Showing papers in "Seminars in Cancer Biology in 1998"

TL;DR: The p53 tumor suppressor is the most commonly mutated gene in human cancer and its activation of expression of a number of target genes including p21WAFI, GADD45, 14-3-3 sigma, bax, Fas/APO1, KILLER/DR5, PIG3, Tsp1, IGF-BP3 and others are reviewed.

TL;DR: A summary of current knowledge concerning the mechanisms of p53-mediated apoptosis is presented in this article, where the pivotal 'choice' between p53induced viable growth arrest and apoptosis are discussed.

TL;DR: The data reviewed is concerned with the in vivo mouse models including p53 knockout mice, transgenic mice harboring various mutant forms of p53 and mice knocked out for cell-cycle- and apoptosis-associated genes situated upstream or downstream from p53, that have been elaborated upon over the last few years.

TL;DR: There are very large differences in the relative importance of the different cancers by world area; some of the factors, environmental and genetic, underlying the geographic distributions, are discussed.

TL;DR: The challenge of understanding the enigmas of this disease will continue into future decades, as the conversion of current knowledge into preventive and therapeutic recommendations is converted.

TL;DR: An etiological model for breast cancer in humans is presented, and it is examined whether it accommodates the patterns of occurrence of this disease and the associated risk factors.

TL;DR: The hypothesis that the pre- and perinatal periods constitute a 'time window' that is of major importance for future cancer risk is supported.

TL;DR: In this review some general aspects of the natural history of HPV are presented followed by a description of the incidence and risk factors for anal, vulvar, and penile cancer.

TL;DR: The potential role of defects in transcriptional regulation of the p53 gene in oncogenic transformation is discussed and the factors that have been demonstrated to regulate promoter activity are discussed.

TL;DR: Short peptides derived from the p53 C-terminus can reactivate at least some mutant p53 proteins and trigger a p53-dependent biological response, which may provide the basis for the design of p 53-reactivating anti-cancer drugs.

TL;DR: It is proposed that the multiple mutations detectable in cancer cells result from a mutator phenotype, in which loss of a genome stability function occurs early during tumor development and predisposes the tumor cell to the accumulation of further mutations.

TL;DR: Comparison of p53 wild type and p53-deficient mice indicates that p53, in fact, determines massive apoptosis occurring shortly after gamma irradiation in radiosensitive tissues, which makes p53 a potential target for therapeutic suppression with the purpose of rescuing normal tissues from the side effects of cancer treatment.

TL;DR: The p53 tumor suppressor gene, its main function is to guard the integrity of the genome, and its role in carcinogenesis and chemotherapy-drug resistance, are reviewed based on acquired knowledge of the structure function of the p53 protein.

TL;DR: In large prospective studies, total fat intake has not been associated with risk of breast cancer, suggesting that international correlations are seriously confounded by differences in other variables related to affluence, including reproductive variables, physical activity, and food availability.

TL;DR: The major risk factors for hepatocellular carcinoma (HCC) are considered to be chronic infection with hepatitis B virus (HBV), hepatitis C virus (HCV) infection, exposure to aflatoxins, and excessive alcohol consumption; tobacco smoking and oral contraceptive use also may be associated with increased risk of HCC.

TL;DR: The current state of knowledge regarding the role of gene-environment interactions in development of colorectal cancer is summarized and areas of particular promise are discussed, as well as the limitations of these studies.

TL;DR: While mice do not necessarily recapitulate all the tumor types found in inherited cancers, they offer the unique opportunity to decipher the critical pathways in tumorigenesis and these findings can then be applied to humans.

TL;DR: The possibility that distinct mutational events can arise from a common precursor will be discussed, as will the possibility that inherited and sporadic cancers can acquire mutator phenotypes at different times in tumor development.

TL;DR: Current evidence of a strong causal link between H. pylori infection and gastric cancer in humans has become less convincing, and recent studies seem to indicate that the strength of the association may vary with type of H.pylori strain, and possibly presence of effect-modifying co-factors in the host and/or the environment.

TL;DR: It is found that tumor DNA can also be directly detected in the serum or plasma of patients with some forms of cancer, and this recent finding is currently being explored but may represent an important contribution to future diagnostic strategies.

TL;DR: A class of tumors may be supermutable with a mutation frequency comparable to that observed in the generation of immune diversity, and this frequency is at least 100 times higher than would be expected for normal tissue.

TL;DR: In this paper, it was shown that the human somatic mutation frequency at approximately 80 years of age in epithelial tissues appears to be more than 10-fold higher than in the human germline.