William M Bonner

William M Bonner,

Clinical Case Manager

Department: Child Protection Team
Business Phone: (352) 527-0978
Business Email: matthewbonner@ufl.edu

Publications

2015
Inactivation of NADPH oxidases NOX4 and NOX5 protects human primary fibroblasts from ionizing radiation-induced DNA damage.
Radiation research. 183(3):262-70 [DOI] 10.1667/RR13799.1. [PMID] 25706776.
2014
Systemic DNA damage accumulation under in vivo tumor growth can be inhibited by the antioxidant Tempol.
Cancer letters. 353(2):248-57 [DOI] 10.1016/j.canlet.2014.07.030. [PMID] 25069035.
2013
Evaluation of the gamma-H2AX assay for radiation biodosimetry in a swine model.
International journal of molecular sciences. 14(7):14119-35 [DOI] 10.3390/ijms140714119. [PMID] 23880859.
2013
Mito-tempol and dexrazoxane exhibit cardioprotective and chemotherapeutic effects through specific protein oxidation and autophagy in a syngeneic breast tumor preclinical model.
PloS one. 8(8) [DOI] 10.1371/journal.pone.0070575. [PMID] 23940596.
2013
NADPH Oxidases NOXs and DUOXs as putative targets for cancer therapy.
Anti-cancer agents in medicinal chemistry. 13(3):502-14 [PMID] 22931418.
2012
A unified phylogeny-based nomenclature for histone variants.
Epigenetics & chromatin. 5 [DOI] 10.1186/1756-8935-5-7. [PMID] 22650316.
2012
Enhanced intrinsic radiosensitivity after treatment with stereotactic radiosurgery for an acoustic neuroma.
Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology. 103(3):410-4 [DOI] 10.1016/j.radonc.2012.03.011. [PMID] 22560711.
2012
SOD2 deficiency promotes aging phenotypes in mouse skin.
Aging. 4(2):116-8 [PMID] 22328603.
2012
Susceptibility to bystander DNA damage is influenced by replication and transcriptional activity.
Nucleic acids research. 40(20):10274-86 [DOI] 10.1093/nar/gks795. [PMID] 22941641.
2012
γ-H2AX and other histone post-translational modifications in the clinic.
Biochimica et biophysica acta. 1819(7):743-56 [DOI] 10.1016/j.bbagrm.2012.02.021. [PMID] 22430255.
2011
DNA damage responses in the prostate: implications for cancer formation?
Cell cycle (Georgetown, Tex.). 10(23) [DOI] 10.4161/cc.10.23.18236. [PMID] 22086112.
2011
H2AX phosphorylation in response to DNA double-strand break formation during bystander signalling: effect of microRNA knockdown.
Radiation protection dosimetry. 143(2-4):264-9 [DOI] 10.1093/rpd/ncq470. [PMID] 21183548.
2011
High salt and DNA double-strand breaks.
Proceedings of the National Academy of Sciences of the United States of America. 108(51):20281-2 [DOI] 10.1073/pnas.1117713109. [PMID] 22160689.
2011
Hypothermia postpones DNA damage repair in irradiated cells and protects against cell killing.
Mutation research. 711(1-2):142-9 [DOI] 10.1016/j.mrfmmm.2010.12.006. [PMID] 21185842.
2011
Para-inflammation mediates systemic DNA damage in response to tumor growth.
Communicative & integrative biology. 4(1):78-81 [DOI] 10.4161/cib.4.1.13942. [PMID] 21509186.
2011
Phase I study of PARP inhibitor ABT-888 in combination with topotecan in adults with refractory solid tumors and lymphomas.
Cancer research. 71(17):5626-34 [DOI] 10.1158/0008-5472.CAN-11-1227. [PMID] 21795476.
2011
Q(γ-H2AX), an analysis method for partial-body radiation exposure using γ-H2AX in nonhuman primate lymphocytes.
Radiation measurements. 46(9):877-881 [PMID] 21949480.
2011
Recent developments in the use of γ-H2AX as a quantitative DNA double-strand break biomarker.
Aging. 3(2):168-74 [PMID] 21325706.
2011
Systemic DNA damage related to cancer.
Cancer research. 71(10):3437-41 [DOI] 10.1158/0008-5472.CAN-10-4579. [PMID] 21558390.
2011
γ-H2AX detection in peripheral blood lymphocytes, splenocytes, bone marrow, xenografts, and skin.
Methods in molecular biology (Clifton, N.J.). 682:249-70 [DOI] 10.1007/978-1-60327-409-8_18. [PMID] 21057933.
2011
γH2AX foci as a measure of DNA damage: a computational approach to automatic analysis.
Mutation research. 711(1-2):49-60 [DOI] 10.1016/j.mrfmmm.2010.12.015. [PMID] 21216255.
2010
Development of a validated immunofluorescence assay for γH2AX as a pharmacodynamic marker of topoisomerase I inhibitor activity.
Clinical cancer research : an official journal of the American Association for Cancer Research. 16(22):5447-57 [DOI] 10.1158/1078-0432.CCR-09-3076. [PMID] 20924131.
2010
DNA-PKcs deficiency leads to persistence of oxidatively induced clustered DNA lesions in human tumor cells.
Free radical biology & medicine. 48(10):1435-43 [DOI] 10.1016/j.freeradbiomed.2010.02.033. [PMID] 20193758.
2010
Histone gammaH2AX and poly(ADP-ribose) as clinical pharmacodynamic biomarkers.
Clinical cancer research : an official journal of the American Association for Cancer Research. 16(18):4532-42 [DOI] 10.1158/1078-0432.CCR-10-0523. [PMID] 20823146.
2010
Impact papers on aging in 2009.
Aging. 2(3):111-21 [PMID] 20351400.
2010
microRNAome changes in bystander three-dimensional human tissue models suggest priming of apoptotic pathways.
Carcinogenesis. 31(10):1882-8 [DOI] 10.1093/carcin/bgq119. [PMID] 20643754.
2010
Role of oxidatively induced DNA lesions in human pathogenesis.
Mutation research. 704(1-3):152-9 [DOI] 10.1016/j.mrrev.2009.12.005. [PMID] 20060490.
2010
The complexity of phosphorylated H2AX foci formation and DNA repair assembly at DNA double-strand breaks.
Cell cycle (Georgetown, Tex.). 9(2):389-97 [PMID] 20046100.
2010
The use of gamma-H2AX as a biodosimeter for total-body radiation exposure in non-human primates.
PloS one. 5(11) [DOI] 10.1371/journal.pone.0015544. [PMID] 21124906.
2010
Tumors induce complex DNA damage in distant proliferative tissues in vivo.
Proceedings of the National Academy of Sciences of the United States of America. 107(42):17992-7 [DOI] 10.1073/pnas.1008260107. [PMID] 20855610.
2010
γH2AX: Applications for the evaluation of telomerase-based cancer therapy.
Cell cycle (Georgetown, Tex.). 9(17):3385-6 [DOI] 10.4161/cc.9.17.13003. [PMID] 20703091.
2009
Accumulation of oxidatively induced clustered DNA lesions in human tumor tissues.
Mutation research. 674(1-2):131-6 [DOI] 10.1016/j.mrgentox.2008.09.010. [PMID] 18948225.
2009
Ataxia telangiectasia mutated activation by transcription- and topoisomerase I-induced DNA double-strand breaks.
EMBO reports. 10(8):887-93 [DOI] 10.1038/embor.2009.97. [PMID] 19557000.
2009
H2AX: functional roles and potential applications.
Chromosoma. 118(6):683-92 [DOI] 10.1007/s00412-009-0234-4. [PMID] 19707781.
2009
Intercellular communication of cellular stress monitored by gamma-H2AX induction.
Carcinogenesis. 30(10):1686-95 [DOI] 10.1093/carcin/bgp192. [PMID] 19651821.
2009
Telomere-dependent and telomere-independent origins of endogenous DNA damage in tumor cells.
Aging. 1(2):212-8 [PMID] 20157510.
2009
The role of DNA damage response pathways in chromosome fragility in Fragile X syndrome.
Nucleic acids research. 37(13):4385-92 [DOI] 10.1093/nar/gkp391. [PMID] 19465392.
2009
γ-H2AX as a biomarker of DNA damage induced by ionizing radiation in human peripheral blood lymphocytes and artificial skin.
Advances in space research : the official journal of the Committee on Space Research (COSPAR). 43(8):1171-1178 [PMID] 20046946.
2008
Both telomeric and non-telomeric DNA damage are determinants of mammalian cellular senescence.
Epigenetics & chromatin. 1(1) [DOI] 10.1186/1756-8935-1-6. [PMID] 19014415.
2008
Delayed kinetics of DNA double-strand break processing in normal and pathological aging.
Aging cell. 7(1):89-100 [PMID] 18005250.
2008
GammaH2AX and cancer.
Nature reviews. Cancer. 8(12):957-67 [DOI] 10.1038/nrc2523. [PMID] 19005492.
2007
Collaborative roles of gammaH2AX and the Rad51 paralog Xrcc3 in homologous recombinational repair.
DNA repair. 6(3):280-92 [PMID] 17123873.
2007
DNA double-strand breaks form in bystander cells after microbeam irradiation of three-dimensional human tissue models.
Cancer research. 67(9):4295-302 [PMID] 17483342.
2007
gamma-H2AX in bystander cells: not just a radiation-triggered event, a cellular response to stress mediated by intercellular communication.
Cell cycle (Georgetown, Tex.). 6(18):2210-2 [PMID] 17881892.
2006
Epigenetic dysregulation underlies radiation-induced transgenerational genome instability in vivo.
International journal of radiation oncology, biology, physics. 66(2):327-30 [PMID] 16965987.
2006
GammaH2AX in cancer cells: a potential biomarker for cancer diagnostics, prediction and recurrence.
Cell cycle (Georgetown, Tex.). 5(24):2909-13 [PMID] 17172873.
2006
Genetic analysis of Saccharomyces cerevisiae H2A serine 129 mutant suggests a functional relationship between H2A and the sister-chromatid cohesion partners Csm3-Tof1 for the repair of topoisomerase I-induced DNA damage.
Genetics. 172(1):67-76 [PMID] 16219777.
2006
Techniques for gamma-H2AX detection.
Methods in enzymology. 409:236-50 [PMID] 16793405.
2006
The phosphorylation status of PAS-B distinguishes HIF-1alpha from HIF-2alpha in NBS1 repression.
The EMBO journal. 25(20):4784-94 [PMID] 17024177.
2005
DNA damage produced by 125I-triplex-forming oligonucleotides as a measure of their successful delivery into cell nuclei.
Annals of the New York Academy of Sciences. 1058:140-50 [PMID] 16394133.
2005
Fractionated low-dose radiation exposure leads to accumulation of DNA damage and profound alterations in DNA and histone methylation in the murine thymus.
Molecular cancer research : MCR. 3(10):553-61 [PMID] 16254189.
2005
Ionizing radiation induces DNA double-strand breaks in bystander primary human fibroblasts.
Oncogene. 24(49):7257-65 [PMID] 16170376.
2004
Assessment of DNA damage produced by 125I-triplex-forming oligonucleotides in cells.
International journal of radiation biology. 80(11-12):927-31 [PMID] 15764404.
2004
Distribution and dynamics of chromatin modification induced by a defined DNA double-strand break.
Current biology : CB. 14(19):1703-11 [PMID] 15458641.
2004
Histone H2AX is phosphorylated at sites of retroviral DNA integration but is dispensable for postintegration repair.
The Journal of biological chemistry. 279(44):45810-4 [PMID] 15308627.
2004
Phenomena leading to cell survival values which deviate from linear-quadratic models.
Mutation research. 568(1):33-9 [PMID] 15530537.
2004
Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks.
Nature cell biology. 6(2):168-70 [PMID] 14755273.
2004
Two-dimensional gel analysis of histones and other H2AX-related methods.
Methods in enzymology. 375:76-88 [PMID] 14870660.
2003
Characteristics of gamma-H2AX foci at DNA double-strand breaks sites.
Biochemistry and cell biology = Biochimie et biologie cellulaire. 81(3):123-9 [PMID] 12897845.
2003
H2AX haploinsufficiency modifies genomic stability and tumor susceptibility.
Cell. 114(3):371-383 [PMID] 12914701.
2003
H2AX is required for chromatin remodeling and inactivation of sex chromosomes in male mouse meiosis.
Developmental cell. 4(4):497-508 [PMID] 12689589.
2003
Histone H2AX in DNA damage and repair.
Cancer biology & therapy. 2(3):233-5 [PMID] 12878854.
2003
Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks.
Nature cell biology. 5(7):675-9 [PMID] 12792649.
2003
Low-dose radiation: thresholds, bystander effects, and adaptive responses.
Proceedings of the National Academy of Sciences of the United States of America. 100(9):4973-5 [PMID] 12704228.
2003
Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes.
The Journal of biological chemistry. 278(22):20303-12 [PMID] 12660252.
2003
Yeast histone 2A serine 129 is essential for the efficient repair of checkpoint-blind DNA damage.
EMBO reports. 4(7):678-84 [PMID] 12792653.
2002
Genomic instability in mice lacking histone H2AX.
Science (New York, N.Y.). 296(5569):922-7 [PMID] 11934988.
2002
Histone H2A variants H2AX and H2AZ.
Current opinion in genetics & development. 12(2):162-9 [PMID] 11893489.
2002
Quantitative detection of (125)IdU-induced DNA double-strand breaks with gamma-H2AX antibody.
Radiation research. 158(4):486-92 [PMID] 12236816.
2002
UV-induced replication arrest in the xeroderma pigmentosum variant leads to DNA double-strand breaks, gamma -H2AX formation, and Mre11 relocalization.
Proceedings of the National Academy of Sciences of the United States of America. 99(1):233-8 [PMID] 11756691.
2001
AID is required to initiate Nbs1/gamma-H2AX focus formation and mutations at sites of class switching.
Nature. 414(6864):660-665 [DOI] 10.1038/414660a. [PMID] 11740565.

Contact Details

Phones:
Business:
(352) 527-0978
Emails:
Addresses:
Business Mailing:
PO BOX 100296
PEDIATRICS CHILD PROTECTION TEAM
GAINESVILLE FL 326100296
Business Street:
1701 SW 16TH ST
GAINESVILLE FL 32608