Molecular model linking Th2 polarized M2 tumour-associated macrophages with deaminase-mediated cancer progression mutation signatures

Scandinavian Journal of Immunology
Jared MamrotRobyn A Lindley

Abstract

A new and diverse range of somatic mutation signatures are observed in late-stage cancers, but the underlying reasons are not fully understood. We advance a "combinatorial association model" for deaminase binding domain (DBD) diversification to explain the generation of previously observed cancer-progression associated mutation signatures. We also propose that changes in the polarization of tumour-associated macrophages (TAMs) are accompanied by the expression of deaminases with a new and diverse range of DBDs, and thus accounting for the generation of new somatic mutation signatures. The mechanism proposed is molecularly reminiscent of combinatorial association of heavy (H) and light (L) protein chains following V(D)J recombination of immunoglobulin molecules (and similarly for protein chains in heterodimers α/β and γ/δ of V(D)Js of T Cell Receptors) required for pathogen antigen recognition by B cells and T cells, respectively. We also discuss whether extracellular vesicles (EVs) emanating from tumour enhancing M2-polarized macrophages represent a likely source of the de novo deaminase DBDs. We conclude that M2-polarized macrophages extruding EVs loaded with deaminase proteins or deaminase-specific transcription/translation r...Continue Reading

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Citations

Apr 17, 2020·Scandinavian Journal of Immunology·Astri FrafjordAlexandre Corthay
Apr 24, 2021·Oncotarget·Jared MamrotRobyn A Lindley
Jun 3, 2021·International Journal of Molecular Sciences·Kyoko OuraTsutomu Masaki
Jun 30, 2021·Journal of Experimental & Clinical Cancer Research : CR·Pablo Hernández-CamareroMacarena Perán

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Methods Mentioned

BETA
deaminations
deamination
exome sequencing

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