We have learned that there is a direct link between specific genes and breast cancer. The next step in breast cancer research is establishing specific genetic malfunction within the cancer cell that is making it abnormal, and how it unfolds into full blown cancer. Then, what is causing gene malfunction and, finally, how it can be prevented, or corrected.

At present, we are still somewhere between the first and second step but, slowly and surely, continuing to move forward.

Every breast cancer is caused by improper DNA function, turning normal breast cells into cancerous. Most breast cancers result either from gene mutations, or from altered gene expression (epigenetic damage) that develop during the lifetime; inherent genetic flaws account for only about 10% of breast cancer cases. Thus, understanding how genes - or their function - get altered, leading to breast cancer, nearly

equals understanding of the disease itself.

Unlike "regular" studies, either direct (clinical) or statistical meta-studies, attempting to filter out what works - or doesn't - for breast cancer patients "statistically", that is, within relatively large groups of people, genetic research is focused on the very core of the disease: specific gene function, which is what is actually happening inside the body. Hopefully not too far from now, it will be possible to track and address this process individually. This would take cancer treatment to another level since, ultimately,

the only reliable treatment is patient-specific;

there is no shoe that fits everyone, and breast cancer treatment certainly isn't an exception to that simple fact.

So, what is this new information about? December 20th issue of The New England Journal of Medicine brings results of the latest breast cancer related genetic research (Breast-Cancer Stromal Cells with TP53 Mutations and Nodal Metastases, Patcos et al., and a comment by T. Liu, Stromal Effects in Breast Cancer). The findings, if proven factual, will enhance our understanding of the breast cancer mechanism, particularly its more mysterious, hormone-negative (not fueled by estrogen or progesterone) varieties.

The main new factor is behavior of stromal breast cells (also called fibroblasts), those forming connective tissue structure. Until now, it was generally assumed that the specific mechanism of breast cells turning cancerous is uniform, spreading through epithelial tumor cells, but not surrounding stromal cells, which are of different genetic origin.

Turns out, not only that stromal breast cells can also become abnormal, but also that

their mutation has different origin than that of epithelial cells.

While the epithelial cells most often turn cancerous due to under-expression of tumor-suppressor BRCA-2 or BRCA-1 genes, the culprit in stromal cells mutation identified in the study was altered tumor-suppressor gene TP53 function (tumor-suppressor genes are those inhibiting cellular division, as opposed to oncogenes, whose activity stimulates the division).

At this point, it is a matter of speculation how exactly genetic mutations of one form inside epithelial breast cells lead into different form of mutation inside surrounding stromal cells. It may be due to the elevated level of "reactive oxygen species" (free radicals) generated by the cancerous epithelial cells, their toxic emission, or some other form of molecular intercellular exchange, causing different, yet gene-specific damage in the surrounding stromal breast cells.

Important implication is that the choice of an effective breast cancer therapy has to be based on the knowledge of actual, specific cancer form. What may work where only epithelial breast cells are affected, may not work when it is accompanied with the stromal cells mutation.

Since the work of Patcos et al. indicated that presence of TP53 mutations in the breast's stroma was a

significant factor in the cancer's lymph-node metastases,

it could be specific to more aggressive, hormone-negative breast cancer forms, most often linked to BRCA-1 gene mutation, affecting disproportionately more younger and African-American women.

While this and some other important possibilities remain speculations at this point, these results are another step forward to better understanding of the link between specific malfunctioning genes and the mechanism through which breast cancer, as well as other cancer types, grow and spread. That could help devise more effective breast cancer therapies in the near future, and bring us one step closer to conquering this merciless modern-day killer. R

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