dc.description.abstract |
Over the past few years, a number of studies have revealed that a significant
number of men with prostate cancer had genetic defects in the DNA damage
repair gene response and mismatch repair genes. Certain of these modifications,
notably gene alterations known as homologous recombination (HRR) genes;
PALB2, CHEK2 BRCA1, BRCA2, ATM, and genes for DNA mismatch repair
(MMR); MLH1, MSH2, MSH6, and PMS2 are connected to a higher risk of
prostate cancer and more severe types of the disease. The DNA damage repair
(DDR) is essential for constructing and diversifying the antigen receptor genes
required for T and B cell development. But this DDR imbalance results in stress on
DNA replication and transcription, accumulation of mutations, and even cell
death, which compromises tissue homeostasis. Due to these impacts of DDR
anomalies, tumor immunity may be impacted, which may encourage the growth
of tumors, the release of inflammatory cytokines, and aberrant immune reactions.
In a similar vein, people who have altered MMR gene may benefit greatly from
immunotherapy. Therefore, for these treatments, mutational genetic testing is
indicated. Mismatch repair gene (MMR) defects are also more prevalent than
previously thought, especially in patients with metastatic disease, high Gleason
scores, and diverse histologies. This review summarizes the current information
on the mutation spectrum and clinical significance of DDR mechanisms, such as
HRR and MMR abnormalities in prostate cancer, and explains how patient
management is evolving as a result of this understanding. |
en_US |