Special Issue "Genetic Susceptibility to Carcinogen-Induced Cancer"
Deadline for manuscript submissions: closed (15 May 2014)
Dr. Joe M. Angel
Division of Pharmacology and Toxicology, The College of Pharmacology, The University of Texas at Austin, 1400 Barbara Jordan Blvd. Austin, TX 78723, USA
Interests: complex traits; tumor susceptibility loci; carcinogenesis
Most human cancers are without a clear inheritance pattern and are believed to be multifactorial, resulting from interactions of genetic and environmental factors. These environmental factors include carcinogens such as chemicals, ultraviolet light, and viruses. Epidemiological studies, as well as animal studies, support the hypothesis that interindividual risk of developing cancer as a result of environmental carcinogen exposure is modified by multiple allelic variants of tumor susceptibility genes. Tumor susceptibility alleles have a low penetrance, can act to increase or decrease risk, and act additively to modify risk of cancer development. They are involved in DNA repair, immune response, carcinogen metabolism, cellular proliferation, differentiation, and death, as well as other cancer-related mechanisms. The mapping and isolation of such low penetrance genes in humans is complicated by the multiplicity of unlinked loci involved. This, together with the absence of clear-cut familial inheritance patterns, necessitates development of sophisticated analytical techniques and animal models to detect candidate genes that underlie tumor susceptibility loci. Rodent cancer models have been useful experimental tools for identifying and characterizing tumor susceptibility genes. Importantly, these genes have also been associated with cancer risk in humans, demonstrating the utility of using rodent models to identify genes that modify susceptibility to cancer. Articles in this Special Issue will address research aimed at identifying and characterizing genes that modify tumor susceptibility in rodent cancer models. In addition, this Special Issue will address the mechanisms by which these genes modify the response to carcinogen exposure.
Dr. Joe M. Angel
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.
- rodent models
- complex traits
- quantitative trait loci
- tumor susceptibility loci
- genetic risk
Review: Cellular Levels of 8-Oxoguanine in either DNA or the Nucleotide Pool Play Pivotal Roles in Carcinogenesis and Survival of Cancer Cells
Int. J. Mol. Sci. 2014, 15(7), 12543-12557; doi:10.3390/ijms150712543
Received: 13 May 2014; in revised form: 23 June 2014 / Accepted: 8 July 2014 / Published: 15 July 2014| PDF Full-text (1243 KB)
Int. J. Mol. Sci. 2014, 15(5), 7958-7973; doi:10.3390/ijms15057958
Received: 3 April 2014; in revised form: 11 April 2014 / Accepted: 21 April 2014 / Published: 7 May 2014| PDF Full-text (444 KB) | HTML Full-text | XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Author: Norihisa Saeki
Affiliation: Division of Genetics, National Cancer Center Research Institute
Abstract: Gastric cancer (GC) is one of the major malignant diseases worldwide, especially in Asia. It is classified into intestinal and diffuse types. While intestinal-type GC (IGC) is almost absolutely caused by Helicobacter pylori (HP) infection, the role of the infection in the diffuse-type GC (DGC) seems to be limited. Recently, genome-wide association studies (GWAS) on Japanese and Chinese populations identified chromosome 1q22 as a GC susceptibility locus which harbors the Mucin 1 gene (MUC1) encoding a cell membrane-bound mucin protein. It is known that in normal gastric mucosa the mucin 1 protein has a role in protecting gastric epithelial cells from a variety of external insults which cause inflammation and carcinogenesis. HP infection is the most definite insult leading to GC and a protective function of mucin 1 protein has been suggested by studies on MUC1 knocked-out mice.
Last update: 25 February 2014