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Richard Press, MD, PhD
Medical Director, Molecular Pathology
Program Director, Molecular Genetic Pathology Fellowhip
Rank: Professor
Clinical Services: Molecular Pathology
Clinical Interests: Molecular diagnostics; Cancer Biomarkers.
Research Interests: Molecular diagnostic biomarkers in cancer & infectious diseases and prevalent genetic alterations in common diseases.
 
Education:
1977-81    Northwestern University, Evanston, IL, BA, Chemistry
1981-87    Case Western Reserve University, Cleveland, OH, PhD, Biochemistry
1981-88    Case Western Reserve University, Cleveland, OH, MD
1988-92    University of Pennsylvania, Philadelphia, Residency, Pathology
1992-93    University of Pennsylvania, Philadelphia, Fellowship, Molecular Pathology
Boards:
Clinical Pathology, 1992
Molecular Genetic Pathology, 2001
Previous Position:
Selected References:
  • Bcr-Abl RNA Levels At and After the Time of a Complete Cytogenetic Remission (CCR) Predict the Duration of CCR In Imatinib-Treated CML Patients. Blood 107: 4250-4256, 2006.
  • Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib. Leukemia 21: 489-493, 2007.
  • HFE C282Y homozygotes ages 25-29 years at HEIRS study initial screening. Genetic Testing 11 (3): 269-275, 2007.
  • A genome-wide linkage scan for iron phenotype quantitative trait loci: The HEIRS Family Study. Clinical Genetics 71: 518-29, 2007.
  • A Half-Log Increase in BCR-ABL RNA Predicts a Higher Risk of Relapse in Patients with Chronic Myeloid Leukemia with an Imatinib-Induced Complete Cytogenetic Response (CCR). Clin Cancer Research, 13 (20): 6136-6143, 2007.
  • An international study to standardize the detection and quantitation of BCR-ABL transcripts from stabilized peripheral blood preparations by quantitative RT-PCR. Haematologica 92: 970-973, 2007.
  • An Intron-Derived Insertion-Truncation Mutation in the BCR-ABL Kinase Domain in CML Patients Undergoing Kinase Inhibitor Therapy. J. Molec Diagn, 10: 177-180, 2008.
  • Characteristics of participants with self-reported hemochromatosis or iron overload at HEIRS Study initial screening. Am J Hematol 83 (2): 126-132, 2008.
  • Characterization of BCR-ABL deletion mutants from patients with chronic myeloid leukemia. Leukemia 22: 1184-90, 2008.
  • Desirable performance characteristics for BCR-ABL measurement on an international reporting scale to allow consistent interpretation of individual patient response and comparison of response rates between clinical trials. Blood 112: 3330-3338, 2008.
  • Laboratory practice guidelines for detecting and reporting BCR-ABL drug resistance mutations in chronic myelogenous leukemia and acute lymphoblastic leukemia. J Mol Diagn 11: 4-11, 2009.
  • Multi-site PCR-based CMV Viral Load Assessment - Assays Demonstrate Linearity and Precision, but Lack Numeric Standardization. J Mol Diagn, 11: 87-92, 2009.
  • Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib. Blood 114: 2598-2605, 2009.
  • HFE, SLC40A1, HAMP, HJV, TFR2, and FTL mutations detected by denaturing high-performance liquid chromatography after iron phenotyping and HFE C282Y and H63D genotyping in 785 HEIRS Study participants. Am J Hematology, 84: 710-714, 2009.
  • Major Molecular Response in CML Patients Treated with Tyrosine Kinase Inhibitors: the Paradigm for Monitoring Targeted Cancer Therapy. The Oncologist 15: 744-749, 2010.
  • BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib. Blood 116 (17): 3278-3285, 2010.
  • Establishment of the 1st World Health Organization International Genetic Reference Panel for quantitation of BCR-ABL mRNA. Blood 116 (22): 111-117, 2010.
  • “Diagnostic Molecular Pathology” chapter (chapter 1), in Essentials of Anatomic Pathology, D Bostwick & L Cheng, editors, 2nd edition, Humana Press, Totowa, NJ, 2006.

Last Updated: 08/09/2010