Friday, January 25, 2013

Take Your Vitamin D- Especially if you are Triple Negative

We have been encouraging No Surrender readers to take their Vitamin D since our inception.
Now, a study we have been following, has yielded great results- especially if you have triple negative breast cancer. We recommend Vitamin D supplementation no matter what your receptors are and suggest that women who do not have breast cancer also supplement to keep their D levels in good range.

Vitamin D Holds Promise in Battling a Deadly Breast Cancer
Wed, 2013-01-23 11:34

In research published in the Jan. 21 issue of The Journal of Cell Biology, a team led by Susana Gonzalo, PhD, assistant professor of biochemistry and molecular biology at Saint Louis University, has discovered a molecular pathway that contributes to triple-negative breast cancer, an often deadly and treatment resistant form of cancer that tends to strike younger women. In addition, Gonzalo and her team identified vitamin D and some protease inhibitors as possible new therapies and discovered a set of three biomarkers that can help to identify patients who could benefit from the treatment.

In the recent breakthrough, which was funded in part by a $500,000 Department of Defense grant, Gonzalo’s lab identified one pathway that is activated in breast cancers with the poorest prognosis, such as those classified as triple-negative. These cancers often strike younger women and are harder to treat than any other type of breast cancer. Women who are born with BRCA1 gene mutations are at increased risk for developing breast and ovarian cancers within their lifetime, and the tumors that arise are frequently the triple-negative type. Although chemotherapy is the most effective treatment for triple-negative breast cancer, it has profound secondary effects. Understanding the biology of triple-negative breast cancers will help to develop less toxic therapeutic strategies.

Experiments performed in Gonzalo's laboratory, in collaboration with the laboratories of Xavier Matias-Guiu and Adriana Duso (IRBLleida, Spain), showed that activation of this novel pathway not only allows tumor cells to grow unchecked, but also explains the reduced sensitivity of these types of tumors to current therapeutic strategies. Importantly, vitamin D plays a role in turning off this pathway, providing a safe and cost-effective strategy to fight these types of tumors.

For molecular biologists like Gonzalo who look for answers below the cellular level to discover why some people develop cancer, the search often involves tracing a chain of events to try to understand cause and effect of the behavior between several genes and the proteins which they express. In order to understand these complex pathways, researchers often turn levels of proteins on or off by expressing one gene or suppressing another. Part of a researcher’s challenge is determining what the function of each component of a pathway is.

The cell employs a complex mechanism to protect genetic information and ensure that damaged DNA is not passed on to daughter cells. Cells have built in checkpoints and fail safes to ensure the accuracy of their DNA code and are able to slow or stop their own proliferation if the information is compromised. Loss of these checkpoints and the accumulation of damaged DNA often leads to cancer.

BRCA1 is a well-established tumor suppressor gene. Women who carry mutations in this gene have a high risk of developing breast and ovarian cancer. Tumors that arise often lack expression of three receptors: estrogen, progesterone and HER2 (thus, “triple-negative”), and do not respond to hormone therapy.

BRCA1 is important because it is involved in repairing DNA double-strand breaks, a kind of DNA damage that is especially dangerous for the integrity of our genome. BRCA1 also is involved in cell-cycle checkpoints after damage, which are control mechanisms during cell proliferation that make sure the DNA information has been accurately replicated and transferred to the daughter cells. Thus, BRCA1 is considered a safeguard of the genome.

Loss of BRCA1 is bad news for the information contained in a cell’s genetic blueprint. It results in genomic instability characterized by unrepaired DNA breaks and chromosomal aberrations that compromise cell viability. How BRCA1-mutated cells are able to form tumors has been a long-standing question. Investigators recently showed that loss of another DNA repair factor, 53BP1, allows proliferation and survival of BRCA1-deficient cells. In addition, decreased levels of 53BP1 were observed in triple-negative breast cancers, and correlated with resistance to drugs at the forefront of cancer treatment, such as PARP inhibitors.

Gonzalo’s team has found a pathway responsible for the loss of 53BP1 in breast cancers with poor prognosis, specifically BRCA1 mutated and triple-negative. It turns out that loss of BRCA1 increases the expression of a protease, known as cathepsin L (CTSL), which causes the degradation of 53BP1. Cells that have lost both BRCA1 and 53BP1 have the ability to repair DNA, maintain the integrity of the genome, and proliferate. Thus, the protease helps cells with faulty BRCA1 to survive.

If lowering the levels of 53BP1 allows BRCA1 deficient cells to thrive and do their worst, increasing the levels of the protein offers a promising strategy for treatment of breast tumors.

So, how to do this? In previous research, Gonzalo’s team showed that vitamin D inhibits CTSL-mediated degradation of 53BP1 in non-tumor cells, as efficiently as specific CTSL inhibitors. This time, they found that treatment of BRCA1-deficient tumor cells with vitamin D restores high levels of 53BP1, which results in increased genomic instability and reduced proliferation.

Importantly, their evidence suggests that vitamin D treatment might restore the sensitivity to PARP inhibitors in patients who become resistant. Thus, a combination of vitamin D and PARP inhibitors could represent a novel therapeutic strategy for breast cancers with poor prognosis.

So, with this chain of events, Gonzalo and colleagues demonstrated a pathway by which triple-negative breast cancers proliferate: BRCA1-deficient cells activate CTSL which minimizes levels of 53BP1 to overcome genomic instability and growth arrest.

In a final exceptionally useful discovery, Gonzalo and collaborators found that high levels of nuclear CTSL and low levels of 53BP1 and nuclear vitamin D receptor (VDR) are a clear marker that identifies certain triple-negative breast cancer patients, biomarkers that offer the potential to customize future breast cancer therapies. In particular, this triple-biomarker signature will allow the identification of patients in whom the pathway is on and who might benefit the most from vitamin D treatment.

Tuesday, January 22, 2013

Friday, January 18, 2013

Lance Armstrong

Back in 2001, September of 2001, when the world had gone mad, I was diagnosed with cancer. I was told to purchase certain books to help me through it. The Breast Book was one. That book did more harm to my psyche than I think the diagnosis did. Why? Because no one knew much about triple negative breast cancer back then other than the oft repeated mantra, "Women with triple negative breast cancer have a poor survival rate and die sooner." I was still in my thirties and was essentially being told there was really nothing I could do to fight my cancer and it seemed to me that the entire cancer establishment was resigned to a defeatist attitude when it came to young women with this particular type of breast cancer.

I put the breast books down. They were outdated and seemed to be talking about people other than me. I did not fit in to their breast cancer patient mold. I refused to be categorized as one of the ones who is on the negative side of the disease. I wanted someone to tell me that no matter how bad your diagnosis, someone has to be on the positive side of the stats, and why shouldn't it be me?

That's when I found the book that made all the difference. It was called,  "It's Not About The Bike" by Lance Armstrong.

I haven't read it since then, I didn't need to. I got its message and I have lived it. He wrote about how he was diagnosed with a cancer that had already spread to his lungs. He wrote about his grueling treatments. He wrote about how he tried to get his life back by riding his bike. When I sat in the chemo room feeling terrible, I "knew" someone who also went through harsh chemo and made it through, stronger, braver and ready to give back.

There was one line in that book that I have lived by since 2001. I will paraphrase it here,
"It is the responsibility of the cured to help others through this disease." While no cancer survivor ever really considers themselves "cured" I have spent the last 11 years paying it forward by helping others through this disease.

For the words in that book,  for the strength it gave me, for the courage I found, and, for all the women I have had the fortune of helping, I am grateful to Lance Armstrong. And I always will be.

Did he admit to doping and bullying and all the other charges against him? I guess so. But I don't care. The Lance Armstrong who helped me was not about the bike. And that is the way I will always view him.

Thursday, January 17, 2013

New Marker Predicts Breast Cancer Recurrence

UAlberta medical researchers find DNA marker that predicts breast cancer recurrence

January 16, 2013

Medical researchers at the University of Alberta tested the DNA of more than 300 women in Alberta and discovered a ‘genetic marker’ method to help accurately profile which women were more apt to have their breast cancer return years later.
Sambasivarao Damaraju, a professor with the Faculty of Medicine & Dentistry, and at the Cross Cancer Institute just published his team’s findings in the peer-reviewed journal, PLoS One.  Using a simple blood test, Damaraju and his team, which included his PhD student Yadav Sapkota, scanned the entire human genome of 369 women who had been diagnosed with breast cancer. Of those, 155 had their cancer come back and 214 did not.
“If we can accurately predict which women are at high risk of breast cancer recurrence, it gives the physicians and oncologists treating those women time to design a more aggressive therapy in hopes of preventing the cancer from coming back,” says Damaraju, who works in the Department of Laboratory Medicine & Pathology. “Treatment strategies could be tailor made for these women based on their genetic make-up and how susceptible it makes them to breast cancer recurrence.”
Damaraju and his team focused their research on good prognosis breast cancer – cancer that has a high success rate in terms of initial recovery and treatment. About 70% of all breast cancers fall into this category. Yet despite the high success rate with initial treatment for this type of breast cancer, the overall numbers of those who died or had their cancer spread in this ‘good prognosis’ group are substantial. The numbers are high simply because so many people have this common ‘good prognosis’ cancer.
Currently, treatment options for breast cancer patients are based on what doctors know about the tumour itself – its size, grade and the absence or presence of certain markers within the tumour. Damaraju noted there are patients who are given an excellent prognosis based on what doctors see within the tumour, yet the cancer comes back. And other women remain cancer free even though their doctors said they had a poor prognosis based on information gleaned from the tumour. Damaraju thinks that this inaccuracy of tumor based markers could be complimented with this DNA marker that can be found through a simple blood test.
Damaraju and his team are continuing their research in this area and would like to reconfirm their findings in a larger study, pending further funding. The results from that study could be published in about three years, and he suspects about two years after that, the DNA predictor test could be tested in prospective clinical studies prior to making them widely available for women.
The research was funded by the Canadian Breast Cancer Foundation – Prairies/NWT region, and the Alberta Cancer Foundation.
“The impact of Dr. Damaraju’s significant discovery on personalized treatment for breast cancer patients is substantial,” says Canadian Breast Cancer Foundation – Prairies/NWT Region CEO Trish Bronsch. “Knowing individual risks of breast cancer and reccurrence provides doctors and oncologists with a better picture in which they can create a treatment plan to fit personal needs. We are very excited to have been able to help fund Dr. Damaraju and his team to this discovery.”
The Alberta Cancer Foundation agreed.
“We are pleased to see donor dollars having a direct impact on outcomes that are important to Albertans--in this case earlier detection and improved treatment options for breast cancer recurrence,” says Myka Osinchuk, CEO of the Alberta Cancer Foundation. “We are excited to follow Dr. Damaraju and his team to ensure those women successfully treated for breast cancer continue to live cancer-free lives.”

Monday, January 14, 2013


The No Surrender Breast Cancer Support forum was started in 2007. It has been an amazing ride since then. We have a wonderful accompanying website that helps women through their breast cancer.

The Support Forum is and always has been a safe place that has been fiercely protected, so that frightened, stressed out breast cancer patients and their families can come to discussed their deepest fears and most intimate treatment details.

Every member has to be approved to prevent spam and hackers.

There are no ads. There is no spam. There is only love, support, sisterhood and heartbreaking posts from beloved sisters who are no longer with us.

Our website is run by us and is totally under our control. However, our Support Forum is hosted by a third party site run by less than scrupulous people. Every year, since 2007, the domain URL associated with the support forum has been on "auto-renew" to ensure our domain stays in ours.
The third party site profited from selling our Domain Name to a loathsome extortionist who gained control of the No Surrender Support Forum domain name. The domain name that women have been turning to for six years. The place where google searches lead newly diagnosed women to help and find friendship of their fellow sisters.

As a result, the third party site owners forced us to purchase a new domain name, profiting yet again.
In the meantime, the loathsome extortionist is now trying to pass himself off as US.

No Surrender is a registered trademark with the United States. It is trademark infringement for this person to pass himself off as us. Action has been taken.

However, we need your help. Please copy and paste the following on any site or twitter or message forum of your own so that women will find us and so, too, will Google search engines:
The authorities have been notified. The United States Trademark Office has been contacted. GoDaddy, where the domain was purchased has been put on notice. BlueHost that hosts the scam, phishing, hacked forum domain has also been put on notice.

Thank you for helping us.

Wednesday, January 9, 2013

Attention Needs To Be Paid to Dr. Watson

Back in the '90s I had the privilege of meeting Dr. Watson and his lovely wife who were honorees for a fundraiser I was organizing. I did a lot of research on Dr. Watson's work. Little did I know at the time that his work would be such an important part of my survival.

Not one to shy away from the glaring light of truth, he has once again stepped forward with what I believe is evidence based, spot on commentary regarding the "war on cancer" and why we are not winning it.

This article appeared today in Reuters.

"The biggest obstacle" to a true war against cancer, Watson wrote, may be "the inherently conservative nature of today's cancer research establishments." As long as that's so, "curing cancer will always be 10 or 20 years away."


NEW YORK (Reuters) - A day after an exhaustive national report on cancer found the United States is making only slow progress against the disease, one of the country's most iconic - and iconoclastic - scientists weighed in on "the war against cancer." And he does not like what he sees.

James Watson, co-discoverer of the double helix structure of DNA, lit into targets large and small. On government officials who oversee cancer research, he wrote in a paper published on Tuesday in the journal Open Biology, "We now have no general of influence, much less power ... leading our country's War on Cancer."

On the $100 million U.S. project to determine the DNA changes that drive nine forms of cancer: It is "not likely to produce the truly breakthrough drugs that we now so desperately need," Watson argued. On the idea that antioxidants such as those in colorful berries fight cancer: "The time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer."

That Watson's impassioned plea came on the heels of the annual cancer report was coincidental. He worked on the paper for months, and it represents the culmination of decades of thinking about the subject. Watson, 84, taught a course on cancer at Harvard University in 1959, three years before he shared the Nobel Prize in medicine for his role in discovering the double helix, which opened the door to understanding the role of genetics in disease.

Other cancer luminaries gave Watson's paper mixed reviews.
"There are a lot of interesting ideas in it, some of them sustainable by existing evidence, others that simply conflict with well-documented findings," said one eminent cancer biologist who asked not to be identified so as not to offend Watson. "As is often the case, he's stirring the pot, most likely in a very productive way."

There is wide agreement, however, that current approaches are not yielding the progress they promised. Much of the decline in cancer mortality in the United States, for instance, reflects the fact that fewer people are smoking, not the benefits of clever new therapies.

"The great hope of the modern targeted approach was that with DNA sequencing we would be able to find what specific genes, when mutated, caused each cancer," said molecular biologist Mark Ptashne of Memorial Sloan-Kettering Cancer Center in New York. The next step was to design a drug to block the runaway proliferation the mutation caused.

But almost none of the resulting treatments cures cancer. "These new therapies work for just a few months," Watson told Reuters in a rare interview. "And we have nothing for major cancers such as the lung, colon and breast that have become metastatic."

The main reason drugs that target genetic glitches are not cures is that cancer cells have a work-around. If one biochemical pathway to growth and proliferation is blocked by a drug such as AstraZeneca's Iressa or Genentech's Tarceva for non-small-cell lung cancer, said cancer biologist Robert Weinberg of MIT, the cancer cells activate a different, equally effective pathway.

That is why Watson advocates a different approach: targeting features that all cancer cells, especially those in metastatic cancers, have in common.

One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.

That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.

"Everyone thought antioxidants were great," he said. "But I'm saying they can prevent us from killing cancer cells."

Research backs him up. A number of studies have shown that taking antioxidants such as vitamin E do not reduce the risk of cancer but can actually increase it, and can even shorten life. But drugs that block antioxidants - "anti-antioxidants" - might make even existing cancer drugs more effective.
Anything that keeps cancer cells full of oxygen radicals "is likely an important component of any effective treatment," said cancer biologist Robert Benezra of Sloan-Kettering.

Watson's anti-antioxidant stance includes one historical irony. The first high-profile proponent of eating lots of antioxidants (specifically, vitamin C) was biochemist Linus Pauling, who died in 1994 at age 93. Watson and his lab mate, Francis Crick, famously beat Pauling to the discovery of the double helix in 1953.

One elusive but promising target, Watson said, is a protein in cells called Myc. It controls more than 1,000 other molecules inside cells, including many involved in cancer. Studies suggest that turning off Myc causes cancer cells to self-destruct in a process called apoptosis.
"The notion that targeting Myc will cure cancer has been around for a long time," said cancer biologist Hans-Guido Wendel of Sloan-Kettering. "Blocking production of Myc is an interesting line of investigation. I think there's promise in that."

Targeting Myc, however, has been a backwater of drug development. "Personalized medicine" that targets a patient's specific cancer-causing mutation attracts the lion's share of research dollars.
"The biggest obstacle" to a true war against cancer, Watson wrote, may be "the inherently conservative nature of today's cancer research establishments." As long as that's so, "curing cancer will always be 10 or 20 years away."

(Reporting by Sharon Begley; Editing by Jilian Mincer and Peter Cooney)

Our Support Forum Has New Address!

If you are a regular to the no surrender support forum and go to the old link of:

Please change your bookmark to the new link of:

And you will find all your friends there! It is the same forum! It just has a different name!