Skip to Main Content

Advertisement

Skip Nav Destination

Issues

In This Issue

In the Spotlight

Science in Society

In Focus

Cancer Hallmarks Review

Research Briefs

A novel Bayesian method to time the occurrence of complex copy number gains was applied to thousands of tumor whole genome sequences, allowing the temporal dynamics between whole genome doubling and other copy number events to be evaluated.

NOTCH3+ cells present in the perivascular stem cell niche promote tumor-initiation, proliferation, and angiogenesis in meningiomas and are a therapeutic vulnerability.

Research Articles

STAG2/LMO2 T-ALL is common in very young children with γδ T-ALL, is high risk, and is characterized by altered chromatin looping, impaired hematopoietic differentiation, and vulnerability to PARP inhibition.

Functional genomic screens in mutant hematopoietic stem cells using an ex vivo co-culture platform nominate KDM3B and an epigenetically regulated signaling pathway as dependencies in a subset of clonal hematopoiesis.

While NK cells naturally lack CD28, incorporating CD28 costimulation into CAR design enhances the antitumor efficacy of CAR-NK cells by recruiting key signaling kinases, underscoring its potential for improving CAR-NK based cancer immunotherapy.

Treatment with an iron chelator sensitizes ovarian tumors to innate immune attack, hindering disease progression and enhancing standard therapy.

Analysis of therapy-resistant leukemia stem cells (LSC) revealed that inhibition of mitochondrial calcium uptake acts to inhibit oxidative phosphorylation, thereby leading to subsequent eradication of LSCs.

This study identifies and characterizes a molecular pathway that causes re-activation of telomerase by high Fe3+-iron, thereby providing novel therapeutic targets for inhibiting this enzyme which drives 90% of human cancers.

Tumor cell-derived signals induce stromal IL33 expression in pancreatic cancer and stromal IL33 promotes pancreatic cancer growth by supporting immunosuppression.

Applying a recordable barcode in a prostate cancer model delineates the clonal architecture, seeding topologies, and routes taken by distinct cancer clones that traverse metastatic sites.

Close Modal

or Create an Account

Close Modal
Close Modal