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Landau, Carter, Stojanov and colleagues characterize genetic clonal evolution in chronic lymphocytic leukaemia and connect the occurrence of clonal evolution to therapy and prognosis.
A recent paper published inBloodindicates that the interaction between AML1–ETO and the transcriptional co-repressor NCOR1 is partly responsible for limiting the leukaemogenic capacity of this fusion gene.
Tumorigenic genetic and epigenetic changes in epithelial cells occur as a result of increased inflammation following the loss of transforming growth factor-β receptor 2 in stromal fibroblasts.
In medulloblastoma, placental growth factor (PLGF) may signal through a non-tyrosine kinase receptor, neuropilin 1 (NRP1), to promote tumour cell survival without having a substantial effect on angiogenesis, thus providing a rationale for targeting this pathway in these tumours.
Pigment epithelium-derived factor (PEDF) has anti-angiogenic, antitumorigenic and antimetastatic properties. If PEDF is to be used for cancer management, a deeper appreciation of its many functions and mechanisms of action is needed, as discussed in this Review.
A new study combines evolutionary simulations with clinical mutation data to suggest that passenger mutations in cancers might have more functional consequences than is often assumed.
The presence of chronic obstructive pulmonary disease (COPD) is linked to an increased risk of developing lung cancer, independently of cigarette smoking dosage. This Review discusses the nature of the link between the two diseases and considers specific mechanisms that operate in both COPD and lung cancer.
A wealth of recent studies has characterized roles for the Hippo pathway in diverse cancer-relevant processes. This Review discusses our latest understanding of Hippo pathway signalling in cancer, including mechanisms of pathway disruption in cancer, and the opportunities and challenges for therapeutic intervention.
A subset of melanoma cells express high levels of PGC1α, which alters their metabolic phenotype compared with melanoma cells that do not express PGC1α.
Eda Yildirim, Jeannie Lee and colleagues present intriguing evidence that the long non-coding RNA X-inactive specific transcript (Xist) is required for maintaining X-chromosome inactivation, and that the loss of Xistafter X inactivation can cause haematopoietic cancers in mice.
The vast majority of the research into cancer metabolism has been limited to a handful of metabolic pathways, with other pathways being sidelined. This Progress article brings to light the potential contribution of fatty acid oxidation to cancer cell function.
The CPEBs regulate polyadenylation — and thus expression — of certain RNAs, including those encoding oncogenes and tumour suppressors. This Opinion article analyses whether the CPEBs are deregulated in cancer and discusses the possible implications for cancer biology.
