BBA - Reviews on Cancer (v.1471, #2)
Mouse models of neurofibromatosis by Andrea I. McClatchey; Karen Cichowski (M73-M80).
Keywords: Neurofibromatosis; Mouse; Malignant peripheral; Nerve sheath tumor;
Regulation of the p53 pathway by Ras, the plot thickens by Martin McMahon; Douglas Woods (M63-M71).
Keywords: Ras; Raf; p53; Cell cycle inhibitor; Senescence;
Centrosome abnormalities, genomic instability and carcinogenic progression by Stefan Duensing; Karl Münger (M81-M88).
Centrosome abnormalities are a frequent finding in various malignant tumors. Since centrosomes form the poles of the mitotic spindle, these abnormalities have been implicated in chromosome missegregation and the generation of aneuploid cells which is commonly found in many human neoplasms. It is a matter of debate, however, whether centrosome alterations can drive cells into aneuploidy or simply reflect loss of genomic integrity by other mechanisms. Since these two models have fundamentally different implications for the diagnostic and prognostic value of centrosome abnormalities, we will discuss the relevance of abnormal centrosomes in the context of different oncogenic events as exemplified by high-risk human papillomavirus-associated carcinogenesis.
Keywords: Centrosome; Genomic instability; Cancer; Human papillomavirus;
A new family of IKK-related kinases may function as IκB kinase kinases by Robert T Peters; Tom Maniatis (M57-M62).
Keywords: IKKϵ; IKK-i; NAK; TBK1; IKKα; IKKβ; IκBα; NF-κB;
The use of common genetic polymorphisms to enhance the epidemiologic study of environmental carcinogens by N. Rothman; S. Wacholder; N.E. Caporaso; M. Garcia-Closas; K. Buetow; J.F. Fraumeni (C1-C10).
Overwhelming evidence indicates that environmental exposures, broadly defined, are responsible for most cancer. There is reason to believe, however, that relatively common polymorphisms in a wide spectrum of genes may modify the effect of these exposures. We discuss the rationale for using common polymorphisms to enhance our understanding of how environmental exposures cause cancer and comment on epidemiologic strategies to assess these effects, including study design, genetic and statistical analysis, and sample size requirements. Special attention is given to sources of potential bias in population studies of gene–environment interactions, including exposure and genotype misclassification and population stratification (i.e., confounding by ethnicity). Nevertheless, by merging epidemiologic and molecular approaches in the twenty-first century, there will be enormous opportunities for unraveling the environmental determinants of cancer. In particular, studies of genetically susceptible subgroups may enable the detection of low levels of risk due to certain common exposures that have eluded traditional epidemiologic methods. Further, by identifying susceptibility genes and their pathways of action, it may be possible to identify previously unsuspected carcinogens. Finally, by gaining a more comprehensive understanding of environmental and genetic risk factors, there should emerge new clinical and public health strategies aimed at preventing and controlling cancer.
Keywords: Cancer; Susceptibility; Environment; Genetics; Gene–environment interaction;
The role of β-tubulin isotypes in resistance to antimitotic drugs by Catherine A. Burkhart; Maria Kavallaris; Susan Band Horwitz (O1-O9).
Keywords: β-Tubulin isotype; Antimitotic agent; Taxol; Vinca alkaloid; Resistance;
Molecular biology and experimental models for hematologic malignant diseases: workshop of the NIH Pathology B Study Section by Arnold B. Rabson; Martin Padarathsingh; Michelle M. Le Beau (R17-R23).
Keywords: Cancer; Hematologic malignancy; Leukemia; Lymphoma; Gene regulation; Chromosomal translocation; Transcription;