Articles in 2015

Stites and Trampontet al. used mathematical modelling with verification in cells and cancer genome data to understand the effects of weakly activating RAS mutations. They found that pairs of mutations within the RAS pathway might be able to act together to create a selective advantage in human tumours.

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.

This study describes a novel approach to increase blood vessels in tumours to enhance drug delivery, uptake and metabolism.

Hosteet al. discuss whether allergic immune responses, which have been observed to be protective against some types of cancer, can be activated to target cancer, and what the mechanism of antitumour allergic responses might be.

Two studies have examined how manipulation of energy availability by cancer cells, mediated by changes in microRNAs (miRNAs), can fuel metastatic colonization.

Two studies offer new possibilities to fight BRAF inhibition resistance.

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.

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.

Tumour cells without mitochondrial DNA acquire mitochondria from host cells to re-establish respiration and tumour-initiating efficacy.

Three papers report on the use of acetate as a nutrient in tumour cells undergoing metabolic stress.

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.

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?

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.