In This Issue
Cancer Discov October 1 2020 10 (10) 1426-1430; DOI:10.1158/2159-8290.CD-ITI10-10
Higher risk of death from COVID-19 among patients with cancer was correlated with male sex, greater age, presence of multiple comorbidities, advanced-stage disease, and active disease; there was no association between risk and anticancer treatment.
Reversion mutations that cause resistance of initially homologous recombination–deficient tumors to PARP inhibitors and platinum-based chemotherapies often affect BRCA1/2 and may lead to susceptibility to immunotherapy.
Poor CD8+ T-cell infiltration, defective antigen presentation, and aberrant upregulation of CCL27 and CCR10 and downregulation of TNFSF9 (all immune system genes) were associated with progression of preinvasive lung carcinoma in situ.
Compared with granulocyte–monocyte progenitor cell–derived acute myeloid leukemia, hematopoietic stem cell–derived leukemia was more resistant to LSD1 inhibition and apoptosis, but resistance was reversed by venetoclax.
In a large observational study in patients with COVID-19 and cancer, survival was not significantly influenced by receipt of COVID-19 treatments, except hydroxychloroquine plus any other treatment, which was associated with reduced survival.
In a phase I trial of patients with advanced solid tumors, combination treatment with the PARP inhibitor olaparib and the AKT inhibitor capivasertib showed early signs of efficacy, supporting preclinical observations of synergy.
CD39-expressing acute myeloid leukemia cells expanded after cytarabine treatment and activated the cell survival–promoting mitochondrial stress response, leading to relapse with chemotherapy-resistant disease.
A new mouse model enabled ascertainment of molecular details of the two pancreatic ductal adenocarcinoma subtypes, revealing that the transition from a slow-growing to a fast-growing tumor is marked by activation of KRAS signaling genes.
Colorectal cancer organoids escaped dependence on WNT signaling via a combination of cancer-associated mutations and priming by TGFβ, abundant in the tumor microenvironment, indicating a possible mechanism of resistance to PORCN inhibitors.