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Tumor suppressor genes in familial adenomatous polyposis

Colorectal cancer (CRC) is mostly due to a series of genetic alterations that are being greatly under the influence of the environmental factors. These changes, mutational or epigenetic modifications at transcriptional forefront and/or post-transcriptional effects via miRNAs, include inactivation an...

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Autores principales: Eshghifar, Nahal, Farrokhi, Naser, Naji, Tahereh, Zali, Mohammadreza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346818/
https://www.ncbi.nlm.nih.gov/pubmed/28331559
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author Eshghifar, Nahal
Farrokhi, Naser
Naji, Tahereh
Zali, Mohammadreza
author_facet Eshghifar, Nahal
Farrokhi, Naser
Naji, Tahereh
Zali, Mohammadreza
author_sort Eshghifar, Nahal
collection PubMed
description Colorectal cancer (CRC) is mostly due to a series of genetic alterations that are being greatly under the influence of the environmental factors. These changes, mutational or epigenetic modifications at transcriptional forefront and/or post-transcriptional effects via miRNAs, include inactivation and the conversion of proto-oncogene to oncogenes, and/or inactivation of tumor suppressor genes (TSG). Here, a thorough review was carried out on the role of TSGs with the focus on the APC as the master regulator, mutated genes and mal-/dysfunctional pathways that lead to one type of hereditary form of the CRC; namely familial adenomatous polyposis (FAP). This review provides a venue towards defining candidate genes that can be used as new PCR-based markers for early diagnosis of FAP. In addition to diagnosis, defining the modes of genetic alterations will open door towards genome editing to either suppress the disease or reduce its progression during the course of action.
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spelling pubmed-53468182017-03-22 Tumor suppressor genes in familial adenomatous polyposis Eshghifar, Nahal Farrokhi, Naser Naji, Tahereh Zali, Mohammadreza Gastroenterol Hepatol Bed Bench Review Article Colorectal cancer (CRC) is mostly due to a series of genetic alterations that are being greatly under the influence of the environmental factors. These changes, mutational or epigenetic modifications at transcriptional forefront and/or post-transcriptional effects via miRNAs, include inactivation and the conversion of proto-oncogene to oncogenes, and/or inactivation of tumor suppressor genes (TSG). Here, a thorough review was carried out on the role of TSGs with the focus on the APC as the master regulator, mutated genes and mal-/dysfunctional pathways that lead to one type of hereditary form of the CRC; namely familial adenomatous polyposis (FAP). This review provides a venue towards defining candidate genes that can be used as new PCR-based markers for early diagnosis of FAP. In addition to diagnosis, defining the modes of genetic alterations will open door towards genome editing to either suppress the disease or reduce its progression during the course of action. Shaheed Beheshti University of Medical Sciences 2017 /pmc/articles/PMC5346818/ /pubmed/28331559 Text en ©2017 RIGLD, Research Institute for Gastroenterology and Liver Diseases This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Eshghifar, Nahal
Farrokhi, Naser
Naji, Tahereh
Zali, Mohammadreza
Tumor suppressor genes in familial adenomatous polyposis
title Tumor suppressor genes in familial adenomatous polyposis
title_full Tumor suppressor genes in familial adenomatous polyposis
title_fullStr Tumor suppressor genes in familial adenomatous polyposis
title_full_unstemmed Tumor suppressor genes in familial adenomatous polyposis
title_short Tumor suppressor genes in familial adenomatous polyposis
title_sort tumor suppressor genes in familial adenomatous polyposis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346818/
https://www.ncbi.nlm.nih.gov/pubmed/28331559
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