DNA crosslinking damage and cancer - a tale of friend and foe

Yaling Huang; Lei Li

doi:10.3978/j.issn.2218-676X.2013.03.01

DNA crosslinking damage and cancer - a tale of friend and foe

Yaling Huang, Lei Li

Research output: Contribution to journal › Review article › peer-review

72 Scopus citations

Abstract

Interstrand crosslinks (ICLs) represent a major challenge for DNA replication and transcription by preventing DNA strand separation. Cells deficient in ICL repair are hypersensitive to a variety of bifunctional alkylating agents and exhibit excessive genomic instability. Patients with deficient ICL repair, such as those with Fanconi anemia, are predisposed to a broad spectrum of cancers. The profound cellular toxicity of ICLs is exploited clinically in cancer chemotherapy. Therefore, understanding the mechanism of ICL repair and its impact on cancer development and treatment is very important. Studies of diseases with defective ICL repair, especially Fanconi anemia, have revealed unique ICL repair mechanisms in humans. In this review, we describe pathways and factors involved in ICL damage response and their implications in cancer development and treatment.

Original language	English (US)
Pages (from-to)	144-154
Number of pages	11
Journal	Translational Cancer Research
Volume	2
Issue number	3
DOIs	https://doi.org/10.3978/j.issn.2218-676X.2013.03.01
State	Published - Jun 1 2013

Keywords

Cancer
DNA repair
Fanconi anemia
Interstrand crosslink

ASJC Scopus subject areas

Oncology
Radiology Nuclear Medicine and imaging
Cancer Research

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10.3978/j.issn.2218-676X.2013.03.01

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title = "DNA crosslinking damage and cancer - a tale of friend and foe",

abstract = "Interstrand crosslinks (ICLs) represent a major challenge for DNA replication and transcription by preventing DNA strand separation. Cells deficient in ICL repair are hypersensitive to a variety of bifunctional alkylating agents and exhibit excessive genomic instability. Patients with deficient ICL repair, such as those with Fanconi anemia, are predisposed to a broad spectrum of cancers. The profound cellular toxicity of ICLs is exploited clinically in cancer chemotherapy. Therefore, understanding the mechanism of ICL repair and its impact on cancer development and treatment is very important. Studies of diseases with defective ICL repair, especially Fanconi anemia, have revealed unique ICL repair mechanisms in humans. In this review, we describe pathways and factors involved in ICL damage response and their implications in cancer development and treatment.",

keywords = "Cancer, DNA repair, Fanconi anemia, Interstrand crosslink",

author = "Yaling Huang and Lei Li",

note = "Funding Information: This research is supported by the National Cancer Institute (CA127945 and CA097175 Project 3 to L.L.). The authors thank Donald R Norwood (Department of Scientific Publication, The University of Texas MD Anderson Cancer Center) for his assistance in English editing",

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T1 - DNA crosslinking damage and cancer - a tale of friend and foe

AU - Huang, Yaling

AU - Li, Lei

N1 - Funding Information: This research is supported by the National Cancer Institute (CA127945 and CA097175 Project 3 to L.L.). The authors thank Donald R Norwood (Department of Scientific Publication, The University of Texas MD Anderson Cancer Center) for his assistance in English editing

PY - 2013/6/1

Y1 - 2013/6/1

N2 - Interstrand crosslinks (ICLs) represent a major challenge for DNA replication and transcription by preventing DNA strand separation. Cells deficient in ICL repair are hypersensitive to a variety of bifunctional alkylating agents and exhibit excessive genomic instability. Patients with deficient ICL repair, such as those with Fanconi anemia, are predisposed to a broad spectrum of cancers. The profound cellular toxicity of ICLs is exploited clinically in cancer chemotherapy. Therefore, understanding the mechanism of ICL repair and its impact on cancer development and treatment is very important. Studies of diseases with defective ICL repair, especially Fanconi anemia, have revealed unique ICL repair mechanisms in humans. In this review, we describe pathways and factors involved in ICL damage response and their implications in cancer development and treatment.

AB - Interstrand crosslinks (ICLs) represent a major challenge for DNA replication and transcription by preventing DNA strand separation. Cells deficient in ICL repair are hypersensitive to a variety of bifunctional alkylating agents and exhibit excessive genomic instability. Patients with deficient ICL repair, such as those with Fanconi anemia, are predisposed to a broad spectrum of cancers. The profound cellular toxicity of ICLs is exploited clinically in cancer chemotherapy. Therefore, understanding the mechanism of ICL repair and its impact on cancer development and treatment is very important. Studies of diseases with defective ICL repair, especially Fanconi anemia, have revealed unique ICL repair mechanisms in humans. In this review, we describe pathways and factors involved in ICL damage response and their implications in cancer development and treatment.

KW - Cancer

KW - DNA repair

KW - Fanconi anemia

KW - Interstrand crosslink

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DNA crosslinking damage and cancer - a tale of friend and foe

Abstract

Keywords

ASJC Scopus subject areas

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