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Scientists Discover Mechanism and Promising Treatment for Aggressive Prostate Tumors

Scientists have identified the mechanism of transition from a normal prostate tumor to an aggressive one, and then successfully tested an experimental treatment on laboratory animals. In all cases, the drug blocked the cancer, and in some cases it led to complete regression of the tumor without side effects. It is important to note that the drug is already being tested in clinical trials for another type of cancer.

Initially, a team from the University of Michigan disclosed a mechanism that explains the reasons for the transformation of an ordinary curable prostate tumor into an aggressive one. Most tumors after treatment are adenocarcinomas or glandular tumors, however, in about 15-20% of cases, despite the success of hormone therapy, some prostate tumors take on a more aggressive identity, for example, become neuroendocrine.

From previous studies, scientists knew that the LSD1 protein was important for the survival of prostate adenocarcinoma tumors. Now they have determined that it is also important for neuroendocrine types – in them it is expressed much more intensively.

Experiments showed that without LSD1, cancer cells survived much worse. Notably, the protein also turned off the p53 tumor suppressor gene, which normally acts as a brake in cancer cells.

The scientists then tested one of the LSD1 inhibitors, the drug seclidemstat, and confirmed their findings: the treatment completely blocked cancer growth in all cases, and in some rodents led to complete tumor regression. However, no toxic side effects were noted.

Currently, seclidemstat is already being tested as part of the first phase of clinical trials for sarcoma, so we can hope for similar studies in people with aggressive prostate cancer soon.

Meanwhile, in other pilot clinical trials, scientists have successfully tested the first drug against cancer metastases. The results showed that in a short time the size of secondary tumor foci can be reduced by half.

2023-08-15 10:09:20

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