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Open Access Journal of Cancer & Oncology Research Article 2 min read

On the Dichotomous Aspect of Cancer Stem Cell

Hugwil AV
ISSN: 2578-4625  10.23880/oajco-16000123  Received: March 29, 2018  Published: April 09, 2018
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Keywords
Dichotomous Stem Cell Soncogenic Vimentin 14-3-3 EMT/MET Prions Pritumumab

Figures

Figure 1: Cancer stem cells are etiologic cells possessing malignant traits e.g. metastasis, invasion and apoptosis resistance. These tumor traits are converted by aberrant altered- vimentin which is the crucial marker of the epithelial- mesenchymal-transition (EMT) of the CSC. During metastasis the reverse transition called the mesenchymal- epithelial-transition (MET) is necessary in order for the circulating tumor cells to colonize the metastasized niche. Reprogramming EMT to MET would be an accomplishment that could lead to cancer recuperation. I have tried to delineate the intervention between Pritumumab and psychological effects on the regulation of tumor growth based on DACSC via the PPIN of TA34 and vimentin. There are two inextricable phases in one state--- dichotomous aspect of cancer stem cell (DACSC) development. Cancer stem cells (CSC) are initiated to grow from normal stem cells (NSC). CSC and NSC are reciprocally participating in EMT/MET when CSCs provoke malignant traits such as metastasis, invasion and anti-apoptosis. Under severe stress, NSC tends to be altered and carcinogenesis during their renewal, which is greatly, influenced by the spatiotemporal architecture of stem cells and their niche cells. Conversely CSC may revert to NSC by losing their carcinogenicity and become susceptible to regular apoptosis from normalized niche, which is implemented by an appropriate condition created by immune surveillance and the autonomous mechanisms for tissue repair which is affected by mental condition in relaxation-transcendency. NSC ordinarily renews for evolutionary adaptation. Simultaneously the state of CSC can adapt to tumor niche created by chronic inflammation and defiance of regular apoptosis. Defective cells that fail the survival game are eliminated by neuro- immune surveillance system, which also initiates the mobilization of stem cells to repair the tissue-gaps epigenetical chromatin assembly/disassembly. Two co- existing phases may frequently be competing at the threshold of carcinogenesis.
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Figure 1: Cancer stem cells are etiologic cells possessing malignant traits e.g. metastasis, invasion and apoptosis resistance. These tumor traits are converted by aberrant altered- vimentin which is the crucial marker of the epithelial- mesenchymal-transition (EMT) of the CSC. During metastasis the reverse transition called the mesenchymal- epithelial-transition (MET) is necessary in order for the circulating tumor cells to colonize the metastasized niche. Reprogramming EMT to MET would be an accomplishment that could lead to cancer recuperation. I have tried to delineate the intervention between Pritumumab and psychological effects on the regulation of tumor growth based on DACSC via the PPIN of TA34 and vimentin. There are two inextricable phases in one state--- dichotomous aspect of cancer stem cell (DACSC) development. Cancer stem cells (CSC) are initiated to grow from normal stem cells (NSC). CSC and NSC are reciprocally participating in EMT/MET when CSCs provoke malignant traits such as metastasis, invasion and anti-apoptosis. Under severe stress, NSC tends to be altered and carcinogenesis during their renewal, which is greatly, influenced by the spatiotemporal architecture of stem cells and their niche cells. Conversely CSC may revert to NSC by losing their carcinogenicity and become susceptible to regular apoptosis from normalized niche, which is implemented by an appropriate condition created by immune surveillance and the autonomous mechanisms for tissue repair which is affected by mental condition in relaxation-transcendency. NSC ordinarily renews for evolutionary adaptation. Simultaneously the state of CSC can adapt to tumor niche created by chronic inflammation and defiance of regular apoptosis. Defective cells that fail the survival game are eliminated by neuro- immune surveillance system, which also initiates the mobilization of stem cells to repair the tissue-gaps epigenetical chromatin assembly/disassembly. Two co- existing phases may frequently be competing at the threshold of carcinogenesis.

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@article{hugwil2018,
  title   = {On the Dichotomous Aspect of Cancer Stem Cell},
  author  = {Hugwil AV},
  journal = {Open Access Journal of Cancer & Oncology},
  year    = {2018},
  volume  = {2},
  number  = {2},
  doi     = {10.23880/oajco-16000123}
}
Hugwil AV (2018). On the Dichotomous Aspect of Cancer Stem Cell. Open Access Journal of Cancer & Oncology, 2(2). https://doi.org/10.23880/oajco-16000123
TY  - JOUR
TI  - On the Dichotomous Aspect of Cancer Stem Cell
AU  - Hugwil AV
JO  - Open Access Journal of Cancer & Oncology
PY  - 2018
VL  - 2
IS  - 2
DO  - 10.23880/oajco-16000123
ER  -