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Correlation between p-STAT3 overexpression and prognosis in lung cancer: A systematic review and meta-analysis

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TLDR
In this paper, a systematic review and meta-analysis was performed to explore the correlation between p-STAT3 overexpression and prognosis in lung cancer patients, and the results indicated that p-stat3 overexposure may serve a biomarker for poor prognosis.
Abstract
Objective Previous studies have shown the correlation between p-STAT3 overexpression and prognosis in a variety of human tumors. However, their correlation in lung cancer remains controversial. We performed a systematic review and meta-analysis to explore the correlation between p-STAT3 overexpression and prognosis in lung cancer patients. Methods We searched PubMed, Embase, Web of Science, CNKI, VIP, and WanFang Data to identify relevant studies. Two reviewers independently screened the literature search results, extracted data, and assessed the methodological quality of the included studies. Then, meta-analysis was performed by using Review Manager 5.3 and STATA 14 software. A random-effect model was employed to evaluate all related pooled results. Statistical heterogeneity of each study was assessed by I2. Publication bias was determined by funnel plot and the Begg’s or Egger’s tests. Results Eventually, 13 studies were included in present meta-analysis. Among these 13 studies, 8 studies were associated with the overall survival of lung cancer and 10 studies with other clinicopathological characteristics. The results of this meta-analysis suggested that p-STAT3 overexpression may be a poor prognosis biomarker in lung cancer (HR: 1.23; 95% CI: 1.04–1.46; P = 0.02). In terms of other clinicopathological characteristics, p-STAT3 overexpression was more frequent to advanced TNM stages ranging from III to IV (OR: 1.92; 95% CI: 1.13–3.27; P = 0.02) and lymphatic node metastasis (OR: 1.81; 95% CI: 1.20–2.72; P = 0.004). But, it was not associated with tumor differentiation (OR: 0.82; 95% CI: 0.44–1.53; P = 0.54). Conclusion p-STAT3 overexpression has significant correlation with poorer overall survival of lung cancer patients, as well as with more advanced TNM stages and lymph node metastasis. Thus, it may serve a biomarker for poor prognosis in lung cancer. Nevertheless, our findings should be confirmed by large prospective studies.

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STAT3 and STAT5 Activation in Solid Cancers.

TL;DR: The role of STAT3/5 activation in solid cancers is reviewed and their association with survival in cancer patients is summarized.
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Silibinin is a direct inhibitor of STAT3.

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STAT3/5 Inhibitors Suppress Proliferation in Bladder Cancer and Enhance Oncolytic Adenovirus Therapy.

TL;DR: Evidence is provided that inhibitors against STAT3/5 are promising as novel mono- and combination therapy in bladder cancer and potential therapeutic strategies by targeting this pathway in BC are explored.
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A novel STAT3 inhibitor W2014-S regresses human non-small cell lung cancer xenografts and sensitizes EGFR-TKI acquired resistance.

TL;DR: This study has provided a novel STAT3 inhibitor with significant anti-tumor activities in NSCLC and suggests that combination ofSTAT3 inhibitor such as W2014-S with gefitinib could serve as a promising strategy to overcome EGFR-TKIs acquired resistance in NSclC patients.
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