mediates tumor angiogenesis by upregulation of VEGF and bFGF in non-small-cell lung cancer

The JAK2/STAT3 signaling pathway plays an important role in the angiogenesis of non-small cell lung cancer.

JAK2/STAT3 signaling operates independent of known driver mutations in non-small cell lung carcinoma and plays critical roles in tumor cell behavior that may not be effectively inhibited by drugs that selectively target these driver mutations.

AGK expression was significantly correlated with JAK2/STAT3 hyperactivation in esophageal squamous cell carcinoma, as well as in lung and breast cancer.

Genetic amplification of the JAK2 gene was correlated with Non-Small Cell lung cancer.

our findings revealed that miR-204 functions as a tumor suppressor in non-small-cell lung carcinoma (NSCLC) by targeting JAK2, and that miR-204 may therefore serve as a biomarker for the diagnosis and treatment of NSCLC.

the up-regulation, mutation and amplification of JAK2 detected in lung adenocarcinoma may participate in lung cancer progression by regulating cancer cells' proliferation, migration and invasion

We describe a subset of non-small-cell lung cancer patients who had JAK2 amplifications resulting in high expression of PD-L1

Mir-204 attenuates angiogenesis in lung adenocarcinoma via JAK2-STAT3 pathway.

We show that MET activation promotes the expression of several negative checkpoint regulators of the immunoresponse, including PD-L1. In addition, we report inactivation of JAK2 in lung cancer cells that prevented the response to IFNgamma.

C-X-C chemokine receptor 2 correlates with unfavorable prognosis and facilitates malignant cell activities via activating JAK2/STAT3 pathway in non-small cell lung cancer.

Study revealed a significantly higher prevalence of PTPRT and JAK2 mutations in lung adenocarcinomas among African Americans compared with European Americans. Patients carrying these mutations have a concomitant increase in IL-6/STAT3 signaling and miR-21 expression.

Low phosphorylation level of JAK2 is associated with lung adenocarcinoma.

Downregulation of SETD7 promotes migration and invasion of lung cancer cells via JAK2/STAT3 pathway.

Aryl hydrocarbon receptor mediates Jak2/STAT3 signaling for non-small cell lung cancer stem cell maintenance.

Mesenchymal stem cells enhance lung cancer initiation through activation of IL-6/JAK2/STAT3 pathway.

PRDX6 promotes lung tumor development via its mediated and CCL5-associated activation of the JAK2/STAT3 pathway.