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.

RIP2: A new target for a potential TNBC drug?

The receptor-interacting protein kinase 2 (RIP2),  known to be involved in  inflammatory processes, also has roles in triple-negative breast cancer metastasis, according to a study in the journal Breast Cancer Research.

The research analyzed data from six breast cancer databases, including The Cancer Genome Atlas and determined that RIP2 was significantly overexpressed in TNBC and correlated with worse progression-free survival.

The results suggest that targeting RIP2 may improve outcomes in advanced breast
cancer patients, in which it is over expressed.

It's another target, folks.  And another target might mean a targeted drug.

I do think RIP is an ominous name, but I guess they weren't looking at that.

You can read the entire study here.

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