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Why do inherited germline mutations in common cancer-associated genes cause a restricted pattern of tissue-specific malignancies, but when somatic mutations occur in these genes they exhibit far less tissue restriction?
Genome sequencing of therapy-related acute myeloid leukaemia (t-AML) has revealed that these malignancies do not have more mutations thande novo AML, and that TP53mutations, which are common in t-AML, are likely to be present before treatment with chemotherapy and expand following treatment.
Yodaet al. have shown that mutations in G protein-β (Gβ) subunits occur in haematological malignancies and can transform cells. Mutant Gβ can also confer resistance to different therapeutic kinase inhibitors.
Madsenet al. have delineated the roles of components of the striatin-interacting phosphatase and kinase (STRIPAK) complex in cancer cell migration and metastasis, which may explain why some of these proteins are overexpressed or mutated in cancer.
YAP and TAZ are the major downstream effectors of the Hippo pathway. This Progress article summarizes the latest findings regarding the biological functions of YAP and TAZ, and their role in connecting the Hippo pathway with other relevant pathways in cancer.
The RUNX transcription factors seem to have dichotomous roles in cancer, sometimes being oncogenic and sometimes acting as tumour suppressors. This Review discusses the many roles of the RUNX family in cancer biology.
The S100 family of proteins modulates cellular responses by acting both as intracellular Ca2+sensors and as extracellular factors. Expression of several members of this family is dysregulated in cancer, and each cancer shows a unique S100 protein profile or signature. In this Review, Anne Bresnick and colleagues highlight new findings regarding the role of S100 proteins in cancer diagnosis and treatment.
Although dysregulation of histone methylation has been widely studied in cancer, accumulating evidence suggests that cancer-relevant non-histone proteins such as p53, RB1 and signal transducer and activator of transcription 3 (STAT3) are also regulated by lysine methylation. This Review summarizes the possible functions of non-histone protein lysine methylation in cancer.
Complementing government and industry funding, philanthropies have made distinct contributions to altering the trajectory of cancer research. This Science and Society article aims to investigate the changing role of philanthropy in fostering cancer research, with emphasis on the work of non-profit institutions.
