Table of contents
May 2008 Vol 8 No 5
From the editors
p319 | doi:10.1038/nrc2388
Research Highlights
Carcinogenesis: Predisposing to behaviour? | PDF (165 KB)
p321 | doi:10.1038/nrc2383
Tumorigenesis: Ready and waiting | PDF (177 KB)
p322 | doi:10.1038/nrc2379
Signalling: Follow your eNOS | PDF (268 KB)
p322 | doi:10.1038/nrc2382
Trial Watch
Don't stop now! | PDF (84 KB)
p322 | doi:10.1038/nrc2387
Therapy: Bad to the bone | PDF (297 KB)
p323 | doi:10.1038/nrc2376
Tumour microenvironment: No changes necessary | PDF (266 KB)
p324 | doi:10.1038/nrc2384
Oncogenes: Sibling rivalry explained | PDF (359 KB)
p324 | doi:10.1038/nrc2385
In the news
The devil with the details | PDF (74 KB)
p324 | doi:10.1038/nrc2386
Signalling: Stress and disease connect at mTORC1 | PDF (282 KB)
p325 | doi:10.1038/nrc2381
Tumour suppressors: Motoring on down | PDF (303 KB)
p326 | doi:10.1038/nrc2377
Metastasis: Bringing up the rear | PDF (373 KB)
p326 | doi:10.1038/nrc2380
Signalling: An oncogene becomes RESTless | PDF (258 KB)
p327 | doi:10.1038/nrc2378
Reviews
Detection, clinical relevance and specific biological properties of disseminating tumour cells
Klaus Pantel, Ruud H. Brakenhoff & Burkhard Brandt
p329 | doi:10.1038/nrc2375
Most cancer deaths are caused by metastatic spread and subsequent growth of tumour cells at distant organs. How are disseminating tumour cells relevant to the biology of early metastatic spread and how might they be used to improve cancer treatment?
Getting to the stem of chronic myeloid leukaemia
Michael Savona & Moshe Talpaz
p341 | doi:10.1038/nrc2368
Imatinib has been an extremely successful treatment for chronic myeloid leukaemia. However, we need to know about the stem cells involved in the disease to understand why relapse is so common when imatinib is stopped.
See also: Correspondence by Williams & Sherr | Author Reply by Savona & Talpaz
Immunotherapy of established (pre)malignant disease by synthetic long peptide vaccines
Cornelis J.M. Melief & Sjoerd H. van der Burg
p351 | doi:10.1038/nrc2373
This Review discusses the recent progress in the treatment of established (pre)malignant disease of viral or non-viral origin with synthetic long peptide vaccines that are capable of inducing robust T-cell responses.
Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival
H. Llewelyn Roderick & Simon J. Cook
p361 | doi:10.1038/nrc2374
Changes in the levels of the second messenger Ca2+ can result in the activation of broadly proliferative or cytotoxic responses. As reviewed here, to tip the balance in their favour, cancer cells often remodel the expression or activity of their Ca2+ signalling apparatus.
Perspectives
Opinion
Fusion of tumour cells with bone marrow-derived cells: a unifying explanation for metastasis
John M. Pawelek & Ashok K. Chakraborty
p377 | doi:10.1038/nrc2371
The causes of metastasis remain elusive. Could the fusion of cancer cells with macrophages or other migratory bone marrow-derived cells (BMDCs) provide an explanation?
Timeline
Wnt signalling and its impact on development and cancer
Alexandra Klaus & Walter Birchmeier
p387 | doi:10.1038/nrc2389
The Wnt signalling pathway has a crucial role in the development of all animal species, and mutations or deregulated expression of components of the Wnt pathway can result in cancer. This Timeline examines the past 25 years of crucial discoveries — from a variety of disciplines — about the components and functions of this pathway.
Science and society
The challenge of cancer control in Africa
Rebecca J. Lingwood, Peter Boyle, Alan Milburn, Twalib Ngoma, John Arbuthnott, Ruth McCaffrey, Stewart H. Kerr & David J. Kerr
p398 | doi:10.1038/nrc2372
The developing world is set to be ravaged by an impending cancer epidemic. How can we help to ensure that cancer patients get the treatment they need in Africa?
Corrigendum: Prostate-specific antigen and prostate cancer: prediction, detection and monitoring (Corrigendum)
Hans Lilja, David Ulmert & Andrew J. Vickers
p403 | doi:10.1038/nrc2395
