Articles related to CHECKPOINT INHIBITORS

With just a few exceptions (p.I157T, p.S428F, and p.T476M), CHEK2 PVs were linked to comparable cancer phenotypes regardless of the variation type. Although CHEK2 PVs were linked to breast, kidney, and thyroid malignancies, they were not linked to colorectal cancer. The prevalent p.I157T, p.S428F, and p.T476M alleles have a weaker connection with breast cancer compared to other CHEK2 PVs and were not related with non-breast malignancies. These findings might help with genetic counseling and care for those with CHEK2 PVs.

An ASCO Reading Room selection Fascinating work defining new therapeutic targets and cutting-edge treatment approaches in gynecological cancer is about to come. In this abstract, the authors go over new therapies for gynecologic cancers, such as endometrial, cervical, ovarian, and uncommon gynecologic tumors, and highlight studies that have improved clinicians’ knowledge of the distinct biology and molecular foundations of different tumors, which is being used to develop potent new therapeutic modalities.

Until a tumor is determined to be TMB-high or MSI-H/MMRd, and thus qualifies for treatment with pembrolizumab or dostarlimab on the basis of cancer site-agnostic approval, there is no justification for the use of single-agent ICB in unselected populations with recurrent EOC. However, the clinical trials carried out up to this point show that ICB can induce long-lasting responses in a relatively small fraction of individuals. These discoveries offer opportunities and challenges to the medical and scientific communities, including the need to use novel technologies to locate predictive biomarkers and create immunotherapies that go beyond ICB to improve the effectiveness of these drugs.

Among doctors and researchers, the 2010 and 2017 versions of the European LeukemiaNet (ELN) recommendations for the diagnosis and treatment of acute myeloid leukemia (AML) in adults are broadly accepted. Researchers now have a better understanding of how AML develops from a molecular perspective, which has led to an update on the classification of the disease. Additionally, genomic diagnostics and the evaluation of measurable residual disease have advanced significantly, and new therapeutic agents like FLT3, IDH1, IDH2, and BCL2 inhibitors have been developed successfully. This update, which contains updated response criteria, therapy suggestions, and a revised ELN genetic risk classification, is a result of these developments.

A Q&A session with Thomas J. Herzog, MD, the Deputy Director at the University of Cincinnati Cancer Center in Ohio, who discusses the PARP inhibitors olaparib (Lynparza, AstraZeneca), niraparib (Zejula, GSK), and rucaparib (Rubraca, Clovis Oncology); the ATHENA-MONO, ENGOT-OV16/NOVA, SOLO2, and ARIEL3 clinical trials; and the implications of the “Dear Health Care Provider” letters that were issued earlier this year regarding PARP inhibitors.

A quartet of current clinical trials involving first-in-class molecules and CRISPR gene editing show great promise. STELLAR investigates a fusion protein in PAH, CodeBreak 200 studies a first-in-class of KRAS inhibitor, EMERGENT-2 focuses on a new treatment for schizophrenia, and NCT04601051 studies a gene editing drug for one form of amyloidosis.