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Director, Molecular Pathology LaboratoryDirector, Molecular Genetic Pathology FellowshipDirector, Resident Rotation in Molecular PathologyClinical Associate Professor of Pathology
- Clinical Pathology
Primary Office: C606 General HospitalIowa City, IA 52242
BA, Biochemistry, Columbia University, New York City, NYMD, University of Iowa Carver College of Medicine, Iowa City, IAPhD, Molecular Biology, University of Iowa Carver College of Medicine, Iowa City, IA
Residency, Clinical Pathology, University of Iowa Carver College of Medicine, Iowa City, IAFellowship, Molecular Genetic Pathology, Hospital of the University of Pennsylvania, Philadelphia, PA
Diplomat in Molecular Genetic Pathology, American Board of PathologyDiplomat in Clinical Pathology, American Board of Pathology
Dr. Bossler's clinical service duties include directing the molecular pathology laboratory, developing and validating new, rapid, and cost effective molecular assays for genetic, neoplastic and infectious disease testing, and interpreting and reporting patient results from clinical molecular testing. His research interest is in understanding the mechanisms and pathways which lead to oncogenesis particularly regarding the association of infection with high risk human papillomavirus (HPV) and the development of squamous cell cancer.
Evaluation of the Bruker Biotyper and Vitek MS matrix-assisted laser desorption ionization-time of flight mass spectrometry systems for identification of nonfermenting gram-negative bacilli isolated from cultures from cystic fibrosis patients.
Journal of clinical microbiology.
2012 June. 50(6):2034-9.
Performance of the COBAS® AmpliPrep/COBAS TaqMan® automated system for hepatitis C virus (HCV) quantification in a multi-center comparison.
Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology.
2011 February. 50(2):100-3.
FSH dystrophy and a subtelomeric 4q haplotype: a new assay and associations with disease.
Journal of medical genetics.
2010 November. 47(11):745-51.
Journal of clinical neuromuscular disease.
2010 March. 11(3):124-6.
Human papillomavirus (HPV) type 18 induces extended growth in primary human cervical, tonsillar, or foreskin keratinocytes more effectively than other high-risk mucosal HPVs.
Journal of virology.
2009 November. 83(22):11784-94.
Impaired PTPN13 phosphatase activity in spontaneous or HPV-induced squamous cell carcinomas potentiates oncogene signaling through the MAP kinase pathway.
2009 November. 28(45):3960-70.
Interferon-beta treatment increases human papillomavirus early gene transcription and viral plasmid genome replication by activating interferon regulatory factor (IRF)-1.
2009 August. 30(8):1336-44.
The PDZ binding motif of human papillomavirus type 16 E6 induces PTPN13 loss, which allows anchorage-independent growth and synergizes with ras for invasive growth.
Journal of virology.
2008 March. 82(5):2493-500.
Deletion of the PDZ motif of HPV16 E6 preventing immortalization and anchorage-independent growth in human tonsil epithelial cells.
Head & neck.
2008 February. 30(2):139-47.
Oligodeoxynucleotide CpG 7909 delivered as intravenous infusion demonstrates immunologic modulation in patients with previously treated non-Hodgkin lymphoma.
Journal of immunotherapy.
Date Last Modified: 07/21/2016 -
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