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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...

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Autores principales: Aliev, Gjumrakch, Obrenovich, Mark E., Tabrez, Shams, Jabir, Nasimudeen R., Reddy, V. Prakash, Li, Yi, Burnstock, Geoffrey, Cacabelos, Ramon, Kamal, Mohammad Amjad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
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.
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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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