Prostate cancer is the most common tumor among men, since it is estimated that one in eight men will be diagnosed with this disease, most of them appearing in elderly men, with 90% of patients over 65. years and the average age of diagnosis of 75 years. Specifically, in Spain it is the third leading cause of cancer death in men, behind lung and colon cancer. And although the majority of patients with prostate cancer will be diagnosed in its early stages, a not inconsiderable number of patients (around 10%) are diagnosed with metastasis, which makes the disease chronic.
Given this scenario, there is now a new reason for hope, since, like prostate-specific antigen (PSA), prostate-specific membrane antigen (PSMA) is a biomarker that can inform doctors about prostate cancer. metastatic from a patient. Specifically, PSMA is a protein on the cell surface of most prostate tumors; scanning it with positron emission tomography (PET) can indicate where in the body the prostate cancer has spread, and it may be targeted with a recently approved radioactive therapy. However, in 15-20% of patients with castration-resistant prostate cancer, PSMA production stops late in the disease.
Now, in a new study published in the scientific journal “Nature Cancer”, scientists at the Dana-Farber Cancer Institute show new light on the mechanism that increases and decreases the expression of PSMA in prostate cancer cells. These findings may help clinicians select PSMA-targeted therapies for specific patientsas the researchers point out.
It has long been known that the androgen receptor (AR), a structure that triggers cell growth in response to the hormone androgen, controls the production of PSMA in prostate cancer cells. In the study published in the journal “Nature Cancer”, researchers led by Himisha BeltranMD, and Martin BakhtPhD, from Dana-Farber, found that PSMA expression is lower in liver metastases than in other parts of the body, independent of androgen receptor expression. They also found that some AR-negative tumors express PSMA and some AR-positive tumors do not, prompting them to look for a control mechanism that does not involve AR. His search revealed that the HOXB13 protein is a key regulator of PSMA: when castration-resistant prostate cancers do not have RA, HOXB13 can control PSMA on its own. This and the discovery of an epigenetic mechanism to suppress PSMA demonstrate that the PSMA control system is more complex than previously thought and that prostate cancer has multiple subtypes that can be optimally treated with specific targeted therapies.
The study authors also identified amino acids that are upregulated in low-PSMA metastatic prostate tumors. The discovery may lead to new biomarkers that complement PSMA imaging to identify prostate cancer subtypes.
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