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The Regulation and Immune Signature of Retrotransposons in Cancer

SIMPLE SUMMARY: A tiny human sample is enough to uncover the complete genome sequence of that individual with the advances in biomedical technologies and data analysis. Jumping genes constituting about half of the human genome, have been implicated in cancer and predisposition to inflammatory reacti...

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Detalles Bibliográficos
Autores principales: Alkailani, Maisa I., Gibbings, Derrick
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10486412/
https://www.ncbi.nlm.nih.gov/pubmed/37686616
http://dx.doi.org/10.3390/cancers15174340
Descripción
Sumario:SIMPLE SUMMARY: A tiny human sample is enough to uncover the complete genome sequence of that individual with the advances in biomedical technologies and data analysis. Jumping genes constituting about half of the human genome, have been implicated in cancer and predisposition to inflammatory reactions. Inflammation may restrict the activity of these genes and reduce the tumor burden. This article summarizes related literature on factors regulating jumping genes and discusses their immune-related evidence made available by genome-wide studies. ABSTRACT: Advances in sequencing technologies and the bioinformatic analysis of big data facilitate the study of jumping genes’ activity in the human genome in cancer from a broad perspective. Retrotransposons, which move from one genomic site to another by a copy-and-paste mechanism, are regulated by various molecular pathways that may be disrupted during tumorigenesis. Active retrotransposons can stimulate type I IFN responses. Although accumulated evidence suggests that retrotransposons can induce inflammation, the research investigating the exact mechanism of triggering these responses is ongoing. Understanding these mechanisms could improve the therapeutic management of cancer through the use of retrotransposon-induced inflammation as a tool to instigate immune responses to tumors.