protein known as SFPR2 has been shown by researchers at the University of North Carolina to inhibit tumor growth in pre-clinical models of triple-negative breast breast cancer, according to research published in the April 19 issue of Molecular Cancer Therapeutics,

The UNC lab first discovered the role of SFRP2 in tumor growth while working to develop an alternative to Avastin (bevacizumab), which targets the protein VEGF. Although Avastin is of benefit to some patients with cancer, not all tumors respond to the drug, and of those that respond, some eventually progress. To find a solution for patients whose tumors are resistant to Avastin, researchers began looking at other proteins that could be used as therapeutic targets. Avastin is not approved by the FDA for use with breast cancer.

“We previously microdissected blood vessels from malignant human breast cancers and compared gene expression to blood vessels microdissected from normal tissue. We found a number of genes that were highly over-expressed in the malignant blood vessels compared to normal. One of those genes was SFRP2,” said research leader Nancy Klauber-DeMore, MD, professor of surgery and a member of UNC Lineberger Comprehensive Cancer Center.

Researchers found that SFRP2 is expressed in a variety of human cancers, including breast, prostate, lung, pancreas, ovarian, colon, kidney tumors, and angiosarcomas. “Demonstrating that a monoclonal antibody to SFRP2 inhibits tumor growth in pre-clinical models opens up a new potential for drug development. This treatment is not presently available for human studies, but our efforts are focused on obtaining funding for further drug development that would lead to a clinical trial” DeMore said.

Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.

Diamonds May Be A TNBC Girl's Best Friend

2013-04-20T12:47:00.002-05:00

From a news release from the University of California:

UCLA researchers have developed a potential new treatment for triple-negative breast cancer that uses nanoscale, diamond-like particles called nanodiamonds.

Nanodiamonds are between 4 and 6 nanometers in diameter and are shaped like tiny soccer balls. Byproducts of conventional mining and refining operations, the particles can form clusters following drug binding and have the ability to precisely deliver cancer drugs to tumors, significantly improving the drugs' desired effect. In the UCLA study, the nanodiamond delivery system has been able to home in on tumor masses in mice with TNBC.

Findings from the study are published online April 15 in the peer-reviewed journal Advanced Materials.

"This study demonstrates the versatility of the nanodiamond as a targeted drug-delivery agent to a tumor site," said Dean Ho, a professor at theUCLA School of Dentistry and co-director of the school's Jane and Jerry Weintraub Center for Reconstructive Biotechnology. Ho is also a member of the California NanoSystems Institute at UCLA, UCLA's Jonsson Comprehensive Cancer Center and the UCLA Department of Bioengineering. "The agent we've developed reduces the toxic side effects that are associated with treatment and mediates significant reductions in tumor size."

The team combined several cancer-fighting components on the nanodiamond surface, including Epirubicin, a chemotherapy drug that is often administered in combination with other cancer drugs. The new compound was then bound to a cell-membrane material coated with antibodies that were targeted toward the epidermal growth factor receptor, which is often highly concentrated on the surfaces of TNBC cells. The resulting agent is a drug-delivery system called a nanodiamond-lipid hybrid compound, or NDLP.

When tested on mice, the agent was shown to notably decrease tumor growth and eliminate the side effects of cancer treatment.

Epirubicin can cause serious side effects, such as heart failure and reduced white blood cell count, and it has been linked to an increased risk for leukemia. In the study, all of the mice that were given Epirubicin alone died well before the completion of the study. But all the mice given Epirubicin through the targeted NDLPs survived the treatment, and some of the tumors regressed until they were no longer visible.

"Triple-negative breast cancer is often very aggressive and hard to treat, making aggressive chemotherapy a requirement," said Dr. Edward K. Chow, co-first author of the study and an assistant professor at the Cancer Science Institute of Singapore. "The targeting and therapeutic efficiency of the nanodiamond-lipid agents were quite remarkable. The simultaneous tumor regression and improved drug tolerance are promising indicators for the continued development of the nanodiamonds toward clinical translation."

The research team is now studying the use of the NDLPs in larger animals. Additional research objectives include determining whether nanodiamonds can enhance the tolerance of a wide spectrum of highly toxic drug compounds, which may improve current treatment options and outcomes. These discoveries will serve as precursors for human trials, the researchers said.

Lymphedema Related to BMI, Higher Stage, and Genes

2013-04-16T18:06:00.000-05:00

A news release from the University of California School of Nursing

The risks of developing lymphedema increased significantly for women who had more advanced breast cancer at the time of diagnosis, more lymph nodes removed or a significantly higher body mass index, and a specific set of genes, according to a study of some 400 women who were tracked over four to five years and published online on April 16, 2013 in PLOS ONE.

The study is the first to evaluate genetic predictors of lymphedema in a large group of women using a type of technology, bioimpedance spectroscopy, to measure increases in fluid in the arm. Bioimpedance spectroscopy is a noninvasive procedure that allows one to measure body composition including an increase in fluid in an arm or a leg.

“The genetic markers found in our study make perfect sense,” said senior author Bradley Aouizerat, PhD, a professor at the UCSF School of Nursing in the department of physiological nursing. “These genes are ‘turned on’ later in the development of our lymph system and blood vessels. They appear to play a role in the ability of our lymphatic system to function on an ongoing basis. It is possible in some individuals who have changes in these genes, that lymphedema could develop after an injury like breast cancer surgery because these genes do not function properly.”

Lymphedema is a swelling or buildup of fluid in the lymphatic tissues, typically in the arms and fingers but also commonly in the patient’s legs and trunk. It can occur after treatment for any form of cancer that affects lymph node drainage. The exact prevalence is unknown, and the onset of the condition can greatly vary, but as many as 56 percent of women who undergo breast cancer surgery develop lymphedema within two years, according to the National Cancer Institute. More than half a million breast cancer survivors in the United States are estimated to be afflicted with the condition.

Lymphedema can be debilitating, causing scarring, discomfort, disfigurement, difficulty in exercising, walking or other daily activities. Some patients are unable to wear their usual clothing or jewelry because of the increased weight and size of their affected limbs. There’s no cure for the condition – treatment generally centers on controlling pain and reducing swelling.

To date, much of the research on lymphedema focused on identifying which women were at greater risk for the development of the condition, and relied only on patient self-reporting or on data from their medical charts.

In the new study, the authors hypothesized that genomic determinants were behind some of the variations in the occurrence of lymphedema as well as the time of onset of the condition.
The study involved 410 women who were at least six months post-treatment for breast cancer surgery on one breast, and either had lymphedema in their upper extremity or did not have the condition.

The women were assessed at the Clinical Research Center at the University of California at San Francisco Medical Center at Mt. Zion, one of eight clinical sites in the Bay Area managed by UCSF’s Clinical and Translational Science Institute.

As part of the research, the women underwent spectroscopy measurements of their arms and genomic DNA was extracted. Genotyping was performed blinded to the women’s lymphedema status.

The researchers found that women with lymphedema had:

More advanced breast cancer at the time of diagnosis;
A higher number of positive lymph nodes;
Were more likely to have a significantly higher body mass index.

The authors also found associations between lymphedema and genes known to play a role in the development of lymphedema—FOXC2 haplotype
A03, LCP2 rs315721, NRP2 rs849530, NRP2 haplotype F01,
SYK rs158689, VCAM1 rs3176861, and VEGFC haplotype B03

“These findings suggest that complex interactions may exist between a variety of patient characteristics and genetic markers that place some women at higher risk for the development of lymphedema,’’ said lead author Christine Miaskowski, RN, PhD, a professor at the UCSF School of Nursing in the department of physiological nursing. “Our hope is that once our findings are confirmed in a future study, we will be able to identify women at higher risk for lymphedema prior to breast cancer surgery, and initiate measures to prevent the development of this devastating condition.”

Omega 3 Fatty Acids in Fish Oil May Slow Triple-Negative

2013-04-13T11:23:00.001-05:00

Eat your fish. Take your Omega 3 supplements. Here's why:

WASHINGTON, DC (April 9, 2013)—Researchers from Fox Chase Cancer Center have found that omega-3 fatty acids and their metabolite products slow or stop the proliferation, or growth in the number of cells, of triple-negative breast cancer cells more effectively than cells from luminal types of the disease. The omega-3s worked against all types of cancerous cells, but the effect was observed to be stronger in triple-negative cell lines, reducing proliferation by as much as 90 percent. The findings were be presented at the AACR Annual Meeting 2013 on Tuesday, April 9.

Omega-3 fatty acids are found in oily fish like sardines and salmon, and also in oils derived from plants like hemp and flax. Previous studies suggest these compounds can negatively affect critical mechanisms in cancer cells, namely those responsible for proliferation and for apoptosis, or programmed cell death. Lead author on the study Thomas J. Pogash, a scientific technician in the Fox Chase Cancer Center lab of Jose Russo, MD, says the new work underscores the important role common compounds found in food may play in keeping cancer at bay.

“Diet can play a critical role in breast cancer prevention,” says Pogash. “When you compare a western diet to a mediterranean diet, which has more omega-3s, you see less cancer in the mediterranean diet. They eat much more fish.”

Breast cancer is a heterogeneous group of cancers comprising diseases that differ on the molecular level. Patients with different types of breast cancer respond differently to treatments. Four distinct categories of the disease are generally recognized. Two of those, luminal A and luminal B, grow in the luminal cells that line milk ducts in the breast and have receptors for estrogen and progesterone (prognosis is generally better for patients with luminal A than with luminal B). A third category includes tumors that test positive for the HER2 receptor.

Tumors in the fourth category, triple-negative, lack receptors for progesterone, estrogen, and a protein called HER2/neu. As a result, this type of disease is insensitive to treatments like trastuzumab, which disrupts the HER2 receptor, and tamoxifen, which targets the estrogen receptor.

Russo notes that no targeted therapies are currently available for patients diagnosed with triple-negative breast cancer. Combination chemotherapies are the standard of care for early-stage disease.

“This type of cancer, which is found more frequently in Latina and African-American women, is highly aggressive and has a low survival rate,” says Russo. “There is not any specific treatment for it.” [Pat's note: It can be aggressive, but only in a minority of cases; the great majority of women survive TNBC and go on to live lovely lives. I am seven years past diagnosis and I am far from unusual.]

When a cancer cell digests omega-3s, the fatty acid is broken down into smaller molecules called metabolites. Russo, Pogash, and their colleagues tested the effect of large omega-3 parent molecules, as well as their smaller metabolic derivatives, on three luminal cell lines and seven lines that included basal-type triple-negative cells.

Omega-3 and its metabolites were observed to inhibit proliferation in all cell lines, but the effect was dramatically more pronounced in the triple-negative cell lines. In addition, the metabolites of omega-3 reduced the motility, or ability to move, by 20-60 percent in the triple-negative basal cell lines.

This study is part of a consortium between Fox Chase Cancer Center and Pennsylvania State University under a five-year grant awarded by the Komen Foundation. Russo is the principal investigator of the project at Fox Chase. Andrea Manni, MD, leader of the Pennsylvania State University team, has extended this work to animal models, studying the anticancer effects of omega-3s and its metabolites on mouse models of triple-negative breast cancer.

Russo and his colleagues are working on two related projects, one on the role of epigenetic events in the mechanism of cell transformation and another on the potential action of peptides of the hormone human chorionic gonadotropin (hCG) on breast cancer prevention.

Metabolic Alterations in Triple-Negative Breast Cancer To Be Cataloged

2013-04-13T11:17:00.002-05:00

WASHINGTON, DC (April 9, 2013)—Researchers at Fox Chase Cancer Center have identified a host of small molecules critical to metabolism in cells of triple-negative breast cancer—one of the least understood groups of breast cancer. These molecules, called metabolites, include key players in energy regulation and lipid synthesis. They could help pave the way for helping researchers differentiate among different forms of the disease and ultimately point to new targets for treatment.

“There’s tremendous excitement in the cancer field for the possibility of manipulating metabolism for therapeutic benefit,” says Jeffrey Peterson, PhD, a cancer biologist at Fox Chase who led the studies.

Patients with triple-negative breast cancer constitute about 15 to 20 percent of all breast cancer cases, though incidence is disproportionately higher among young and African-American women. In triple-negative breast cancer, tumor cells lack receptors for two hormones—progesterone and estrogen—and a protein called HER2/neu. This type of cancer is notoriously difficult to treat and does not respond to some of the most effective treatments available for other types of breast cancer, like trastuzumab, which interferes with the HER2receptor in HER2+ breast cancer, or endocrine therapies like tamoxifen.

Triple-negative breast cancer is not one well-defined disease. It’s a large group of diseases that all lack the three receptors but may differ from each other in critical ways, from individual molecules all the way up to clinical prognosis and treatment options. Peterson says that cataloging the small molecules involved in cellular metabolism may help researchers differentiate among these different cancers lacking the three receptors.

“One of our hopes is to understand how this heterogeneous disease can be classified into subtypes,” says Peterson. “We’d like to be able to define each subtype and a biomarker for each of those subtypes, based on the specific metabolites altered in that subtype.”

Like healthy cells, tumor cells take food from the blood and turn it into energy, but their metabolic processes differ from those of healthy cells. In recent years scientists have begun to try to find ways to exploit these differences to selectively kill cancer cells, with the ultimate goal of developing new therapies. Peterson and his colleagues used cutting edge technology, including liquid chromatography-mass spectrometry, to survey the amounts of a wide range of metabolites in cells from nine widely-used cell lines of triple-negative breast cancer.

They also zoomed in to study particular, targeted metabolites more closely. Broad metabolic profiling is new technology, and Peterson and his colleagues are among the first teams of researchers to apply it to the study of triple-negative disease.

They looked at both the metabolic “footprints” and “fingerprints” of the cells. The metabolic “footprint” includes the metabolites that go in to a cell from the surrounding media — or come out the other end of the process. The metabolic “fingerprint” shows all the molecules that work inside the cell during metabolic processes.

“We basically remove all the cells from the media, and then extract all of their small metabolites(less than 1500 dalton) and analyze those,” Peterson says.

He says this catalog of metabolites from these cell lines is a good first step toward using metabolic markers to better understand the disease. Since triple-negative breast cancer is heterogeneous, the next step, he says, is to replicate the study in other cell lines and validate potential biomarkers.

This study grew out of another ongoing project by Peterson and his team. He was the lead author on a paper, published in the journal Nature Biotechnologyin 2011, introducing a new technique to study the action of kinases—which are a class of enzymes that control cellular metabolism. Once that tool was developed, he decided to apply it to the poorly understood triple-negative breast cancer. In another study he’s presenting at the AACR Annual Meeting 2013, Peterson and colleagues show how this technique can be used to identify small molecules that block the kinases important to the growth of triple-negative disease.

“Those small molecules may be the starting point for new therapies,” he says. Ultimately, he says, he’d like to combine the metabolite and kinase studies to develop targeted therapies that stymy the metabolism of cancer cells.

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.

Short Bouts of Exercise As Good As Formal Regimens

2013-04-11T10:42:00.000-05:00

[NOTE: This is a news release from January from Oregon State University. I found it while researching other things. It offers a good perspective on exercise and how to make it work. Exercise is important in fighting TNBC. Tied with a healthy diet, it can lead to weight loss, which is a key to reducing risk of recurrence.]

New research at Oregon State University suggests the health benefits of small amounts of activity – even as small as one- and two-minute increments that add up to 30 minutes per day – can be just as beneficial as longer bouts of physical exercise achieved by a trip to the gym.

The nationally representative study of more than 6,000 American adults shows that an active lifestyle approach, as opposed to structured exercise, may be just as beneficial in improving health outcomes, including preventing metabolic syndrome, high blood pressure, and high cholesterol.

“Our results suggest that engaging in an active lifestyle approach, compared to a structured exercise approach, may be just as beneficial in improving various health outcomes,” said Paul Loprinzi, lead author of the study. “We encourage people to seek out opportunities to be active when the choice is available. For example, rather than sitting while talking on the phone, use this opportunity to get in some activity by pacing around while talking.”

Perhaps just as importantly, the researchers found that 43 percent of those who participated in the “short bouts” of exercise met physical activity guidelines of 30 minutes day. In comparison, less than 10 percent of those in the longer exercise bouts met those federal guidelines for exercise.

Loprinzi, who is an assistant professor at Bellarmine University, conducted the research as a doctoral student working in the lab of Brad Cardinal at Oregon State University. Cardinal, a professor of exercise and sport science, is co-author of the study, which is in the current issue of the American Journal of Health Promotion.

“You hear that less than 10 percent of Americans exercise and it gives the perception that people are lazy,” Cardinal said. “Our research shows that more than 40 percent of adults achieved the exercise guidelines, by making movement a way of life.”

Cardinal, who has studied the “lifestyle exercise” model for more than 20 years, said one of the most common barriers people cite to getting enough exercise is lack of time. He said the results of this study are promising, and show that simply building movement into everyday activities can have meaningful health benefits.

“This is a more natural way to exercise, just to walk more and move around a bit more,” Cardinal said. “We are designed by nature as beings who are supposed to move. People get it in their minds, if I don’t get that 30 minutes, I might as well not exercise at all. Our results really challenge that perception and give people meaningful, realistic options for meeting the physical activity guidelines.”

For example, Cardinal said instead of driving half a mile, try biking or walking the same distance; instead of using a riding lawn mower, use a push lawn mower. Instead of sitting through TV commercials, try doing some sit-ups, push-ups, or jumping jacks during the commercial breaks; and instead of sitting and being a spectator at a child's sporting event, try walking around during the halftime break.

The researchers said the participants in this study wore accelerometers, which is an objective tool to measure physical activity. Those who participated in the short bouts of activity could be moving as few as one or two minutes at a time. The people in the “short bouts” group had positive results in areas such as blood pressure, cholesterol, metabolic syndrome, and waist circumference.

For instance, the study showed those in the shorter exercise group who met physical activity guidelines had an 89 percent chance of not having metabolic syndrome, compared to 87 percent for those meeting guidelines using the structured exercise approach.

Loprinzi said the one area where small bursts of activity did not seem to equal the benefits of longer, sustained exercise was in Body Mass Index, or BMI. However, the researchers cautioned that these findings do not necessarily mean that short bouts of activity do not help with weight loss, especially since they did find a benefit on weight circumference.

“There are inherent limitations in BMI as a surrogate measure of fat and health in general,” Cardinal said. “People can still be ‘fit’ and ‘fat.’”

The researchers emphasized that for health benefits, people should seek out opportunities to be physically active.

“In our society, you will always be presented with things that entice you to sit or be less active because of technology, like using a leaf blower instead of a rake,” Cardinal said. “Making physical activity a way of life is more cost-effective than an expensive gym membership. You may be more likely to stick with it, and over the long term, you’ll be healthier, more mobile and just feel better all around.”

A Moment of Beauty

2013-04-08T22:43:00.002-05:00

Carolyn Justin Baer took this photograph of Lake Tahoe, where she lived with her husband Bob. Justin's family selected this photo for her obituary after she died of triple-negative breast cancer March 21, 2013. I considered Justin a friend, even though I had never met her, and I wrote about our friendship for Psychology Today. But I had not known, until I saw this photograph, that she was such a talented artist. This amazing shot is a memory of a moment in time, of the beauty that Justin saw and captured, the beauty she left behind with us. (See more of Justin's remarkable work here.)

Genetic Details of Triple-Negative Breast Cancer

2013-04-08T07:47:00.002-05:00

Beyond its most basic definition—negative for receptors for estrogen, progesterone and Her2/neu—triple-negative breast cancer has unique genetic characteristics. Research published April 1, 2013 in the journal Cancer Research has outlined some of TNBC’s genetic associations. Researchers keep getting closer to finding what makes TNBC tick. Once they know that, they can target it. Put a big red bull’s eye on its nasty old back.

Some details of the research:

• TNBC is more likely to be associated with TOX3, ESR1, RAD51L1, TERT, 19p13.1, 20q11, MDM4, 2p24.1, and FTO.

• 70 percent of those with the BRCA1 mutation who get breast cancer get TNBC.

• 16 to 23 percent of those with the BRCA2 mutation who get breast cancer get TNBC.

• Variations in the 19p13.1 locus and the MDM4 locus have been associated with TNBC, but not other forms of breast cancer, meaning that these are TNBC-specific.

• TNBC accounts for 12 to 24 percent of all breast cancers.

The Tale of Two Treats

2013-03-24T16:18:00.000-05:00

We went for a walk yesterday right before lunch, then stopped at the gas station. Note to self: Don't do that anymore. The gas station has Diet Coke and potato chips. And I am hungry and more vulnerable to food temptations of lunchtime. I have written about Diet Coke before—it is one of the food addictions I have worked hard to overcome. I give myself a C+ on that. I now have a Diet Coke 3-4 times a week instead of 8-10. My success is up and down. Sometimes I can go weeks without one. And I always feel better. So, long way of getting to the fact that I succumbed yesterday and had a fountain Diet Coke. Here's what I need to remember about that: They never taste good enough for all the bad they do. That needs to be my mantra.

Then there were the chips. But at least I chose the healthier ones. And here's a cautionary note: standard potato chips have about 80 percent more calories and fats that baked ones. The data:

Baked Lays: 160 calories in a 1.375 oz. bag; 4 percent of your daily value of fat, and no trans or saturated fats; and 8 percent of your DV of sodium.

Cape Cod Kettle Cooked: 270 calories in a 1.875 oz. bag; 21 percent of your daily value of fat, 5 percent DV of saturated fat, and no trans fats; and 14 percent of your DV of sodium.

So, if you're going to fall off the wagon with a treat, your choice of treats can make a big difference.

I had the chips with a healthy vegetarian sandwich sandwich: low-fat whole wheat bread, avocado, red pepper, romaine, and hummus. So there's that.

Enough About Diet

2013-03-22T14:26:00.000-05:00

My blogs about my diet are not working as well as I had hoped. My goal was to create a sense of community, with readers joining in on a healthy eating bandwagon. But reader response was lackluster. And then I had missteps in my own diet, so I felt like a bit of a fraud. But I also thought maybe that made it more authentic. Whatever the case, the product, process, and response were all uninspiring.

So I am going to continue my diet but not the daily posts, and I may do a recap when it is over. We'll see. (I have lost a pound, so something worked.) Anybody who wants to join me can email me and I will help encourage you. I am all about encouraging people.

The message I want to send in all this:

• Diet is important in fighting TNBC; losing weight appears to be the essential factor.

• It's a real pain to eat healthy all the time. Others are better at it than I am.

• Remembering how much better I feel and look when I eat well keeps me motivated.
• Remembering is difficult when I am being lured by fats and sweets.

• Success in anything comes in smalls bits and starts. When you lose weight slowly and steadily, you are more likely to keep it off.

• Moderation in all things should be your goal.

Now off to chew on a carrot.

[Here's yesterday's diet—I already had this prepared, so figured I might as well post it.]
March 21, 2013

Green Drink: Pure Synergy: 45 calories, no fats

Breakfast:

•1/2 cup Cascadian Farm Organic cereal: 67 calories, no trans or saturated fats

•1/4 cup Almond Breeze almond milk: 10 calories, no trans or saturated fats

Lunch:

Veggie Sandwich:

• Sara Lee 45 calorie whole wheat bread: 90 calories, no trans or saturated fats

• 1/3 red bell pepper: 23 calories, no trans or saturated fats

•low fat cream cheese: 70 calories, 4 grams of saturated fat, no trans

• 1 leaf of romaine lettuce: 1 calories, no fats

Sandwich total: 183 calories, 4 grams saturated fats

•small apple: 116 calories, trace saturated, no trans fats

• Organic hot chocolate with almond milk: 110 calories

Snack:

• 1 cup broccoli: 25 calories, no trans or saturated fats

• 2 tbsp. Roasted Garlic Hummus: 60 calories, no trans or saturated fats

• 16 whole almonds: 82 calories. 2 percent daily value saturated fats, no trans fats

Juice:

• 2 carrots (52 calories), 1 stalk of kale (34 calories), 1/8 red cabbage (14 calories), 1/2 apple (58 calories): 158 calories

Dinner:

• Baked acorn squash with apples: 315 calories

NOTE: I make sure to keep hydrated during the day, but don't actually measure whether I get the recommended 64 ounces or not. I feel livelier when I am hydrated. Often, when I start losing energy, I have a tall drink of water and I feel better.

TOTAL:

1172 calories

5 grams saturated fats—25 percent daily value

2+ servings of fruits, 2+ serving of vegetables, plus juice and green drink

Stats: I've lost a pound so far. We'll see if I keep it off, but it feels like progress.

March 20, 2013: What I Ate (Day 3)

2013-03-21T13:04:00.000-05:00

Green Drink

Pure Synergy: 45 calories, no fats

Breakfast:

Smoothie:

•1 cup fresh blueberries (frozen, then thawed): 70 calories, 0.2 grams saturated fat, no trans fats

• I peach: 51 calories, trace of saturated fat, no trans fats.

•1/2 cup Almond Breeze almond milk: 20 calories, no trans or saturated fats

• 1 cup orange juice: 112 calories, no trans or saturated fats

Total for smoothie: 253 calories, trace of saturated, no trans fats

Snack:

•Blueberry muffin with low fat milk: 162 calories, 6 percent daily value saturated fat, no trans fats.

• Coffee (black): 2 calories

Lunch:

• California roll (sushi—9 pieces): 360 calories, no trans or saturated fats

Snack:

• air-popped popcorn: 93 calories

• Powdered cheddar cheese: 50 calories, 5 percent of saturated fats, no trans fats

Juice:

• 2 carrots (52 calories), 1 stalk of kale (34 calories), 1/8 red cabbage (14 calories), 1/2 apple (58 calories): 158 calories

Dinner:

• Berry smoothie: 150 calories (estimate)

Exercise:

1 hour qigong: 200 calories

TOTAL:

1273 calories

12 percent daily value of saturated fats

4+ servings of fruits, 1 serving of vegetables, plus juice and green drink

1273 calories consumed minus 200 burned = 1073

Stats

This was a two-smoothie day, which put me a little heavy on fruit—that’s not a good habit, as fruit is high in sugars. They’re natural, but it is still not good to overdo. The evening smoothie was a healthy treat after my qigong class and it was small. I had the morning smoothie because I was going out to coffee at a friend’s and I wanted to make sure I got enough nutrients, knowing I would not have a healthy snack. I did get a low-fat muffin, so it was a little lower in fat, but it still was not nutrient-rich. It is difficult to eat healthy while eating out or at a friend's house.

As for exercise, I found several estimates for qigong that were higher than I used. I love this exercise, but I think it was a bit modest in terms of calorie burning.

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.

March 19, 2013: What I Ate (Day Two)

2013-03-20T09:09:00.000-05:00

March 19, 2013

Green Drink

Pure Synergy: 45 calories, no fats

Breakfast:

•1/2 cup fresh blueberries (frozen, then thawed): 35 calories, 0.1 gram saturated fat, no trans fats

•1/2 cup Cascadian Farm Organic cereal: 67 calories, no trans or saturated fats

•1/4 cup Almond Breeze almond milk: 10 calories, no trans or saturated fats

Snack:

•1 banana: 105 calories, 1 percent daily value of saturated fats, no trans fats

• 8 whole almonds: 41 calories. 1 percent daily value saturated fats, no trans fats

Lunch:

•Tasty Taco original (aka: Fell Off the Wagon): 520 calories, 12 grams of saturated fat, no trans fats

• 1/2 cup red grapes: 60 calories, no trans or saturated fats

Snack:

• 1 cup broccoli: 25 calories, no trans or saturated fats

• 2 tbsp. Roasted Garlic Hummus: 60 calories, no trans or saturated fats

Juice:

• 2 carrots (52 calories), 1 stalk of kale (34 calories), 1/8 red cabbage (14 calories), 1/2 apple (58 calories): 158 calories

Dinner:

• California roll (sushi): 255 calories, no trans or saturated fats

• 5 oz merlot: 122 calories, no trans or saturated fats

• sourdough bread: 160 calories, no trans or saturated fats

• butter: 72 calories, 26 percent daily value of saturated fat, no trans fats.

Exercise:

55 minutes brisk walking (burned 236 calories)

TOTAL:

1735 calories

27 percent daily value of saturated fats

3 servings of fruits, 2+ servings of vegetables, plus juice and green drink

1735 calories consumed minus 236 burned = 1509

Stats

At my height (5' 9.5"), I could consume 1693 calories a day and stay at the same weight (168 pounds), so today was a bit of a wash. Exercise did help. The lunchtime taco did not.

Writing this all down, however, is an excellent exercise—it helps keep me on track and makes me acknowledge reality. Hope it helps some of you.

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.

Genes Related to the Metabolism of Fats Linked to Triple-Negative Breast Cancer

2013-03-19T14:24:00.005-05:00

News Release from the American Association for Cancer Research

PHILADELPHIA — The overexpression or underexpression of a newly identified set of genes related to lipid metabolism may help physicians identify whether or not a woman is at risk for hormone receptor-positive or hormone receptor-negative breast cancer and to subsequently tailor prevention strategies appropriately, according to data published in Cancer Prevention Research, a journal of the American Association for Cancer Research.

Researchers sought to find a way to identify women at risk for estrogen receptor-negative breast cancer by examining gene expression in the unaffected breasts of women who had a primary breast cancer of known estrogen-receptor status.

They used this approach because prior research has indicated that if women who have had cancer in one breast subsequently develop a cancer in their second breast, the second cancer is likely to have hormone-receptor status that resembles the first cancer.

Using this logic, Khan and colleagues performed fine-needle aspiration on the unaffected breasts of 15 women with estrogen receptor-positive breast cancer and 15 women with estrogen receptor-negative breast cancer. They validated their results in a second group of women: 12 with estrogen receptor-positive disease, 12 with estrogen receptor-negative disease and 12 healthy controls. The cases in each set were matched by age, race and menopausal status.

The researchers identified 13 genes with significantly higher expression levels in samples from estrogen receptor-negative women. Eight of these genes were associated with lipid metabolism.

“This was interesting because obesity is a breast cancer risk factor for postmenopausal women, but obese women are generally thought to be at increased risk for hormone-sensitive cancer,” said Seema A. Khan, M.D., co-leader of the Breast Cancer Program at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University in Chicago. “We were surprised to see that some of these genes that are associated with lipid metabolism, or the metabolism of fats, are actually more highly expressed in the unaffected breasts of women with estrogen receptor-negative breast cancer.”

The researchers also found significant overexpression of four of the genes associated with lipid metabolism — DHRS2, HMGCS2, HPGD and ACSL3 — in estrogen receptor-negative samples when compared with healthy women. In estrogen receptor-positive samples, two different lipid metabolism-associated genes — UGT2B11 and APOD — were underexpressed.

“It will be a few more steps before this information is practically useful, but we are hoping that it can take us to a place where we can obtain a breast sample from healthy women, see that they are at risk for a certain type of breast cancer and tailor the prevention strategy accordingly,” Khan said.

Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Read more about metabolism and TNBC in my book, Surviving Triple-Negative Breast Cancer.

March 18, 2013: What I Ate

2013-03-19T11:24:00.003-05:00

Breakfast:
•1/2 cup fresh blueberries (frozen, then thawed): 35 calories, 0.1 gram saturated fat, no trans fats
•1/2 cup Cascadian Farm Organic cereal: 67 calories, no trans or saturated fats
•1/4 cup Almond Breeze almond milk: 10 calories, no trans or saturated fats
Snack:
•1 banana: 105 calories, 1 percent daily value of saturated fats, no trans fats
• 8 whole almonds: 41 calories. 1 percent daily value saturated fats, no trans fats

Lunch:
•Leftover crab cake sandwich (crab cake 160 calories, 11 percent daily value saturated fat, no trans fat; English muffin 135 calories, 1 percent daily value of saturated fat, no trans fat) 295 calories, 12 percent daily value of saturated fat, no trans fats.
• 1/2 fresh red bell pepper: 23 calories, no trans or saturated fats
• 1/2 cup red grapes: 60 calories, no trans or saturated fats

Snack:
• 1 cup broccoli 25 calories, no trans or saturated fats
• 2 tbsp. Roasted Garlic Hummus: 60 calories, no trans or saturated fats

Juice:
• 2 carrots (52 calories), 1 stalk of kale (34 calories), 1/8 red cabbage (14 calories), 1/2 apple (58 calories): 158 calories

Dinner:
• Mexican Seitan Fajitas on whole wheat tortillas (Seitan, 100 calories, no trans or saturated fats; whole grain tortilla, 130 calories, no trans or saturated fats; bell pepper and onion: 25 calories, no trans or saturated fats), 255 calories, no trans or saturated fats.
• 1/4 bar Lily's almond dark chocolate bar with stevia: 43 calories, 10 percent daily value of saturated fats, no trans fats.

Exercise:
30 minutes brisk walking

TOTAL:
1177 calories
24 percent daily value of saturated fats
3 servings of fruits, 2+ servings of vegetables, plus juice

Stats
I am 5' 9.5" and now weigh 168 pounds, which gives me a body mass index (BMI) that's right at the edge of normal and overweight. I want to weigh 160. If I reduce my caloric intake to 1193.8 calories per day I will lose one pound per week without exercise, according to About.com's Weight Management Calculator. I will use that amount, but also continue my exercise.

So, if I can keep this up, I am OK. (And, yes, I am not technically overweight yet, but this is a slippery slope, and I have fallen down it once, ending up 50 pounds overweight. I do not want that to happen again.)

Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.

Let's Lose Weight Together

2013-03-19T10:11:00.002-05:00

I love French fries, potato chips, pastries, coffee in my cream, enchiladas with green chili, tacos, and you get the point. This food is truly addictive. According to The Extraordinary Science of Addictive Junk Food, in The New York Times Magazine, food companies know just how to grab us where we're most vulnerable—with crunchy goodness that taps into brain receptors through sugar, salt or fat. All this makes our blood sugars spike and leads to our craving more. And our consumption of these foods is supported with staggering marketing efforts.

One scientist, who spent 30 years developing fast food, commented in the article, "I feel sorry for the public."

So if you have been having trouble losing weight—or if, like me, you have been gaining it—stop feeling guilty. We're working against some serious forces. It can take a truckload of effort to fight our impulse to eat these taste-good, feel-bad treats.

But I am going to do it. Here is my plan.

I have been somewhat lax in my healthy eating habits lately. I sort of fell off a cliff once I allowed myself unlimited access to French fries. It was all uphill on the scale from there. And downhill on my health. I have gained ten pounds in two years and it is time to get back on the health train. So, in an effort to keep me honest, I am going public with my diet. I will publish what I eat each day, so I can motivate myself to do what is good for me. If you want to join me, just add your notes to the comments section. Or join me silently.

[Here's how I did the first day.]

There's a great deal of evidence that being overweight is a risk for triple-negative breast cancer. And the only real way to lose weight is by modifying our diet and increasing our exercise. No fads, no quick fixes, just modifying what we eat and how much we move. I will maintain my goal of four hours of exercise a week—I have been OK with that one—but I will strive to:

• Focus on a plant-based diet high in vegetables, fruits, grains, nuts, and seeds.
• Eat at least five servings of fruits and vegetables a day.
• Reduce the amount of saturated and trans fats in my diet—these come from fried and processed food, plus meats, cheese, butter, and ice cream. This will be difficult.

We'll see how this goes. I'll do it for two weeks and see what progress I make.

I hope you can join me. I hope I can be a good model.

Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.

SOX11 and p53 May Spell Unique Development of Triple-Negative Breast Cancer

2013-03-19T09:31:00.001-05:00

Could you create a breast cancer tumor in mature mice by reactivating how embryonic breast cancer cells develop? And, if you could, what would you learn?

In a study published in the journal Breast Cancer Research, scientists discovered that basal-like breast cancers with the BRCA1 mutation—many of them triple-negative breast cancers—grow differently than other cancers. In fact, the way they grow predicts the prognosis of the tumor.

The protein p53 was found to be active in development of these cancers, which supports much previous research. The also determined that a progenitor cell, SOX11, may play a significant role. A progenitor cel is active in cell development and regulation. In this research, SOX11 was also

• highly expressed in some mammary tumors with the BRCA1 mutation.

• found to regulate breast cancer cell proliferation and cell survival.

This is an initial study, but it gets us closer to understanding the genetic profile of triple-negative breast cancer.

Please consider a donation to Positives About Negative to keep this site going. This work is entirely supported by readers. Just click on the Donate button in the right of the page. Thank you!

Read more about diet and TNBC in my book, Surviving Triple-Negative Breast Cancer.