Yale study identifies how cancer drug inhibits DNA repair in cancer cells
According to Yale research, a cancer drug thought to be of limited use may be able to stop certain cancer cells from repairing their DNA in order to survive.
Authors: Morgans AK, Szymaniak BM Abstract The landscape of genetic testing for prostate cancer is rapidly evolving. There is increasing evidence that individuals with germline mutations in DNA-repair genes are more responsive to targeted therapies. Due to potential implications for treatment, these genes should be taken into consideration when determining the scope of genetic testing. PMID: 31629435 [PubMed - in process]
Authors: Carroll PR, Witte JS, Parsons JK Abstract Men with germline mutations in DNA repair genes are at an increased risk of prostate cancer. These germline mutations are commonly seen in conjunction with somatic DNA repair gene mutations in prostate tumors. This indicates that men with a personal or family history of prostate cancer-as well as other cancer syndromes arising from mutations in DNA repair genes-should be considered for genetic testing and counseling. PMID: 31629425 [PubMed - in process]
This article summarizes a presentation at the 2019 Philadelphia Consensus Conference focused on the latest data at the intersection of germline and tumor genetic testing for prostate cancer patients. PMID: 31629422 [PubMed - in process]
Authors: Knudsen KE Abstract Despite significant advances in understanding the biology of advanced prostate cancer and approval of novel therapeutic agents, there is no durable cure for metastatic disease. Recent findings unmasked the importance of androgen receptor (AR) signaling in regulation of DNA repair, and alterations of the AR-DNA repair factor axis were shown to promote aggressive phenotypes including metastasis. These and related findings underscore the importance of determining impact AR-DNA repair factor alterations on prostate cancer progression. PMID: 31629421 [PubMed - in process]
Authors: Cheng HH Abstract Recent studies demonstrate that the prevalence of germline mutations in DNA repair genes in metastatic prostate cancer is higher than previously recognized, and is higher than in localized disease and in unaffected men. This is compelling evidence that specific gene dysfunction is critical in prostate cancer initiation and/or evolution to metastases. Applications to treatment in advanced disease are imminent, and further investigation in early-stage disease, as well as in diverse and at-risk populations will help maximize clinical benefit. PMID: 31629420 [PubMed - in process]
Authors: Boyle J, Cooney KA Abstract Germline pathogenic mutations in DNA repair genes have been linked to prostate cancer risk and aggressiveness. This observation was facilitated by tumor sequencing of men with advanced prostate cancer and has important implications for clinical management. In addition, cascade testing will identify at-risk individuals who should be assessed for cancer risk. PMID: 31629416 [PubMed - in process]
Synchronous cancer in patients with abdominal aortic aneurysm (AAA) increases their morbidity and mortality after AAA repair. However, little is known about the history of cancer in AAA patients and its impact on mortality after AAA repair. We analyzed the incidence and type of cancer history in patients who underwent AAA repair and difference in short- and long-term mortality.
In this study, AT1-AAs were detected in the sera of patients with peripheral arterial disease (PAD) and the positive rate was 44.44% vs. 17.46% in non-PAD volunteers. In addition, analysis showed that AT1-AAs level was positively correlated with PAD. To reveal the causal relationship between AT1-AAs and vascular aging, an AT1-AAs-positive rat model was established by active immunization. The carotid pulse wave velocity was higher, and the aortic endothelium-dependent vasodilatation was attenuated significantly in the immunized rats. Morphological staining showed thickening of the aortic wall. Histological examination showe...
Publication date: Available online 19 October 2019Source: Seminars in Cancer BiologyAuthor(s): Patricia Rousselle, Jean Yves ScoazecAbstractLaminin 332 is crucial in the biology of epithelia. This large extracellular matrix protein consists of the heterotrimeric assembly of three subunits – α3, β3, and γ2 – and its multifunctionality relies on a number of extracellular proteolytic processing events. Laminin 332 is central to normal epithelium homeostasis by sustaining cell adhesion, polarity, proliferation, and differentiation. It also supports a major function in epithelial tissue formation, r...
Publication date: Available online 18 October 2019Source: Molecular MetabolismAuthor(s): Matthieu Lacroix, Romain Riscal, Giuseppe Arena, Laetitia Karine Linares, Laurent Le CamAbstractBackgroundThe TP53 gene is one of the most commonly inactivated tumor suppressors in human cancers. p53 functions during cancer progression have been linked to a variety of transcriptional and non-transcriptional activities that lead to the tight control of cell proliferation, senescence, DNA repair, and cell death. However, converging evidence indicates that p53 also plays a major role in metabolism in both normal and cancer cells.Scope of ...