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Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion
Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649749/ https://www.ncbi.nlm.nih.gov/pubmed/23691268 http://dx.doi.org/10.1155/2013/962984 |
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author | Aliev, Gjumrakch Obrenovich, Mark E. Tabrez, Shams Jabir, Nasimudeen R. Reddy, V. Prakash Li, Yi Burnstock, Geoffrey Cacabelos, Ramon Kamal, Mohammad Amjad |
author_facet | Aliev, Gjumrakch Obrenovich, Mark E. Tabrez, Shams Jabir, Nasimudeen R. Reddy, V. Prakash Li, Yi Burnstock, Geoffrey Cacabelos, Ramon Kamal, Mohammad Amjad |
author_sort | Aliev, Gjumrakch |
collection | PubMed |
description | Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors and metastatic colorectal cancer. One of the key features of tumors is the deficiency in tissue energy that accompanies mitochondrial lesions and formation of the hypoxic smaller sized mitochondria with ultrastructural abnormalities. We speculate that mitochondrial involvement may play a significant role in the etiopathogenesis of cancer. Recent studies also demonstrate a potential link between AD and cancer, and anticancer drugs are being explored for the inhibition of AD-like pathology in transgenic mice. Severity of the cancer growth, metastasis, and brain pathology in AD (in animal models that mimic human AD) correlate with the degree of mitochondrial ultrastructural abnormalities. Recent advances in the cell-cycle reentry of the terminally differentiated neuronal cells indicate that NO-dependent mitochondrial abnormal activities and mitotic cell division are not the only important pathogenic factors in pathogenesis of cancer and AD, but open a new window for the development of novel treatment strategies for these devastating diseases. |
format | Online Article Text |
id | pubmed-3649749 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-36497492013-05-20 Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion Aliev, Gjumrakch Obrenovich, Mark E. Tabrez, Shams Jabir, Nasimudeen R. Reddy, V. Prakash Li, Yi Burnstock, Geoffrey Cacabelos, Ramon Kamal, Mohammad Amjad Oxid Med Cell Longev Review Article Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors and metastatic colorectal cancer. One of the key features of tumors is the deficiency in tissue energy that accompanies mitochondrial lesions and formation of the hypoxic smaller sized mitochondria with ultrastructural abnormalities. We speculate that mitochondrial involvement may play a significant role in the etiopathogenesis of cancer. Recent studies also demonstrate a potential link between AD and cancer, and anticancer drugs are being explored for the inhibition of AD-like pathology in transgenic mice. Severity of the cancer growth, metastasis, and brain pathology in AD (in animal models that mimic human AD) correlate with the degree of mitochondrial ultrastructural abnormalities. Recent advances in the cell-cycle reentry of the terminally differentiated neuronal cells indicate that NO-dependent mitochondrial abnormal activities and mitotic cell division are not the only important pathogenic factors in pathogenesis of cancer and AD, but open a new window for the development of novel treatment strategies for these devastating diseases. Hindawi Publishing Corporation 2013 2013-04-03 /pmc/articles/PMC3649749/ /pubmed/23691268 http://dx.doi.org/10.1155/2013/962984 Text en Copyright © 2013 Gjumrakch Aliev et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Aliev, Gjumrakch Obrenovich, Mark E. Tabrez, Shams Jabir, Nasimudeen R. Reddy, V. Prakash Li, Yi Burnstock, Geoffrey Cacabelos, Ramon Kamal, Mohammad Amjad Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title | Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title_full | Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title_fullStr | Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title_full_unstemmed | Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title_short | Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion |
title_sort | link between cancer and alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial dna overproliferation and deletion |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649749/ https://www.ncbi.nlm.nih.gov/pubmed/23691268 http://dx.doi.org/10.1155/2013/962984 |
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