A recent study has found that a specific gene in cancerous prostate tumors indicates when patients are at high-risk for the cancer to spread, suggesting that targeting this gene can help patients live longer.
Researchers have discovered how a gene involved in regulating hormone receptors may contribute to drug resistance in some prostate cancer patients.
Cancers most commonly arise because of a series of two to five mutations in different genes that combine to cause a tumor. Evidence from a growing number of experiments focused on truncal mutations -- the first mutations in a given sequence -- suggests a new direction in understanding the origins of cancer.
Unlike healthy tissues, tumors thrive in low-oxygen environments, often acquiring the ability to resist treatment and spread to other sites in the body. Despite being a well-known cause of therapy resistance and metastasis, the impact of low oxygen, known as hypoxia, on tumor cells is poorly understood. As reported today in Nature Genetics, researchers have discovered molecular hallmarks of hypoxia in the first-ever pan-cancer analysis of low oxygen in human tumors, with a special focus on prostate cancer.
The study has potential implications for families with members suffering from these types of tumours who are at an increased risk of developing cancer. The finding is based on PROREPAIR-B, a prospective multi-centre observational cohort study that followed up more than 400 patients with metastatic prostate cancer, aimed to identify genetic markers associated with its progression and treatment response. Further studies will evaluate whether patients with BRCA2 mutations can undergo treatments used in patients with ovarian and breast cancer.
Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Spain, have discovered a new mechanism controlling the expression of a set of genes important for cell proliferation and tumor progression. Their research, which has been published in Molecular Cell, responds to a very fundamental question about how key genes lead to tumors growth by maintaining their active expression. This finding opens the possibility to better target and develop new therapies for certain types of cancer.
This review concerned the recent updates on the structure-activity relationships of flavonoids as P-gp inhibitors, the molecular mechanisms of their action and their ability to overcome P-gp-mediated MDR in preclinical studies.
This review illustrates a perspective on prostate cancer imaging summarizing current imaging approaches with a special focus on Prostate Specific Membrane Antigen (PSMA), Bombesin (BN) and Androgen Receptor (AR) targeted imaging using Positron Emission Tomography (PET) and Single Positron Emission Computed Tomography (SPECT) based on 99mTc and other radiotracers.
Northwestern Medicine scientists have discovered two successful therapies that slowed the progression of pediatric leukemia in mice, according to three studies published over the last two years in the journal Cell, and the final paper published Dec. 20 in Genes & Development. When a key protein responsible for leukemia, MLL, is stabilized, it slows the progression of the leukemia, the most recent study found.
An analysis of the NRG Oncology clinical trial NRG-RTOG 9202 showed that the interval of time to biochemical failure (IBF), or the time it takes for previously treated cancer to return as indicated by prostate specific antigen (PSA) rise, could be used as a surrogate endpoint for locally advanced prostate cancer.