Cancer stem cells: Tracing clones | PDF (124 KB)

p579 | doi:10.1038/nrc3354

Three papers have used lineage tracing to examine the contribution of individual cells to tumour growth.

Tumour suppressors: At the SHARP end of metastasis | PDF (112 KB)

p580 | doi:10.1038/nrc3347

A new study uncovers a tumour suppressor role for SHARP1.

Micrornas: Lines of communication | PDF (1,792 KB)

p580 | doi:10.1038/nrc3348

Tumour cell-derived miRNAs carried in microvesicles can communicate with endothelial cells to activate angiogenesis through Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signalling.

Migration: VEGF suppresses invasion | PDF (578 KB)

p581 | doi:10.1038/nrc3345

Blocking vascular endothelial growth factor (VEGF) can promote the invasive growth of glioblastoma through a mechanism that involves MET and VEGF receptor 2.

Genomics: Viral vista | PDF (417 KB)

p582 | doi:10.1038/nrc3346

Looking at the effects of proteins encoded by DNA tumour viruses on the host genome could aid the interpretation of high-throughput sequencing data from cancer samples.

Medulloblastoma: Pump up the volume | PDF (139 KB)

p583 | doi:10.1038/nrc3353

The voltage-gated potassium channel EAG2 is overexpressed in medulloblastoma and contributes to tumorigenesis by regulating cell volume dynamics during mitosis.

Therapeutics: Holding JAK back | PDF (127 KB)

p583 | doi:10.1038/nrc3357

A new study characterizes mechanisms of tolerance to JAK2 inhibitors.

Immunology: TIM3 suppresses antitumour DCs | PDF (144 KB)

p584 | doi:10.1038/nrc3349

Chiba and colleagues characterize the role of TIM3 in suppressing innate antitumour immune responses.

Metastasis: No sympathy? | PDF (160 KB)

p584 | doi:10.1038/nrc3351

Stimulation of the sympathetic nervous system through prolonged emotional stress might increase bone metastases in patients with breast cancer owing to effects on the bone marrow microenvironment.

Glioblastoma: Transforming fusions induce aneuploidy | PDF (251 KB)

p585 | doi:10.1038/nrc3350

A recurrent oncogenic fusion of fibroblast growth factor receptor (FGFR) and transforming acidic coiled-coil (TACC) proteins in a subset of glioblastomas can directly interfere with cell division and induce aneuploidy, and this can be inhibited by FGFR kinase inhibitors.

The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance

Peter Bouwman & Jos Jonkers

p587 | doi:10.1038/nrc3342

DNA damage response signalling pathways are often altered in tumours, which can affect their response to chemotherapy and targeted therapies. This Review discusses the mechanisms by which altered DNA damage responses elicit such therapy resistance.

• Abstract
• Full Text
• PDF (716 KB)
• Supplementary information

The role of mutations in epigenetic regulators in myeloid malignancies

Alan H. Shih, Omar Abdel-Wahab, Jay P. Patel & Ross L. Levine

p599 | doi:10.1038/nrc3343

Alterations to epigenetic regulators are a recently characterized class of oncogenic changes in myeloid malignancies. This Review discusses what these alterations mean for leukaemogenesis.

• Abstract
• Full Text
• PDF (885 KB)

MicroRNAs in the p53 network: micromanagement of tumour suppression

Heiko Hermeking

p613 | doi:10.1038/nrc3318

This Review discusses how microRNAs (miRNAs) are intricately involved in p53 signalling, from the regulation of p53 expression and activity to contributing to various tumour suppressor effector functions of p53. Evidence for the importance of these miRNAs from cancer-specific alterations, and the implications for diagnostics and therapeutics, are also considered.

• Abstract
• Full Text
• PDF (587 KB)

Aiding and abetting roles of NOX oxidases in cellular transformation

Karen Block & Yves Gorin

p627 | doi:10.1038/nrc3339

NADPH oxidases of the NOX family are reactive oxygen species-generating enzymes that regulate redox-sensitive signalling pathways. In this Review, the authors discuss primary targets and redox-linked signalling systems that are influenced by NOX-derived ROS and the biological role that NOX oxidases might have in the aetiology of cancer.

• Abstract
• Full Text
• PDF (468 KB)