Journal
FRONTIERS IN ONCOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.695770
Keywords
lung cancer; mesothelioma; type I interferon; CDKN2A (p16); homozygous deletion; immunotherapy; STING
Categories
Funding
- La Ligue Regionale Grand Ouest contre le Cancer [CSIRGO: CD16, CD22, CD44, CD49, CD72, CD79, CD85]
- La Ligue Nationale contre le Cancer
- L'association ARSMESO44
- ''La fondation ARC, L'Agence Nationale pour la Recherche [ANR-16-CE18-0016]
- National Research Agency via the investment of the future program [ANR-11-LABX-0016-01]
- Ligue contre le Cancer
- Agence Nationale de la Recherche (ANR) [ANR-16-CE18-0016] Funding Source: Agence Nationale de la Recherche (ANR)
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The review discusses the potential impact of homozygous deletion of IFN I genes on thoracic cancers therapy, advocating for better consideration of this genetic alteration in patient monitoring.
Homozygous deletion (HD) of the tumor suppressor gene CDKN2A is the most frequent genetic alteration in malignant pleural mesothelioma and is also frequent in non-small cell lung cancers. This HD is often accompanied by the HD of the type I interferons (IFN I) genes that are located closed to the CDKN2A gene on the p21.3 region of chromosome 9. IFN I genes encode sixteen cytokines (IFN-alpha, IFN-beta horizontal ellipsis ) that are implicated in cellular antiviral and antitumor defense and in the induction of the immune response. In this review, we discuss the potential influence of IFN I genes HD on thoracic cancers therapy and speak in favor of better taking these HD into account in patients monitoring.
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