David Van Mater

Overview:

I am a pediatric oncologist with a specific interest in hereditary cancer syndromes and sarcoma. I am also director of the Duke Comprehensive Neurofibromatosis Clinic where I see children and adults with neurofibromatosis type I and II, in addition to schwannomatosis.

Positions:

Assistant Professor of Pediatrics

Pediatrics, Hematology-Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

MD./PhD. 2006

University of Michigan, Ann Arbor

Pediatrics Internship and Residency, Pediatrics

University of Michigan, Ann Arbor

Pediatric Hematology/Oncology Fellowship, Pediatrics

Duke University School of Medicine

Grants:

Dissecting the role of injury is sarcoma formation

Administered By
Pediatrics, Hematology-Oncology
Awarded By
Sarcoma Alliance for Research Through Collaboration
Role
Principal Investigator
Start Date
End Date

Dissecting the role of injury is sarcoma formation

Administered By
Pediatrics, Hematology-Oncology
Awarded By
Sarcoma Alliance for Research Through Collaboration
Role
Principal Investigator
Start Date
End Date

Phase I study of PD-0332991 for pediatric patiens with retinoblastoma protein (RB)-positive recurrent or refractory central nervous system (CNS) tumors.

Administered By
Pediatrics, Hematology-Oncology
Awarded By
Pfizer, Inc.
Role
Principal Investigator
Start Date
End Date

MAIN STUDY: Developing Evidence-Based Crieteria for Initiating Treatment fo NF1-OPG.

Administered By
Pediatrics, Hematology-Oncology
Awarded By
Children's Tumor Foundation
Role
Principal Investigator
Start Date
End Date

Visual Field Outcomes in Pediatric Patients with NF1-associated Optic Pathway Gliomas

Administered By
Pediatrics, Hematology-Oncology
Awarded By
Boston Children's Hospital
Role
Principal Investigator
Start Date
End Date

Publications:

A phase I trial of the CDK 4/6 inhibitor palbociclib in pediatric patients with progressive brain tumors: A Pediatric Brain Tumor Consortium study (PBTC-042).

BACKGROUND: Disruption of cell-cycle regulators is a potential therapeutic target for brain tumors in children and adolescents. The aim of this study was to determine the maximum tolerated dose (MTD) and describe toxicities related to palbociclib, a selective cyclin-dependent kinase 4/6 (CDK4/6) inhibitor in pediatric patients with progressive/refractory brain tumors with intact retinoblastoma protein. METHODS: Palbociclib was administered orally starting at 50 mg/m2 daily for the first 21 days of a 28-day course. Dose escalation was according to the Rolling-6 statistical design in less heavily (stratum I) and heavily pretreated (stratum II) patients, and MTD was determined separately for each group. Pharmacokinetic studies were performed during the first course, and pharmacodynamic studies were conducted to evaluate relationships between drug levels and toxicities. RESULTS: A total of 21 patients were enrolled on stratum I and 14 patients on stratum II. The MTD for both strata was 75 mg/m2 . Palbociclib absorption (mean Tmax between 4.9 and 6.6 h) and elimination (mean half-life between 11.3 and 19.5 h) were assessed. The most common toxicity was myelosuppression. Higher palbociclib exposure was associated with grade 3/4 neutropenia and leukopenia. Dose limiting toxicities included grade 4 neutropenia and grade 3 thrombocytopenia and dehydration. No patients had an objective response to palbociclib therapy. CONCLUSIONS: Palbociclib was safely administered to children and adolescents at a dosage of 75 mg/m2 for 21 consecutive days followed by seven days of rest in both strata. Future studies will establish its optimal utilization in pediatric patients with brain tumors.
Authors
Van Mater, D; Gururangan, S; Becher, O; Campagne, O; Leary, S; Phillips, JJ; Huang, J; Lin, T; Poussaint, TY; Goldman, S; Baxter, P; Dhall, G; Robinson, G; DeWire-Schottmiller, M; Hwang, EI; Stewart, CF; Onar-Thomas, A; Dunkel, IJ; Fouladi, M
MLA Citation
Van Mater, David, et al. “A phase I trial of the CDK 4/6 inhibitor palbociclib in pediatric patients with progressive brain tumors: A Pediatric Brain Tumor Consortium study (PBTC-042).Pediatr Blood Cancer, vol. 68, no. 4, Apr. 2021, p. e28879. Pubmed, doi:10.1002/pbc.28879.
URI
https://scholars.duke.edu/individual/pub1471176
PMID
33405376
Source
pubmed
Published In
Pediatr Blood Cancer
Volume
68
Published Date
Start Page
e28879
DOI
10.1002/pbc.28879

Molecular and phenotypic diversity of CBL-mutated juvenile myelomonocytic leukemia.

Mutations in the gene CBL were first identified in adults with various myeloid malignancies. Some patients with juvenile myelomonocytic leukemia (JMML) were also noted to harbor mutations in CBL, but were found to have generally less aggressive disease courses compared to other forms of Ras pathway-mutant JMML. Importantly, and in contrast to most reports in adults, the majority of CBL mutations in JMML patients are germline with acquired uniparental disomy occurring in affected marrow cells. Here, we systematically studied a large cohort of 33 JMML patients with CBL mutations and found this disease to be highly diverse in presentation and overall outcome. Moreover, we discovered somatically-acquired CBL mutations in 15% of pediatric patients who presented with more aggressive disease. Neither clinical features nor methylation profiling were able to distinguish somatic CBL patients from germline CBL patients, highlighting the need for germline testing. Overall, we demonstrate that disease courses are quite heterogeneous even among germline CBL patients. Prospective clinical trials are warranted to find ideal treatment strategies for this diverse cohort of patients.
Authors
Hecht, A; Meyer, JA; Behnert, A; Wong, E; Chehab, F; Olshen, A; Hechmer, A; Aftandilian, C; Bhat, R; Choi, SW; Chonat, S; Farrar, JE; Fluchel, M; Frangoul, H; Han, JH; Kolb, EA; Kuo, DJ; MacMillan, ML; Maese, L; Maloney, KW; Narendran, A; Oshrine, B; Schultz, KR; Sulis, ML; Van Mater, D; Tasian, SK; Hofmann, W-K; Loh, ML; Stieglitz, E
MLA Citation
Hecht, Anna, et al. “Molecular and phenotypic diversity of CBL-mutated juvenile myelomonocytic leukemia.Haematologica, vol. Online ahead of print, Dec. 2020. Pubmed, doi:10.3324/haematol.2020.270595.
URI
https://scholars.duke.edu/individual/pub1472590
PMID
33375775
Source
pubmed
Published In
Haematologica
Volume
Online ahead of print
Published Date
DOI
10.3324/haematol.2020.270595

Receptor tyrosine kinase inhibitors for the treatment of osteosarcoma and Ewing sarcoma.

Adjuvant chemotherapy for osteosarcoma and Ewing sarcoma consists of conventional cytotoxic regimens that have changed little over the past decades. There is an urgent need for agents that are more effective and have less long-term toxicity. Receptor tyrosine kinases regulate cell growth and proliferation of these tumors, and small-molecule inhibitors for many of these kinases are now available. In this article, we review published phase II trials for patients with recurrent disease and highlight the pathways targeted by available agents, as well as the toxicity and efficacy results seen to date. We also discuss the difficulties in identifying biomarkers to facilitate rational patient selection, as well as published and proposed strategies for how these inhibitors can be combined with conventional chemotherapy or other targeted agents. It is hoped future trials can capitalize on this growing experience to optimize the use of this exciting class of agents.
Authors
MLA Citation
Just, Marissa A., et al. “Receptor tyrosine kinase inhibitors for the treatment of osteosarcoma and Ewing sarcoma.Pediatr Blood Cancer, vol. 68, no. 8, Aug. 2021, p. e29084. Pubmed, doi:10.1002/pbc.29084.
URI
https://scholars.duke.edu/individual/pub1482407
PMID
33894051
Source
pubmed
Published In
Pediatr Blood Cancer
Volume
68
Published Date
Start Page
e29084
DOI
10.1002/pbc.29084

Sweet Syndrome in Pediatric Acute Myeloid Leukemia.

Authors
Keskinyan, VS; Noyd, DH; Underwood, CM; Van Mater, D
MLA Citation
Keskinyan, Vahakn S., et al. “Sweet Syndrome in Pediatric Acute Myeloid Leukemia.J Pediatr Hematol Oncol, vol. 43, no. 1, Jan. 2021, pp. 31–32. Pubmed, doi:10.1097/MPH.0000000000001900.
URI
https://scholars.duke.edu/individual/pub1462119
PMID
32925399
Source
pubmed
Published In
Journal of Pediatric Hematology/Oncology
Volume
43
Published Date
Start Page
31
End Page
32
DOI
10.1097/MPH.0000000000001900

Genitourinary manifestations of hereditary cancer predisposition syndromes in children

Several hereditary cancer predisposition syndromes are associated with genitourinary (GU) manifestations in children. The GU manifestation may be the first symptom of a more global syndrome to arise, which places the pediatric urologist in a unique position to impact the health of the child. Some GU manifestations are pathognomonic for a particular hereditary cancer predisposition syndrome, which can prompt genetic testing and enhanced surveillance for other features of the condition. In other cases, knowledge of an underlying hereditary cancer predisposition syndrome alters treatment decisions. This review focuses on hereditary cancer predisposition syndromes that impact the GU tract and are likely to be seen by a pediatric urologist.
Authors
Gillespie, NJ; van Mater, D
MLA Citation
Gillespie, N. J., and D. van Mater. “Genitourinary manifestations of hereditary cancer predisposition syndromes in children.” Translational Andrology and Urology, vol. 9, no. 5, Oct. 2020, pp. 2331–47. Scopus, doi:10.21037/tau-2019-pum-09.
URI
https://scholars.duke.edu/individual/pub1465208
Source
scopus
Published In
Translational Andrology and Urology
Volume
9
Published Date
Start Page
2331
End Page
2347
DOI
10.21037/tau-2019-pum-09

Research Areas:

Neurofibromatosis
Neurofibromatosis 1
Neurofibromatosis 2
Neurofibromatosis in children
Oncology
Sarcoma
Tumors in children