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DNA-repair, cell killing and normal tissue damage.

Standard

DNA-repair, cell killing and normal tissue damage. / Dahm-Daphi, Jochen; Dikomey, E; Brammer, I.

in: STRAHLENTHER ONKOL, Jahrgang 174, Nr. 3, 3, 1998, S. 8-11.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Dahm-Daphi, J, Dikomey, E & Brammer, I 1998, 'DNA-repair, cell killing and normal tissue damage.', STRAHLENTHER ONKOL, Jg. 174, Nr. 3, 3, S. 8-11. <http://www.ncbi.nlm.nih.gov/pubmed/9830448?dopt=Citation>

APA

Dahm-Daphi, J., Dikomey, E., & Brammer, I. (1998). DNA-repair, cell killing and normal tissue damage. STRAHLENTHER ONKOL, 174(3), 8-11. [3]. http://www.ncbi.nlm.nih.gov/pubmed/9830448?dopt=Citation

Vancouver

Dahm-Daphi J, Dikomey E, Brammer I. DNA-repair, cell killing and normal tissue damage. STRAHLENTHER ONKOL. 1998;174(3):8-11. 3.

Bibtex

@article{6fa7b616c956457ea9a96ea63bb22a4f,
title = "DNA-repair, cell killing and normal tissue damage.",
abstract = "BACKGROUND: Side effects of radiotherapy in normal tissue is determined by a variety of factors of which cellular and genetic contributions are described here. MATERIAL AND METHODS: Review. RESULTS: Normal tissue damage after irradiation is largely due to loss of cellular proliferative capacity. This can be due to mitotic cell death, apoptosis, or terminal differentiation. Dead or differentiated cells release cytokines which additionally modulate the tissue response. DNA damage, in particular non-reparable or misrepaired double-strand breaks are considered the basic lesion leading to G1-arrest and ultimately to cell inactivation. CONCLUSION: Evidence for genetic bases of normal tissue response, cell killing and DNA-repair capacity is presented. However, a direct link of all 3 endpoints has not yet been proved directly.",
author = "Jochen Dahm-Daphi and E Dikomey and I Brammer",
year = "1998",
language = "Deutsch",
volume = "174",
pages = "8--11",
journal = "STRAHLENTHER ONKOL",
issn = "0179-7158",
publisher = "Urban und Vogel",
number = "3",

}

RIS

TY - JOUR

T1 - DNA-repair, cell killing and normal tissue damage.

AU - Dahm-Daphi, Jochen

AU - Dikomey, E

AU - Brammer, I

PY - 1998

Y1 - 1998

N2 - BACKGROUND: Side effects of radiotherapy in normal tissue is determined by a variety of factors of which cellular and genetic contributions are described here. MATERIAL AND METHODS: Review. RESULTS: Normal tissue damage after irradiation is largely due to loss of cellular proliferative capacity. This can be due to mitotic cell death, apoptosis, or terminal differentiation. Dead or differentiated cells release cytokines which additionally modulate the tissue response. DNA damage, in particular non-reparable or misrepaired double-strand breaks are considered the basic lesion leading to G1-arrest and ultimately to cell inactivation. CONCLUSION: Evidence for genetic bases of normal tissue response, cell killing and DNA-repair capacity is presented. However, a direct link of all 3 endpoints has not yet been proved directly.

AB - BACKGROUND: Side effects of radiotherapy in normal tissue is determined by a variety of factors of which cellular and genetic contributions are described here. MATERIAL AND METHODS: Review. RESULTS: Normal tissue damage after irradiation is largely due to loss of cellular proliferative capacity. This can be due to mitotic cell death, apoptosis, or terminal differentiation. Dead or differentiated cells release cytokines which additionally modulate the tissue response. DNA damage, in particular non-reparable or misrepaired double-strand breaks are considered the basic lesion leading to G1-arrest and ultimately to cell inactivation. CONCLUSION: Evidence for genetic bases of normal tissue response, cell killing and DNA-repair capacity is presented. However, a direct link of all 3 endpoints has not yet been proved directly.

M3 - SCORING: Zeitschriftenaufsatz

VL - 174

SP - 8

EP - 11

JO - STRAHLENTHER ONKOL

JF - STRAHLENTHER ONKOL

SN - 0179-7158

IS - 3

M1 - 3

ER -