Genetics Lead the Way to Targeted TNBC Treatment: 17q25.3

The q25.3 region of chromosome 17 may be another genetic marker that defines subtypes of triple-negative breast cancer and, therefore, could lead to the golden grail: targeted treatment, especially for those forms of TNBC linked to the BRCA1 mutation.  In research published in the journal Breast Cancer Research, 17q25.3 was detected in 86 percent of the mutated TNBC tumors.

This is significant because, as the researchers note, the BRCA1 mutation is closely linked to TNBC, with  as many as  90 percent of tumors with the mutation being triple negative.  This does not mean, however, that all TNBC tumors have the BRCA1 mutation.  In fact, only 10 to 20 percent of all TNBC tumors have the BRCA1 mutation.  I explain this link in my book on TNBC.

Identifying patients with the BRCA1 mutation will ultimately help select patients who could benefit from  selective treatments 17q25.3.   First, though, we need those treatments.  Baby steps, friends.  But at least they are steps.

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For more details on triple-negative breast cancer, check out my book, Surviving Triple-Negative Breast Cancer.

Protein Successfully Stops TNBC in Mice

A team at the University of Kansas School of Medicine has identified a potential target for treating triple-negative breast cancer: atypical protein kinase C signaling. In a recent paper, published in the journal Cell Death and Differentiation, Soumen Paul, Ph.D and his colleagues conclude that this finding holds "tremendous" promise for treating breast cancer.

The researchers analyzed tissue samples of breast cancer that had spread to the liver, lung and other organs and found that atypical protein kinase c lambda/iota, which is known to influence cell growth, was highly expressed and phosphorylated in metastatic breast cancers.

In tests conducted on mice, the researchers depleted the protein in a line of triple-negative breast cancer and found that this significantly slowed the breast tumor growth.

Previous studies have implicated the atypical protein kinase c lambda/iota in the other cancers, they say, but no prior study had indicated any role in breast cancer metastasis. 

"We have been able to show that this protein is highly expressed in metastatic triple-negative breast cancer, and when we are depleting it from triple-negative breast cancer cells, we found that the cancer cells are not metastasizing," Dr. Paul said. "The tumor growth is slowing down. This is giving us an opportunity for a targeted therapy."

The next step would be to begin clinical trials on humans, but that could be years away.

Source: The University of Kansas

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For more details on triple-negative breast cancer, check out my book, Surviving Triple-Negative Breast Cancer.