Monday, December 16, 2013

Extremely Good News for TNBC

From SABCS: A new drug combo is showing great effectiveness in the battle against triple negative breast cancer. It is still in trial, but with such good results, they are hoping to accelerate it.

Neoadjuvant Veliparib Plus Carboplatin Holds Promise for TNBC

SAN ANTONIO—Adding carboplatin and veliparib to standard neoadjuvant chemotherapy improves pathologic complete response (pCR) among women with triple-negative breast cancer (TNBC), according to the first set of efficacy results from the adaptively randomized multidrug I-SPY 2 clinical trial. The findings were presented at the 2013 San Antonio Breast Cancer Symposium.

“The results predict that the veliparib/carboplatin regimen is highly likely to be superior to the control (standard) regimen for triple-negative breast cancer in a phase 3 trial,” reported Hope Rugo, MD, professor of medicine and director of breast oncology and clinical trials education at the UCSF Helen Diller Family Comprehensive Cancer Center in San Francisco, CA.

“Adaptive randomization successfully identified a biomarker signature for veliparib plus carbo on the basis of a modest number of patients,” she added. “There is a suggestion that hormone receptor–positive, HER2-negative tumors benefit little from this regimen and inclusion of tumors in this subset would therefore dilute its effect in a subsequent trial.”

A total of 71 study participants (38 women with TNBC and 33 with hormone receptor (HR)–positive and HER2-negative breast cancer) were enrolled and randomly assigned to receive veliparib plus carboplatin in combination with standard neoadjuvant paclitaxel; 44 patients with HER2-negative breast cancer were concurrently randomly assigned to standard adjuvant chemotherapy.

pCR was defined as no residual tumor in breast or lymph nodes at the time of surgery. The estimated pCR rates for patients with TNBC are 26% for standard neoadjuvant therapy versus 52% for those administered veliparib, carboplatin, and standard paclitaxel, Dr. Rugo reported. For HER2-negative tumors, those numbers are 33% and 22%, respectively, she said.

Toxicity was “moderately elevated, as expected, but well-managed with dose reductions and delays,” Dr. Rugo said.

These findings also indicate that the innovative adaptive-randomization design of the I-SPY 2 multidrug trial “can generate results that will power phase 3 registration trials,” Dr. Rugo added. The adaptive randomization design of the trial uses a computer algorithm to detect which patients respond better to which therapies as a trial proceeds; patients are randomly assigned to standard neoadjuvant (presurgical) anthracycline- and paclitaxel-based chemotherapy, or neoadjuvant paclitaxel in combination with a novel agent, followed by anthracycline-based chemotherapy.

Then, as the trial progresses and data accumulates on how different tumor subtypes respond to distinct investigational agents, the adaptive trial design allows women to be “assigned with higher probability to therapies that are performing better for patients of their subtypes,” Dr. Rugo explained.

“Each new patient benefits from information from the previous patient.”

“By identifying which patients benefit, we can reduce trial size, accelerate drug development, and avoid overtreatment in the majority of patients, which is the future of drug development,” she said.
Adaptive randomization “is a new way of getting new drugs to market rapidly,” agreed panel moderator Peter Ravdin, MD, PhD, clinical professor of oncology at the University of Texas Health Science Center in San Antonio, TX.

Analyses are now underway to define additional pCR-predictive biomarkers, Dr. Rugo said. Future studies will need to compare survival outcomes with pCR data prior to US Food and Drug Administration approval, she cautioned.


  1. Rugo HS et al. S5-02. Presented at: San Antonio Breast Cancer Symposium 2013. Dec. 10-14, 2013; San Antonio.

Wednesday, October 2, 2013

The Other Awareness

 I have been packing to move. For a few hours this morning I tackled my storage closet. There was one box way in the back with writing on it that said "Circle Girls- Do NOT throw out."

I opened it up and in it were letters and cards from the sisters I have come to know over the years through my breast cancer network. There was a group of us called Circle Girls in one location and they moved over to the No Surrender site when it was started. "Circle Girls" refers to circling the wagons to protect ourselves from cancer, where we sit around a warm fire, in a circle of friendship, understanding,  love and much laughter.

I found the cards they all sent me when I was diagnosed for the second time. I found CDs we had burned for fun music. I also found letters and notes from sisters who we lost over the years.  These women were very dear to me and their deaths left a void in all of our lives.

Among all the "Awareness" this month, this part of breast cancer doesn't get talked about much. Instead you see Danika Patrick's hot pink race car; a Real Housewife from Orange County naked with only her special pink purse covering her healthy breasts,  and TV reporters all decked out in pink telling us all to "feel our boobies! "

The NSBCF has an awareness campaign all year long. It is for African American women who are young, much younger than the government tells us to get our first mammogram, to get screened through many different modalities. Because if they develop breast cancer it will most likely be the harder to treat triple negative breast cancer and one that you want to treat at its earliest stage. You can find it here :

You would really have to be living under a rock to not be "aware" of breast cancer today. There is almost no mention, however, of the millions of women who are dealing with breast cancer every day and who are in treatment for the rest of their lives. These women have metastatic disease.

Metastatic breast cancer is cancer that has spread beyond the breast to distant sites. It could be the bone, the lung, the liver, the brain and many other places. When someone has "mets" they are continually scanned for progression of their disease. If their scan is stable, that means they may get a chemo break for a while. If there is some growth but no further spread they actually find themselves being happy if the lung lesion "only" grew 2 centimeters. A finding that would normally terrify someone. It is often said that non-metastatic women live with "the new normal." Metastatic women live in "a new reality" and it is a scary, stressful and heartbreaking realty.

We need more treatments for advanced disease. We need to find a way to stop the spread of breast cancer throughout the body. We need these women to be able to live their lives without the shadow of The Beast breathing down their necks, every hour of every day of every year.

All the beautiful women I saved the letters and cards from who left this earth had metastatic disease.

I have recommended a good place to send your donations to before and I will recommend them again, it is The Cold Spring Harbor Laboratory. It is my belief that they are a research organization that will find the key that will open the door that will lead us all out of the hell of breast cancer - in fact all cancers.  Here is their link:

This October, don't pink. Instead, on October 13th take a moment to recognize Metastatic Breast Cancer Awareness Day by sending a donation to an accredited research organization.

People never know what to say to others who have serious diseases. It's simple: We are here for you. We will fight for you. We love you.

Tuesday, October 1, 2013

The Answer for Those of Us Who Lost Our Medical Coverage?

Concierge medicine certainly seems like it may be our best hope. The problem for cancer patients/survivors is what about our oncology team? That question needs to be answered. But if you had a private plan and were told by your carrier that you were being dropped, and the exchange in your state will either not cover you or the premium will be three times what you were currently paying, this may be something to consider.

Concierge Medicine Gains Ground

Published: Sep 28, 2013

SAN DIEGO -- Concierge doctors are spreading the word that it's possible to operate a direct primary care practice, make a living, and avoid one of the biggest headaches for family medicine physicians -- dealing with health insurance companies.

Multiple sessions at the American Academy of Family Physicians (AAFP) scientific assembly informed attendees about the growing world of direct primary care, sometimes called concierge, boutique, or retainer-based medicine. These practices charge patients a monthly or annual membership fee for unlimited office access, and bill patients for the tests and supplies they use.
When Doug Nunamaker, MD, and Josh Umbehr, MD, ended their 45-minute AAFP talk about their direct primary practice in Wichita, Kan., the two had barely walked off stage when they were besieged by a couple dozen doctors wanting more information.

Nunamaker and Umbehr opened Atlas MD, a direct primary care practice, in 2009 shortly after Umbehr left residency. They charge $50 a month in membership fees for adults ages 20 to 44, with fees ranging from $10 to $100 a month for pediatric and older patients.

They describe their payment structure on the Atlas MD website as a "direct fee-for-services arrangement [that] frees us from the typical contractual agreements that prevent physicians from offering wholesale prices on laboratory tests, imaging, and medications."

The practice quickly grew to about 600 patients in the first couple of years, with a monthly revenue of $30,000 in membership fees. The only marketing has been word of mouth.

They said patients loved the open access to their physicians. Patients are encouraged to email, call, or text their doctors with questions. The office has no office staff, and the physicians answer the phones, which they said "freaks out" patients at times.

Nunamaker and Umbehr said they loved not having to deal with insurance payers for such issues as prior authorizations or rejected claims.

The practice has added three physicians along with one full-time nurse and one part-time nurse. They said they now count 1,300 patients in their practice for $65,000 in monthly revenue from membership fees.

The practice of direct primary care is growing, but the web of providers is so fragmented that even those in the field don't know how many physicians or practices work in this way, said Sharon George, MD, who owns a one-physician direct primary care practice in Irvine, Calif.

"It's definitely growing," she added. "You don't have to leave medicine if you're frustrated. You have your medical degree."

The Direct Primary Care Coalition formed as Congress was debating the Affordable Care Act (ACA). At that time, the coalition estimated there were between 30 and 50 practices in the U.S., with around 100,000 patients.

But Erika Bliss, MD, told MedPage Today that it's likely there are more concierge doctors -- and patients who use their services -- practicing today.

Bliss, a leader of the coalition and chief executive of the five-location concierge practice Qliance, based in Seattle, said she receives Google alerts monthly about a new concierge practice or converting practice, and now estimates one direct primary care practice in nearly every state.

"This model allows you to be the kind of doctor you always wanted to be, and allows you to develop lasting, trusting relationships with patients. [You] actually get to help them ... by being able to spend more time with them [with] minimal interference from an outdated and dysfunctional payment system," she told MedPage Today in a phone interview.

The first Direct Primary Care National Summit will take place in October in St. Louis.
"If people are interested, maybe now is the time for an association that would serve to pull together knowledge and experience ... on how to do direct primary care," Bliss said.

In March, the AAFP board of directors issued a position statement in favor of the direct primary care model (DPC), saying it empowers the physician-patient relationship.

"The DPC contract fee structure can enable physicians to spend more time with their patients, both in face-to-face visits, and through telephonic or electronic communications mediums should they choose, since they are not bound by insurance reimbursement restrictions," the statement read. "For these reasons, the DPC model is consistent with the AAFP's advocacy of the [patient-centered medical home] and a blended payment method of paying family medicine practices."

However, one of the common criticisms of direct primary care is that it's an unsustainable model. Given the current shortage of primary care doctors, will there be enough concierge providers to see patients under ACA coverage expansion?

Direct primary care can help keep family doctors from retiring or moving to hospitalists jobs, Umbehr said, adding that it also offers a more rewarding lifestyle to encourage students to go into family medicine.

Umbehr pointed out that "the current model is the cause of the physician shortage. To blame direct primary care is [to blame] the victim of a crime. The only way we're going to prevent the physician shortage is by making it fun to be a doctor, reward physicians, and make their work rewarding."
As for how patients access specialty services in the concierge system, Umbehr added that concierge doctors can work directly with specialists in their area, helping patients obtain services.

For example, his practice is able to negotiate $900 colonoscopies and $225 head CT scans for their patients when appropriate.

George said that many of her patients have insurance coverage, either through Medicare or privately, that gives them access to a specialist when needed.

Umbehr said he has seen patient habits change when they are billed directly for services; they may not always opt for the most expensive medicine or test.

"When you put the choices in front of the patient, you'll see the decisions change because it's their money," he said.

This Cancer Survivor's Experience with "Affordable Care"

I had a private plan. I paid a lot of money for it. But as a person who has had breast cancer twice, I am grateful I had the coverage.

I received a letter a while back that my carrier was canceling my policy due to the "Affordable Care Act." I was told to go to the New York Health Care Exchange.

I have.

I am not eligible for coverage.
If I can find a new individual plan, the exchange informed me I will be paying twice what I was paying and it will not be for the same coverage I was protected by. What's more, my doctors, the very team that is responsible for saving my life, may not be on the plans I will be permitted to enroll in.

So for everyone out there who thinks that the "Affordable Health Care Act" is good for you: think again. It may be good for a young person with no medical problems who did not have insurance. Although according the Wall Street Journal, it will be very expensive for some, depending on where they live. Read the comprehensive report  at this link:

Ask a metastatic breast cancer patient who is on Medicare who has now lost her oncologist because of the "Affordable Health Care Act."

Ask the person who is now being denied life-saving/prolonging chemotherapy because of the "Affordable Health Care Act."

Ask the physician who is scrambling to find a way to treat patients the way they should be treated.

I am not political. I am not a right wing extremist. I am not anything but a person who has a health history a mile long and who has now lost  her health insurance and doctors due to the "Affordable Health Care Act."

Yes. Today is historic. Today is the day that patient centered medical care died. 

Closing the government is not the answer. Fixing the government is.

Monday, September 30, 2013

October. Again.

This one is for my sisters. We know better than anyone what it feels like to be told we have breast cancer. We know the cold, dark fear those words bring us. We know the panic when we look up our stats on scary websites. We know how much the surgery hurts and how much chemo truly does suck. We know what it is like to lose our hair, our lashes, our nails, our breasts, our fertility, and our way of life.

There is not much an outsider can do but be a friend to us. What does that mean? Give us a lift to the hospital when we have to have yet another surgery. Bring us something to eat when we are too weak to cook for ourselves. Call us up and talk about anything but cancer. Treat us like we are still human, still women, and still the same strong, intelligent people we were a month ago.

Things that give us hope are evidence-based information about our disease and ways to fight it. Give us grown up information for the adults we are. Do not suddenly treat us like children.

What not to give a woman with breast cancer:   A pink bear. A pink ribbon in any form. A pink tee shirt to remind everyone that, A. We may not be looking too great in a tee shirt at the moment and B. Why in hell would we want to advertise our illness? And the most important thing?  Who profited from that bear, ribbon, and tee shirt and all the other insidious pink crap that has suddenly defined every woman with a serious, adult, no bull-shit disease called cancer? Why are women with this particular affliction suddenly reduced to simpering, pink washed nitwits?

If you have money to spend on making some large corporation with a pink marketing plan rich, keep it. If you want to help us send your money to a true research organization that is actively working on finding a way to help us.  Or you could send a donation to an organization that helps women get through their cancer.  For the former, I recommend The Cold Spring Harbor Laboratory. For the latter, I naturally recommend the No Surrender Breast Cancer Foundation. But there are many, many places that your money can go to that are not hijacking a serious illness to make money off of women suffering.

Tomorrow is the beginning of Pink Hell Month. Don't get sucked into buying that pink salad spinner. THINK. DON'T PINK.

On behalf of all of us locked in pink jail, thank you in advance.

Friday, September 6, 2013

We Will Prevail

This post is for every woman who has just been diagnosed with triple negative breast cancer.

I was told that I had this type of breast cancer twelve years ago. Twelve years ago they did not know much about it except that it was bad, it had a poor survival rate and there was nothing I could do after the chemo and radiation was over. They didn't even call it "triple negative" back then. It was called "estrogen and progesterone negative breast cancer."

Twelve years ago they also told me that I wouldn't be here to write about it today.

This post is for those of you who feel that there is no hope because not only do you have breast cancer, you have the "bad" one.

Keep strong. Do what your doctors tell you to do. TNBC responds well to chemotherapy. Think of it as your ally not your enemy. When you are done with your chemo and radiation and surgeries, take care of yourself. Exercise. Eat a low fat diet. Make sure your vitamin D blood levels are at the optimal range. Stop eating so much red meat and start eating a whole foods diet based on fruits and vegetables. Stop eating processed foods and switch to whole grains. Add ground flax seeds to your diet. And then live your life looking forward, not back. And do not, under any circumstances, look at outdated stats that say you are not going to make it.

You will get through this.

Twelve years ago all I wanted was to speak to someone who had been through it all and was on the other side of it. I'm here for you right now. I am not alone. There are lots of us many years out of our TNBC diagnosis.

"May our strength give you strength
May our faith give you faith
May our hope give you hope
May our love give you love"

                                                      Into the Fire, Bruce Springsteen

Wednesday, August 7, 2013

Please Don't Take Away My Healthcare

Today it happened. I have been dreading this day. I was informed by my health insurance carrier that they will be dropping me as of January 1, 2014. The health insurance company that helped me pay for two bouts with breast cancer including surgeries too numerous to count; two separate rounds of chemotherapy, the first in 2001-2002 and the second in 2007-2008; almost 100 radiation treatments; and the medication that is helping to keep me alive today.

When I called my insurance carrier to ask what I could do to protect myself, I was told they simply do not know. They don't know if I can purchase a back up plan that will cover costly treatments not covered by the government. They don't know what will be available. They don't know how much it will cost me. They just don't know. It is not their fault, they are waiting on word from the federal government to tell them what to do.

I have friends who are on the federal plans of medicare and medicaid and they are already being refused the chemotherapy that will help them survive their disease. My health insurance carrier told me that I may be refused treatments based on an algorithm that decides on who should live and who should die. We are facing elderly people who will be denied treatments if their life expectancy is low. If you are a person with advanced disease, you will be denied treatment so you die sooner because your life expectancy does not warrant approval for life-extending medicine.

This information came from an insurance carrier not some pundit.

The Affordable Health Care Act: What is affordable? If you are forced to take the government plan, at what price? At what cost? Who lives and who dies? Who gets treatment and who is denied? If you try to pay for chemotherapy yourself, how do you find the money? Chemotherapy runs in the hundreds of thousands of dollars. And then there are the doctors. They cannot afford to stay in practice nor are they allowed to prescribe medicine to patients who don't fit into the algorithm. With so much cutting back, what happens to the research that can be done to help us fight disease?

The worst part is, no one knows what will happen. Not the insurance carriers and not the legislators. I could not be told how much it would cost me to supplement the Affordable Health Care plan to make sure I can get the treatment I need. They weren't even sure I would be permitted to. There was some mention of being able to shop for insurance, but I can do that now and I found a plan that has cost me quite a bit of money, but has also saved my life.

This is not a political post. This is a panicked one. One written by someone who has had cancer twice and is alive because of surgeries, nine different chemotherapy drugs, multiple radiation treatments and the grace of God. Being denied my healthcare coverage, coverage I paid dearly for, leaves me only with God's grace to protect me.

My faith is strong. It got me through my illnesses and helped me stay brave when I was watching the chemotherapy drugs run from the IV into my bloodstream. I knew it was toxic, but I knew it was the only chance I had to fight my cancers.  Now a governing body that thinks it is bigger than God has decided to take it away from me.

If you work for a company then you should be grateful because you are somewhat protected. If you are a single payer, then you will be getting the letter I did and you will understand this post. If you are a physician, I don't know how you will do your life's work the way you had set out to do it. How will you be able to help your patients when you are told it is against the law to do so?

Before you can become a doctor you must take the oath:
"First, do no harm."
Politicians don't take that oath. Never has that been more evident than now.

Saturday, July 13, 2013

A Possible Cure May Have Been Found.

For those of us who have been touched by cancer- we have it, we've had it, it came back, we are trying to live with advanced disease, or we love someone with it... this tiny lab in the UK has been working for the past 20 years on this treatment, and now it looks like it may work. We've prayed for this day, let us continue to pray the rest of the studies and clinical trials continue to prove that we may finally have victory over the beast.

Exclusive: Cancer - A cure just got closer thanks to a tiny British company - and the result could change lives of millions

The UK Independent
by Steve Connor, Sunday, 14 July 2013

A revolution is brewing on an English business park as scientists harness our natural-born killers – the T cells – to target malign tumours  

A single-storey workshop on a nondescript business park in Oxfordshire is not the sort of place where you would expect scientific revolutions to take place. But behind the white-painted walls of this small start-up company, scientists are talking about the impossible – a potential cure for cancer.
For the past 20 years, the former academics who set up Immunocore have worked hard on realising their dream of developing a totally new approach to cancer treatment, and finally it looks as if their endeavours are beginning to pay off. In the past three weeks, the company has signed contracts with two of the biggest players in the pharmaceuticals industry which could lead to hundreds of millions of pounds flowing into the firm's unique research on cancer immunotherapy – using the body's own immune system to fight tumour cells.

Immunocore is probably the only company in the world that has developed a way of harnessing the power of the immune system's natural-born killer cells: the T-cells of the blood which nature has designed over millions of years of evolution to seek out and kill invading pathogens, such as viruses and bacteria. T-cells are not nearly as good at finding and killing cancer cells, but the hard-nosed executives of the drugs industry – who are notoriously cautious when it comes to investments – believe Immunocore may have found a way around this so that cancer patients in future are able to fend off their disease with their own immune defences.

"Immunotherapy is radically different," said Bent Jakobsen, the Danish-born chief scientific officer of Immunocore who started to study T-cells 20 years ago while working at the Medical Research Council's Laboratory of Molecular Biology in Cambridge.

"It doesn't do away with the other cancer treatments by any means, but it adds something to the arsenal that has one unique feature – it may have the potency to actually cure cancer," Dr Jakobsen said.

It is this potency that has attracted the attention of Genentech in California, owned by the Swiss giant Roche, and Britain's GlaxoSmithKline. Both companies have independently signed deals with Immunocore that could result in up to half a billion pounds being invested in new cancer treatments based on its unique T-cell therapy.

It is no understatement to say that cancer immunotherapy, or immuno-oncology as it is technically called, represents a sea change in terms of cancer treatment. Cancer in the past has been largely treated by slicing (surgery), poisoning (chemotherapy) or burning (radiotherapy). All are burdened with the inherent problem of how to spare healthy tissue from irreparable damage while ensuring that every cancer cell is killed, deactivated or removed.

Now there is another approach based on the immune system, a complex web of cells, tissues and organs that constantly strive to keep the body free of disease, which almost certainly includes keeping cancerous cells in check.

For many years, scientists have realised that the immune system plays a key role in cancer prevention. There is ample evidence of this, not least from patients who are immune-suppressed in some way – they are more likely than other patients to develop cancer.

The immune system has two basic ways of fighting invading pathogens and the body's own cells that have gone awry. One involves the release of free-floating proteins, or antibodies, that lock on to an invader, triggering other immune cells to come in and sweep them away.

Many organisations have tried to develop anti-cancer treatments based on antibodies, with limited success, Dr Jakobsen said. Part of the problem is that antibodies are not really designed to recognise cells. What Immunocore has done is to build a therapy around the second arm of the immune system, known as cellular immunity, where T-cells seek out and destroy invading pathogens.

"There are a lot of companies working with antibodies but we are virtually the only company in the world that has managed to work with T-cells. It has taken 20 years and from that point we are unique," Dr Jakobsen said.

Immunocore has found a way of designing small protein molecules, which it calls ImmTACs, that effectively act as double-ended glue. At one end they stick to cancer cells, strongly and very specifically, leaving healthy cells untouched. At the other end they stick to T-cells.

The technology is based on the "T-cell receptor", the protein that sticks out of the surface of the T-cell and binds to its enemy target. Immunocore's ImmTACs are effectively independent T-cell receptors that are "bispecific", meaning they bind strongly to cancer cells at one end, and T-cells at the other – so introducing cancer cells to their nemesis.

"What we can do is to use that scaffold of the T-cell receptor to make something that is very good at recognising cancer even if it doesn't exist naturally," said Dr Jakobsen. "Although T-cells are not very keen at recognising cancer, we can force them to do so. The potential you have if you can engineer T-cell receptors is quite enormous. You can find any type of cell and any kind of target. This means the approach can in theory be used against any cancer, whether it is tumours of the prostate, breast, liver or the pancreas.

The key to the success of the technique is being able to distinguish between a cancer cell and a normal, healthy cell. Immunocore's drug does this by recognising small proteins or peptides that stick out from the surface membrane of cancer cells. All cells extrude peptides on their membranes and these peptides act like a shop window, telling scientists what is going on within the cell, and whether it is cancerous or not.

"All these little peptides tell you the story of the cell. The forest of them on the cell surface is a sort of display saying 'I am this kind of cell. This is my identity and this is everything going on inside me'," Dr Jakobsen explained.

Immunocore is building up a database of peptide targets on cancer cells in order to design T-cell receptors that can target them, leaving healthy cells alone and so minimising possible side effects – or that is the hope.

The first phase clinical trial of the company's therapy, carried out on a small number of patients in Britain and the United States with advanced melanoma, has shown that people can tolerate the drug reasonably well and preliminary results suggest there are "early signs of anti-tumour activity", the company said.

A danger with deploying T-cells against cancer is their potency. Yet it is this very potency that it is so exciting because it could lead to a cure for metastatic disease that has spread around the body, Dr Jakobsen said. "You can never make a single-mechanism drug that would come anywhere near a T-cell in terms of its potency.

"If you want to make an impact on cancer you need something that is incredibly potent – but when something goes wrong, it goes badly wrong. I think the honest truth about all cancer treatments is that no matter how much we test and do beforehand, it will continue to go wrong sometimes."

One infamous case of something going disastrously wrong was a clinical trial in 2006 at Northwick Park Hospital in London where scientists were testing a powerful immuno-regulatory drug on six volunteers. All suffered serious side effects caused by the overstimulation of their immune systems.
But Dr Jakobsen said the clinical trial of Immunocore's T-cell drug, as well as future trials, are inherently safe because they are based on incremental rises in dose. All indications suggest it will lead to the expected breakthrough.

He added: "All the pharma companies have come to the realisation that immunotherapy may hold the ultimate key to cancer; it is the missing link in cancer treatment that can give cures. They have seen this technology develop. It has come over the mountain top, if you like. With our melanoma trial they have seen it is safe – and it is working."

T-cell therapy
Using the body's immune system to fight cancer is one of the most promising areas of therapy, and could prove particularly helpful in the treatment of metastatic disease, when the cancer has spread from its original site.

The immune system is complex and is composed of many kinds of cells, proteins and chemical messengers that modulate how it works. Scientists are working on ways of exploiting the immune defences to recognise and eliminate cells that have become cancerous.

One of the most interesting examples is ipilimumab, a "monoclonal antibody" made by Bristol-Myers-Squib. It recognises and binds to a molecule, called CTLA-4, which is found on the T-cells of the immune system. CTLA-4 normally keeps T-cells from proliferating, but in the presence of ipilimumab, it becomes blocked, allowing T-cells to increase in numbers, so leading them to attack cancer cells.

Other drugs based on monoclonal antibodies are designed to attack tumours more directly. When they bind to a cancerous cell, it serves as a signal for other cells of the immune system to come in and sweep the cancer cells away.

The trouble is that cancer cells are notoriously mutational. Eliminating 99.9 per cent of cancer cells in a patient may be an improvement, but it still leaves 0.1 per cent that could "escape".

One hope of using T-cells, is that this possibility of escape is narrowed down, or even eliminated. Of course, these are still early days. This is only just beginning to go through the first clinical trials. It could take five or 10 years before we know whether or not they work.

Monday, May 13, 2013

Our Lee

It happens with so many things we come across in our lives. We live in many places, but there is that special one that holds a warm place in our heart. It may not have been big and fancy, but we loved it for what it was. It happens with our pets. We all adore our furry friends, but there is that one little guy who you will always feel the closest to. Sometimes, it even happens with our friends. We all have different kinds of friends. There are the old friends we've known forever, who know all of our secrets, and even though we may not see them for ages we can pick up our last conversation right where we last left off.  When meet new friends they are interesting and the "newness" of them is exciting.  We feel blessed to have all of our friends in our lives.  And, sometimes, if we are very lucky, we have a friend in our life like Lee.

Lee was beautiful. That word is not even adequate. She was stunning. Lee was funny and had a very quick sense of humor. Lee was a mom who devoted her life to her amazing girls. Lee was a wife and friend to her loving husband. Lee could drive one girl to a sporting event, take the other to a music lesson, run home and put a healthful, delicious dinner in the oven, get out her trusted Dyson and vacuum like no one's business and be finished in time to pick up each girl and greet her husband with a wonderful family dinner in a sparkling house as he returned home from a long business trip.

Lee was my friend. She was a true friend to so many. Her friendships spanned in person friends and also included an vast array of women she met on our online support forum for women with breast cancer. Lee also had breast cancer -  a terribly aggressive form of the disease that she did everything in her power to fight. And she had quite a fight these last few months. The cancer was relentless but Lee fought every curve ball it could throw at her. On Mother's Day, Lee left this earth. Just a few days ago she was picking out her daughter's prom dresses. Now she is gone. In the wake of her loss are countless women who loved her deeply because Lee was one of those very special people who touch you in a way that is so rare. She is irreplaceable and unforgettable.

This has been a kick in the stomach to all of us. It feels like someone took the sun away.  She warmed us with her friendship and her cheerfulness. She just made us feel better simply by being present in our lives.

But the cold we are feeling right now won't last long because Lee won't let it. In fact, with Lee watching over us from above, the sun will shine a little brighter, the stars will become clearer in the night sky, and the breezes will be softer. She will find ways for us to smile at the smallest of things. You'll see. Look for the extraordinary and beautiful around you, when you see something truly heartwarming, you'll know that Lee put it there for you.

I will miss our Lee terribly. I will try to do everything to continue her legacy of love and friendship.

Lee, I love you my sweet sister. Rest well you dear, sweet, gentle soul.

Thursday, March 14, 2013



Young women are presenting with breast cancer that has already advanced. Would that be happening if they were screened younger and able to treat their cancers earlier? At The No Surrender Breast Cancer Foundation, we believe that young women need to be screened before the age of forty utilizing all techniques, including ultrasound and breast MRI. Tumors must be found small, before they have spread. While there are no guarantees that finding a tumor early will prevent it from spreading, the greatest chance a woman has to fight it from spreading is treating it while it is still localized.

Our Before Forty Initiative is educating young women to become aware of their risks and to be armed with the knowledge they need to demand early screening. We will continue to fight until the "Guidelines" that prevent young women from obtaining life saving screening are changed.

Metastatic Breast Cancer Incidence is Rising 

Among Young Women

IMNG Medical Media, 2013 Feb 26, MA Moon

The incidence of breast cancer presenting with distant involvement has risen significantly over the past 30 years among young women, and this trend shows no signs of abating, according to a report in the Feb. 27 issue of JAMA.

In contrast, the rate of locoregional breast cancer has not increased in this age group, and the incidence of all stages of the disease have not shown any increasing trends among older women, said Dr. Rebecca H. Johnson of Seattle Children’s Hospital and the University of Washington, Seattle, and her associates.

This trajectory “predicts that an increasing number of young women in the United States will present with metastatic breast cancer in an age group that already has the worst prognosis, no recommended routine screening practice, the least health insurance, and the most potential years of life” lost, the investigators noted.

They used data from three of the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) registries to examine time trends in breast cancer between 1976 and 2009. They found a steady, and possibly accelerating, rise in the rate of women aged 25-39 years presenting with metastatic breast cancer, from 1.53/100,000 in 1976 to 2.90/100,000 in 2009.

“No other age group had statistically significant increases, either for distant, regional, or localized disease at diagnosis,” Dr. Johnson and her colleagues said (JAMA 2013;309:800-5).
In a different analysis of the data, the category of metastatic breast cancer as a proportion of all invasive breast cancer in this age group rose from 4.4% in the 1970s to 4.8% in the 1980s, 5.5% in the 1990s, and 7.2% in the early 2000s.

This trend was evident in women of all races/ethnicities, in women residing in both urban and nonurban regions, and in women with estrogen receptor–positive and estrogen receptor–negative tumors. “Non-Hispanic white and African-American individuals appear to have been more affected by the increase, as have women with the ER-positive subtype of the disease,” they said.
“The absolute increase of 1.37/100,000 over 34 years is relatively small, but the trend shows no evidence of abatement and may indicate increasing epidemiologic and clinical significance,” the researchers said.

These findings must be corroborated in other studies. If they are confirmed, they will be particularly concerning “because young age itself is an independent adverse prognostic factor for breast cancer.
“The most recent national 5-year survival data for distant disease for 25- to 39-year-old women is only 31% ... compared with a 5-year survival of 87% for women with locoregional breast cancer,” they added.
Dr. Johnson reported having served on a board for Critical Mass Young Adult Cancer Alliance and having served as a speaker at the Leukemia and Lymphoma Society AYA Survivorship Conference. One of her colleagues reported being a consultant and speaker for Sigma-Tau Pharmaceuticals; another researcher’s salary was funded by the Seattle Children’s Guild Association Teen Cancer Grant. No other disclosures were reported.

Your Heart: After Cancer

Important information about chest radiation and heart disease.

We have warned about this in the past, but a new study confirms earlier ones.

Bottom line: Keep an eye on your cholesterol, it elevates after chemotherapy; exercise at least 5 times a week; keep your weight down. Make sure you have your cholesterol checked when you go to your oncologist (since you probably see that doc more than any other one)


Radiotherapy for breast cancer often involves some incidental exposure of the heart to ionizing radiation. The effect of this exposure on the subsequent risk of ischemic heart disease is uncertain.



We conducted a population-based case–control study of major coronary events (i.e., myocardial infarction, coronary revascularization, or death from ischemic heart disease) in 2168 women who underwent radiotherapy for breast cancer between 1958 and 2001 in Sweden and Denmark; the study included 963 women with major coronary events and 1205 controls. Individual patient information was obtained from hospital records. For each woman, the mean radiation doses to the whole heart and to the left anterior descending coronary artery were estimated from her radiotherapy chart.


The overall average of the mean doses to the whole heart was 4.9 Gy (range, 0.03 to 27.72) Rates of major coronary events increased linearly with the mean dose to the heart by 7.4% per gray (95% confidence interval, 2.9 tp 14.5 with no apparent threshold.

The increase started withing the first 5 years after radiotherapy and continued into the third decade after radiotherapy. The proportional increase in the rate of major coronary events per gray was similar in women with and women without cardiac risk factors at the time of radiotherapy.


Exposure of the heart to ionizing radiation during radiotherapy for breast cancer increases the subsequent rate of ischemic heart disease. The increase is proportional to the mean dose to the heart, begins within a few years after exposure, and continues for at least 20 years. Women with preexisting cardiac risk factors have greater absolute increases in risk from radiotherapy than other women. (Funded by Cancer Research UK and others.)

Supported by funding to the Oxford University Clinical Trial Service Unit from Cancer Research UK, the British Heart Foundation, and the U.K. Medical Research Council and by grants from the European Commission (FI6R-012796), the U.K. Department of Health (RRX 108), the British Heart Foundation Centre for Research Excellence (CRE RE/08/004, to Dr. Cutter), and the Oxford National Institute for Health Research Biomedical Research Centre (to Dr. Rahimi).

Disclosure forms provided by the authors are available with the full text of this article at
No potential conflict of interest relevant to this article was reported.
We thank research nurses Ann-Sofie Andersson and Milka Krestelica in Sweden and Liselotte Jeppesen in Denmark for data abstraction; and Ulrich H. Koehler in Denmark for data management.

Source Information

From the Clinical Trial Service Unit (S.C.D., P.M., D.C., R.P., C.T.) and the George Centre for Healthcare Innovation (K.R.), University of Oxford, Oxford, and the Department of Medical Physics, Royal Surrey County Hospital and Surrey University, Guildford (A.N.) — both in the United Kingdom; the Department of Oncology, Odense University Hospital, Institute of Clinical Research, University of Southern Denmark, Odense (M.E.), the Oncology Department, Aalborg Hospital, Aalborg (D.B.), and the Danish Breast Cancer Cooperative Group, Rigshospitalet, Copenhagen (M.-B.J.) — all in Denmark; the Department of Medical Epidemiology and Biostatistics (A.M.B., P.H.) and the Division of Cardiovascular Epidemiology, Institute of Environmental Medicine and Division of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd Hospital (B.G.), Karolinska Institutet, and the Departments of Oncology (U.B.-G.) and Medical Physics (G.G.), Karolinska University Hospital — all in Stockholm; and the H. Lee Moffitt Cancer Center and Research Institute, University of Southern Florida, Tampa (C.C.).
Address reprint requests to Dr. Darby at the Clinical Trial Service Unit, Richard Doll Bldg., Old Road Campus, Oxford OX3 7LF, United Kingdom, or at .

Friday, March 8, 2013

March 8th, International Women's Day

The No Surrender Breast Cancer Foundation is proud to be a member of International Women's Day, as we salute survivors across the world with our
There & Back: A Celebration of Survival Gala.
Photo's to come.
We Salute YOU!

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!