Is Pakistani Herbal Tea a New Cancer-Fighter?

Folks in rural Pakistan might be on to something.  They have long used extracts from a common herbal tea ingredient, the plant Fagonia cretica, known as virgin's mantle, to treat breast cancer. Now researchers at Aston University, Birmingham, England, and Russells Hall Hospital, Dudley, England, have evidence that this is more than folklore—an extract of the plant might actually work to repair cell damage in cancer cells without affecting healthy cells.  So far, their studies have been confined to laboratory analysis, but they hope to now determine what elements in the plant are the active cancer-fighters, with the hope of eventually beginning clinical trials.

In previous laboratory research, virgin's mantle repaired damage caused by p53 expression, which is associated with triple-negative breast cancer.  

In a news release, Professor Helen Griffith of Aston said,  "More research is needed to establish the role of the extract in cancer management and It now needs to be demonstrated that this extract is as effective in killing cancer cells inside the body as it is within laboratory."

Virgin's mantle is found in arid regions of Pakistan, India, Africa and parts of Europe.

Sharing Good News One Case at a Time

Here's one face of TNBC as I have seen it this week:

A reader wrote that his 36-year-old wife, who had been diagnosed in February with stage 3b TNBC, just got a glowing report from the doctor after a mastectomy and 8 rounds of ACT: Her chances of long-term survival are excellent.  They are meeting with the radiation oncologist soon.

So thanks to Walt for keeping me current and lifting my spirits.    When I first heard from him in late March, they were reeling from the diagnosis, and she was sleeping off the anti-nausea drugs. (I stopped taking them because they did little for nausea and made me feel worse.)

Walt says they modified their diet after her diagnosis.  Here's what he says about their new approach: 

I started juicing for us nightly.  I usually throw in: Kale, carrots, celery, blue berries, ginger, cucumber, and apple.... Also, we've dropped milk from our diet, and switched to decaf coffee and decaf tea.  Otherwise, we were pretty healthy before so not much has changed—oh, less red meat (but that wasn't a lot to start with).

That is similar to my approach, but I do have some milk—always low-fat organic. And I have my blueberries whole in the morning, not as party of my nightly juice.

I love hearing from readers and will start sharing bits of it with all of you who are on the same journey.

More Genetic Research Helping Define TNBC: Oncogene FAM83B

NEWS RELEASE

Newswise — A team of researchers at Case Western Reserve University School of Medicine, led by Dr. Mark W. Jackson, have developed a novel method to identify genes that, when overexpressed, make normal cells behave like cancer cells. Using this method, the Jackson laboratory has identified a new oncogene, which is a gene that contributes to the development of cancer, named FAM83B.

“We made our discovery in a model of breast cancer,” said Mark W. Jackson, Ph.D., Assistant Professor, Department of Pathology, Case Western Reserve University School of Medicine, Case Comprehensive Cancer Center. "Using an unbiased screening approach, we let the biology of cancer formation tell us what genes are important and FAM83B was one of the genes that came out of our screen. When FAM83B was overproduced in normal breast cells, it transformed the normal cells, causing them to behave like breast cancer," stated Jackson.

There are relatively few oncogenes that are critical to breast cancer growth, and only one other breast cancer oncogene has been identified in the last 6 years. Breast cancers are classified clinically into subgroups based on the presence of specific proteins, including estrogen receptor (ER), progesterone receptor (PR), and HER2.

"Analysis of breast cancer revealed that elevated FAM83B expression is associated with the more aggressive, triple negative subgroup which lacks ER, PR and HER2,” said Jackson. “In short, patients with triple-negative breast cancer would benefit most from the development of new therapeutics.”

Novel oncogenes provide opportunities for drug development that may expand the number of therapies available for eradicating cancer and extending the life of patients. "Our discovery provides the foundation for developing new therapies that can inhibit FAM83B in these aggressive cancers, which have traditionally been difficult to treat." We are currently trying to identify drugs that that can inhibit the function of FAM83B." stated Jackson.

This study will appear in The Journal of Clinical Investigationand will be co-published with a discovery from the laboratory of Dr. Mina Bissell at Lawrence Berkley National Laboratories. Dr. Bissell’s laboratory discovered an oncogene called FAM83A. Both FAM83A and FAM83B belong to an eight member family of genes that both laboratories propose may drive tumor formation and therapeutic resistance.

Dr. Jackson is the principal investigator leading a multidisciplinary team with investigators that include: Rocky Cipriano, James Graham, Kristy Miskimen, Benjamin Bryson, Ronald Bruntz, Sarah Scott, H. Alex Brown and George Stark. Additional support for the research came from the Case Comprehensive Cancer Center, the United States National Institutes of Health (R01CA138421 to M.W.J; T32CA059366 to R.C), the Department of Defense Breast Cancer Research Program (M.W.J), the American Cancer Society (RSG-10-072-01-TBG to M.W.J) and the McDonnell Foundation (to H.A.B).

The pharmaceutical company EntreMed has announced a Phase 2 study of ENMD-2076 in triple-negative breast cancer.  

Jennifer R. Diamond, MD, of the University of Colorado, says, 

"We are encouraged by the data from the Phase 1 study of ENMD-2076 in patients with advanced solid tumors, including triple-negative breast cancer. ENMD-2076 has also demonstrated significant anti-tumor activity against preclinical models of breast cancer with more robust activity against triple-negative breast cancer alone or in combination with standard chemotherapies. This single-agent Phase 2 study is designed to determine the activity of ENMD-2076 by the clinical benefit rate in patients with previously treated locally advanced or metastatic triple-negative breast cancer."

For more information, check out the news release.

What We Can Learn From Hospice Patients

NOTE:  The article below is essentially a press release about a new book, and I don't normally share these things until I can read the book.  However, I like what Gourgey has to say about the qualities of dying patients--essentially they demonstrate how we all should live, especially the part about love not being self-interested.  

Does our society hold too narrow a view of what defines strength? 

The things many would point to as indicators – youth, wealth, a fully capable body – fall short, says Charles Gourgey, a veteran hospice music therapist and author of Judeochristianity: The Meaning and Discovery of Faith (www.judeochristianity.org), a book that explores the unifying faith elements of Judaism and Christianity. 

“Youth is ephemeral, abundant wealth is for just a few, and we all experience some kind of disability, usually at several points in our lives,” he says. “A car accident, the loss of a job or a home, grief over a loved one’s dying: such things can happen to anyone and easily destroy our happiness.” 

Gourgey says some of the greatest strength he’s ever seen was demonstrated by certain of his patients facing imminent death. 

“Some people have complete love and grace when facing death – it’s how they’ve lived their lives, and at the end of their lives, it’s what supports them,” he says. “Those who, at the end, are peaceful, grateful and confident share some common characteristics.” 

They are: 

• Their love is non-self-interested. When we have awareness of and deepest respect and reverence for the individuality of others, we overcome the high walls of ego and experience a tremendous sense of freedom, says Gourgey. He says he continues to be inspired by patients who cared more for the well-being of others, including their fellow hospice patients, than themselves while facing their own mortality. Non-self-interested love – loving others for themselves without expecting or needing anything in return – is the greatest form of love, he says. 

• They had an unwavering faith that transcended religious dogma. Faith is the knowledge that there is more to life than the apparent randomness of the material world; a sense that we are known to a greater reality and will return to that reality. No matter what their religion, the patients who were most at peace with their life’s journey were those who had faith in something higher than themselves. The problem with many concepts of faith, Gourgey continues, is that people attach specific doctrines to it, which means some people will always be excluded. A unifying faith – that all people are connected and love is the force that binds us – allows for trust, compassion and caring. 

• They were motivated by an innate sense of what is good. They didn’t get mad at themselves; they didn’t beat themselves up for mistakes they might have made in the past. That’s because they were always guided by their sense of what is good, and they made their choices with that in mind. That did not prevent them from making some bad choices or mistakes over the course of their lives, Gourgey says. But when they erred, they addressed the problem with the same loving compassion they extended to others. “Their compassion overcame even any self-hate they may have experienced.”

Many patients left lasting impressions on Gourgey, and taught him valuable life lessons. He remembers one in particular. 

“She was in hospice, a retired nurse who had developed a rare, incurable disease,” he recalls. “She would go around every day, checking to see what she could do for the other patients. She fetched blankets for a 104-year-old lady who always complained of cold feet. She sat with and listened to patients who needed company and someone to talk to. She had an attentive awareness about her, like she was fully in touch with her soul.” 

Gourgey was with the woman when she died. 

“She was radiant, she just glowed. She kept repeating how grateful she was for her life,” he says. “It was as if the life of love she’d lived was there to transport and support her at the end.” 

About Charles “Carlos” GourgeyCharles “Carlos” Gourgey, PhD, LCAT, MT-BC, is a board-certified and New York state-licensed music therapist. He has more than 20 years of experience working in hospices and nursing homes, and for 10 years was music therapist for Cabrini Hospice in New York City. He has published articles on psychology and religion in various journals.

Botanical Formula Shows Promise in Fighting Metastatic TNBC

A botanical formula that includes medicinal mushroom, flavonoids, botanicals, and extracts of cruciferous vegetables may be effective against triple-negative metastases, according to a study published in the  journal Oncology Reports.

The study was conducted at the Cancer Research Laboratory, Methodist Research Institute, Indiana University Health. It was presented at the annual meeting of the American Academy for Cancer Research.  Its publication in Oncology Reports marks the third peer-reviewed study demonstrating the anticancer effects of the formula.

Researchers implanted triple-negative human breast cancer cells in the breast tissue of mice.  The tested group was given the formula orally for four weeks; the control group received no treatment.  

According to a news release from Indiana University Health:

The cancer metastasized to the lungs in only 20 percent of the treated group as compared to 70% of the untreated, control group. Furthermore, in the treatment group that did metastasize, the number and size of the lesions was dramatically reduced in comparison to the control group. 

Gene analysis showed that the formula down regulated (suppressed and reduced) two genes implicated in cancer metastasis -- PLAU (urokinase plasminogen activator, uPA) and CXCR4 (C-X-C chemokine receptor-4). These results further substantiate previous cancer cell studies published on this formula, which similarly demonstrated a down regulation of these cancer promoting genes. 

The  formula includes ingredients that have been shown in previous research to have anti-cancer properties:

• Medicinal mushrooms Trametes versicolor, Ganoderma lucidum, Phellinus linteus reduce cancer growth and invasiveness.• Extracts from the botanicals Scutellaria barbata, Astragalus membranaceus and Curcuma longa induce programmed cell death (apoptosis) and reduce cancer metastasis.•The flavonoid, quercetin, reduces cancer cell proliferation and helps suppress tumor growth.• DIM (3, 3'-Diindolylmethane), an active component of cruciferous vegetables, reduces cancer growth, migration and invasiveness.

      Source: Jiang J, Thyagarajan-Sahu A, Loganathan J, Eliaz I, Terry C, Sandusky GE, Sliva D. BreastDefend prevents breast-to-lung cancer metastases in an orthotopic animal model of triple-negative human breast cancer. Oncol Rep. 2012 Jul 26. doi: 10.3892/or.2012.1936.

Protein Kinase Thwarts TNBC Cell Migration and Invasion

NEWS RELEASE

ScienceDaily (Aug. 1, 2012) — By identifying a key protein that tells certain breast cancer cells when and how to move, researchers at Michigan State University hope to better understand the process by which breast cancer spreads, or metastasizes.
When breast cancer metastasizes, cancer cells break away from a primary tumor and move to other organs in the body, including the lungs, liver and brain. In work published recently in the journal Cancer Research, MSU researchers Kathy Gallo and Jian Chen show a protein called MLK3 (mixed lineage kinase 3) is a critical driver of breast cancer cell migration and invasion.More importantly, Chen and Gallo showed that in triple-negative breast tumor cells, which are more aggressive and for which targeted therapies are needed, it is possible to thwart that cell migration and invasion."While the classical approach to cancer drugs has been to find drugs that kill tumor cells, there recently also is an interest in finding drugs that interrupt metastasis," said Gallo, a professor in MSU's Department of Physiology. "The hope is that such drugs in combination with conventional therapies may lead to better outcomes in patients."As part of their study, Gallo and Chen, a biochemistry graduate student, also found that eliminating MLK3 prevented tumors in animals from metastasizing to the lungs, providing the foundation for future research on targeting MLK3 pathways as an approach to preventing the spread of cancer.The researchers identified how key cellular proteins were instructed by the MLK3 protein -- through the addition of molecular tags called phosphates -- to interact with one another, leading cancer cells to move. Specifically, MLK3 promotes the addition of phosphates to another protein called paxillin, which is known to control how cells move.Gallo and Chen then stopped cell movement in breast cancer models by eliminating MLK3 altogether or using a drug called CEP-1347 to block MLK3's ability to add phosphates to other proteins. The experimental results indicate that when certain cancer cells lose MLK3, the ability to add phosphates is impaired, eventually crippling the cell migration machinery and diminishing cell movement."Our research suggests that the intracellular pathways involving MLK3 that control cell movement could provide new targets for the treatment of patients with metastatic cancer," Chen said. "Drugs developed for combating the MLK3 activity may be useful in reducing the spread of breast cancer."Gallo added that MLK3 is a protein kinase, and these types of proteins have proven to be good drug targets in cancers and other diseases."While drugs such as chemotherapy kill all cells, research has shown drugs that inhibit kinases often can be effective with fewer side effects," she said.The next step for the researchers is to test whether an MLK3 inhibitor can prevent cancer from metastasizing in animal models."Cancer is a very complex collection of diseases, but we believe that certain types of cancers may be sensitive to MLK inhibitors," Gallo said, "and targeting MLK3 may provide a very useful weapon in the fight against cancer."The team's research was supported by grants from the Department of Defense's Breast Cancer Research Program and the Elsa U. Pardee Foundation. The MLK inhibitor, CEP-1347, was provided by Cephalon Inc., a wholly owned, indirect subsidiary of Teva Pharmaceuticals Industries Ltd.

Drug Combo May Stop TNBC Growth

From Medical Daily

Two drugs approved by the Food and Drug Administration for blood cancer treatment may also be used to treat triple negative breast and kidney cancer. researchers say.

The drugs are romidepsin and decitabine. Together they can activate a gene sFRP1 (secreted frizzled related protein one) that can stop the growth of cancer cells. 

"We now have the basis for a clinical trial aimed at providing effective therapy for two drug-resistant cancers and perhaps many more tumor types in the future," said Dr. John Copland, biologist from Mayo Clinic. The trials were conducted on cell lines of cancers where the combination of drugs was effective in halting the cell growth. 

"Individually, each drug did not induce any form of cell death but, together, they killed all of the different cell lines of kidney and triple negative breast cancer that we tested in the laboratory," said Simon Cooper, a Mayo Clinic molecular biologist who specializes in renal cancer and lead author of the study. 

Nearly, 80,000 people are affected each year by these two types of cancers in the United States.

It was observed that certain types of cancer suppress the gene sFRP1. Activation of this gene by the drugs can stop the growth of cancer cells. Even cancers that affect colon, ovary and lungs grow by suppressing this gene.
Researchers say that this gene could act as a biomarker to test the effectiveness of the combination drug therapy on certain kinds of cancers. 

"But now, not only do we have a very promising lead on future therapy, but if this combination treatment works as we hope it does, we will have a biomarker to be able to test which patients might benefit the most. In other words, a biopsy test could identify patients whose tumors had lost sFRP1 function," said Edith Perez, MD, deputy director of Mayo Clinic Cancer Center and co-author of the study. The combination therapy can help fight cancers that have become resistant to other drugs and as these drugs are clinically approved the human trial phase would be faster.

 "This type of interdisciplinary preclinical research effort is important, not only because of the value of the science, but also because the drugs are already in the clinic and that will facilitate translational efforts and hopefully confirm the preclinical findings in patients with advanced malignancies," said Michael Menefee, MD, an oncologist and co-author of the study.  

The study was published in Molecular Cancer Therapeutics. 

Tumor Suppressor Gene Linked to Improved Response to Chemo in TNBC and Other Breast Cancer Patients

NEWS RELEASE

PHILADELPHIA—Breast cancer patients whose tumors lacked the retinoblastoma tumor suppressor gene (RB) had an improved pathological response to neoadjuvant chemotherapy, researchers atThomas Jefferson University Hospital and the Kimmel Cancer Center at Jefferson report in a retrospective study published in a recent online issue of Clinical Cancer Research.

Many breast cancer patients undergo neoadjuvant therapy to reduce the size or extent of the cancer before surgical intervention. Complete response of the tumor to such treatment signifies an improved overall prognosis. Today, no marker is applied to identify tumors which will respond to such treatment, and as a result, only a subset of patients exhibit benefit from it.

"We found that loss of RB was associated with better pathological response rates in breast cancer patients—at various stages and representing multiple molecular subtypes—who were administered neoadjuvant chemotherapy," said Agnieszka Witkiewicz, M.D., Associate Professor of Pathology, Anatomy and Cell Biology at Thomas Jefferson University.

Erik Knudsen, Ph.D, Professor of Cancer Biology and the Hilary Koprowski Chair in Cancer Biology, was excited that discoveries from his life-long research on the RB-pathway were making their way into the clinic.

"This represents a potential new biomarker that could be used to tailor treatment plans for women considering neoadjuvant therapy and is a testament to the importance of cancer research," he said.

For the study, researchers, including Gordon Schwartz, M.D., Director of the Jefferson Breast Care Center and Adam Ertel, Ph.D., Bioinformatics Specialist, Department of Cancer Biology, performed a combination of gene expression profiling to identify those with RB loss and direct histological analysis in over 1,000 breast cancer patients who had undergone neoadjuvant therapy. These patients represented distinct subtypes of breast cancer and were treated with multiple different therapeutic regimens.

RB loss was associated, the team found, with an improved response to all the neoadjuvant regimens investigated in the major subtypes of breast cancer.

"Together, these data indicate that the loss of RB, which occurs relatively frequently in locally advanced disease, could be a useful tool for defining patients who experience an improved response to neoadjuvant chemotherapy," said Dr. Witkiewicz. "Based on these findings, we have initiated a prospective clinical trial at Jefferson, evaluating the association of RB and another marker, PTEN, with the response to neoadjuvant chemotherapy."

###

The clinical trial is open to patients who have a diagnosis of triple negative breast cancer and are eligible for neoadjuvant chemotherapy. (clinicaltrials.gov/ct2/show/NCT01514565).

Seeing the Trees in The Forest, And Where We Fit In

A little evergreen tree has died alongside our road and, as we walked by it yesterday, my husband wondered why.  All the other trees around it are healthy and it did not look like it had been hit by lightning or damaged by wind or attacked by bugs.

The tree is about eight feet tall, so it lived several years.  We are in the Rocky Mountains and this little guy took root on its own, taking seed and growing in that place by the road.

The trees all around it are scrub oak, so maybe the soil was not right for an evergreen.  Maybe it just grew in the wrong place, in soil that could not sustain it.  Still, there are evergreens nearby that soar to the sky, so maybe this little tree was just too weak to begin with.

Could we have done something to save it?  If we were in the city, would we have babied it and maybe kept it alive?  Or would it have died sooner there?

These are the same questions we ponder about why some people get sick, why one disease affects one person more than others, why people who live healthy lives still can’t beat some illnesses, yet people with deplorable habits keep going and going.

It’s the old nature versus nurture argument.  Bad genes or bad environment?  Or both?

I am sort of over being angry at people who have dodged major illnesses—largely because, frankly, there aren’t that many of them.  Seems like most people I know have something to contend with—debilitating arthritis, diabetes, heart disease, Alzheimer’s.  But when I first got cancer I did look around at people who obviously were not living as healthy as I was and wondered, Why me and not them? And then I realized that I had no idea what they were dealing with and I should just stop being so angry and judgmental and get over myself.  It was not their fault I got sick.

Still, you have to wonder about this poker game we all play with our health.  Some seem to be dealt a good hand to begin with, some make the best of a poor hand, some try but can’t make a straight out of a pair of twos, and some look at their cards and just fold. 

I have one friend who never exercises and has a diet full of fat, yet she is in her mid-80s, hale, hearty, and youthful-looking.  Another smoked all his life, drank, and never exercised, yet he is pushing 80 and has nothing seriously wrong physically, although I do think he looks back at his life with serious regret.  Still, the big C didn’t get him, nor did any major illness.  I wouldn’t swap places with him, though, even if I knew my cancer would return.

I also know a wide variety of cancer patients—fighters who refuse to let the disease get the upper hand, questioners who search for their own information rather than listening to the docs, accommodators who go along with whatever the doctor says, worriers who can’t get beyond the fact that they might die.  Most of us are a mix of these traits, fighting one day, living in worry the next.  But we are all built differently, both physically and mentally, so we all react to our disease differently.  Nobody is right, nobody is wrong.  We’re all just us, being our own little trees fighting our own little battles.

We cannot escape our genes—they make us prone to certain diseases, give us the strength to fight others, and offer a blueprint for either a long or a short life.  Still, we can change some of that—the science of epigenetics demonstrates that lifestyle and environmental factors can influence our genetic makeup so that, by improving things such as diet and physical activity and by avoiding unhealthy environmental pollutants including stress, bad air, and chemicals, we can eventually build a healthier DNA.

I was born into a history of cancer.  My grandmother and both of my parents had forms of cancer, although none of them had breast cancer.  I was the pioneer there.  But both parents lived into their 80s and remained in their home until they died, surrounded by their family.  So, I might have a tendency toward cancer, but perhaps my genes also mean I will hang around for a couple more decades.  And my particular mix of nature and nurture has given me an ability to love, to laugh, to process health information in a way that might make me proactive, and to keep going, assuming all will be well, at least at some level.

Maybe I won’t end up as one of the stronger trees in the forest, maybe I will be the gnarled, crooked one.  Maybe disease might slow me, but I feel I am rooted deeply in decent soil—family, friends, community—so I am going to push on, grow how I can, and, in the process, help shade and nurture the other trees around me.

  

Do You Have A Survivorship Care Plan?

When most breast cancer patients finish treatment, docs set up a schedule of regular visits for mammograms, blood work, and general physical monitoring.  In the best cases, they also help you develop a survivorship plan (SCP) to help navigate life as a whole after cancer.  The report, From Cancer Patient to Cancer Survivor: Lost in Translation, written in 2005, offers a blueprint for this transitional period.  In the introduction, the authors note:

Despite the increase in survivors...primary care physicians and other health care providers often are not extremely familiar with the consequences of cancer, and seldom receive explicit guidance from oncologists. Furthermore, the lack of clear evidence for what constitutes best practices in caring for patients with a history of cancer contributes to wide variation in care.

The report's recommendations acknowledge the the period after cancer treatment  should be seen as a "distinct phase of cancer care."   This means going beyond tests and helping patients deal with the fact that they have had cancer and are likely terrified that it will return.  Cancer care may last a lifetime.


Access to affordable health care is a constant in the group's recommendations, which is especially apt as we await the  U.S. Supreme Court's ruling on the Affordable Care Act.  If the act is struck down, require Congress to implement some of its aspects, such as allowing covering for people with preexisting conditions and eliminating lifetime caps on coverage.  Those who have gone through cancer treatment know that good healthcare is a lifesaver.  And the need for care does not stop when treatment ends—nor does the cost get any more reasonable.

Summer 2012: My Life Right Now

We drive up a rutted mountain road, going 15 miles an hour, feeling we are speeding as we dodge rocks and pines and locust trees full of pink blossoms. The road follows a small creek that rushes down the mountain, sliding over rocky beds and through lush grass. We stop to say hello to our nearest neighbors, two miles away.  And then we head here, to our wee cabin, settled in a mountain valley that ends in a 12,000-foot peak. 

It is our little piece of paradise.  From the cabin, we see mountains, trees, and meadow—not one house, not a sign of another human being.  My brother lives a quarter of a mile past us, but we cannot see his house, although we occasionally hear his dogs as they send bears up the trees and scare turkeys off into the meadow. I like the dogs and I love having my brother this close.

Our cabin is 480 square feet, one cozy room plus bath   The kitchen consists of antique cabinets and a skirted sink, something Laura Ingalls might relate to.  Except for the propane refrigerator and stove.

Our bedroom is tucked into a corner, with a four-poster walnut bed I bought at the Salvation Army in 1970, a few months before we were married—and it was an antique then.  Our living room and dining room are a hodgepodge of furniture from antique and junk shops and castoffs from our Iowa house and my parents’ home.  A wooden camping cooler my dad made is our coffee table and the desk is from our son’s room.  He refinished it sometime in the 80s.

We start the day with hot tea on the deck, then a hike, then breakfast on the deck.  Then Joe goes off to putter in the yard or cut down trees, or work in his little shop (aka shed) and I go inside to write or to putz around the cabin, rearranging this, moving that. At night, I have a hot magnesium drink as a nightcap and sit on the deck listening to the creek and watching the stars—you really can see billions and billions from here.

We have no light pollution because we have no lights. We are off the grid here, with solar power, propane gas, and well water.  Oh, and a compost toilet, which is far less nasty than you might think.  In fact, it is quite efficient and has no smell (as long as the fan is working).  Every week, though, we have to dump its drum, which makes our stay in paradise seem a little less idyllic.

Also on the downside is our Internet connection, which is dial-up and simply does not work.   Last year, satellite service came to the mountain but we have not yet signed on—we are waiting to see how it works, and reluctant to sign onto an expensive monthly contract for a place we live in for slightly more than three months. 

So the frequency of my blog posts drops every summer, as I simply don’t have the technology to effectively connect, and I have to wait until I go to town to do anything of any consequence online.  And my Facebook status updates get bunched together—several on one day, none for the rest of the week—for the same reason.

This is a beautiful place and it is ideal writing territory, so I am starting to work on my next book.  This location is not so great for communicating with the frequency with which we are all accustomed.  So my apologies for posting in bits and spurts.  Know that you are all on my mind as I relax and recharge.  And if you are heading north up I-25 between Trinidad and Walsenburg, Colorado, look to your left at the mountain looming there.  I am in its foothills.  Maybe writing.  Maybe staring at a pile of rocks called the East Spanish Peak.  

PHOTO:   This guy walked through the meadow across from out cabin the other day.  My husband Joe caught him, plus some early-morning rays.   NOTE:  And by "caught him" I meant on the camera.

More targeted therapy potential for TNBC: Protein RSK2

NEWS RELEASE

The Canadian Breast Cancer Foundation – BC/Yukon Region (CBCF) is thrilled to announce a game-changing discovery in triple-negative breast cancer (TNBC). This breakthrough points to one of the first personalized therapies for the treatment of TNBC and reports that RSK inhibition has the potential to block TNBC recurrence.

The breakthrough research of Canadian Breast Cancer Foundation – BC/Yukon Region’s (CBCF) Doctoral Breast Cancer Research Fellows Kristen Reipas and Dr. Anna Stratford will today be published in the highly recognized medical journal, Stem Cells.

Supported by University of British Columbia (UBC) Associate Professor in the Faculty of Medicine, Dr. Sandra Dunn, trainees Ms. Reipas and Dr. Stratford have identified a protein critical to the survival of triple-negative breast cancer (TNBC) patients. This breakthrough research has the potential to cure TNBC by targeting a protein called RSK2, which eliminates TNBC cells completely. The study, published June 5, 2012 in Stem Cells medical journal, reports that RSK2 inhibitors have the ability to kill all of the cells including cancer stem cells which give rise to cancer recurrence. This cutting-edge discovery will potentially personalize the treatment of TNBC on an international scale.

"RSK2 inhibition provides a novel therapeutic avenue for TNBC and holds the promise of being one of the first targeted therapies for this challenging form of breast cancer," says Dr. Sandra Dunn, UBC.

TNBC is diagnosed in approximately 400,000 women worldwide and is considered the most difficult breast cancer subtype to treat due to lack of effective therapies. Dr. Dunn’s laboratory at the Child & Family Research Institute at BC Children’s Hospital led the project in collaboration with scientists from Breakthrough Breast Cancer UK and the University of Aukland NZ.

This project began four years ago when UBC Post Doctorate Fellow Dr. Stratford of the Child & Family Research Institute was awarded $214,000 by CBCF BC/Yukon to support her research on this project entitled “The regulation of the Y-box binding protein-1 (YB-1) by p90 ribosomal S6 kinase (RSK) in triple-negative breast cancer.”

In addition, a doctoral candidate in the Experimental Medicine Program at UBC, Kristen Reipas was awarded $35,000 in support of this research study, entitled “Targeting Y-box binding protein-1 eliminates tumor-initiating cells and reduces relapse in triple-negative breast cancer.”

The BC/Yukon Region of CBCF is proud to award the Breast Cancer Research Postgraduate Fellowships every year to the most qualified breast cancer research projects across the province. These awards are intended for qualified health care professionals, MD graduates or recent PhD graduates to provide assistance in launching a career as independent, social, clinical or basic science investigator in breast cancer research.

Canadian Breast Cancer Foundation – BC/Yukon Region

The BC/Yukon Region of CBCF was established in 1992 to make a difference in breast cancer research and breast health for the BC population. Every year CBCF, along with its donors, sponsors and partners, raises funds to support unique and innovative initiatives in prevention, early detection, treatment, research and emerging issues in the health care workforce.

Will biomarkers help ID women with TNBC who benefit from taxanes?

NEWS RELEASE

CHICAGO, June 2, 2012 /PRNewswire via COMTEX/ -- TLE3 Biomarker Over-expressed in HER2-positive, Hormone Receptor-positive, and Triple-negative Breast Cancers --

EGFR status May Facilitate Therapeutic Decision-making in Head and Neck Cancer --

In a poster presentation today, Gargi Basu, Ph.D., and colleagues at Caris Life Sciences, presented results from the first study providing a comprehensive review of transducin-like enhancer of split 3 (TLE3) expression in breast cancer subtypes. They described TLE3 as a transcriptional repressor that influences tumor growth and microtubule stability; its expression in epithelial tumor cells may reflect that these cells require the expression of TL3 to maintain their undifferentiated state. The expression of TLE3 is also associated with response to taxane therapy in patients with breast cancer.

Working with tumor cells collected from 978 breast cancer patients, the investigators employed two different technological platforms used in Caris Target Now -immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) - to gather information on four biomarkers: TLE3 (M-201), ER(1D5), PR(PgR636), and human epidermal growth factor receptor 2 (HER2)/neu (Polyclonal). IHC analysis of the four biomarkers was conducted at the protein level, and FISH was used to determine amplification of HER2/neu. Samples were then sub-classified as hormone receptor (HR)-positive (i.e., estrogen receptor [ER]-positive and/or progesterone receptor [PR]- positive), HER2-positive (either at the protein level or amplified by FISH), or triple-negative (i.e., lacking in ER, PR, and HER2/neu).

Overall, 351 (36%) of the patients were HR-positive, 150 (15%) were HER2-positive, and 477 (49%) were triple-negative. TLE3 was expressed in 82% of the HR-positive patients, 73% of the HER2-positive patients, and 61% of the triple-negative patients. To further investigate TLE3 expression in the patient subtypes, Dr. Basu and colleagues performed a pairwise Fisher's Exact Test between the various pairs; this analysis revealed that for all pairs, the ratios of TLE3-expressing individuals were significantly different. The largest difference was observed between the HR-positives and the triple-negatives (82% vs. 61%, respectively; p=2.509e-10), suggesting that the HR-positives have a higher likelihood of responding to taxane therapy. The HER2-positives, at 73%, had a ratio that was significantly higher than the triple-negatives and significantly lower than the HR-positives.

"We found TLE3 to be over-expressed in the majority of patients with HER2-positive and hormone receptor-positive breast cancer," Dr. Basu observed. "Interestingly, the comparatively low over-expression of TLE3 in the triple-negative subtype makes it especially important to identify those patients in this group who are most likely to respond to taxane therapy. If physicians are provided with such knowledge prior to starting therapy, their chances of selecting appropriate regimens for patients with these subtypes of breast cancer may be greatly improved."

Micro RNAs may explain why African-Amercan and Caucasian Women React Differently to the Same Treatment

NEW RELEASE

Chicago, IL (PRWEB) June 02, 2012

Researchers and doctors at the North Shore-LIJ Health System and the Feinstein Institute for Medical Research have discovered a potential explanation for why breast cancer is not experienced the same way with African American and Caucasian patients. This data will be presented at the 2012 American Society of Clinical Oncology (ASCO) Annual Meeting to be held from Friday through Tuesday (June 1-5) in Chicago, IL.

Breast cancer is more common in Caucasian women than in African American women; however, African American women experience a more aggressive form of breast cancer that occurs almost a decade earlier than Caucasian women. Because of this, African American women have a lower breast cancer survival rate than Caucasian women. To explore the reasons why, researchers and doctors at the North Shore-LIJ Health System and the Feinstein Institute for Medical Research conducted a study to determine 1) why the expression of a genetic marker embedded in deoxyribonucleic acid (DNA), called microRNA, differs between African American and Caucasian women, and 2) if variation in microRNAs may explain the observed survival difference between African American and Caucasian women.

In this study, microRNA profiles from the blood of 32 female patients were collected before removal of breast tumors. The mean age of the patients was 50 years, ranging from age 31 to 68, and 10 of the patients had stage III triple-negative breast cancer (five were African American and five were Caucasian), 10 patients had stage III estrogen-receptor or progesterone-receptor positive breast cancer (five were African American and five were Caucasian), and 12 patients were controls (six were African American and six were Caucasian). Triple-negative breast cancer refers to any breast cancer that does not express three receptors known to advance most breast cancers; estrogen receptors, progesterone receptors and human epidermal growth factor receptor 2 (HER2). Although triple-negative breast cancer is estrogen-receptor negative, progesterone-receptor negative and HER2 negative, and the most successful treatments for breast cancer target these receptors, triple-negative breast cancer typically responds to chemotherapy.

The study found that, 1) female Caucasian patients who had triple-negative breast cancer overexpressed 20 microRNAs (15 times higher than the controls), and none of the microRNAs these patients had were found in any of the African American patients, 2) female African American breast cancer patients overexpressed only six microRNAs (15 times higher than the controls), and none of these microRNAs were detected in Caucasian patients who had triple-negative breast cancer, and 3) four microRNAs in African American patients and eight microRNAs in Caucasian patients were not previously reported in association with breast cancer, which suggests that they may be connected to how the patient reacts to cancer.

“The striking difference in the patterns of microRNA expression between African American and Caucasian breast cancer patients may provide insight into answering why, when receiving similar treatments, outcomes are different between African Americans and Caucasians,” said Iuliana Shapira, MD, director of the Cancer Genetics Program at the North Shore-LIJ Health System’s Monter Cancer Center. “Breast cancer patients who have the most devastating outcome may carry the microRNAs that promote cancer. What we saw in this study is that Caucasian women may carry microRNAs that protect against cancer while African American women do not express those microRNAs. The lack of expressing these microRNAs in African Americans could be the cause of poor outcomes seen in these women. Methods to increase microRNAs in the blood before surgery for cancer, such as giving chemotherapy before surgery for cancer, may improve survival rates in African American women with triple-negative breast cancer.”

About The Feinstein Institute for Medical Research
Headquartered in Manhasset, NY, The Feinstein Institute for Medical Research is home to international scientific leaders in cancer research, Parkinson's disease, Alzheimer’s disease, psychiatric disorders, rheumatoid arthritis, lupus, sepsis, inflammatory bowel disease, human genetics, pulmonary hypertension, leukemia, neuroimmunology, and medicinal chemistry. The Feinstein Institute, part of the North Shore-LIJ Health System, ranks in the top 5th percentile of all National Institutes of Health grants awarded to research centers. For more information visithttp://www.FeinsteinInstitute.org.