STAT3

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Reverted 4 edits by Pasteur immunology (talk): Same citespam, new sock account

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Increased activity of STAT3 in cancer cells, leads to changes in the function of protein complexes that control expression of inflammatory genes, with result profound change in the secretome and the cell phenotypes, their activity in the tumor, and their capacity for metastasis.<ref>{{cite journal|last1=Vlahopoulos|first1=SA | title= Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode. | journal = Cancer Biology & Medicine | date = August 2017 | pmid = 28884042 | doi = 10.20892/j.issn.2095-3941.2017.0029 | volume = 14 |issue=3 | pages = 254–270 | pmc = 5570602}}</ref>Increased activity of STAT3 in cancer cells, leads to changes in the function of protein complexes that control expression of inflammatory genes, with result profound change in the secretome and the cell phenotypes, their activity in the tumor, and their capacity for metastasis.<ref>{{cite journal|last1=Vlahopoulos|first1=SA | title= Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode. | journal = Cancer Biology & Medicine | date = August 2017 | pmid = 28884042 | doi = 10.20892/j.issn.2095-3941.2017.0029 | volume = 14 |issue=3 | pages = 254–270 | pmc = 5570602}}</ref>
Using a combination of targeted biological therapy and cytotoxic chemotherapy has proven to be a successful approach in overcoming resistance to treatment. By simultaneously blocking Src kinase and epidermal growth factor receptor with gemcitabine, researchers have effectively countered the resistance mediated by STAT3, leading to inhibition of pancreatic tumor growth.<ref>{{cite journal | vauthors = Nagaraj NS, Washington MK, Merchant NB | title = Combined blockade of Src kinase and epidermal growth factor receptor with gemcitabine overcomes STAT3-mediated resistance of inhibition of pancreatic tumor growth | journal = Clin Cancer Res | volume = 17 | issue = 3 | pages = 483-93 | date = 2011 | pmid= 21266529 | doi = 10.1158/1078-0432.CCR-10-1670}}</ref> Furthermore, blocking STAT3 through the use of small molecules such as FLLL32, either independently or in combination with Trastuzumab (Herceptin), effectively impedes the progression of cancer cells. Targeting STAT3 inhibition holds immense potential for cancer treatment including those used for [[breast cancer]].<ref name="pmid138441231">{{cite journal | vauthors = Jahangiri AH, Ezzeddini R, Zounemat Kermani N, Bahrami F, Salek Farrokhi A | title = Combination of STAT3 inhibitor with Herceptin reduced immune checkpoints expression and provoked anti‐breast cancer immunity: An in vitro study | journal = Scandinavian Journal of Immunology | volume = 98 | issue = 3 | pages = e13300 | date = September 2023 | pmid = 38441231 | doi = 10.1111/sji.13300 | url = https://www.researchgate.net/public...anti-breast_cancer_immunity_An_in-vitro_study}}</ref>
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