Inserting A549 the incorporation of cDNA into lung cancer (non-small cell) lines as well as tumor genomic clones repressor gene cancer of the lungs 1 (TSLC-1) helps these cell lines reverse tumor enlargement trends. Signal transducer and transcription activator 3 (STAT3) were phosphorylated chronically in 22 percent to 65 percent cancers of the non-small cell lung cancer. Tyrosine kinase receptors, for example EGFR (EGF stands for epidermal growth factor.), MET receptors as well as cytokine receptors, activate STAT3. IL-6, for example non-receptor kinases, as well as SRC were found to be involved as well. In resected NSCLC, overexpression of total or phosphorylated STAT-3 results in a poor prognosis. Gene expression and cell cycle variations show TSLC1 downstream pathways that serve as a bridge between the two repression of tumor products in A549 cells. The activation of STAT3 by stromal cells can be beneficial to NSCLC cell oncogenic outcomes.
| Published in | Journal of Gynecology and Obstetrics (Volume 10, Issue 2) |
| DOI | 10.11648/j.jgo.20221002.18 |
| Page(s) | 108-119 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2022. Published by Science Publishing Group |
Endometrial Cancer, Tumor, Gene Expression, STAT-3, TSLC-1, NSCLC, Growth Factors, Pathways
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APA Style
Sadik Yusuf Musse. (2022). TSLC-1 and STAT-3 Expression and Its Implication in Cervical Adenocarcinoma. Journal of Gynecology and Obstetrics, 10(2), 108-119. https://doi.org/10.11648/j.jgo.20221002.18
ACS Style
Sadik Yusuf Musse. TSLC-1 and STAT-3 Expression and Its Implication in Cervical Adenocarcinoma. J. Gynecol. Obstet. 2022, 10(2), 108-119. doi: 10.11648/j.jgo.20221002.18
AMA Style
Sadik Yusuf Musse. TSLC-1 and STAT-3 Expression and Its Implication in Cervical Adenocarcinoma. J Gynecol Obstet. 2022;10(2):108-119. doi: 10.11648/j.jgo.20221002.18
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Download@article{10.11648/j.jgo.20221002.18,
author = {Sadik Yusuf Musse},
title = {TSLC-1 and STAT-3 Expression and Its Implication in Cervical Adenocarcinoma},
journal = {Journal of Gynecology and Obstetrics},
volume = {10},
number = {2},
pages = {108-119},
doi = {10.11648/j.jgo.20221002.18},
url = {https://doi.org/10.11648/j.jgo.20221002.18},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.jgo.20221002.18},
abstract = {Inserting A549 the incorporation of cDNA into lung cancer (non-small cell) lines as well as tumor genomic clones repressor gene cancer of the lungs 1 (TSLC-1) helps these cell lines reverse tumor enlargement trends. Signal transducer and transcription activator 3 (STAT3) were phosphorylated chronically in 22 percent to 65 percent cancers of the non-small cell lung cancer. Tyrosine kinase receptors, for example EGFR (EGF stands for epidermal growth factor.), MET receptors as well as cytokine receptors, activate STAT3. IL-6, for example non-receptor kinases, as well as SRC were found to be involved as well. In resected NSCLC, overexpression of total or phosphorylated STAT-3 results in a poor prognosis. Gene expression and cell cycle variations show TSLC1 downstream pathways that serve as a bridge between the two repression of tumor products in A549 cells. The activation of STAT3 by stromal cells can be beneficial to NSCLC cell oncogenic outcomes.},
year = {2022}
}
TY - JOUR T1 - TSLC-1 and STAT-3 Expression and Its Implication in Cervical Adenocarcinoma AU - Sadik Yusuf Musse Y1 - 2022/03/23 PY - 2022 N1 - https://doi.org/10.11648/j.jgo.20221002.18 DO - 10.11648/j.jgo.20221002.18 T2 - Journal of Gynecology and Obstetrics JF - Journal of Gynecology and Obstetrics JO - Journal of Gynecology and Obstetrics SP - 108 EP - 119 PB - Science Publishing Group SN - 2376-7820 UR - https://doi.org/10.11648/j.jgo.20221002.18 AB - Inserting A549 the incorporation of cDNA into lung cancer (non-small cell) lines as well as tumor genomic clones repressor gene cancer of the lungs 1 (TSLC-1) helps these cell lines reverse tumor enlargement trends. Signal transducer and transcription activator 3 (STAT3) were phosphorylated chronically in 22 percent to 65 percent cancers of the non-small cell lung cancer. Tyrosine kinase receptors, for example EGFR (EGF stands for epidermal growth factor.), MET receptors as well as cytokine receptors, activate STAT3. IL-6, for example non-receptor kinases, as well as SRC were found to be involved as well. In resected NSCLC, overexpression of total or phosphorylated STAT-3 results in a poor prognosis. Gene expression and cell cycle variations show TSLC1 downstream pathways that serve as a bridge between the two repression of tumor products in A549 cells. The activation of STAT3 by stromal cells can be beneficial to NSCLC cell oncogenic outcomes. VL - 10 IS - 2 ER -
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