One study describes how prostate cancer cells mimic bone when they metastasize

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Researchers of the Cancer Institute of Duke University (United States) have described how cancer cells in the prostate develop the ability to mimic bone-forming cells called osteoblasts, allowing them to proliferate in the bone microenvironment.

Prostate cancer often becomes lethal as it spreads to the bones, and the process behind this deadly feature could potentially turn against you as a target for radiation targeting bones and new therapies.

Attacking these cells with radio-233, a radioactive isotope that selectively attacks the cells of these bone metastases, has been shown to prolong the life of patients. But a better understanding of how the radius works in the bone was needed. The mapping of this process of imitation could lead to a more effective use of radio-233 and the development of new therapies to treat or prevent the spread of prostate cancer to the bones, according to the scientists explain in their work, published in the journal 'Plos One'.

“Given that most men who die of prostate cancer have bone metastases, this work is critical to help understand this process,” says lead author Andrew Armstrong, who with his team recruited a small group of 20 men with symptomatic metastatic bone prostate cancer.

By analyzing the circulating tumor cells of the participants, they found that bone-forming enzymes appeared to be expressed frequently, and that genetic alterations in the bone-forming pathways were also common in these prostate cancer cells. They then validated these new genetic findings in a separate multicenter trial that involved a larger group of more than 40 men with prostate cancer and bone metastases.

After treatment with radio-223, the researchers found that the radioactive isotope was concentrated in bone metastases, but the tumor cells were still circulating and the cancer progressed within six months of therapy. They also found a range of complex genetic alterations in these tumor cells that probably allowed them to persist and develop resistance to radiation over time.

“Osteomymesis may contribute in part to the spread of prostate cancer to bones, but also to the uptake of radio-223 into bone metastases, which could improve the therapeutic benefit of radiation therapy to the bones. By mapping this lethal pathway of bone metastasis from prostate cancer, the study points to new targets and, therefore, to critical areas of research to design better targeted therapies for tumors, “concludes Armstrong.


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