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Breast Cancer Is Hard To Treat: What Protects These Tumor-Iniating Cells?

Update Date: Jan 20, 2017 10:00 AM EST
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Breast cancer is one of the types of cancer that is very difficult to treat because the tumor cells may come back and recur. A team of scientists has identified a protein that may play a pivotal role in maintaining a population of tumor-initiating cells (TICs), which are cells resistant to treatment.

Investigators at the Massachusetts General Hospital have recognized a protein, called G3BP2, affects the survival and proliferative potential of breast cancer cells. This protein is responsible for regulating the ratio of TICs to non-TICs within a tumor.

"We also found that G3BP2 regulates breast tumor initiation in a way that leads to the increased expression of Oct-4 and Nanog, transcription factors contributing to the pluripotency of embryonic stem cells," Igor Garkavtsev, lead author of the study, said in a press release.

Breast cancers are usually made up of different cell types. It is believed that TICs are capable of generating a full range of cancer cells. TICs also seem to resist common therapies used to treat breast cancer and finding ways to target these cells could pave the way for the development of new therapies that may reduce the risk of recurrence and treatment-resistance.

"Malignant breast tumors consist of supporting stromal cells and epithelial cancerous cells. The cancer cell population is fueled by a reservoir of tumor-initiating cells, and these cells can give rise to the bulk of the tumor," the researchers wrote in the study published in the journal Proceedings of the National Academy of Sciences (PNAS).

"Some breast cancer cell populations with vast proliferative potential may be intrinsically resistant to standard anticancer therapy," they added.

After various experiments, a more detailed analysis showed that G3BP2 regulates breast tumor initiation by controlling the levels of TICs in tumors.

"The possibility that some breast cancer cells with vast proliferative potential may be intrinsically resistant to standard therapies may partially explain why tumors relapse after treatment," Garkavtsev explained.

"Our identification of compound C108 and the discovery of G3BP2 as a potential regulator of TICs open opportunities for further exploration of the mechanisms of breast cancer initiation and the development of novel therapies," Garkavtsev added.

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