FRONT PAGES: A New Drug Can Put Cancer Cells To Sleep And Prevent Them From Spreading

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(*_ Newswise) — A new therapeutic approach prevents metastatic tumor growth in mice by putting them in a dormant condition, where they are unable proliferate. The study, published November 23 in the Journal of Experimental Medicine (JEM), could lead to new treatments that prevent the recurrence or spread of various cancer types, including breast cancer and head and neck squamous cell carcinoma (HNSCC).

Many cancer patients experience a relapse after treatment. They develop new tumors in the same area or spread to other areas of their body. Secondary tumors can be resistant to treatment. They are usually caused by individual tumor cells, which may stay dormant for long time periods before they are reactivated and start growing again. Researchers may be able to prevent patient relapse by finding a way for cancer cells to remain dormant.

A previous study , Maria Soledad Sosa, from the Icahn School of Medicine in Mount Sinai, and Julio A. Aguirre–Ghiso, now with Albert Einstein College of Medicine discovered that a protein called the NR2F1 controls the ability of cancer cells remain dormant. This receptor protein can enter the cell nucleus to turn on many genes or disable them to activate a program that stops cancer cells proliferating. Dormant disseminated tumor cells have elevated levels of NR2F1, while primary tumors have low levels. The levels of the NR2F1 proteins then drop once cancer cells begin to proliferate again, forming recurrent or metastatic tumours.

” We thought activating NR2F1 with a small molecule could make it attractive as a clinical strategy to induce cell dormancy in cancer cells and prevent recurrence or metastasis,” Aguirre Ghiso explained.

In the new JEM study, Sosa and Aguirre-Ghiso’s teams used a computer-based screening approach to identify a drug, named C26, that activates NR2F1. The researchers found that treating patient-derived HNSCC cells with C26 boosted the levels of NR2F1 and arrested cell proliferation.

The researchers then tested whether C26 would prevent metastasis in mice. Patients-derived HNSCC cells are often injected into animals to form large primary tumors. These tumors spread to the lungs even after the original tumor has been removed. Treatment with C26 reduced the size of primary tumors, and, after surgery, further doses of C26 completely blocked the growth of metastatic tumors. Instead, only a few disseminated and dormant cancer cells were found in the rodent’s lungs. They were unable to reproduce even after the treatment was stopped.

Sosa and Aguirre-Ghiso’s teams determined that, by activating NR2F1, C26 forces cancer cells into a long-lived state of dormancy characterized by a unique pattern of gene activity. Cancer patients whose tumors display a similar pattern of gene activity tend to go longer without relapsing, suggesting that inducing this dormancy program with C26-type drugs could be effective in humans.

“Drugs which activate NR2F1 may be especially useful in breast cancer,” Sosa says. “NR2F1 is highly enriched in ER-positive tumors when compared to ER-negative tumors, and activating NR2F1 might be able to suppress reawakening of dormant cancer cells kept in that state by anti-estrogen therapies.” However, because C26 treatment elevates the levels of NR2F1, the approach may also be useful for other cancers with inherently low levels of the receptor protein.

“Overall, our study reveals a mechanism-based and rationally designed strategy to exploit NR2F1-activated dormancy as a therapeutic option to prevent metastatic relapse,” Aguirre-Ghiso says.

Khalil et al. 2021. J. Exp. Med. https://rupress.org/jem/article-lookup/doi/10.1084/jem. 20210836?PR

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About Journal of Experimental Medicine

Journal of Experimental Medicine (JEM) publishes peer-reviewed research on immunology, cancer biology, stem cell biology, microbial pathogenesis, vascular biology, and neurobiology. Editorial decisions regarding research manuscripts are made in collaboration between academic editors and professional scientists. Established in 1896, JEM is published by Rockefeller University Press, a department of The Rockefeller University in New York. For more information, visit jem.org.

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