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Neurofibromatosis type 1 (NF1) is a cancer predisposition syndrome, and somaticNF1 mutations are also common in tumours. The neurofibromin protein (encoded by NF1) is a RAS GTPase-activating protein that activates RAS–MAPK signalling when lost. This Review discusses NF1 disease, neurofibromin signalling pathways and recent developments in NF1 therapeutics.
Heterogeneous expression of the epidermal growth factor receptor (EGFR) in glioblastoma poses an important challenge for the effective use of EGFR-targeted therapies. In this Opinion article, Furnariet al. highlight the possible mechanisms underlying EGFR heterogeneity, and the importance in understanding these mechanisms to improve treatment outcome in glioblastoma.
This Opinion article advocates therapeutically targeting the niches that harbour dormant disseminated tumour cells in order to make them susceptible to cytotoxic agents. Similar strategies have sensitized leukaemic cells and latent HIV to therapy, and such an approach might delay or even prevent metastasis.
Caveolar lipid rafts are distinct regions of the cell membrane that can mediate diverse signalling events, including the regulation of autophagy, responses to oxidative stress and metabolism. What are the implications of caveolae in cancer cells and associated stromal cells?
Haematological malignancies have provided both initial proofs of concept and an informative testing ground for various immune-based cancer therapeutics. The immune-cell origin of many of the blood malignancies provides a unique opportunity both to understand the mechanisms of cancer immune responsiveness and immune evasion, and to exploit the unique therapeutic opportunities they provide.
Protein-linked DNA breaks can be formed through the abortive activity of topoisomerases — this Review discusses the roles of such breaks during transcription and in triggering gene deletions and translocations in cancer.
Mutations in the gene encoding DNA methyltransferase 3A (DNMT3A) have been reported in patients with various haematological malignancies, suggesting that DNMT3A could be a tumour suppressor. In this Review, Yanget al. put data from basic science studies into clinical context, opening stimulating discussions regarding possible new therapeutic avenues.
Lynch syndrome is caused by heterozygous mutations and epimutations in mismatch repair genes, which lead to specific pathologies, including increased risk of multiple types of cancer and microsatellite instability. Lynch syndrome has been pivotal to the history of understanding hereditary cancer-prone syndromes and continues to lead the way in our understanding of the risk and treatment of familial cancers.
There is evidence that African-American women with triple-negative breast cancer (TNBC) have worse clinical outcomes than women of European descent with TNBC. However, it is unclear whether survival differences persist after adjusting for health disparities. Understanding the relative contributions of biology and disparities is crucial for improving the poor survival of African-American women with TNBC.
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.
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.
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.
