Browse our latest Cancer Biology articles

Six computationally designed and in vitro optimized protein inhibitors serve as molecular probes to reveal BCL2 profiles of different human cancers.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

A new tumor suppressor function of p21, needed at each undamaged duplication cycle, ensures the adequate execution of the DNA replication program thereby protecting the genome integrity.

An effector of AMPK is essential for the kinase and its pharmacological activators, including Metformin, to strengthen cell-cell junctions and preserve epithelial cell polarity and barrier functions in the face of energetic stress, as well as to suppress oncogenesis.

Engineered T cell receptors enable targeted immunotherapy with a reduced risk of harmful autoimmunity.

The earliest steps of tumor initiation in the cerebellum are regulated by critical interactions between pre-tumor cells and stromal cells, which can be manipulated by targeting the Norrin/Frizzled4 signaling axis.

Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.

Carbonyl stress mediated by Methylglyoxal affects Hsp90 activity, inhibits the Hippo pathway and promotes tumor growth and metastasis in breast cancer.

Clinical analysis corroborated with experimental data demonstrate that Δ133p53β, a naturally occurring isoform of p53 protein, induces a pro-metastatic program and is a clinical indicator of metastasis, independently of TP53 mutation status.

A unique two-step mechanism of plasma membrane recruitment and activation governs G-protein-coupled receptor mediated PI3K signaling.