Investigating reproducibility in preclinical cancer research.

Lactate in pancreatic cancer micro-environment can lead to TET enzyme activation and loss of DNA methylation seen in cancer associated fibroblasts.

NIFK promotes lung cancer metastasis via Runx1-dependent repression of CK1α, which activates TCF4/β-catenin signaling.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

DECR1, a rate-limiting enzyme for polyunsaturated fatty acid (PUFA) β-oxidation, is an androgen-repressed gene in prostate cancer cells that limits oxidative stress to promote cancer cell survival.

A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.

Treatment with precision nanomedicine in combination with an anti-angiogenic peptide enhance anti-tumor efficacy while minimizing toxicities in a pre-clinical glioblastoma model, making this approach a promising and important therapeutic alternative for patients.

Overexpression of BAG2—a novel mutant p53 binding protein—in tumors inhibits MDM2-mediated mutant p53 degradation, which leads to the accumulation of mutant p53 protein and promotes tumorigenesis.

Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.