Last year was a lively one for research on triple-negative breast cancer. Below is my list of the year’s top studies—all pointing toward understanding what makes TNBC tick, which will ultimately lead to treatment and a reduction in the risk of recurrence. Remember, though, that the road from research to clinical practice can be long and rocky, so most of these treatments won’t be immediately available. Still, this list points to a rich reservoir of inquiry and information—which is good news for those of us on the TNBC Road and for those who follow us.
Bisphosphonatessuch as Zometa and Reclast reduced the risk of bone metastases following breast cancer in post-menopausal women by 34 percent in research presented at the 2013 San Antonio Breast Cancer Symposium. And they reduced the risk of death in that same group by 17 percent, regardless of receptor status, node involvement or previous chemotherapy. More.
Genetic Details of Triple-Negative Breast Cancer
Beyond its most basic definition—negative for receptors for estrogen, progesterone and Her2/neu—triple-negative breast cancer has unique genetic characteristics. Research published in the journal Cancer Researchhas outlined some of TNBC’s genetic associations. Once they know what it is rather than what it isn’t, they can target it. Put a big red bull’s eye on its nasty old back. More.
New Drug Regimens Can Lead to Improved Outcomes for Women with Stages II and III TNBC Adding the chemotherapy drug carboplatin to standard treatment improved outcomes for women with triple-negative breast cancer in two studies presented at the 2013 San Antonio Breast Cancer Symposium. Both measured pathological complete response (pCR), which is recognized as a positive marker for overall survival. The second study also showed improved outcomes using bevacizumab (Avastin). More.
Tumor-infiltrating lymphocytes may become an additional factor in determining which types of triple-negative breast cancer respond best to chemotherapy. Seventy-five percent of tumors with the highest levels of lymphocytes—researchers call this lymphocyte predominate breast cancer (LPBC)—had a pathological complete response to doxorubicin and taxane plus carboplatin when compared to non-LPBC tumors. The results came from the GeparSixto trial (GBG 66) in Germany. More.
High Fat Diet in Puberty Linked to Basal-Like Breast Cancer
Young women who eat excess amounts of saturated fats during their teenage years increase their risk of basal-like breast cancer, according to a study published in Breast Cancer Research. Many basal-like tumors are also triple-negative. More
Metformin: New Agent Against TNBC?
The diabetes drug Metformin can effectively reduce breast cancer risk that is associated with insulin resistance and was directly correlated with Ki67 status, according to research in the British Journal of Cancer. TNBC has shown links to insulin resistance in previous studies, and many TNBC tumors are positive for Ki67, so this could be additional support for considering metformin as a treatment for TNBC. More.
Restorative Yoga Can Help Trim Fat
Yoga’s health benefits may go beyond stress reduction – a study funded by the National Institutes of Health (NIH) found that for overweight women, restorative yoga may offer a way to actually trim subcutaneous fat. Obesity is a risk factor for breast cancer, including TNBC. The benefits of restorative yoga – a form of the practice that emphasizes relaxation over flowing movements or challenging balance poses – compared favorably with simple stretching when tested among a group of women who were clinically obese. More.
New Imaging Technique Can Determine Cancer Subtype and Response to Treatment
An optical imaging technique that measures metabolic activity in cancer cells can accurately differentiate breast cancer subtypes, and it can detect responses to treatment as early as two days after therapy administration, according to a study published in Cancer Research, a journal of the American Association for Cancer Research. More.
Existing Drugs Kill TNBC Drugs By Targeting Their Own Waste
Triple-negative breast cancers may be vulnerable to drugs that attack the proteasome, a cellular structure that acts as the cell’s waste disposal, breaking down damaged or unneeded proteins, according to a new paper in Cancer Cell. In lab tests, researchers selectively “turned off” genes in triple-negative tumor cells. When turned off, the cells die. These data suggest that triple-negative breast cancers may respond to treatment with drugs similar to bortezomib (Velcade), which is used in multiple myeloma. More.
Protein May Be Path to Targeted TNBC Treatment
A protein called Numb (seriously) may promote the death of cancer cells by binding to and stabilizing the tumor suppressor protein p53, which is implicated in many cases of triple-negative breast cancer, according to research published in the May 23rd issue of Molecular Cell. When Numb is reduced by the Set8 enzyme , it will no longer protect p53. More.
HMGA1 Turns TNBC Cells Back to More Normal and Slows Their Growth
Researchers at Johns Hopkins have identified a gene that, when repressed in tumor cells, puts a halt to cell growth and a range of processes needed for tumors to enlarge and spread to distant sites. The researchers hope that this so-called “master regulator” gene may be the key to developing a new treatment for tumors resistant to current drugs. More.
Diamonds May Be A TNBC Girl’s Best Friend
UCLA researchers have developed a potential new treatment for triple-negative breast cancer that uses nanoscale, diamond-like particles called nanodiamonds. Nanodiamonds are between 4 and 6 nanometers in diameter and are shaped like tiny soccer balls. Byproducts of conventional mining and refining operations, the particles can form clusters following drug binding and have the ability to precisely deliver cancer drugs to tumors, significantly improving the drugs’ desired effect. In the UCLA study, the nanodiamond delivery system has been able to home in on tumor masses in mice with TNBC. More.
Omega 3 Fatty Acids in Fish Oil May Slow Triple-Negative
Researchers from Fox Chase Cancer Center have found that omega-3 fatty acids and their metabolite products slow or stop the proliferation, or growth in the number of cells, of triple-negative breast cancer cells more effectively than cells from luminal types of the disease. The omega-3s worked against all types of cancerous cells, but the effect was observed to be stronger in triple-negative cell lines, reducing proliferation by as much as 90 percent. More.
SOX11 and p53 May Spell Unique Development of Triple-Negative Breast Cancer
Could you create a breast cancer tumor in mature mice by reactivating how embryonic breast cancer cells develop? And, if you could, what would you learn? In a study published in the journal Breast Cancer Research, scientists discovered that basal-like breast cancers with the BRCA1 mutation—many of them triple-negative breast cancers—grow differently than other cancers. In fact, the way they grow predicts the prognosis of the tumor. More.
Could Copper Depletion Be a Cure for Metastatic TNBC?
An anti-copper drug compound that disables the ability of bone marrow cells from setting up a “home” in organs to receive and nurture migrating cancer tumor cells has shown surprising benefit for metastatic triple-negative breast cancer. Results of a phase II clinical trial conducted by researchers at Weill Cornell Medical College and reported in the Annals of Oncology shows that patients who are copper depleted show a significantly reduced risk of relapse. In fact, only two of 11 study participants with a history of advanced triple-negative breast cancer relapsed within 10 months after using the anti-copper drug, tetrathiomolybdate (TM). More.
Scientists Map TNBC’s Metastatic Path
Cancer Scientists at Weill Cornell Medical College have discovered the molecular switch that allows triple negative breast cancer cells to grow the amoeba-like protrusions they need to crawl away from a primary tumor and metastasize throughout the body. Their findings, published in Cancer Cell, suggest a novel approach for developing agents to treat cancer once it has spread. More.
Protease May Help Define New Subset of TNBC—and Lead to Treatment.
Researchers at St, Louis University have found a molecular signature that may define a particular subset of triple-negative breast cancer, which can ultimate lead to target therapy for that group of patients. In specific, they have uncovered a pathway responsible for the loss of 53BP1 in TNBC tumors related to the BRCA1 mutation. Loss of BRCA1, they discovered, increases the expression of the protease cathepsin L (CTSL), which causes the degradation of 53BP1. Cells that have lost both BRCA1 and 53BP1 have the ability to repair DNA and proliferate. That means the protease helps cancer cells with faulty BRCA1 survive—it is a defined bad guy in TNBC growth. And, when we know who the bad guy is, we can stop looking at ways to stop him in his mean old tracks. More