Latest Articles Include:
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- Nat Rev Cancer 11(2):77 (2011)
- Genomics: Driving cancer biology | PDF (194 KB)
- Nat Rev Cancer 11(2):79 (2011)
Identifying genes as drivers of tumorigenesis from cancer genomics analyses is a crucial challenge. Dana Pe'er and colleagues have developed a new algorithm, copy number and expression in cancer (CONEXIC), to identify genes that exhibit copy number alterations (CNAs) that drive tumorigenesis. - Medulloblastoma: Origins | PDF (256 KB)
- Nat Rev Cancer 11(2):80 (2011)
The term medulloblastoma covers a range of distinct brain tumour subtypes that arise in childhood and have long been associated with the cerebellum. However, Paul Gibson and colleagues have found that one subtype, characterized by mutations in the Wnt pathway, actually arises in the brain stem. - Metabolism: Choose your carbon source | PDF (134 KB)
- Nat Rev Cancer 11(2):80 (2011)
Glucose and glutamine are the primary carbon sources for ATP production and biosynthesis in proliferating mammalian cells, but how their uptake and metabolism is coordinated according to supply is poorly understood. A recent report uncovers new mechanistic details of this regulation, indicating that flux through the hexosamine pathway is a crucial determinant of glutamine uptake. - Going up | PDF (92 KB)
- Nat Rev Cancer 11(2):80 (2011)
A recent report from researchers at the National Cancer Institute (NCI) in the United States has shown that the costs of caring for cancer patients in the United States could increase by as much as 66% by 2020. The reasons for this increase were outlined by Dr Robin Yabroff of the NCI who was involved in the study, "We are expecting to see a lot more cancer in the future ... mostly in the elderly. - Epigenetics | Melanoma | Metabolism | Breast cancer | PDF (118 KB)
- Nat Rev Cancer 11(2):81 (2011)
TRIM24 links a non-canonical histone signature to breast cancer Tsai, W.-W.et al. Nature 468, 927–932 (2010) - Cell signalling: Weighing up TGFβ signals | PDF (144 KB)
- Nat Rev Cancer 11(2):82 (2011)
Signalling through the Hippo pathway allows sensing of local cell density and subsequent control of cell growth, proliferation and apoptosis. The transcriptional regulators TAZ and YAP are key components in this response, and Varelas et al. - Genome instability: Chrombling into pieces | PDF (149 KB)
- Nat Rev Cancer 11(2):82 (2011)
It is generally assumed that tumours evolve through a progressive acquisition of mutations in the genome that allow cells to evade apoptosis, proliferate, invade and metastasize. However, in some instances one single event can lead to multiple coexisting mutations — the loss of telomeres results in end-to-end chromosome fusions that lead to chromosomal rearrangements. - Signalling: REX rules | PDF (202 KB)
- Nat Rev Cancer 11(2):83 (2011)
Many of the signalling pathways that are disrupted in breast cancer, such as the ERBB family of tyrosine kinase receptors, have been characterized, but the precise downstream effector pathways are still being identified. Two recent papers have identified a RAC-guanine nucleotide exchange factor (GEF) that is required for breast cancer progression. - Regulation of cancer cell metabolism
- Nat Rev Cancer 11(2):85 (2011)
Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. However, the initial hypotheses that were based on these observations proved inadequate to explain tumorigenesis, and the oncogene revolution pushed tumour metabolism to the margins of cancer research. In recent years, interest has been renewed as it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology. - DNA polymerases and cancer
- Nat Rev Cancer 11(2):96 (2011)
There are 15 different DNA polymerases encoded in mammalian genomes, which are specialized for replication, repair or the tolerance of DNA damage. New evidence is emerging for lesion-specific and tissue-specific functions of DNA polymerases. Many point mutations that occur in cancer cells arise from the error-generating activities of DNA polymerases. However, the ability of some of these enzymes to bypass DNA damage may actually defend against chromosome instability in cells, and at least one DNA polymerase, Pol ζ, is a suppressor of spontaneous tumorigenesis. Because DNA polymerases can help cancer cells tolerate DNA damage, some of these enzymes might be viable targets for therapeutic strategies. - Wilms' tumours: about tumour suppressor genes, an oncogene and a chameleon gene
- Nat Rev Cancer 11(2):111 (2011)
Genes identified as being mutated in Wilms' tumour include TP53, a classic tumour suppressor gene (TSG); CTNNB1 (encoding β-catenin), a classic oncogene; WTX, which accumulating data indicate is a TSG; and WT1, which is inactivated in some Wilms' tumours, similar to a TSG. However, WT1 does not always conform to the TSG label, and some data indicate that WT1 enhances cell survival and proliferation, like an oncogene. Is WT1 a chameleon, functioning as either a TSG or an oncogene, depending on cellular context? Are these labels even appropriate for describing and understanding the function of WT1? - Contribution of platelets to tumour metastasis
- Nat Rev Cancer 11(2):123 (2011)
Extensive experimental evidence shows that platelets support tumour metastasis. The activation of platelets and the coagulation system have a crucial role in the progression of cancer. Within the circulatory system, platelets guard tumour cells from immune elimination and promote their arrest at the endothelium, supporting the establishment of secondary lesions. These contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy. - Mouse models of advanced spontaneous metastasis for experimental therapeutics
- Nat Rev Cancer 11(2):135 (2011)
An enduring problem in cancer research is the failure to reproduce highly encouraging preclinical therapeutic findings using transplanted or spontaneous primary tumours in mice in clinical trials of patients with advanced metastatic disease. There are several reasons for this, including the failure to model established, visceral metastatic disease. We therefore developed various models of aggressive multi-organ spontaneous metastasis after surgical resection of orthotopically transplanted human tumour xenografts. In this Opinion article we provide a personal perspective summarizing the prospect of their increased clinical relevance. This includes the reduced efficacy of certain targeted anticancer drugs, the late emergence of spontaneous brain metastases and the clinical trial results evaluating a highly effective therapeutic strategy previously tested using such models. - Cancer-related direct-to-consumer advertising: a critical review
- Nat Rev Cancer 11(2):142 (2011)
The direct-to-consumer advertising (DTCA) phenomenon has received attention because of its attempt to reach out to consumers by bypassing important gatekeepers such as physicians. The emergence of new information platforms and the introduction of genetic tests directly to the consumer have heightened the concern with DTCA and its potential consequences. These effects of DTCA are particularly important given the communication inequalities among social groups, with class, race and ethnicity influencing how people access, seek, process and act on information. This Science and Society article reviews the major issues regarding general and cancer-related DTCA and also offers data from a national survey in the United States as an example of the communication inequalities in genetic testing awareness.
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