Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Genetic Susceptibility to Carcinogen-Induced Cancer
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Genetic Susceptibility to Carcinogen-Induced Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (15 May 2014) | Viewed by 26445

Special Issue Editor

Dr. Joe M. Angel

E-Mail Website
Guest Editor
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

Special Issue Information

Dear Colleagues,

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
Guest Editor

Submission

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 semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF.


Keywords

  • rodent models
  • complex traits
  • quantitative trait loci
  • tumor susceptibility loci
  • genetic risk
  • carcinogenesis

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

1243 KiB  
Review
Cellular Levels of 8-Oxoguanine in either DNA or the Nucleotide Pool Play Pivotal Roles in Carcinogenesis and Survival of Cancer Cells
by Yusaku Nakabeppu
Int. J. Mol. Sci. 2014, 15(7), 12543-12557; https://doi.org/10.3390/ijms150712543 - 15 Jul 2014
Cited by 150 | Viewed by 19216
Abstract
8-Oxoguanine, a major oxidized base lesion formed by reactive oxygen species, causes G to T transversion mutations or leads to cell death in mammals if it accumulates in DNA. 8-Oxoguanine can originate as 8-oxo-dGTP, formed in the nucleotide pool, or by direct oxidation [...] Read more.
8-Oxoguanine, a major oxidized base lesion formed by reactive oxygen species, causes G to T transversion mutations or leads to cell death in mammals if it accumulates in DNA. 8-Oxoguanine can originate as 8-oxo-dGTP, formed in the nucleotide pool, or by direct oxidation of the DNA guanine base. MTH1, also known as NUDT1, with 8-oxo-dGTP hydrolyzing activity, 8-oxoguanine DNA glycosylase (OGG1) an 8-oxoG DNA glycosylase, and MutY homolog (MUTYH) with adenine DNA glycosylase activity, minimize the accumulation of 8-oxoG in DNA; deficiencies in these enzymes increase spontaneous and induced tumorigenesis susceptibility. However, different tissue types have different tumorigenesis susceptibilities. These can be reversed by combined deficiencies in the defense systems, because cell death induced by accumulation of 8-oxoG in DNA is dependent on MUTYH, which can be suppressed by MTH1 and OGG1. In cancer cells encountering high oxidative stress levels, a high level of 8-oxo-dGTP accumulates in the nucleotide pool, and cells therefore express increased levels of MTH1 in order to eliminate 8-oxo-dGTP. Suppression of MTH1 may be an efficient strategy for killing cancer cells; however, because MTH1 and OGG1 protect normal tissues from oxidative-stress-induced cell death, it is important that MTH1 inhibition does not increase the risk of healthy tissue degeneration. Full article
(This article belongs to the Special Issue Genetic Susceptibility to Carcinogen-Induced Cancer)
►▼ Show Figures

Graphical abstract

444 KiB  
Review
Mucin 1 Gene (MUC1) and Gastric-Cancer Susceptibility
by Norihisa Saeki, Hiromi Sakamoto and Teruhiko Yoshida
Int. J. Mol. Sci. 2014, 15(5), 7958-7973; https://doi.org/10.3390/ijms15057958 - 07 May 2014
Cited by 27 | Viewed by 6867
Abstract
Gastric cancer (GC) is one of the major malignant diseases worldwide, especially in Asia. It is classified into intestinal and diffuse types. While the intestinal-type GC (IGC) is almost certainly caused by Helicobacter pylori (HP) infection, its role in the diffuse-type GC (DGC) [...] Read more.
Gastric cancer (GC) is one of the major malignant diseases worldwide, especially in Asia. It is classified into intestinal and diffuse types. While the intestinal-type GC (IGC) is almost certainly caused by Helicobacter pylori (HP) infection, its role in the diffuse-type GC (DGC) appears limited. Recently, genome-wide association studies (GWAS) on Japanese and Chinese populations identified chromosome 1q22 as a GC susceptibility locus which harbors mucin 1 gene (MUC1) encoding a cell membrane-bound mucin protein. MUC1 has been known as an oncogene with an anti-apoptotic function in cancer cells; however, in normal gastric mucosa, it is anticipated that 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. Full article
(This article belongs to the Special Issue Genetic Susceptibility to Carcinogen-Induced Cancer)
►▼ Show Figures

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop