Reasons for treatment resistance in prostate cancer found

Subject : Science and Technology

Context:

Prostate cancer cell dynamics at a single-cell resolution across the time span of the disease — from its beginning to the point of androgen independence, where the tumour no longer responds to hormone, deprivation therapy has now been characterised.

Research analysis:

Researchers have found that a gene called Pten, which codes for a tumour-suppressing enzyme, is inactive in the majority of advanced prostate cancer patients.
This suggests that basal cells can transform into intermediate cells (expansion of these cells causes prostate cancer) upon Pten deletion.
In the intermediate cells, the researchers discovered that a 5-gene signature is specifically enriched.
Using two datasets of bulk RNA-sequencing from prostate cancer patients, they showed that the signature is associated with treatment resistance and poor clinical outcomes.

Significance of the findings:

An expansion of intermediate cells correlates with resistance to treatment and poor clinical outcomes in humans.
These cells are castration-resistant, meaning they continue to grow in the absence of testosterone and could explain how prostate tumours become resistant to hormone-related treatments.
These findings suggest that a 5-gene signature derived from prostate cancer may have importance in understanding human disease.
The presence of this gene signature may serve as a useful prognostic tool for predicting treatment resistance and outcomes in patients.

Prostate cancer:

It is cancer in a man’s prostate, a small walnut-sized gland that produces seminal fluid.
- The prostate gland epithelium — a type of body tissue that forms the surface of glands and organs — is typically composed of two types of epithelial cells: basal cells and highly differentiated luminal cells (cells which have altered in form).
Prostate cancer is the most diagnosed form of cancer and the second-leading cause of cancer-related deaths in males in the U.S.
This is due to incomplete knowledge of the cellular drivers behind the disease’s progression and the risk of progressing to castration-resistant prostate cancer (CRPC).