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Vascular anomalies are frequent in patients with PHTS. Loss of the PTEN gene in endothelial cells causes PHTS-related vascular malformations, which are reduced by PI3K signaling inhibitors in a novel mouse model as well as in patients.

Research Articles

In the U.S., incidence rates of some cancers have increased in 15- to 49-year-olds with concomitant increases in older age groups, suggesting that changes in risk factor prevalence and/or improvements in detection could impact risk across age ranges.

Single-cell analyses of a spontaneous glioblastoma mouse model and tumor-free subventricular zone tissues from patients identify precancerous cells, arising via an oligodendrocyte progenitor lineage, that initiate gliomagenesis and drive intratumoral heterogeneity.

RAS inhibition reveals how RAS mutations dictate oncogenic signaling and response to therapy, suggests codon-specific treatments against multiple cancers, and explains the high frequency of RASQ61 mutations in EGFR inhibitor–resistant colorectal cancer.

In human and murine melanomas, HPGDS identifies a subset of immunosuppressive tumor-associated macrophages, whereas HPGDS downregulation through TNFα release by activated CD8+ T cells signals efficient anti–PD-1 treatment.

Phospholipase signaling drives stress granule formation in a cell cycle–dependent manner, generating tumor cell sensitivity to phospholipase inhibition in combination with G2-stalling chemotherapeutics in orthotopic models of pancreatic ductal adenocarcinoma.

IL1RAP blockade reverses IL1-induced systemic immunosuppression in HPV16+ cancers, enabling efficacy of a therapeutic vaccine, and survival benefit is further enhanced in combination with anti-CTLA4 in a preclinical model.

The cell-intrinsic antiproliferative effects of HIF2 inhibitors in kidney cancer are caused by loss of cyclin D1 activity, and upregulation of cyclin D2 or D3 are potential resistance mechanisms.

Tumor-related IL6/IL1β-dependent induction of hepatic PCSK9 downregulates hepatic LDL receptor (LDLR) expression, activating RORγ-dependent expansion of suppressive protumor myeloid populations and favoring tumor progression.

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