Chairman, Department of Therapeutic Radiology, Yale University
Radiation Oncology
Dr. Peter M. Glazer, MD
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Dr. Peter M. Glazer is an expert in the field of Radiation Oncology. He went to medical school at Yale University School of Medicine. Yale University School of Medicine is a top medical college. Yale University School of Medicine is ranked 7/57 in Research/PrimaryCare. Peter M. Glazer, MD is a published physician. He has 97 papers published. The most current publication "Chromosomal mutations induced by triplex-forming oligonucleotides in mammalian cells."
Publications
- LKB1 preserves genome integrity by stimulating BRCA1 expression.
- MicroRNA silencing for cancer therapy targeted to the tumour microenvironment.
- Modified Poly(lactic-co-glycolic Acid) Nanoparticles for Enhanced Cellular Uptake and Gene Editing in the Lung.
- Single-Stranded γPNAs for In Vivo Site-Specific Genome Editing via Watson-Crick Recognition.
- Hypoxic stress facilitates acute activation and chronic downregulation of fanconi anemia proteins.
- Silencing of the DNA Mismatch Repair Gene MLH1 Induced by Hypoxic Stress in a Pathway Dependent on the Histone Demethylase LSD1.
- The cytotoxicity of (-)-lomaiviticin A arises from induction of double-strand breaks in DNA.
- microRNAs in Cancer Cell Response to Ionizing Radiation.
- Radiation sensitivity and sensitization in melanoma.
- Nanoparticle for delivery of antisense γPNA oligomers targeting CCR5.
- Triplex-forming Peptide Nucleic Acids Induce Heritable Elevations in Gamma-globin Expression in Hematopoietic Progenitor Cells.
- Hypoxia-induced protein CAIX is associated with somatic loss of BRCA1 protein and pathway activity in triple negative breast cancer.
- Molecular and cellular pharmacology of the hypoxia-activated prodrug TH-302.
- Preclinical Evaluation of Laromustine for use in Combination with Radiation Therapy in the Treatment of Solid Tumors.
- Inhibition of hypoxia-induced miR-155 radiosensitizes hypoxic lung cancer cells.
- Targeted disruption of the CCR5 gene in human hematopoietic stem cells stimulated by peptide nucleic acids.
- Radiation Resistance in Cancer Therapy: Meeting Summary and Research Opportunities Report of an NCI Workshop held September 1-3, 2010.
- New translational possibilities for microenvironmental modulation of radiosensitivity.
- Functional and physical interaction between the mismatch repair and FA-BRCA pathways.
- Reduced Level of Ribonucleotide Reductase R2 Subunits Increases Dependence on Homologous Recombination Repair of Cisplatin-Induced DNA Damage.
- Targeted Gene Modification of Hematopoietic Progenitor Cells in Mice Following Systemic Administration of a PNA-peptide Conjugate.
- Radiation Resistance in Cancer Therapy: Meeting Summary and Research Opportunities: Report of an NCI Workshop held September 1-3, 2010.
- Hypoxia-Induced Epigenetic Regulation and Silencing of the BRCA1 Promoter.
- Polymer delivery systems for site-specific genome editing.
- Nanoparticles deliver triplex-forming PNAs for site-specific genomic recombination in CD34+ human hematopoietic progenitors.
- The tumor microenvironment and DNA repair.
- Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130.
- Potentiation of temozolomide cytotoxicity by inhibition of DNA polymerase beta is accentuated by BRCA2 mutation.
- "Micro"-management of DNA repair genes by hypoxia.
- Src-Induced cisplatin resistance mediated by cell-to-cell communication.
- Repair of DNA lesions associated with triplex-forming oligonucleotides.
- MicroRNA regulation of DNA repair gene expression in hypoxic stress.
- Correction of a splice-site mutation in the beta-globin gene stimulated by triplex-forming peptide nucleic acids.
- Chronic hypoxia decreases synthesis of homologous recombination proteins to offset chemoresistance and radioresistance.
- Triplex-mediated gene modification.
- Repair and recombination induced by triple helix DNA.
- CHK2-dependent phosphorylation of BRCA1 in hypoxia.
- Basal repression of BRCA1 by multiple E2Fs and pocket proteins at adjacent E2F sites.
- Triplex-stimulated intermolecular recombination at a single-copy genomic target.
- Targeted cross-linking of the human beta-globin gene in living cells mediated by a triple helix forming oligonucleotide.
- Site-specific gene modification by PNAs conjugated to psoralen.
- Hypoxia-induced down-regulation of BRCA1 expression by E2Fs.
- Hypoxia-induced phosphorylation of Chk2 in an ataxia telangiectasia mutated-dependent manner.
- Alterations in DNA repair gene expression under hypoxia: elucidating the mechanisms of hypoxia-induced genetic instability.
- Targeted genome modification via triple helix formation.
- Gene therapy for autosomal dominant disorders of keratin.
- Distance and affinity dependence of triplex-induced recombination.
- Down-regulation of Rad51 and decreased homologous recombination in hypoxic cancer cells.
- Cell-interdependent cisplatin killing by Ku/DNA-dependent protein kinase signaling transduced through gap junctions.
- Targeted gene modification using triplex-forming oligonucleotides.
- Setting standards in gene repair.
- The potential for gene repair via triple helix formation.
- Decreased expression of the DNA mismatch repair gene Mlh1 under hypoxic stress in mammalian cells.
- Transcription dependence of chromosomal gene targeting by triplex-forming oligonucleotides.
- Site-directed recombination via bifunctional PNA-DNA conjugates.
- IGF1 receptor expression protects against microenvironmental stress found in the solid tumor.
- Human XPA and RPA DNA repair proteins participate in specific recognition of triplex-induced helical distortions.
- Therapeutic genome mutagenesis using synthetic donor DNA and triplex-forming molecules.
- Triplex-mediated genome targeting and editing.
- Hypoxia and DNA Repair.
- Site-specific Genome Editing in PBMCs With PLGA Nanoparticle-delivered PNAs Confers HIV-1 Resistance in Humanized Mice.
- Cognitive rehabilitation in the elderly: effects on memory.
- Development of a statewide hospital plan for radiologic emergencies.
- The tyrphostin AG1024 accelerates the degradation of phosphorylated forms of retinoblastoma protein (pRb) and restores pRb tumor suppressive function in melanoma cells.
- MicroRNA-210 regulates mitochondrial free radical response to hypoxia and krebs cycle in cancer cells by targeting iron sulfur cluster protein ISCU.
- Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (II).
- Directed gene modification via triple helix formation.
- Intracellular generation of single-stranded DNA for chromosomal triplex formation and induced recombination.
- Genomic instability in cancer.
- Triplex forming oligonucleotides: sequence-specific tools for gene targeting.
- Gene targeting via triple-helix formation.
- Chromosome targeting at short polypurine sites by cationic triplex-forming oligonucleotides.
- Hypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice.
- Triplex-induced recombination in human cell-free extracts. Dependence on XPA and HsRad51.
- ATM-dependent expression of the insulin-like growth factor-I receptor in a pathway regulating radiation response.
- Specific mutations induced by triplex-forming oligonucleotides in mice.
- Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways.
- Diminished DNA repair and elevated mutagenesis in mammalian cells exposed to hypoxia and low pH.
- High-frequency intrachromosomal gene conversion induced by triplex-forming oligonucleotides microinjected into mouse cells.
- Cyclin D1 expression and early breast cancer recurrence following lumpectomy and radiation.
- Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts.
- Prognostic significance of cyclin D1 protein levels in early-stage larynx cancer treated with primary radiation.
- Activation of human gamma-globin gene expression via triplex-forming oligonucleotide (TFO)-directed mutations in the gamma-globin gene 5'' flanking region.
- Mutant p53 protein overexpression in women with ipsilateral breast tumor recurrence following lumpectomy and radiation therapy.
- Triple-helix formation induces recombination in mammalian cells via a nucleotide excision repair-dependent pathway.
- BRCA1/BRCA2 in breast-conserving therapy.
- BRCA1/BRCA2 germline mutations in locally recurrent breast cancer patients after lumpectomy and radiation therapy: implications for breast-conserving management in pat...
- The Tyr-265-to-Cys mutator mutant of DNA polymerase beta induces a mutator phenotype in mouse LN12 cells.
- Peptide nucleic acid (PNA) binding-mediated induction of human gamma-globin gene expression.
- Different mutator phenotypes in Mlh1- versus Pms2-deficient mice.
- Targeted correction of an episomal gene in mammalian cells by a short DNA fragment tethered to a triplex-forming oligonucleotide.
- Triplex formation by oligonucleotides containing 5-(1-propynyl)-2'-deoxyuridine: decreased magnesium dependence and improved intracellular gene targeting.
- Chromosomal mutations induced by triplex-forming oligonucleotides in mammalian cells.
- Expression of AP-2 transcription factors in human breast cancer correlates with the regulation of multiple growth factor signalling pathways.
- Targeted gene knockout mediated by triple helix forming oligonucleotides.
- Mutagenesis induced by the tumor microenvironment.
Schools
Yale University
St Vincent39s Med Center
Yale
Doctors Specialties
- Radiation Oncology
Accepted Insurances
Education
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Yale-New Haven Hospital -
Yale University School of Medicine
Hospital
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Yale-New Haven Hospital
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