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Related Concept Videos

lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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STING Pathway Expression Identifies NSCLC With an Immune-Responsive Phenotype.

Carminia M Della Corte1, Triparna Sen2, Carl M Gay3

  • 1Departments of Thoracic/Head & Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas; Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.

Journal of Thoracic Oncology : Official Publication of the International Association for the Study of Lung Cancer
|February 19, 2020
PubMed
Summary
This summary is machine-generated.

Stimulator of interferon genes (STING) pathway activation in non-small cell lung cancer (NSCLC) predicts immunotherapy response and is boosted by cisplatin. This suggests STING activation may be a biomarker for improved chemoimmunotherapy outcomes.

Keywords:
Immune checkpointsImmunotherapyInnate immunityLung cancerSTING

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Area of Science:

  • Oncology
  • Immunology
  • Cancer Genomics

Background:

  • Chemoimmunotherapy combining platinum chemotherapy and immune checkpoint inhibitors (ICIs) is standard for NSCLC, but responses vary.
  • Predictive biomarkers for ICI monotherapy (e.g., PD-L1, tumor mutational burden) have unclear relevance in chemoimmunotherapy.
  • The stimulator of interferon genes (STING) innate immune pathway enhances immunotherapy response in small cell lung cancer (SCLC).

Purpose of the Study:

  • To investigate if STING pathway activation can predict and underlie antitumor immunity in NSCLC.
  • To explore the relationship between STING activation and response biomarkers in NSCLC.

Main Methods:

  • Analysis of transcriptomic and proteomic profiles from 1320 NSCLC patients (treatment-naive and relapsed) and The Cancer Genome Atlas.
  • Stratification of tumors based on STING activation markers (cGAS, phospho-STING, CCL5, CXCL10).
  • Correlation of STING activation with immunotherapy response biomarkers in patient tumors and preclinical NSCLC models treated with platinum.

Main Results:

  • STING activation in NSCLC correlates with intrinsic DNA damage, immune checkpoints, and chemokines.
  • Low STING/immune gene expression linked to STK11 mutations, but a TP53 comutated subset showed high STING/immune gene expression.
  • Cisplatin treatment enhanced STING pathway activation and PD-L1 expression in preclinical NSCLC models.

Conclusions:

  • STING pathway activation in NSCLC predicts immunotherapy response features.
  • Cisplatin treatment enhances STING activation and PD-L1 expression, suggesting a mechanism for improved chemoimmunotherapy.
  • STING activation may serve as a predictive biomarker for enhanced response to NSCLC chemoimmunotherapy.