Dr. Jose Cancelas, MD PhD

Headshot of Dr. Jose Cancelas

Jose Cancelas, MD, PhD, is Professor of Pediatrics at the University of Cincinnati College of Medicine, is Director of Hoxworth Blood Center and holds the Beatrice C. Lampkin Chair for Stem Cell and Hematotherapy. He is also leader of the Stem Cell group of the Cancer & Blood Diseases Institute of Cincinnati Children's Hospital Medical Center (CCHMC). 

Dr. Cancelas is a physician-scientist with broad background in hematology, stem cell biology, hematopoietic malignancies, cell therapies and transfusion medicine. His long-standing interest in hematopoiesis began during his doctoral and postdoctoral work in the Cancer Research Institute of Barcelona, the Erasmus University of Rotterdam and CCHMC and Hoxworth Blood Center, University of Cincinnati. During his training and as an independent investigator Jose developed methods and proof-of-concept for analysis of signaling pathways in hematopoietic/cancer stem cell activity in vivo. 

He has published over 170 peer-reviewed manuscripts in the areas of hematopoiesis and transfusion/cell therapies. His laboratory is funded by the NIH, US DoD and different private foundations and corporations. He has trained over 40 MD, MD PhD, and PhD professionals who are currently working in Hematology/ Oncology and Transfusion Medicine programs in USA, Europe and Asia. 

As Medical Director for both Cell Therapies at the Hoxworth Blood Center and the Cell Manipulation Laboratory of the Cancer & Blood Diseases of CCHMC, Dr. Cancelas’ work focuses on developing new blood and cell therapy products with augmented efficacy and/or safety profiles in the areas of transfusion, stem cell transplantation and immunotherapy. His clinical group has optimized methods of progenitor (Cancelas JA et al., Transfusion 2016;56:2824) and granulocyte collection for transfusion in neutropenic patients (Cancelas JA et al., Transfusion 2015; 55:748) and validated novel methods to preserve and store T lymphocytes (Worsham DN et al., Transfusion 2017;57:1555), and red cells and platelets (Cancelas JA et al., Transfusion 2017;57:1218; Cancelas JA et al. Vox Sang, 2017;112:210 Dumont LJ, Cancelas JA, et al. Transfusion. 2015;55:485; Cancelas JA et al., Transfusion. 2015;55:491; Dumont LJ, Cancelas JA, et al. Transfusion. 2013;53:972; Dumont LJ, Cancelas JA, et al. Transfusion. 2013;53:128; Cancelas JA, et al. Transfusion. 2011;51:1460, 2011;51:2228, 2011;51:2367; Bandarenko N, Cancelas JA et al., Transfusion. 2007;47:680; AuBuchon JP, Cancelas JA, et al. Transfusion. 2006;46:1311). 

His basic biology laboratory has contributed to the elucidation of the cellular and molecular mechanisms of hematopoietic stem cell (HSC) and granulocyte progenitor activity through the Rho family of GTPases in normal hematopoiesis and provided the basis for understanding the physiological cell-autonomous and microenvironment/cytokine dependent mechanisms that control HSC activity in the BM microenvironment (Gu Y et al., Science 2003;302:445; Cancelas JA et al., Nat. Med., 2005;11:886; Sengupta A et al., PNAS 2011; 108:9957; Gonzalez-Nieto D et al., Blood 2012;119:5144; Taniguchi-Ishikawa et al., PNAS 2012;109:9071; Taniguchi-Ishikawa et al., Nature Comm. 2013;4:art. No. 1660; Chang KH et al, Cell Reports, 2014;9:2084-9; Chang KH et al., Nature Comm., 2015;6;art. No. 5914). He has identified the mechanisms controlling malignant transformation by BCR-ABL and FIP1L1/PDGFRa (Yamada Y et al., Blood 2006;107:4071; Thomas EK et al., Cancer Cell 2007;22:898; Yamada Y et al., Blood 2008;112:2500; Sengupta A et al., Blood 2010;116:81; Chang KH et al., Blood 2012;120:800; Sengupta A et al., Blood 2012;119:494; Zhang C et al., Oncotarget 2018;9:29665; Nayak RC et al., Nature Comm., 2019;10:45). In normal and pathological myelopoiesis, his group defined the mechanisms that control oncogenic tyrosine kinase signals dependent transformation in leukemic progenitors through intrinsic and microenvironment-dependent signaling (Yamada Y et al., Blood 2006;107:4071; Thomas EK et al., Cancer Cell 2007;12:467; Yamada Y et al., Blood 2008;112:2500; Kesarwani et al. Nat. Med. 2017;23:472).

Through hematopoietic differentiation of human induced pluripotent stem cells (iPSC) from patients with severe congenital neutropenia, his laboratory is trying to identify the pathogenetic mechanisms of neutropenia in patients with ELANE mutations resulting in neutrophil elastase intracellular mislocalization, endoplasmic reticulum stress and apoptosis along with a non-cell autonomous effect on myeloid progenitors responsible to a bias towards monocytosis (Tidwell T et al., Blood 2014;123:562; Nayak RC et al., JCI 2015;125:3103). His laboratory has also developed specific methods for the characterization of iPSC from the NHLBI progenitor cell biology consortium (Salomonis N et al., Stem Cell Rep., 2016;7:110; Daily K et al., Sci. Data, 2017; 4:170030).