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Two studies reported inNature have identified a mutation in microphthalmia-associated transcription factor (MITF) that predisposes to familial melanoma, as well as to sporadic melanoma and renal cell carcinoma.
The treatment of patients with refractory non-small-cell lung cancer with a low-dose DNA methyltransferase inhibitor and a histone deacetylase inhibitor shows promise for a subset of patients.
Johanna Joyce and colleagues show that tumour-associated macrophages protect breast tumour cells from cell death mediated by various chemotherapeutic agents.
Two papers inNature Geneticsshow that the isocitrate dehydrogenases IDH1 and IDH2 are mutated in two subtypes of the cancer-prone enchondromatosis syndrome.
The α-subunits that form the oxygen-sensitive component of the hypoxia-inducible factor (HIF) transcription factor have unique and overlapping roles in mediating cellular responses to hypoxia. Surprisingly, they can also have opposing roles, and the differences between HIF1α and HIF2α are discussed in this Review.
The regulation of cell polarity has pleiotropic effects on cell morphology and function, which has implications for tumorigenesis and tumour progression. This Review discusses how polarity complexes affect tumour cell biology and their crosstalk with other important cancer pathways.
Metastasis accounts for the vast majority of cancer deaths. The potential of using nanoparticles to diagnose and to treat metastatic cancer is highlighted in this Review.
Human cell engineering has made considerable progress, but where to insert foreign sequences in the human genome to maximize safety and efficacy is still uncertain. This Opinion article discusses genomic safe harbours, which are chromosomal locations where therapeutic transgenes can integrate and function without perturbing endogenous gene activity or promoting cancer.
Recent evidence indicates that successful cancer clones must have overcome programmed cell removal. In this Opinion article, the authors explore the role of programmed cell removal in both normal and neoplastic cells.
Inherited inactivating mutations inBRCA1 or BRCA2seem to cause a similar predisposition to breast and ovarian cancer, but a closer look reveals many differences as well. This Perspective discusses the similarities and differences between BRCA1 and BRCA2 and their effects on cancer phenotypes.
