Research Highlights in 2011

A new study reveals that activation of PI3K–AKT signalling is capable of inducing a state that is superficially similar to RAS-induced senescence. However, cooperative activation of both pathways promotes senescence bypass and tumour progression.

This paper shows that activation of the JNK pathway mediates engulfment of premalignant cells by surrounding normal cells in cell competition.

Sequencing of multiple myeloma genomes leads to the identification of novel mutations and potential new therapeutic targets.

Michael Wigler and colleagues sequence single nuclei from two advanced breast carcinomas and a matched metastasis to investigate tumour evolution.

Inhibition of Myc activity in tumour cells induces the collapse of the tumour microenvironment.

A new study suggests that activation of SRC may underlie multiple mechanisms of resistance to the targeted breast cancer therapy, trastuzumab.

Reducing the number of macrophages in primary breast cancers in mice increases sensitivity to paclitaxel through a mechanism involving CD8⁺ T cells, and patients with breast cancer who have a higher ratio of CD68 (a macrophage marker) mRNA levels to CD8mRNA levels have a reduced rate of pathological complete response.

Three papers show that oncogenic RAS induces autophagy.

Three papers show that HiPSCs differ at the genetic and epigenetic levels compared with HESCs.

Angelika Amon and colleagues have isolated drugs that selectively target aneuploid cells.

Galon and colleagues correlate different subsets of T cells with clinical outcome of patients with colorectal cancer.

CD4⁺regulatory T cells promote mammary tumour metastasis through intratumoural RANKL expression.

The DNA repair protein 53BP1 marks regions of under-replicated DNA in the G1 phase of the cell cycle.

A new study suggests that internalization of one cell into another (entosis) may not have the tumour-suppressive effect that it was assumed to have. Instead, entosis leads to aneuploidy and can have tumour-promoting effects.

Two papers describe how wounds 'call' stem cells with the ability to initiate tumours out of their niches.

Charlotte Kuperwasser and colleagues show that BRCA1 regulates SNAI2, which suppresses luminal cell differentiation, leading to the development of basal-like breast cancers.

Nuclear PTEN positively regulates APC–CDH1 in a phosphatase-independent manner.

A new study identifies the selective overexpression of satellite repeats in various cancers.

Canine tumours steal mitochondria from their hosts.

Three papers report the involvement of SLX4 in the Fanconi anaemia DNA repair pathway, and two papers show that mutations inSLX4cause a new subtype of Fanconi anaemia.