Sensitization of tumor to 212Pb radioimmunotherapy by gemcitabine involves initial abrogation of G2 arrest and blocked DNA damage repair by interference with Rad51

International Journal of Radiation Oncology Biology Physics

Volumn 85, Issue 4, 2013, Pages 1119-1126

  Yong, Kwon Joong ^a   Milenic, Diane E ^a   Baidoo, Kwamena E ^a   Brechbiel, Martin W ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CHROMATIN REMODELING; CHROMATIN STRUCTURE; DNA DOUBLE-STRAND BREAKS; HUMAN COLON CANCER; METHODS AND MATERIALS; PARTICLE RADIATION THERAPIES; RADIOIMMUNOTHERAPY; THERAPEUTIC EFFICACY;

BIOSYNTHESIS; CELL DEATH; CHROMOSOMES; DISEASES; DNA; MONOCLONAL ANTIBODIES; RADIOTHERAPY; TUMORS;

LEAD;

[2 (4 ISOTHIOCYANATOBRENZYL) 1,4,7,10 TETRAAZA 1,4,7,10 TETRA(2 CARBAMONYLMETHYL)CYCLODODECANE]TRASTUZUMAB PB 212; ANTIBODY CONJUGATE; CHECKPOINT KINASE 1; CYCLIN DEPENDENT KINASE INHIBITOR 1; GEMCITABINE; LEAD 212; RAD51 PROTEIN; TRASTUZUMAB; UNCLASSIFIED DRUG; 2-(4-ISOTHIOCYANATOBENZYL)-1,4,7,10--TETRAAZA-1,4,7,10-TETRA-(2-CARBAMOYLMETHYL)CYCLODODECANE; 2 (4 ISOTHIOCYANATOBENZYL) 1,4,7,10 TETRAAZA 1,4,7,10 TETRA (2 CARBAMOYLMETHYL)CYCLODODECANE; ANTINEOPLASTIC AGENT; CDKN1A PROTEIN, HUMAN; CYCLIN DEPENDENT KINASE INHIBITOR 1A; DEOXYCYTIDINE; DRUG DERIVATIVE; HETEROCYCLIC COMPOUND; ISOTHIOCYANIC ACID DERIVATIVE; LEAD; MONOCLONAL ANTIBODY; PROTEIN KINASE; RADIOSENSITIZING AGENT;

ALPHA RADIATION; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CHROMATIN; CHROMATIN ASSEMBLY AND DISASSEMBLY; CHROMATIN STRUCTURE; COLON CANCER; CONTROLLED STUDY; DNA REPAIR; DNA SYNTHESIS; DOUBLE STRANDED DNA BREAK; DOWN REGULATION; DRUG EFFICACY; DRUG MECHANISM; DRUG POTENTIATION; ENZYME PHOSPHORYLATION; FEMALE; G2 PHASE CELL CYCLE CHECKPOINT; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; RADIOIMMUNOTHERAPY; S PHASE CELL CYCLE CHECKPOINT; SENSITIZATION; TUMOR XENOGRAFT; ANIMAL; CELL CYCLE G2 PHASE; CELL DEATH; DRUG ANTAGONISM; DRUG EFFECT; DRUG SCREENING; GENETICS; IMMUNOLOGY; LINEAR ENERGY TRANSFER; METABOLISM; METHODOLOGY; MITOSIS; MULTIMODALITY CANCER THERAPY; NICK END LABELING; NUDE MOUSE; PERITONEUM TUMOR; PHOSPHORYLATION; PHYSIOLOGY; RADIATION EXPOSURE; TUMOR CELL LINE;

ANIMALS; ANTIBODIES, MONOCLONAL, HUMANIZED; ANTINEOPLASTIC AGENTS; APOPTOSIS; CELL DEATH; CELL LINE, TUMOR; CHROMATIN; COMBINED MODALITY THERAPY; CYCLIN-DEPENDENT KINASE INHIBITOR P21; DEOXYCYTIDINE; DNA REPAIR; DRUG SYNERGISM; FEMALE; G2 PHASE; HETEROCYCLIC COMPOUNDS; HUMANS; IN SITU NICK-END LABELING; ISOTHIOCYANATES; LEAD RADIOISOTOPES; LINEAR ENERGY TRANSFER; MICE; MICE, NUDE; MITOSIS; PERITONEAL NEOPLASMS; PHOSPHORYLATION; PROTEIN KINASES; RAD51 RECOMBINASE; RADIATION-SENSITIZING AGENTS; RADIOIMMUNOTHERAPY; XENOGRAFT MODEL ANTITUMOR ASSAYS;

MLCS; MLOWN;

EID: 84875214677     PISSN: 03603016     EISSN: 1879355X     Source Type: Journal    
DOI: 10.1016/j.ijrobp.2012.09.015     Document Type: Article

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