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Article

FHIT loss-induced DNA damage creates optimal APOBEC substrates: Insights into APOBEC-mediated mutagenesis.

Oncotarget - 20 Feb 2015

Waters Catherine E, Saldivar Joshua C, Amin Zaynab A, Schrock Morgan S, Huebner Kay

Abstract excerpt

APOBEC cytidine deaminase activity is a major source of hypermutation in cancer. But previous studies have shown that the TC context signature of these enzymes is not observed in sizable fractions of cancers with overexpression of APOBEC, suggesting that cooperating factors that contribute to this mutagenesis should be identified. The fragile histidine triad protein (Fhit) is a tumor suppressor and DNA caretaker...

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Source

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Identifiers

PMID: 25401976
DOI: 10.18632/oncotarget.2636
PMCID: PMC4413662

Genes

FHIT

Provenance

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