Diversity of Triple Negative
First an apology: I never made it to the computer to post a blog yesterday. Somehow the day got completely away from her, and, at 11 PM when our guests had left, I just did not have the energy to deal with it. So (lucky you), I will do two today.
This first one is about the diversity of triple negative breast cancer, and the increasing scientific awareness that one size does not fit all for treatment of this variant either (as it does not for any other kind). You likely have noticed that the very central challenge of cancer treatment is that the more is known, the more complicated and difficult it becomes.
Since the general direction of cancer research is towards better understanding of individual tumors and selecting treatments that are likely to be targeted and specifically helpful, it makes sense that triple negative breast cancers are being studied in this way. The term "triple negative" is relatively new; I think that I first heard it a dozen or so years ago. Of course, this particicular tumor type has been around, but it was not so clearly understood and labeled. What it means for treatment is that neither the herceptin type drugs (which attack the her2 target) or the anti-estrogen drugs will be helpful. This leaves chemotherapy, and these tumors are often especially sensitive to drugs. Knowing that, the goal is to find the drugs that are the most helpful.
Here is a
OncologyStat® One Source, Many Resources.® By Elsevier
Diversity of Triple-Negative Breast Cancer Complicates Treatment
IMNG Medical Media. 2013 Feb 13, HS Rugo
Treatment of triple-negative breast cancer, so named because it lacks estrogen receptors, progesterone receptors, and HER2 overexpression, is one of the most challenging areas of breast oncology. Not only do patients with this aggressive cancer have some of the shortest absolute survival times, but they also are the only group for whom we still have no targeted therapies.
It is becoming increasingly clear that effectively treating triple-negative disease will require recognition of its diversity. Viewing it as a single entity is inherently flawed, an oversimplified way of referring to a disease that's incredibly heterogeneous and complicated. And that's probably been our biggest challenge in the design of clinical trials for this cancer.
Gene expression profiling is helping to tease apart molecular subtypes of triple-negative breast cancers (Mol. Oncol.2011;5:5-23). These subtypes often have distinctly different behavior and treatment responses.We are also learning more about the overlap between triple negativity and mutation of the BRCA1 tumor suppressor gene.About 90% of BRCA1-mutated breast cancers have a triple-negative phenotype. But interestingly, most triple-negative tumors have normal BRCA1 function. Recent data suggest that a subset of these tumors may have posttranslational modifications that affect BRCA1 function, so if you look for the DNA mutation, you won't find it. Sporadic basal-like tumors and hereditary BRCA1 tumors have a similar phenotype, so a defect in BRCA1 may have a role in these sporadic basal-like tumors.
Recent clinical trials are adding to our arsenal several new drugs - and a few old ones - from different classes that target vulnerabilities of triple-negative breast cancer and offer promise for improving outcomes in this hard-to-treat disease.
Here is the link to read more of this good article from Oncology Stat: