Prostate Cancer And DNA Mutation: New Connections Revealed

Specific mutations in the DNA of men with metastatic prostate cancer have been shown to play a larger role in the disease than previously thought. Researchers hope that this finding will help change standard therapy guidelines and open the door to drugs currently being used for other cancers.

The new study, published in the New England Journal of Medicine, examined inherited mutations in DNA repair genes.

These gene mutations were already known to occur more frequently in prostate cancer patients than the general population.

However, the present study demonstrated that mutations in DNA repair genes were even more prevalent in people with metastatic prostate cancer, specifically.

Read more: Prostate Cancer And DNA Mutation: New Connections Revealed

Gene mutation research gives a new perspective on prostate cancer.

Source: medicalnewstoday

Scissor protein responsible for cancer spread

Aggressive cancer cells have been found to express higher amounts of a certain protein by scientists at the University of Bergen.

PITPNC1 controls a process where cancer cells secrete molecules which cut through proteins outside cell walls like scissors. This allows the cancerous cells to then enter the tissue and begin dividing and multiplying at a new site.

Dr Nils Halberg, a researcher at the University of Bergen said: “We discovered that the aggressive cancer cells that are spreading in colon, breast, and skin cancer contained a much higher portion of the protein PITPNC1, than the non-aggressive cancer cells.”

Using this knowledge, scientists can predict which cancer cells are becoming more aggressive and are likely to metastasize.

Read more: Scissor protein responsible for cancer spread

Source: labnews

Targeting Tumor Metastasis

Tumour metastasis, the movement of tumour cells from a primary site to progressively colonize distant organs, is a major contributor to the deaths of cancer patients. Therapeutic goals are the prevention of an initial metastasis in high-risk patients, shrinkage of established lesions and prevention of additional metastases in patients with limited disease. Instead of being autonomous, tumour cells engage in bidirectional interactions with metastatic microenvironments to alter antitumour immunity, the extracellular milieu, genomic stability, survival signalling, chemotherapeutic resistance and proliferative cycles. Can targeting of these interactions significantly improve patient outcomes? In this Review preclinical research, combination therapies and clinical trial designs are re-examined.

Metastases, or the consequences of their treatment, are the greatest contributors to deaths from cancer. Clinical metastatic disease results from several selective forces. Pathways that fuel initial tumorigenesis, described as the 'trunk' of a cancer evolutionary tree, can also endow tumour cells with metastatic properties and de novo drug resistance. Two types of 'limb' pathway emerge from the tree trunk: events that induce acquired resistance to therapy and pathways that induce or accelerate metastasis to distant organs1. Cancer therapy has largely concentrated on druggable targets in the trunk tumorigenesis pathways, such as receptor tyrosine kinases, and uses sequential and combination therapies to minimize drug resistance.

Read more: Targeting Tumor Metastasis

Source: NatureReviewsCancer