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Two papers recently published in Nature Medicine and Science Signaling highlight the various interdependent or independent ways by which YAP and TAZ can affect tumour growth.
Lee, Singh et al. find that cancer-specific intronic polyadenylation events occur frequently in tumour suppressor genes in chronic lymphocytic leukaemia (CLL) and generate truncated proteins that could act as CLL drivers.
D’Amico et al. show that, in the presence of oncogenic RAS mutations, STAT3 acts as a tumour modifier by regulating the epithelial differentiation of pancreatic and lung cancer cells via p63.
Seehawer, Heinzmann et al. show that lineage commitment in liver cancer is independent of oncogenic driver expression and is instead dictated by the type of cell death occurring in the nearby liver microenvironment.
Keren et al. have used multiplexed imaging in intact samples from breast cancer patients to gain insights into the architecture of the tumour immune microenvironment.
Yang et al. have used genetically engineered mouse models of small cell lung cancer to show that the same genomic alterations in different cells of origin lead to the formation of tumours that follow distinct evolutionary paths to metastasis.
This Review discusses how cells with stem cell characteristics often serve as the tumour cell of origin, as they are preferentially primed for transformation. Furthermore, the activation of stem cell programmes can be crucial for promoting cancer progression and therapy resistance.
This Review discusses new insights into molecular mechanisms that link the dysregulation of polyamine metabolism with carcinogenesis and strategies for targeting this pathway for cancer therapy.
This Review discusses the 2018 Catalogue of Somatic Mutations in Cancer (COSMIC) Cancer Gene Census (CGC), an expert-curated description of human cancer genes, which has recently been expanded to include functional descriptions of how each gene contributes to cancer.
This Opinion discusses the potential of fasting and fasting-mimicking diets to help overcome toxicities induced by anticancer therapy. The differential response of normal and cancer cells undergoing starvation is argued to make normal cells less sensitive to therapy-induced toxicity, while cancer cells become more sensitive to therapy-induced cell death.
