@article{borst_targeted_2013,
	title = {Targeted radiosensitization by the {Chk1} inhibitor {SAR}-020106},
	volume = {85},
	issn = {1879-355X},
	doi = {10.1016/j.ijrobp.2012.08.006},
	abstract = {PURPOSE: To explore the activity of a potent Chk1 inhibitor (SAR-020106) in combination with radiation.
METHODS AND MATERIALS: Colony and mechanistic in vitro assays and a xenograft in vivo model.
RESULTS: SAR-020106 suppressed-radiation-induced G2/M arrest and reduced clonogenic survival only in p53-deficient tumor cells. SAR-020106 promoted mitotic entry following irradiation in all cell lines, but p53-deficient cells were likely to undergo apoptosis or become aneuploid, while p53 wild-type cells underwent a postmitotic G1 arrest followed by subsequent normal cell cycle re-entry. Following combined treatment with SAR-020106 and radiation, homologous-recombination-mediated DNA damage repair was inhibited in all cell lines. A significant increase in the number of pan-γH2AX-staining apoptotic cells was observed only in p53-deficient cell lines. Efficacy was confirmed in vivo in a clinically relevant human head-and-neck cell carcinoma xenograft model.
CONCLUSION: The Chk1 inhibitor SAR-020106 is a potent radiosensitizer in tumor cell lines defective in p53 signaling.},
	language = {eng},
	number = {4},
	journal = {International Journal of Radiation Oncology, Biology, Physics},
	author = {Borst, Gerben R. and McLaughlin, Martin and Kyula, Joan N. and Neijenhuis, Sari and Khan, Aadil and Good, James and Zaidi, Shane and Powell, Ned G. and Meier, Pascal and Collins, Ian and Garrett, Michelle D. and Verheij, Marcel and Harrington, Kevin J.},
	month = mar,
	year = {2013},
	keywords = {Animals, Apoptosis, Cell Line, Tumor, Cell cycle, Checkpoint Kinase 1, Cyclin-Dependent Kinase Inhibitor p21, DNA Damage, DNA Repair, G2 Phase, HeLa Cells, Histones, Humans, Immunohistochemistry, Isoquinolines, Mice, Mice, Nude, Microscopy, Mitosis, Papillomaviridae, Protein Kinases, Pyrazines, Radiation Tolerance, Radiation-Sensitizing Agents, Time-Lapse Imaging, Tumor Stem Cell Assay, Tumor Suppressor Protein p53},
	pages = {1110--1118},
}

{"_id":"3jKBhes9MPSGE5Efh","bibbaseid":"borst-mclaughlin-kyula-neijenhuis-khan-good-zaidi-powell-etal-targetedradiosensitizationbythechk1inhibitorsar020106-2013","author_short":["Borst, G. R.","McLaughlin, M.","Kyula, J. N.","Neijenhuis, S.","Khan, A.","Good, J.","Zaidi, S.","Powell, N. G.","Meier, P.","Collins, I.","Garrett, M. D.","Verheij, M.","Harrington, K. J."],"bibdata":{"bibtype":"article","type":"article","title":"Targeted radiosensitization by the Chk1 inhibitor SAR-020106","volume":"85","issn":"1879-355X","doi":"10.1016/j.ijrobp.2012.08.006","abstract":"PURPOSE: To explore the activity of a potent Chk1 inhibitor (SAR-020106) in combination with radiation. METHODS AND MATERIALS: Colony and mechanistic in vitro assays and a xenograft in vivo model. RESULTS: SAR-020106 suppressed-radiation-induced G2/M arrest and reduced clonogenic survival only in p53-deficient tumor cells. SAR-020106 promoted mitotic entry following irradiation in all cell lines, but p53-deficient cells were likely to undergo apoptosis or become aneuploid, while p53 wild-type cells underwent a postmitotic G1 arrest followed by subsequent normal cell cycle re-entry. Following combined treatment with SAR-020106 and radiation, homologous-recombination-mediated DNA damage repair was inhibited in all cell lines. A significant increase in the number of pan-γH2AX-staining apoptotic cells was observed only in p53-deficient cell lines. Efficacy was confirmed in vivo in a clinically relevant human head-and-neck cell carcinoma xenograft model. CONCLUSION: The Chk1 inhibitor SAR-020106 is a potent radiosensitizer in tumor cell lines defective in p53 signaling.","language":"eng","number":"4","journal":"International Journal of Radiation Oncology, Biology, Physics","author":[{"propositions":[],"lastnames":["Borst"],"firstnames":["Gerben","R."],"suffixes":[]},{"propositions":[],"lastnames":["McLaughlin"],"firstnames":["Martin"],"suffixes":[]},{"propositions":[],"lastnames":["Kyula"],"firstnames":["Joan","N."],"suffixes":[]},{"propositions":[],"lastnames":["Neijenhuis"],"firstnames":["Sari"],"suffixes":[]},{"propositions":[],"lastnames":["Khan"],"firstnames":["Aadil"],"suffixes":[]},{"propositions":[],"lastnames":["Good"],"firstnames":["James"],"suffixes":[]},{"propositions":[],"lastnames":["Zaidi"],"firstnames":["Shane"],"suffixes":[]},{"propositions":[],"lastnames":["Powell"],"firstnames":["Ned","G."],"suffixes":[]},{"propositions":[],"lastnames":["Meier"],"firstnames":["Pascal"],"suffixes":[]},{"propositions":[],"lastnames":["Collins"],"firstnames":["Ian"],"suffixes":[]},{"propositions":[],"lastnames":["Garrett"],"firstnames":["Michelle","D."],"suffixes":[]},{"propositions":[],"lastnames":["Verheij"],"firstnames":["Marcel"],"suffixes":[]},{"propositions":[],"lastnames":["Harrington"],"firstnames":["Kevin","J."],"suffixes":[]}],"month":"March","year":"2013","keywords":"Animals, Apoptosis, Cell Line, Tumor, Cell cycle, Checkpoint Kinase 1, Cyclin-Dependent Kinase Inhibitor p21, DNA Damage, DNA Repair, G2 Phase, HeLa Cells, Histones, Humans, Immunohistochemistry, Isoquinolines, Mice, Mice, Nude, Microscopy, Mitosis, Papillomaviridae, Protein Kinases, Pyrazines, Radiation Tolerance, Radiation-Sensitizing Agents, Time-Lapse Imaging, Tumor Stem Cell Assay, Tumor Suppressor Protein p53","pages":"1110–1118","bibtex":"@article{borst_targeted_2013,\n\ttitle = {Targeted radiosensitization by the {Chk1} inhibitor {SAR}-020106},\n\tvolume = {85},\n\tissn = {1879-355X},\n\tdoi = {10.1016/j.ijrobp.2012.08.006},\n\tabstract = {PURPOSE: To explore the activity of a potent Chk1 inhibitor (SAR-020106) in combination with radiation.\nMETHODS AND MATERIALS: Colony and mechanistic in vitro assays and a xenograft in vivo model.\nRESULTS: SAR-020106 suppressed-radiation-induced G2/M arrest and reduced clonogenic survival only in p53-deficient tumor cells. SAR-020106 promoted mitotic entry following irradiation in all cell lines, but p53-deficient cells were likely to undergo apoptosis or become aneuploid, while p53 wild-type cells underwent a postmitotic G1 arrest followed by subsequent normal cell cycle re-entry. Following combined treatment with SAR-020106 and radiation, homologous-recombination-mediated DNA damage repair was inhibited in all cell lines. A significant increase in the number of pan-γH2AX-staining apoptotic cells was observed only in p53-deficient cell lines. Efficacy was confirmed in vivo in a clinically relevant human head-and-neck cell carcinoma xenograft model.\nCONCLUSION: The Chk1 inhibitor SAR-020106 is a potent radiosensitizer in tumor cell lines defective in p53 signaling.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {International Journal of Radiation Oncology, Biology, Physics},\n\tauthor = {Borst, Gerben R. and McLaughlin, Martin and Kyula, Joan N. and Neijenhuis, Sari and Khan, Aadil and Good, James and Zaidi, Shane and Powell, Ned G. and Meier, Pascal and Collins, Ian and Garrett, Michelle D. and Verheij, Marcel and Harrington, Kevin J.},\n\tmonth = mar,\n\tyear = {2013},\n\tkeywords = {Animals, Apoptosis, Cell Line, Tumor, Cell cycle, Checkpoint Kinase 1, Cyclin-Dependent Kinase Inhibitor p21, DNA Damage, DNA Repair, G2 Phase, HeLa Cells, Histones, Humans, Immunohistochemistry, Isoquinolines, Mice, Mice, Nude, Microscopy, Mitosis, Papillomaviridae, Protein Kinases, Pyrazines, Radiation Tolerance, Radiation-Sensitizing Agents, Time-Lapse Imaging, Tumor Stem Cell Assay, Tumor Suppressor Protein p53},\n\tpages = {1110--1118},\n}\n\n","author_short":["Borst, G. R.","McLaughlin, M.","Kyula, J. N.","Neijenhuis, S.","Khan, A.","Good, J.","Zaidi, S.","Powell, N. G.","Meier, P.","Collins, I.","Garrett, M. D.","Verheij, M.","Harrington, K. J."],"key":"borst_targeted_2013","id":"borst_targeted_2013","bibbaseid":"borst-mclaughlin-kyula-neijenhuis-khan-good-zaidi-powell-etal-targetedradiosensitizationbythechk1inhibitorsar020106-2013","role":"author","urls":{},"keyword":["Animals","Apoptosis","Cell Line","Tumor","Cell cycle","Checkpoint Kinase 1","Cyclin-Dependent Kinase Inhibitor p21","DNA Damage","DNA Repair","G2 Phase","HeLa Cells","Histones","Humans","Immunohistochemistry","Isoquinolines","Mice","Mice","Nude","Microscopy","Mitosis","Papillomaviridae","Protein Kinases","Pyrazines","Radiation Tolerance","Radiation-Sensitizing Agents","Time-Lapse Imaging","Tumor Stem Cell Assay","Tumor Suppressor Protein p53"],"metadata":{"authorlinks":{}}},"bibtype":"article","biburl":"https://bibbase.org/zotero/tplas","dataSources":["YLgywGcXWx96vKKaB"],"keywords":["animals","apoptosis","cell line","tumor","cell cycle","checkpoint kinase 1","cyclin-dependent kinase inhibitor p21","dna damage","dna repair","g2 phase","hela cells","histones","humans","immunohistochemistry","isoquinolines","mice","mice","nude","microscopy","mitosis","papillomaviridae","protein kinases","pyrazines","radiation tolerance","radiation-sensitizing agents","time-lapse imaging","tumor stem cell assay","tumor suppressor protein p53"],"search_terms":["targeted","radiosensitization","chk1","inhibitor","sar","020106","borst","mclaughlin","kyula","neijenhuis","khan","good","zaidi","powell","meier","collins","garrett","verheij","harrington"],"title":"Targeted radiosensitization by the Chk1 inhibitor SAR-020106","year":2013}