Table of contents
From the editors
p481 | doi:10.1038/nrc2338
Research Highlights
Metastasis: Regressing to self-renewal | PDF (272 KB)
p483 | doi:10.1038/nrc2423
Signalling: Survival of the sweetest | PDF (300 KB)
p484 | doi:10.1038/nrc2424
Tumorigenesis: Combined effort | PDF (227 KB)
p484 | doi:10.1038/nrc2426
In the news
Weighing benefits and risks | PDF (77 KB)
p484 | doi:10.1038/nrc2435
Cell cycle: Stop start | PDF (288 KB)
p485 | doi:10.1038/nrc2421
Genetics: Looking at the big picture | PDF (163 KB)
p486 | doi:10.1038/nrc2422
Tumour suppressor: Confirming DLC1 | PDF (201 KB)
p486 | doi:10.1038/nrc2425
Trial Watch
Vaccinating the brain | Positively platinum | PDF (85 KB)
p486 | doi:10.1038/nrc2436
In brief
Chemotherapy | Immunotherapy | DNA repair | PDF (91 KB)
p487 | doi:10.1038/nrc2430
Tumorigenesis: Some HIFs are more equal than others | PDF (304 KB)
p488 | doi:10.1038/nrc2427
Senescence: Hold that thought | PDF (263 KB)
p488 | doi:10.1038/nrc2429
Tumorigenesis: Too much of a good thing | PDF (258 KB)
p489 | doi:10.1038/nrc2428
Progress
Targeting the oncogene and kinome chaperone CDC37
Phillip J. Gray, Jr, Thomas Prince, Jinrong Cheng, Mary Ann Stevenson & Stuart K. Calderwood
p491 | doi:10.1038/nrc2420
CDC37 is oncogenic because it stabilizes the structures of mutated or overexpressed oncogenic kinases. Targeting this chaperone activity, on which many tumours depend, is therefore an attractive option for broad-based therapy.
Reviews
Recurrent gene fusions in prostate cancer
Chandan Kumar-Sinha, Scott A. Tomlins & Arul M. Chinnaiyan
p497 | doi:10.1038/nrc2402
Gene fusions have long been known to have an important role in leukaemias, but they have recently been identified in a majority of prostate cancers. Understanding their role in this disease could lead to better targeted therapies.
Article series: Senescence
Living on a break: cellular senescence as a DNA-damage response
Fabrizio d'Adda di Fagagna
p512 | doi:10.1038/nrc2440
Cellular senescence is associated with ageing and cancer in vivo and has a proven tumour suppressive function. This Review discusses the evidence indicating that DNA damage and the engagement of the DNA-damage response pathways are common to both ageing and cancer.
MYB function in normal and cancer cells
Robert G. Ramsay & Thomas J. Gonda
p523 | doi:10.1038/nrc2439
The transcription factor MYB seems to have key roles as a regulator of epithelial stem and progenitor cells. Therefore, MYB is an oncogene that is involved in some human leukaemias, and could also be involved in epithelial cancers such as colorectal cancer and breast cancer.
Perspectives
Opinion
Revisiting the biological roles of PAI2 (SERPINB2) in cancer
David R. Croucher, Darren N. Saunders, Sergei Lobov & Marie Ranson
p535 | doi:10.1038/nrc2400
Of the two main urokinase plasminogen activator inhibitors, high tumour levels of the type 1 inhibitor promote tumour progression, whereas high levels of the type 2 inhibitor decrease tumour growth and metastasis. What might be the basis of this paradoxical action?
Opinion
Exploring the role of cancer stem cells in radioresistance
Michael Baumann, Mechthild Krause & Richard Hill
p545 | doi:10.1038/nrc2419
Cancer stem cell content and the intrinsic radiosensitivity of cancer stem cells is thought to vary between tumours, thereby affecting their radiocurability. What do we know about cancer stem cells in radioresistance and how might this information be used?
See also: | Correspondence by Maurice et.al | Correspondence by Baumann et.al |
Science and society
Banking on cord blood stem cells
Michael J. Sullivan
p555 | doi:10.1038/nrc2418
The controversy surrounding private, for–profit umbilical cord blood banks continues unabated. What is the scientific rationale for banking your child's cord blood for its potential future use against malignancy? Michael sullivan investigates.
See also: | Correspondence by Nietfeld | Correspondence by Harris | Author's Reply by Sullivan | Correspondence by Patrinos |
Correspondence
Correspondence: BCR–ABL and CDKN2A: a dropped connection
Richard T. Williams & Charles J. Sherr
p563 | doi:10.1038/nrc2368-c1
Author Reply: Cell-cycle deregulation in progressive CML
Michael Savona & Moshe Talpaz
p563 | doi:10.1038/nrc2368-c2
