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Chris Ryder, MD, PhD

 
Specialty: Pathology
Program: Pathology

Overview

Dr. Ryder received his MD and PhD in Pharmacology from Case Western Reserve University School of Medicine. He completed a Residency in Clinical Pathology and Hematopathology Fellowship at University Hospitals Cleveland Medical Center/Case Western Reserve University. Dr. Ryder joins us from University Hospitals Cleveland Medical Center/Case Western Reserve University, where he was, an Assistant Professor in the Department of Pathology. Dr. Ryder’s clinical interests include multimodal approaches to establish accurate diagnosis and prognostic stratification of myeloid malignancies by synthesizing morphological, immunophenotypic and genomic data. Dr. Ryder has a background in the study of leukemia cell biology, with a focus on cell death pathways. His current interests include understanding the pathophysiology of myeloid leukemogenesis and developing improved methodologies to aid in the diagnosis and risk stratification of myeloid malignancies, including molecular genetics, flow cytometry and other laboratory techniques.


Education & Training

Fellowship:

  • University Hospitals Cleveland Medical Center / Case Western Reserve University - Hematopathology

Residency:

  • University Hospitals Cleveland Medical Center / Case Western Reserve University - Clinical Pathology

Medical School:

  • Case Western Reserve University School of Medicine - MD, PhD
Participating Trials

If you believe you are eligible for one of these trials or studies, please call
813-745-6100 or toll-free 1-800-679-0775.

Publications

  • Ryder CB, Oduro KA, Moore EM. Monoclonal B-cell lymphocytosis in the bone marrow: revisiting the criteria for chronic lymphocytic leukemia/small lymphocytic lymphoma. Hum Pathol. 2022 Jul.125:108-116. Pubmedid: 35472399.
  • Ryder CB, Kondolf HC, O'Keefe ME, Zhou B, Abbott DW. Chemical Modulation of Gasdermin-Mediated Pyroptosis and Therapeutic Potential. J Mol Biol. 2022 Feb.434(4):167183. Pubmedid: 34358546. Pmcid: PMC8810912.
  • Nirmalanantham P, Sakhi R, Beck R, Oduro K, Gadde R, Ryder C, Yoest J, Sadri N, Meyerson HJ. Flow Cytometric Findings in Clonal Cytopenia of Undetermined Significance. Am J Clin Pathol. 2022 Feb.157(2):219-230. Pubmedid: 34542558.
  • Narla G, Sangodkar J, Ryder CB. The impact of phosphatases on proliferative and survival signaling in cancer. Cell Mol Life Sci. 2018 Aug.75(15):2695-2718. Pubmedid: 29725697. Pmcid: PMC6023766.
  • Ryder CB, Schmotzer CL. Circulating tumor DNA: the future of personalized medicine in oncology?. Clin Chem. 2015 Feb.61(2):443-444. Pubmedid: 25789399.
  • Rosko AE, McColl KS, Zhong F, Ryder CB, Chang MJ, Sattar A, Caimi PF, Hill BT, Al-Harbi S, Almasan A, Distelhorst CW. Acidosis Sensing Receptor GPR65 Correlates with Anti-Apoptotic Bcl-2 Family Member Expression in CLL Cells: Potential Implications for the CLL Microenvironment. J Leuk (Los Angel). 2014 Dec.2(5). Pubmedid: 25984552. Pmcid: PMC4431653.
  • Ryder CB, McColl K, Distelhorst CW. Acidosis blocks CCAAT/enhancer-binding protein homologous protein (CHOP)- and c-Jun-mediated induction of p53-upregulated mediator of apoptosis (PUMA) during amino acid starvation. Biochem Bioph Res Co. 2013 Jan.430(4):1283-1288. Pubmedid: 23261451. Pmcid: PMC3601792.
  • Sun W, Liu K, Ryu H, Kang DW, Kim YS, Kim MS, Cho Y, Bhondwe RS, Thorat SA, Kim HS, Pearce LV, Pavlyukovets VA, Tran R, Morgan MA, Lazar J, Ryder CB, Toth A, Blumberg PM, Lee J. 2-(4-Methylsulfonylaminophenyl) propanamide TRPV1 antagonists: Structure-activity relationships in the B and C-regions. Bioorg Med Chem. 2012 Feb.20(3):1310-1318. Pubmedid: 22227463. Pmcid: PMC6988731.
  • Ryder C, McColl K, Zhong F, Distelhorst CW. Acidosis promotes Bcl-2 family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor Gpr65 signaling to Mek/Erk. J Biol Chem. 2012 Aug.287(33):27863-27875. Pubmedid: 22685289. Pmcid: PMC3431637.
  • Zhong F, Harr MW, Bultynck G, Monaco G, Parys JB, De Smedt H, Rong YP, Molitoris JK, Lam M, Ryder C, Matsuyama S, Distelhorst CW. Induction of Ca²+-driven apoptosis in chronic lymphocytic leukemia cells by peptide-mediated disruption of Bcl-2-IP3 receptor interaction. Blood. 2011 Mar.117(10):2924-2934. Pubmedid: 21193695. Pmcid: PMC3062302.

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