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Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion.

Aliev G, Obrenovich ME, Tabrez S, Jabir NR, Reddy VP, Li Y, Burnstock G, Cacabelos R, Kamal MA - Oxid Med Cell Longev (2013)

Bottom Line: Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD).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.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.

View Article: PubMed Central - PubMed

Affiliation: GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, No. 328, San Antonio, TX 78229, USA. aliev03@gmail.com

ABSTRACT
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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Electron Microscopic Peroxidase-anti-Peroxidase immunocytochemical determination of the distribution of NOS1 immunolabeling features in control (a) and metastatic colorectal cancer liver tumor tissues (b)–(d). (a) NOS1 immunopositive EC (indicated by asterisk) were seen in control liver microvessels. Vacuoles are indicated by single arrow X4 000. (b) Tumor vessel endothelium (indicated by asterisk) showed no staining for NOS1 antibody. X20,000. (c) NOS1 immunopositive white blood cells (indicated by asterisk) were attached to vessel endothelium in tumor growth regions. X6,000. (d) NOS1 immunopositive myofibroblast (smooth muscle cell) were seen in metastatic liver tumor tissues. X10,000. Reprinted with permission of J Submicrosc Cytol Pathol [2].
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fig3: Electron Microscopic Peroxidase-anti-Peroxidase immunocytochemical determination of the distribution of NOS1 immunolabeling features in control (a) and metastatic colorectal cancer liver tumor tissues (b)–(d). (a) NOS1 immunopositive EC (indicated by asterisk) were seen in control liver microvessels. Vacuoles are indicated by single arrow X4 000. (b) Tumor vessel endothelium (indicated by asterisk) showed no staining for NOS1 antibody. X20,000. (c) NOS1 immunopositive white blood cells (indicated by asterisk) were attached to vessel endothelium in tumor growth regions. X6,000. (d) NOS1 immunopositive myofibroblast (smooth muscle cell) were seen in metastatic liver tumor tissues. X10,000. Reprinted with permission of J Submicrosc Cytol Pathol [2].

Mentions: Electron Microscopic PAP techniques determination of the distribution of NOS1 immunolabeling features in control (Figure 3(a)) and metastatic colorectal cancer liver tumor tissues (Figures 3(b)–3(d) showed that NOS1 immunopositive EC were seen in control liver microvessels. In contrary to these observations, tumor vessel endothelium showed no staining for NOS1 antibody (Figure 3(b)). However, presence of the NOS1 immunopositive white blood cells was attached to vessel endothelium in tumor growth regions often observed (Figure 3(c)). In addition, NOS1 immunopositive myofibroblast (smooth muscle cell) was also seen in metastatic liver tumor tissues (Figure 3(d)).


Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion.

Aliev G, Obrenovich ME, Tabrez S, Jabir NR, Reddy VP, Li Y, Burnstock G, Cacabelos R, Kamal MA - Oxid Med Cell Longev (2013)

Electron Microscopic Peroxidase-anti-Peroxidase immunocytochemical determination of the distribution of NOS1 immunolabeling features in control (a) and metastatic colorectal cancer liver tumor tissues (b)–(d). (a) NOS1 immunopositive EC (indicated by asterisk) were seen in control liver microvessels. Vacuoles are indicated by single arrow X4 000. (b) Tumor vessel endothelium (indicated by asterisk) showed no staining for NOS1 antibody. X20,000. (c) NOS1 immunopositive white blood cells (indicated by asterisk) were attached to vessel endothelium in tumor growth regions. X6,000. (d) NOS1 immunopositive myofibroblast (smooth muscle cell) were seen in metastatic liver tumor tissues. X10,000. Reprinted with permission of J Submicrosc Cytol Pathol [2].
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3649749&req=5

fig3: Electron Microscopic Peroxidase-anti-Peroxidase immunocytochemical determination of the distribution of NOS1 immunolabeling features in control (a) and metastatic colorectal cancer liver tumor tissues (b)–(d). (a) NOS1 immunopositive EC (indicated by asterisk) were seen in control liver microvessels. Vacuoles are indicated by single arrow X4 000. (b) Tumor vessel endothelium (indicated by asterisk) showed no staining for NOS1 antibody. X20,000. (c) NOS1 immunopositive white blood cells (indicated by asterisk) were attached to vessel endothelium in tumor growth regions. X6,000. (d) NOS1 immunopositive myofibroblast (smooth muscle cell) were seen in metastatic liver tumor tissues. X10,000. Reprinted with permission of J Submicrosc Cytol Pathol [2].
Mentions: Electron Microscopic PAP techniques determination of the distribution of NOS1 immunolabeling features in control (Figure 3(a)) and metastatic colorectal cancer liver tumor tissues (Figures 3(b)–3(d) showed that NOS1 immunopositive EC were seen in control liver microvessels. In contrary to these observations, tumor vessel endothelium showed no staining for NOS1 antibody (Figure 3(b)). However, presence of the NOS1 immunopositive white blood cells was attached to vessel endothelium in tumor growth regions often observed (Figure 3(c)). In addition, NOS1 immunopositive myofibroblast (smooth muscle cell) was also seen in metastatic liver tumor tissues (Figure 3(d)).

Bottom Line: Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD).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.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.

View Article: PubMed Central - PubMed

Affiliation: GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, No. 328, San Antonio, TX 78229, USA. aliev03@gmail.com

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus