Research ExplorerPublicationsBiomarkers and mechanisms of FANCD2 function

Biomarkers and mechanisms of FANCD2 function

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Biomarkers and mechanisms of FANCD2 function. / Willers, Henning; Kachnic, Lisa A; Luo, Chen-Mei; Li, Li; Purschke, Martin; Borgmann, Kerstin; Held, Kathryn D; Powell, Simon N.

In: J BIOMED BIOTECHNOL, Vol. 2008, 01.01.2008, p. 821529.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Willers, H, Kachnic, LA, Luo, C-M, Li, L, Purschke, M, Borgmann, K, Held, KD & Powell, SN 2008, 'Biomarkers and mechanisms of FANCD2 function', J BIOMED BIOTECHNOL, vol. 2008, pp. 821529. https://doi.org/10.1155/2008/821529

APA

Willers, H., Kachnic, L. A., Luo, C-M., Li, L., Purschke, M., Borgmann, K., Held, K. D., & Powell, S. N. (2008). Biomarkers and mechanisms of FANCD2 function. J BIOMED BIOTECHNOL, 2008, 821529. https://doi.org/10.1155/2008/821529

Vancouver

Willers H, Kachnic LA, Luo C-M, Li L, Purschke M, Borgmann K et al. Biomarkers and mechanisms of FANCD2 function. J BIOMED BIOTECHNOL. 2008 Jan 1;2008:821529. https://doi.org/10.1155/2008/821529

Bibtex

@article{0fd87c125a1341bda3671b3d862fe916,
title = "Biomarkers and mechanisms of FANCD2 function",
abstract = "Genetic or epigenetic inactivation of the pathway formed by the Fanconi anemia (FA) and BRCA1 proteins occurs in several cancer types, making the affected tumors potentially hypersensitive to DNA cross-linkers and other chemotherapeutic agents. It has been proposed that the inability of FA/BRCA-defective cells to form subnuclear foci of effector proteins, such as FANCD2, can be used as a biomarker to aid individualization of chemotherapy. We show that FANCD2 inactivation not only renders cells sensitive to cross-links, but also oxidative stress, a common effect of cancer therapeutics. Oxidative stress sensitivity does not correlate with FANCD2 or RAD51 foci formation, but associates with increased gammaH2AX foci levels and apoptosis. Therefore, FANCD2 may protect cells against cross-links and oxidative stress through distinct mechanisms, consistent with the growing notion that the pathway is not linear. Our data emphasize the need for multiple biomarkers, such as gammaH2AX, FANCD2, and RAD51, to capture all pathway activities.",
keywords = "Biological Markers, Cell Line, Fanconi Anemia, Fanconi Anemia Complementation Group D2 Protein, Fibroblasts, Histones, Humans, Oxidative Stress, Rad51 Recombinase, Signal Transduction",
author = "Henning Willers and Kachnic, {Lisa A} and Chen-Mei Luo and Li Li and Martin Purschke and Kerstin Borgmann and Held, {Kathryn D} and Powell, {Simon N}",
year = "2008",
month = jan,
day = "1",
doi = "10.1155/2008/821529",
language = "English",
volume = "2008",
pages = "821529",

}

RIS

TY - JOUR

T1 - Biomarkers and mechanisms of FANCD2 function

AU - Willers, Henning

AU - Kachnic, Lisa A

AU - Luo, Chen-Mei

AU - Li, Li

AU - Purschke, Martin

AU - Borgmann, Kerstin

AU - Held, Kathryn D

AU - Powell, Simon N

PY - 2008/1/1

Y1 - 2008/1/1

N2 - Genetic or epigenetic inactivation of the pathway formed by the Fanconi anemia (FA) and BRCA1 proteins occurs in several cancer types, making the affected tumors potentially hypersensitive to DNA cross-linkers and other chemotherapeutic agents. It has been proposed that the inability of FA/BRCA-defective cells to form subnuclear foci of effector proteins, such as FANCD2, can be used as a biomarker to aid individualization of chemotherapy. We show that FANCD2 inactivation not only renders cells sensitive to cross-links, but also oxidative stress, a common effect of cancer therapeutics. Oxidative stress sensitivity does not correlate with FANCD2 or RAD51 foci formation, but associates with increased gammaH2AX foci levels and apoptosis. Therefore, FANCD2 may protect cells against cross-links and oxidative stress through distinct mechanisms, consistent with the growing notion that the pathway is not linear. Our data emphasize the need for multiple biomarkers, such as gammaH2AX, FANCD2, and RAD51, to capture all pathway activities.

AB - Genetic or epigenetic inactivation of the pathway formed by the Fanconi anemia (FA) and BRCA1 proteins occurs in several cancer types, making the affected tumors potentially hypersensitive to DNA cross-linkers and other chemotherapeutic agents. It has been proposed that the inability of FA/BRCA-defective cells to form subnuclear foci of effector proteins, such as FANCD2, can be used as a biomarker to aid individualization of chemotherapy. We show that FANCD2 inactivation not only renders cells sensitive to cross-links, but also oxidative stress, a common effect of cancer therapeutics. Oxidative stress sensitivity does not correlate with FANCD2 or RAD51 foci formation, but associates with increased gammaH2AX foci levels and apoptosis. Therefore, FANCD2 may protect cells against cross-links and oxidative stress through distinct mechanisms, consistent with the growing notion that the pathway is not linear. Our data emphasize the need for multiple biomarkers, such as gammaH2AX, FANCD2, and RAD51, to capture all pathway activities.

KW - Biological Markers

KW - Cell Line

KW - Fanconi Anemia

KW - Fanconi Anemia Complementation Group D2 Protein

KW - Fibroblasts

KW - Histones

KW - Humans

KW - Oxidative Stress

KW - Rad51 Recombinase

KW - Signal Transduction

U2 - 10.1155/2008/821529

DO - 10.1155/2008/821529

M3 - SCORING: Journal article

C2 - 18483568

VL - 2008

SP - 821529

ER -