
Raúl Montiel-Esparza
Affiliate, Dean's Office Operations - Dean Other
Fellow in Pediatrics - Hematology & Oncology
Bio
Raúl Montiel-Esparza, MD is a board-certified pediatric hematologist/oncologist and currently the inaugural pediatric Stem Cell Transplantation and Cellular Therapy clinical fellow at Stanford University School of Medicine. Dr. Montiel-Esparza grew up in central Mexico and earned his MD with honors from Tecnológico de Monterrey Escuela de Medicina. He completed a postdoctoral research fellowship in cancer immunology in the Luznik Lab at Johns Hopkins University followed by his residency in Pediatrics at UT Southwestern Medical Center. He has presented his work on Acute Myeloid Leukemia and Graft-versus-Host disease multiple times at national conferences and has several publications and co-authorships. His experiences as a clinician, scientist, and advocate have ultimately inspired him to explore graft engineering strategies in haploidentical stem-cell transplantation to ameliorate Graft-versus-Host disease in the Bertaina Lab at Stanford. His preliminary research recently granted him the 2022 inaugural underrepresented in medicine new investigator award from the American Society for Transplantation and Cellular Therapy (ASTCT). Ultimately, decreasing barriers to stem cell transplantation and improving donor availability in Latin America is in alignment with his future career goals.
Clinical Focus
- Fellow
- Pediatric Hematology/Oncology
- Haploidentical stem cell transplantation
Honors & Awards
-
Underrepresented Minority New Investigator Award, American Society for Transplantation and Cellular Therapy (ASTCT) (2022)
-
Pete and Arline Harman Endowed Fellow, Stanford Maternal and Child Health Research Institute (MCHRI) (2020-2022)
Professional Education
-
Board Certification, American Board of Pediatrics, Pediatric Hematology/Oncology (2023)
-
Fellowship, Stanford University School of Medicine, Pediatric Hematology/Oncology (2022)
-
Board Certification, American Board of Pediatrics, Pediatrics (2020)
-
Residency, University of Texas Southwestern Medical Center. Dallas, TX., Pediatrics (2019)
-
Postdoctoral research fellow, Johns Hopkins University. Baltimore, MD., Cancer immunology (2016)
-
MD, Escuela de Medicina Tecnológico de Monterrey (ITESM). Monterrey, N.L. México. (2013)
Graduate and Fellowship Programs
-
Pediatric Hem/Onc (Fellowship Program)
All Publications
-
Viral-specific T cells for Cytomegalovirus retinitis following hematopoietic stem cell transplantation: A success story.
Pediatric blood & cancer
2023: e30429
Abstract
Cytomegalovirus retinitis (CMVR) following hematopoietic stem cell transplantation (HCT) for a primary immunodeficiency is a rare but highly morbid condition with potential irreversible consequences despite optimal antiviral pharmacotherapy. Viral-specific T cells (VSTs) pose a promising and safe approach eradicating intractable viral disease. We describe the case of a 21-month-old male with Wiskott-Aldrich syndrome (WAS) and CMVR post HCT with sustained long-term virologic and clinical response after CMV-specific T-cell therapy. This case highlights the need to consider VST as an adjunct upfront strategy in refractory CMVR and for routine ophthalmologic screening and surveillance in high-risk patients post HCT.
View details for DOI 10.1002/pbc.30429
View details for PubMedID 37243390
-
Culturally Adapted Motivational Interviewing for Pediatric Acute Lymphoblastic Leukemia Adherence: Feasibility and Acceptability
CLINICAL PRACTICE IN PEDIATRIC PSYCHOLOGY
2022
View details for DOI 10.1037/cpp0000447
View details for Web of Science ID 000830744900001
-
Role of Cytokine Secretion Signatures of Donor-derived T Cells and Recipient Serum Cytokine Profiles as Predictive Biomarkers of Acute Graft-Versus-Host Disease in alpha beta T-cell/CD19 B-cell Depleted Hematopoietic Stem Cell Transplant Pediatric Recipients
WILEY. 2022
View details for Web of Science ID 000788322300433
-
POTENTIAL BIOMARKERS OF ACUTE GVHD IN ALPHA/BETA T-CELL/B-CELL DEPLETED HSCT PEDIATRIC RECIPIENTS
WILEY. 2022
View details for Web of Science ID 000788322300258
-
Combinatorial Cytokine Secretion Signature of Donor-Derived T Cells Infused with the Graft: A New Potential Biomarker of Acute Graft-Versus-Host Disease in.ss t-Cell/CD19 B-Cell Depleted Hematopoietic Stem Cell Transplant Recipients
AMER SOC HEMATOLOGY. 2021
View details for DOI 10.1182/blood-2021-149948
View details for Web of Science ID 000736398806151
-
Use of cardiac radiation therapy as bridging therapy to CAR-T for relapsed pediatric B-cell acute lymphoblastic leukemia.
Pediatric blood & cancer
2020: e28870
Abstract
The use of radiotherapy as bridging therapy to chimeric antigen receptor T-cell therapy (CAR-T) in pre-B acute lymphoblastic leukemia (B-ALL) has been minimally explored. Here, we present a boy with B-ALL who relapsed after allogeneic bone marrow transplant with disseminated disease, including significant symptomatic cardiovascular and gastrointestinal (GI) involvement. The cardiac and GI leukemic infiltrates were successfully treated with bridging radiation therapy (BRT) prior to CAR-T infusion. Using this approach, he successfully tolerated CAR-T with no evidence of disease or sequelae on 3-month follow-up. This is the first reported case of safe and effective delivery of cardiac BRT in B-ALL.
View details for DOI 10.1002/pbc.28870
View details for PubMedID 33355997
-
Use of Chimeric Antigen Receptor Modified T Cells With Extensive Leukemic Myocardial Involvement
JACC: CARDIOONCOLOGY
2020; 2 (4): 666–70
View details for DOI 10.1016/j.jaccao.2020.08.009
View details for Web of Science ID 000613114700018
-
Use of Chimeric Antigen Receptor Modified T Cells With Extensive Leukemic Myocardial Involvement.
JACC. CardioOncology
2020; 2 (4): 666-670
View details for DOI 10.1016/j.jaccao.2020.08.009
View details for PubMedID 34396279
View details for PubMedCentralID PMC8352108
-
Delayed cancer diagnoses and high mortality in children during the COVID-19 pandemic.
Pediatric blood & cancer
2020: e28427
View details for DOI 10.1002/pbc.28427
View details for PubMedID 32588960
-
Immunomodulation with pomalidomide at early lymphocyte recovery after induction chemotherapy in newly diagnosed AML and high-risk MDS
LEUKEMIA
2020
Abstract
An immunosuppressive microenvironment promoting leukemia cell immune escape plays an important role in the pathogenesis of AML. Through its interaction with cereblon, a substrate receptor for the E3 ubiquitin ligase complex, pomalidomide leads to selective ubiquitination of transcription factors Aiolos and Ikaros thereby promoting immune modulation. In this phase I trial, 51 newly diagnosed non-favorable risk AML and high-risk MDS patients were enrolled and treated with AcDVP16 (cytarabine 667 mg/m2/day IV continuous infusion days 1-3, daunorubicin 45 mg/m2 IV days 1-3, etoposide 400 mg/m2 IV days 8-10) induction therapy followed by dose- and duration-escalation pomalidomide beginning at early lymphocyte recovery. Forty-three patients (AML: n = 39, MDS: n = 4) received pomalidomide. The maximum tolerated dose of pomalidomide was 4 mg for 21 consecutive days. The overall complete remission (CR + CRi) rate, median overall survival, and disease-free survival were 75%, 27.1 and 20.6 months, respectively. Subset analyses revealed 86% CR/CRi rate in AML patients with unfavorable-risk karyotype treated with pomalidomide. Pomalidomide significantly decreased Aiolos expression in both CD4+ and CD8+ peripheral blood and bone marrow T cells, promoted T cell differentiation, proliferation, and heightened their cytokine production. Finally, pomalidomide induced distinct gene expression changes in immune function-related ontologies in CD4+ and CD8+ T cells.
View details for DOI 10.1038/s41375-019-0693-4
View details for Web of Science ID 000508141700001
View details for PubMedID 31900407
- Use of Chimeric Antigen Receptor Modified T Cells With Extensive Leukemic Myocardial Involvement JACC: CardioOncology 2020; 2 (4)
-
A Novel Case of Carcinoid Tumor in a Pediatric Patient With Short Bowel Syndrome Secondary to Gastroschisis
J Pediatr Gastroenterol Nutr
2020; 1 (2)
View details for DOI 10.1097/PG9.0000000000000023
-
A Signature of T Cell Exhaustion Is Enriched in the Bone Marrow (BM) of AML Patients and Shared with Immune Exhaustion Signatures of Solid Tumors
AMER SOC HEMATOLOGY. 2019
View details for DOI 10.1182/blood-2019-128742
View details for Web of Science ID 000577160406092
-
Connecting the Dots From Fever of Unknown Origin to Myelodysplastic Syndrome: GATA2 Haploinsufficiency.
Journal of pediatric hematology/oncology
2019
Abstract
Leukemia-predisposing conditions, such as GATA2 haploinsufficiency, are known for their high penetrance and expressivity profiles. These disorders pose a difficult diagnostic challenge to even the most experienced clinician when they first present. We describe the case of a 17-year-old male presenting with features of nontuberculous mycobacterial infection, pulmonary fibrinoid granulomatous vasculitis, and myelodysplasia in the setting of a pathogenic GATA2 frameshift mutation confirmed by next-generation sequencing. The broad differential for GATA2 haploinsufficiency requires prompt recognition of key clinical features and laboratory abnormalities towards directing diagnosis and guiding appropriate and perhaps life-saving therapy.
View details for DOI 10.1097/MPH.0000000000001505
View details for PubMedID 31033783
-
Effective Immunomodulation with Pomalidomide Beginning at Early Lymphocyte Recovery during Induction Timed Sequential Therapy (TST) for Acute Myeloid Leukemia (AML) and High-Risk Myelodysplasia (HR-MDS)
AMER SOC HEMATOLOGY. 2018
View details for DOI 10.1182/blood-2018-99-114961
View details for Web of Science ID 000454837601044
-
Signatures of CD8(+) T cell dysfunction in AML patients and their reversibility with response to chemotherapy
JCI INSIGHT
2018; 3 (21)
Abstract
Our understanding of phenotypic and functional signatures of CD8+ T cell dysfunction in acute myeloid leukemia (AML) is limited. Deciphering these deranged T cell functional states and how they are impacted by induction chemotherapy is essential for incorporation of novel immune-based strategies to restore and maintain antileukemia immunity.We utilized high-dimensional immunophenotyping, gene expression, and functional studies to characterize peripheral blood and bone marrow CD8+ T cells in 72 AML patients at diagnosis and after induction chemotherapy.Our data suggest that multiple aspects of deranged T cell function are operative in AML at diagnosis, with exhaustion and senescence being the dominant processes. Following treatment, the phenotypic and transcriptional profile of CD8+ T cells diverged between responders and nonresponders. Response to therapy correlated with upregulation of costimulatory, and downregulation of apoptotic and inhibitory, T cell signaling pathways, indicative of restoration of T cell function. In functional studies, AML blasts directly altered CD8+ T cell viability, expansion, co-signaling and senescence marker expression. This CD8+ T cell dysfunction was in part reversible upon PD-1 blockade or OX40 costimulation in vitro.Our findings highlight the uniqueness of AML in sculpting CD8+ T cell responses and the plasticity of their signatures upon chemotherapy response, providing a compelling rationale for integration of novel immunotherapies to augment antileukemia immunity.This work was supported by the Leukemia & Lymphoma Society grant no. 6449-13; NIH grants UM1-CA186691 and R01-HL110907-01; the American Society for Blood and Marrow Transplantation New Investigator Award/Gabrielle's Angel Foundation; the Vienna Fund for Innovative Cancer Research; and by fellowships from the Wenner-Gren Foundation and the Swedish Society for Medical Research.
View details for DOI 10.1172/jci.insight.120974
View details for Web of Science ID 000449225900004
View details for PubMedID 30385732
View details for PubMedCentralID PMC6238744
-
Acute Myeloid Leukemia (AML) Blasts Influence the Gene Expression Signature and Co-Signaling Receptor Expression of CD8(+) T Cells
AMER SOC HEMATOLOGY. 2016
View details for DOI 10.1182/blood.V128.22.1700.1700
View details for Web of Science ID 000394452306011
-
Phase 1 Study of Pomalidomide Given at the Time of Early Lymphocyte Recovery after Induction Timed Sequential Chemotherapy in Newly Diagnosed Acute Myeloid Leukemia (AML) and High-Risk Myelodysplastic Syndrome (HR-MDS)
AMER SOC HEMATOLOGY. 2016
View details for DOI 10.1182/blood.V128.22.2820.2820
View details for Web of Science ID 000394452305092
-
Immune Modulation with Pomalidomide after Induction Chemotherapy in Newly Diagnosed Acute Myeloid Leukemia (AML)
AMER SOC HEMATOLOGY. 2015
View details for Web of Science ID 000368019004151
-
Tracking Effector T Cell Dynamics and Immune Inhibitory Receptors in Patients with Acute Myeloid Leukemia (AML)
AMER SOC HEMATOLOGY. 2015
View details for Web of Science ID 000368021800106