David Van Mater

Overview:

I am a pediatric oncologist with a specific interest in hereditary cancer syndromes and sarcoma. I 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:

Combination therapy with sorafenib and celecoxib for pediatric patients with desmoid tumor.

Authors
Robles, J; Keskinyan, VS; Thompson, M; Davis, JT; Mater, DV
MLA Citation
Robles, Joanna, et al. “Combination therapy with sorafenib and celecoxib for pediatric patients with desmoid tumor.Pediatr Hematol Oncol, vol. 37, no. 5, Aug. 2020, pp. 445–49. Pubmed, doi:10.1080/08880018.2020.1735591.
URI
https://scholars.duke.edu/individual/pub1434261
PMID
32129687
Source
pubmed
Published In
Pediatr Hematol Oncol
Volume
37
Published Date
Start Page
445
End Page
449
DOI
10.1080/08880018.2020.1735591

Somatic Mosaicism of IDH1 R132H Predisposes to Anaplastic Astrocytoma: A Case of Two Siblings.

Anaplastic astrocytomas are aggressive glial cancers that present poor prognosis and high recurrence. Heterozygous IDH1 R132H mutations are common in adolescent and young adult anaplastic astrocytomas. In a majority of cases, the IDH1 R132H mutation is unique to the tumor, although rare cases of anaplastic astrocytoma have been described in patients with mosaic IDH1 mutations (Ollier disease or Maffucci syndrome). Here, we present two siblings with IDH1 R132H mutant high grade astrocytomas diagnosed at 14 and 26 years of age. Analysis of IDHR132H mutations in the siblings' tumors and non-neoplastic tissues, including healthy regions of the brain, cheek cells, and primary teeth indicate mosaicism of IDHR132H. Whole exome sequencing of the tumor tissue did not reveal any other common mutations between the two siblings. This study demonstrates the first example of IDH1 R132H mosaicism, acquired during early development, that provides an alternative mechanism of cancer predisposition.
Authors
Lee, S; Kambhampati, M; Almira-Suarez, MI; Ho, C-Y; Panditharatna, E; Berger, SI; Turner, J; Van Mater, D; Kilburn, L; Packer, RJ; Myseros, JS; Vilain, E; Nazarian, J; Bornhorst, M
MLA Citation
Lee, Sulgi, et al. “Somatic Mosaicism of IDH1 R132H Predisposes to Anaplastic Astrocytoma: A Case of Two Siblings.Front Oncol, vol. 9, 2019, p. 1507. Pubmed, doi:10.3389/fonc.2019.01507.
URI
https://scholars.duke.edu/individual/pub1432118
PMID
32010615
Source
pubmed
Published In
Frontiers in Oncology
Volume
9
Published Date
Start Page
1507
DOI
10.3389/fonc.2019.01507

Injury promotes sarcoma development in a genetically and temporally restricted manner.

Cancer results from the accumulation of genetic mutations in a susceptible cell of origin. We and others have also shown that injury promotes sarcoma development, but how injury cooperates with genetic mutations at the earliest stages of tumor formation is not known. Here, we utilized dual recombinase technology to dissect the complex interplay of the timing of KrasG12D activation, p53 deletion, and muscle injury in sarcomagenesis using a primary mouse model of soft tissue sarcoma. When mutations in oncogenic Kras and p53 are separated by 3 weeks, few sarcomas develop without injury. However, the transformation potential of these tumor-initiating cells can be unmasked by muscle injury. In the absence of Kras mutations, injury of the muscle with global deletion of p53 results in sarcomas with amplification of chromosomal regions encompassing the Met or Yap1 gene. These findings demonstrate a complex interplay between the timing of genetic mutations and perturbations in the tumor microenvironment, which provides insight into the earliest stages of sarcoma development.
Authors
Van Mater, D; Xu, E; Reddy, A; Añó, L; Sachdeva, M; Huang, W; Williams, N; Ma, Y; Love, C; Happ, L; Dave, S; Kirsch, DG
MLA Citation
Van Mater, David, et al. “Injury promotes sarcoma development in a genetically and temporally restricted manner.Jci Insight, vol. 3, no. 20, Oct. 2018. Pubmed, doi:10.1172/jci.insight.123687.
URI
https://scholars.duke.edu/individual/pub1355049
PMID
30333301
Source
pubmed
Published In
Jci Insight
Volume
3
Published Date
DOI
10.1172/jci.insight.123687

Disproportionate relationship between APOBEC-1 expression and apolipoprotein B mRNA editing activity.

Apolipoprotein B (apoB) mRNA editing is a site-specific (nucleotide 6666) cytidine to uridine transition catalyzed by a cytidine deaminase, APOBEC-1, in the context of a multiprotein complex referred to as the C/U editosome. This report quantifies for the first time the effect of altering APOBEC-1 protein abundance on the proportion of edited apoB mRNAs using transfected McArdle rat hepatoma cells which had been sorted by flow cytometry into populations expressing different levels of green fluorescent protein-APOBEC-1 chimera, GFP-APOBEC. A correlation was observed in which increased expression of GFP-APOBEC protein resulted in a higher proportion of edited apoB mRNA. The number of enzyme molecules required to increase the proportion of edited apoB RNAs was disproportionately high relative to that which might have been predicted from a typical catalytic relationship. Moreover, editing of apoB mRNA at inappropriate sites (promiscuous editing) occurred in response to overexpressing GFP-APOBEC. The data suggest that experimental manipulation of APOBEC-1 abundance in the absence of other regulatory considerations will always result in some level of promiscuous editing. Coordinate expression of APOBEC-1 and the auxiliary proteins and/or regulation of their interactions may be required to increase editing activity without losing editing-site fidelity.
Authors
Siddiqui, JF; Van Mater, D; Sowden, MP; Smith, HC
MLA Citation
Siddiqui, J. F., et al. “Disproportionate relationship between APOBEC-1 expression and apolipoprotein B mRNA editing activity.Exp Cell Res, vol. 252, no. 1, Oct. 1999, pp. 154–64. Pubmed, doi:10.1006/excr.1999.4598.
URI
https://scholars.duke.edu/individual/pub1114006
PMID
10502408
Source
pubmed
Published In
Experimental Cell Research
Volume
252
Published Date
Start Page
154
End Page
164
DOI
10.1006/excr.1999.4598

Calvarial mass as a presenting feature of neurofibromatosis type 2 in a pediatric patient.

Authors
Narine, KY; Oh, CC; Fuchs, HE; Van Mater, D
MLA Citation
Narine, Kalindi Y., et al. “Calvarial mass as a presenting feature of neurofibromatosis type 2 in a pediatric patient.Am J Med Genet A, vol. 176, no. 1, Jan. 2018, pp. 246–47. Pubmed, doi:10.1002/ajmg.a.38505.
URI
https://scholars.duke.edu/individual/pub1286028
PMID
29130639
Source
pubmed
Published In
Am J Med Genet A
Volume
176
Published Date
Start Page
246
End Page
247
DOI
10.1002/ajmg.a.38505

Research Areas:

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