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Journal Article
Exploring the basis of heterogeneity of cancer aggressiveness among the mutated POLE variants
2024
Overview
Germline pathogenic variants in the exonuclease domain of the replicative DNA polymerase Pol ε encoded by the
POLE
gene, predispose essentially to colorectal and endometrial tumors by inducing an ultramutator phenotype. It is still unclear whether all the
POLE
alterations influence similar strength tumorigenesis, immune microenvironment, and treatment response. In this review, we summarize the current understanding of the mechanisms and consequences of
POLE
mutations in human malignancies; we highlight the heterogeneity of mutation rate and cancer aggressiveness among POLE variants, propose some mechanistic basis underlining such heterogeneity, and discuss novel considerations for the choice and efficacy of therapies of POLE tumors.
Publisher
Life Science Alliance LLC
Subject
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - pathology
/ DNA Polymerase II - genetics
/ DNA Polymerase II - metabolism
/ Endometrial Neoplasms - genetics
/ Endometrial Neoplasms - pathology
/ Female
/ Humans
/ Mutation
/ Poly-ADP-Ribose Binding Proteins
/ Poly-ADP-Ribose Binding Proteins - genetics
/ Poly-ADP-Ribose Binding Proteins - metabolism
/ Review
/ Reviews
