Comment on “A Novel Thymoma-Associated Immunodeficiency with Increased Naive T Cells and Reduced CD247 Expression”

Welsh, James S.; Howard, Steven

doi:10.4049/jimmunol.1501667

Cited by 1 publication

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References 5 publications

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“…The mechanisms that elicit severe combined deficiency of CD4 and CD8 T cells [28] or the acquired hypoexpression of CD247 (encoding the CD3 zeta-chain) are unclear. CD247 hypoexpression entails susceptibility to infections [26] and, hypothetically, the increased prevalence of non-thymic cancers in thymoma patients [29]. Chronic mucocutaneous candidiasis in thymoma patients results from defective Autoimmune Regulator Gene (AIRE) expression in thymomas [11][12][13].…”

Section: Immunodeficiency In Thymoma Patientsmentioning

confidence: 99%

Molecular pathology of thymomas: implications for diagnosis and therapy

et al. 2021

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Thymomas exhibit a unique genomic landscape, comprising the lowest on average total mutational burden among adult human cancers; a unique point mutation in the GTF2I gene in WHO type A and AB thymomas (and rarely others); almost unique KMT2A-MAML2 translocations in rare WHO type B2 and B3 thymomas; a unique YAP1-MAML2 translocation in almost all metaplastic thymomas; and unique miRNA profiles in relation to GTF2I mutational status and WHO histotypes. While most thymomas can be diagnosed solely on the basis of morphological features, mutational analyses can solve challenging differential diagnostic problems. No molecular biomarkers have been identified that predict the response of unresectable thymomas to chemotherapy or agents with known molecular targets. Despite the common and strong expression of PDL1 in thymomas, immune checkpoint inhibitors are rarely applicable due to the poor predictability of common, life-threatening autoimmune side effects that are related to the unrivaled propensity of thymomas towards autoimmunity.

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