Browse our latest Cancer Biology articles

A putative therapeutic target undergoing clinical trials in breast cancer is non-essential and the drug used in those trials blocks cell division through an off-target effect.

Partial copy loss of spliceosome genes are common non-driver gene dependencies in cancer.

The loss of genes that encode RNA splicing factors weakens cancer cells in a way that could be exploited by new approaches to treatment.

Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

Tumor-growth-factor-beta signaling helps cancer cells to evolve and become resistant to drugs by down-regulating accurate DNA repair.

A new mechanism connects the loss of TGFβ signaling with invasion and metastasis in highly malignant transition zone tumors.

A new luciferase and fluorescent reporter system enables rapid and efficient in-cell profiling of the majority of protein kinase oncogenes known to date.

Loss of KEAP1 modulates sensitivity to targeted therapies in lung cancer.

Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.

Stromal cell levels and localization of active α₅β₁-integrin are regulated by desmoplastic extracellular matrix control of α_vβ₅-integrin signaling, and predict clinical outcomes for pancreatic and renal cancer patients.