Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1)
By M. Marzec, Qian Zhang, Ami Goradia, Puthiyaveettil N. Raghunath, Xiaobin Liu, M. Paessler, Hong Y. Wang, M. Wysocka, Mangeng Cheng, B. Ruggeri and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2008
726 citations recorded by the source corpus.
Subfields: Immunology, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/65d372020e57ee799771efcd2d9aa548bd73ff99
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Citations in the corpus
- Control of PD-L1 Expression by Oncogenic Activation of the AKT-mTOR Pathway in Non-Small Cell Lung Cancer. (2016, background): “lymphomas carrying NPM–ALK fusions induce PD-L1 expression through STAT3 activation (13).”
- Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR-Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients with EGFR Mutation (2015, background): “Similarly, constitutive activation of nucleophosmin– anaplastic lymphoma kinase was reported to drive PD-L1 expression through signal transducer and activator of transcription-3 (STAT3) in lymphoma.(23) More recently, we found Epstein–Barr virus driven latent membrane protein 1 , a well-recognized i”
- PD-L1 Expression as a Predictive Biomarker in Cancer Immunotherapy (2015, background): “STAT3 upregulation, via upstream activation of ALK, results in induction of PDL1 and tumor evasion in T-cell lymphoma (58).”
- Regulatory mechanisms of PD-1/PD-L1 in cancers (2024, background): “It also inhibits the elevated PD-L1 protein expression caused by NPM/ALK (nucleophosmin/anaplastic lymphoma kinase) mutations by silencing STAT3 [217].”
- EGFR Mutations and ALK Rearrangements Are Associated with Low Response Rates to PD-1 Pathway Blockade in Non-Small Cell Lung Cancer (NSCLC): A Retrospective Analysis (2016, background): “For example, Marzec and colleagues observed that NPM–ALK rearrangements induce PD-L1 expression in anaplastic large cell lymphoma as a result of downstream activation of STAT3 (20).”
- Interferon Receptor Signaling Pathways Regulating PD-L1 and PD-L2 Expression (2017, neutral): “…did not reveal direct binding of this factor at the PD-L1 promoter in M381 melanoma cells (Figure S5B), which is different from the reported binding of STAT3 to the PD-L1 promoter in a chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) T cell lymphoma (ALK-TCL) (Marzec et al., 2008).”
- Immune checkpoint blockade: a common denominator approach to cancer therapy (2015, background): “Intrinsic resistance refers to the constitutive expression of PD-L1 by tumor cells because of genetic alterations or activation of certain signaling pathways, such as the AKT pathway and STAT3, which are commonly activated in many cancers (Parsa et al., 2007; Marzec et al., 2008).”
- Association of PD-1, PD-1 ligands, and other features of the tumor immune microenvironment with response to anti-PD-1 therapy (2014, neutral): “497 Present 4 (31) 4 (100) 0 (0) 4 (100) 0 (0) CD4:CD8 (n 1⁄4 29) CD4 CD8 13 (45) 10 (77) 3 (23) 0.”
- Mechanisms controlling PD-L1 expression in cancer (2019, background): “The EGFR pathway is involved in the regulation of PD-L1 expression via the IL-6/JAK/STAT3 signaling pathway in EGFRmutated non-small cell lung cancer.”
- The blockade of immune checkpoints in cancer immunotherapy (2012, background): “Similarly, constitutive anaplastic lymphoma kinase (ALK) signalling, which is observed in certain lymphomas and occasionally in lung cancer, has been reported to drive PDL1 expression through signal transducer and activator of transcription 3 (STAT3) signallin”
- Regulation of PD-L1: a novel role of pro-survival signalling in cancer. (2016, background): “Yu H, Pardoll D, Jove R. STATs in cancer inflammation and immunity: a leading role for STAT3.”
- PD-L1 Expression is Characteristic of a Subset of Aggressive B-Cell Lymphomas and Virus-Associated Malignancies (2013, neutral): “In cell lines, increased 9p24 copy number is associated with increased PD-L1 expression due to both direct amplification of CD274, and through increased JAK2 andenhanced JAK–STAT signaling (6, 7).”