Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We emphasize the deleterious gene alterations in components of the major histocompatibility complex (HLA-I or B2M) and of the response to IFNγ (such as JAK2) which are mutually exclusive and can affect up to one fifth of the NSCLCs.
|
31253869 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study aimed to investigate the correlation of C-X-C chemokine receptor 2 (CXCR2) with clinicopathological characteristics and survival in non-small cell lung cancer (NSCLC) patients and further explore its effect on proliferation, apoptosis, invasion, stemness, chemosensitivity as well as JAK2/STAT3 pathway in NSCLC cells.
|
31731888 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We evaluated the JAK1/JAK2 inhibitor ruxolitinib plus pemetrexed/cisplatin first-line in patients with stage IIIB/IV or recurrent nonsquamous NSCLC with systemic inflammation (modified Glasgow prognostic score [mGPS] 1/2).
|
29681434 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We further discovered that TGR5 knockdown prevented JAK2 and STAT3 phosphorylation and repressed the expression of STAT3 target genes, thus inhibiting cell proliferation, migration and invasion in NSCLC.
|
29074425 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Overexpression of miR-4443 may promote the resistance of NSCLC cells to EPI by targeting INPP4A and regulating the activation of JAK2/STAT3 pathway. miR-4443 may serve as a drug target for NSCLC.
|
30001772 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings suggest potential dual roles for JAK2 inhibitors, both as a novel monotherapy in NSCLCs resistant to genotoxic therapies, and in tandem with immune checkpoint inhibition.<i></i>.
|
29467274 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Acquired resistance of ELTN results in extremely poor prognoses of non-small cell lung cancer (NSCLC) patients, wherein activation of the JAK2/STAT3 signaling pathway has been proven to induce acquired ELTN resistance.
|
30483119 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
By using quantitative (real-time) PCR, western blot analysis, and immunocytochemical staining, three non-small cell lung cancer (NSCLC) cell lines (A427, A549 and NCI-H358) were analyzed for the expression of EpoR and its specific downstream signaling pathways [Janus kinase 2 (Jak2)-signal transducer and activator of transcription 5 (STAT5), phosphatidylinositol-3-kinase (PI3K)-Akt, mitogen-activated protein (MAP) kinase].
|
29345289 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Nicotine increased the levels of α5-nAChR mRNA and protein in NSCLC cell lines and activated the JAK2/STAT3 signaling cascade.
|
28750889 |
2017 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Taken together, this study demonstrated the clinical utility of targeted NGS with a focused hotspot cancer gene panel in NSCLCs and identified activating mutations in JAK2 and JAK3 with clinical implications inferred through integrative analysis of cancer genetic, genomic, and pharmacogenomic data.
|
29082853 |
2017 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Synergistic effect of pacritinib with erlotinib on JAK2-mediated resistance in epidermal gowth factor receptor mutation-positive non-small cell lung Cancer.
|
27180268 |
2016 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results reveal a mechanism whereby JAK2 inhibition overcomes acquired resistance to EGFR inhibitors and support the use of combination therapy with JAK and EGFR inhibitors for the treatment of EGFR-dependent NSCLC.
|
27025877 |
2016 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our findings revealed that miR-204 functions as a tumor suppressor in NSCLC by targeting JAK2, and that miR-204 may therefore serve as a biomarker for the diagnosis and treatment of NSCLC.
|
27323056 |
2016 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, as an inhibitor of JAK2/3-STAT3 signaling, physalin A, has potent anti-tumor activities, which may facilitate the development of a therapeutic strategy for treating NSCLC.
|
26843613 |
2016 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These data demonstrate that JAK2/STAT3 signaling operates independent of known driver mutations in NSCLC and plays critical roles in tumor cell behavior that may not be effectively inhibited by drugs that selectively target these driver mutations.
|
22319590 |
2012 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
JAK2/STAT3 signaling pathway activation mediates tumor angiogenesis by upregulation of VEGF and bFGF in non-small-cell lung cancer.
|
21333372 |
2011 |