Nucleotide excision repair and response and survival to chemotherapy in colorectal cancer patients

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Nucleotide excision repair and response and survival to chemotherapy in colorectal cancer patients. / Kap, Elisabeth J; Popanda, Odilia; Chang-Claude, Jenny.

In: PHARMACOGENOMICS, Vol. 17, No. 7, 05.2016, p. 755-94.

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@article{589c74b7ad9e4883a89573f655c5946d,
title = "Nucleotide excision repair and response and survival to chemotherapy in colorectal cancer patients",
abstract = "Several new chemotherapeutic agents have become available for the treatment of colorectal cancer, which has led to increased complexity in treatment planning. Treatment decision making for individual patients could be facilitated if guided by predictive and prognostic markers. As most cytotoxic drugs induce DNA damage, the DNA damage repair pathways hold potential for yielding such biomarkers. Here, we review the current evidence of a possible involvement of the nucleotide excision repair pathway in the efficacy of chemotherapeutic agents used in the treatment of colorectal cancer. Although a large number of studies have been conducted, they are generally of moderate size and heterogeneous in design. Up to date no firm conclusions can be drawn to translate these results into the clinic. We recommend further comprehensive investigations of the nucleotide excision repair pathway in large patient studies that include both discovery and validation cohorts.",
author = "Kap, {Elisabeth J} and Odilia Popanda and Jenny Chang-Claude",
year = "2016",
month = may,
doi = "10.2217/pgs-2015-0017",
language = "English",
volume = "17",
pages = "755--94",
journal = "PHARMACOGENOMICS",
issn = "1462-2416",
publisher = "Future Medicine Ltd",
number = "7",

}

RIS

TY - JOUR

T1 - Nucleotide excision repair and response and survival to chemotherapy in colorectal cancer patients

AU - Kap, Elisabeth J

AU - Popanda, Odilia

AU - Chang-Claude, Jenny

PY - 2016/5

Y1 - 2016/5

N2 - Several new chemotherapeutic agents have become available for the treatment of colorectal cancer, which has led to increased complexity in treatment planning. Treatment decision making for individual patients could be facilitated if guided by predictive and prognostic markers. As most cytotoxic drugs induce DNA damage, the DNA damage repair pathways hold potential for yielding such biomarkers. Here, we review the current evidence of a possible involvement of the nucleotide excision repair pathway in the efficacy of chemotherapeutic agents used in the treatment of colorectal cancer. Although a large number of studies have been conducted, they are generally of moderate size and heterogeneous in design. Up to date no firm conclusions can be drawn to translate these results into the clinic. We recommend further comprehensive investigations of the nucleotide excision repair pathway in large patient studies that include both discovery and validation cohorts.

AB - Several new chemotherapeutic agents have become available for the treatment of colorectal cancer, which has led to increased complexity in treatment planning. Treatment decision making for individual patients could be facilitated if guided by predictive and prognostic markers. As most cytotoxic drugs induce DNA damage, the DNA damage repair pathways hold potential for yielding such biomarkers. Here, we review the current evidence of a possible involvement of the nucleotide excision repair pathway in the efficacy of chemotherapeutic agents used in the treatment of colorectal cancer. Although a large number of studies have been conducted, they are generally of moderate size and heterogeneous in design. Up to date no firm conclusions can be drawn to translate these results into the clinic. We recommend further comprehensive investigations of the nucleotide excision repair pathway in large patient studies that include both discovery and validation cohorts.

U2 - 10.2217/pgs-2015-0017

DO - 10.2217/pgs-2015-0017

M3 - SCORING: Journal article

C2 - 27183147

VL - 17

SP - 755

EP - 794

JO - PHARMACOGENOMICS

JF - PHARMACOGENOMICS

SN - 1462-2416

IS - 7

ER -