Browse our latest Cancer Biology articles

In the pancreas, reciprocal interactions between epithelial cells and myeloid cells determine the balance between tissue repair and carcinogenesis by regulating acinar cell plasticity through differential activation of EGFR/MAPK signaling.

53BP1 and BRCA1 antagonistically control a temporal choice of two distinct pathways to restart stalled replication forks in a DNA double stand repair-independent manner.

Application of machine learning to serum miRNA profiles generated through next generation sequencing identifies a biologically relevant miRNA signature which can be deployed as a qPCR test to assist the diagnosis of epithelial ovarian cancer.

ESRP1 is central to intestinal barrier integrity in mice and humans and alterations in ESRP1 function or expression contribute to intestinal pathology, partly through modified expression of ESRP1-specific GPR137 isoforms.

Loading of CD95 and CD95L-derived sequences into the RNA-induced silencing complex elicits a distinct form of RNAi-mediated cell death of cancer cells that results from the targeting of multiple survival genes.

The glial developmental factor, Daam2, promotes glioma tumorigenesis by degrading the VHL tumor suppressor, illustrating how dysregulation of gliogenic factors can impact tumor suppressor activity and promote glioma tumorigenesis.

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.

Targeting the activation of the androgen receptor N-terminal domain by the cochaperone Bag-1L provides a new approach for inhibiting androgen receptor function to treat prostate cancer.

Activation of the NRF2 antioxidant program leads to an imbalance in central carbon metabolism and sensitizes cancers to glutaminase inhibition.

The oncogenic Ras^V12 keeps cells mutant for the tumor suppressor scribble in an undead-like condition, which is required for an amplification loop that promotes tumorigenesis.