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Edited bone marrow cells trigger "striking" tumor regression in mice

Edited bone marrow cells trigger "striking" tumor regression in mice
Scientists have used edited bone marrow cells to trigger powerful immune responses that attack cancer cells in mice
Scientists have used edited bone marrow cells to trigger powerful immune responses that attack cancer cells in mice
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Scientists have used edited bone marrow cells to trigger powerful immune responses that attack cancer cells in mice
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Scientists have used edited bone marrow cells to trigger powerful immune responses that attack cancer cells in mice

Immunotherapy is an increasingly powerful form of cancer treatment where the patient's own immune system is equipped with heightened abilities to take down the disease, and one promising arm of this is known as adoptive cell therapy. This involves using altered versions of a patient's own cells to trigger a more strong-handed response from their own immune system. Scientists at Johns Hopkins Kimmel Cancer Center are reporting an exciting advance in this area, demonstrating that engineered bone marrow cells can slow the growth of prostate and pancreatic cancers in mice.

The study builds on previous research where scientists demonstrated that a range of cancers, including melanomas, colon cancer and brain cancer, grow much more slowly in mice that are lacking a certain gene, known as p50, which seems to activate a stronger immune response. The Johns Hopkins researchers sought to further validate these earlier findings, while expanding the utility of a promising form of cancer therapy.

To do this, the team worked with what are known as immature myeloid cells, a type of white blood cell, which previous research had indicated could help switch on immune responses that fight tumors. In this case, the immature myeloid cells were taken from the bone marrow of mice engineered to lack the p50 gene, as a way of comparing them to the behavior of cells taken from mice who had the p50 gene in tact.

The team inoculated the p50-deficient mice with human prostate and pancreatic cancer cells, along with another group of regular mice. Both groups were pre-treated with a common cancer drug called 5-fluorouracil, and the team found that when this was combined with the p50-deficient myeloid cells, it produced significantly greater results.

In these mice, the tumors grew at least three times more slowly in 13 out of 14 pancreatic cancers (93 percent) and in eight out of 15 pancreatic cancers (53 percent). In some cases, the combination treatment induced a significant regression among mice with pancreatic cancer, with an up to tenfold reduction in tumor size which the scientists describe as "striking."

These outcomes add to the growing body of research suggesting the myeloid cells that are p50 deficient could benefit a range of cancer treatments, by stirring the body's immune system into action.

"Seven different cancers – prostate cancer, pancreatic cancer, brain cancer, melanoma, colon cancer, sarcoma and neuroblastoma – tested by us and others grew slower in mice lacking p50," says study co-author and pediatric oncologist Alan Friedman.

The research was published Journal for ImmunoTherapy of Cancer.

Source: Johns Hopkins Medicine

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