Zachary Reitman

Overview:

Dr. Reitman’s clinical interests include radiotherapy for primary and metastatic tumors of the brain and spine.  He is also interested in basic and translational research studies to develop new treatment approaches for pediatric and adult brain tumors.  He uses genomic analysis, radiation biology studies, and genetically engineered animal models of cancer to carry out this research

Positions:

Assistant Professor of Radiation Oncology

Radiation Oncology
School of Medicine

Assistant Professor of Pathology

Pathology
School of Medicine

Assistant Professor in Neurosurgery

Neurosurgery
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 2012

Duke University School of Medicine

M.D. 2014

Duke University School of Medicine

Internship, Internal Medicine

Union Memorial Hospital

Resident, Radiation Oncology

Massachusetts General Hospital

Grants:

Prioritizing PPM1D mutations as a target for new DIPG therapies

Administered By
Radiation Oncology
Awarded By
Michael Mosier Defeat DIPG Foundation
Role
Principal Investigator
Start Date
End Date

Generation of a genetically-modified microorganism for adipic acid production

Administered By
Pathology
Awarded By
North Carolina Biotechnology Center
Role
Principal Investigator
Start Date
End Date

Identifying brainstem glioma subtypes that can be radiosensitized by ATM inhibition

Administered By
Radiation Oncology
Awarded By
Pediatric Brain Tumor Foundation
Role
Principal Investigator
Start Date
End Date

Enhancing the efficacy of radiation therapy for DIPG

Administered By
Radiation Oncology
Awarded By
Michael Mosier Defeat DIPG Foundation
Role
Principal Investigator
Start Date
End Date

Enhancing the efficacy of radiation therapy for brainstem gliomas

Administered By
Radiation Oncology
Awarded By
St. Baldrick's Foundation
Role
PI-Fellow
Start Date
End Date

Publications:

Relationship Between Time of First Publication and Subsequent Publication Success Among Non-PhD Physician-Scientists.

BACKGROUND: Studies have shown that publication of work during medical school and residency is associated with higher numbers of later publications and citations of published research. However, it is unknown whether this association exists for non-PhD physician-scientists and whether the association persists later into their careers. METHODS: We extracted publication records from the curricula vitae (CVs) of 102 corresponding authors of articles published in 2008 in the New England Journal of Medicine and JAMA, and obtained those authors' citation records from Web of Science. We used regression models to examine the association between time of first publication and later publication and citation rates for the entire postgraduate career and a recent 2-year period. RESULTS: After adjusting for time since medical school graduation, sex, location of medical school (United States or not United States), and additional non-PhD degrees, we found that authors who first published before graduating from medical school had a greater mean number of publications after medical school and during the period from 2006 to 2007 (164 and 28, respectively) than those who first published during the 5 years afterward (111 and 19, respectively) and those who first published more than 5 years after graduation (59 and 13, respectively). Similarly, authors who first published before graduating from medical school had a greater mean number of citations of their published work since graduation and of publications from 2006 to 2007 (4634 and 333, respectively) than those who first published during the 5 years afterward (2936 and 183, respectively) and those who first published more than 5 years after graduation (1512 and 143, respectively). CONCLUSIONS: Early publication is associated with higher numbers of publications and more citations of published research among non-PhD physician-scientists. This association persists well into a researcher's career.
Authors
Riggs, KR; Reitman, ZJ; Mielenz, TJ; Goodman, PC
MLA Citation
Riggs, Kevin R., et al. “Relationship Between Time of First Publication and Subsequent Publication Success Among Non-PhD Physician-Scientists.J Grad Med Educ, vol. 4, no. 2, June 2012, pp. 196–201. Pubmed, doi:10.4300/JGME-D-11-00068.1.
URI
https://scholars.duke.edu/individual/pub1507962
PMID
23730441
Source
pubmed
Published In
Journal of Graduate Medical Education
Volume
4
Published Date
Start Page
196
End Page
201
DOI
10.4300/JGME-D-11-00068.1

Epigenetic STING silencing is developmentally conserved in gliomas and can be rescued by methyltransferase inhibition.

Authors
Low, JT; Chandramohan, V; Bowie, ML; Brown, MC; Waitkus, MS; Briley, A; Stevenson, K; Fuller, R; Reitman, ZJ; Muscat, AM; Hariharan, S; Hostettler, J; Danehower, S; Baker, A; Khasraw, M; Wong, NC; Gregory, S; Nair, SK; Heimberger, A; Gromeier, M; Bigner, DD; Ashley, DM
MLA Citation
Low, Justin T., et al. “Epigenetic STING silencing is developmentally conserved in gliomas and can be rescued by methyltransferase inhibition.Cancer Cell, vol. 40, no. 5, May 2022, pp. 439–40. Pubmed, doi:10.1016/j.ccell.2022.04.009.
URI
https://scholars.duke.edu/individual/pub1519621
PMID
35487217
Source
pubmed
Published In
Cancer Cell
Volume
40
Published Date
Start Page
439
End Page
440
DOI
10.1016/j.ccell.2022.04.009

Smaller protein, larger therapeutic potential: PPM1D as a new therapeutic target in brainstem glioma.

Authors
MLA Citation
Reitman, Zachary J. “Smaller protein, larger therapeutic potential: PPM1D as a new therapeutic target in brainstem glioma.Pharmacogenomics, vol. 15, no. 13, Sept. 2014, pp. 1639–41. Pubmed, doi:10.2217/pgs.14.123.
URI
https://scholars.duke.edu/individual/pub1507961
PMID
25410889
Source
pubmed
Published In
Pharmacogenomics
Volume
15
Published Date
Start Page
1639
End Page
1641
DOI
10.2217/pgs.14.123

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation.

The role of PPM1D mutations in de novo gliomagenesis has not been systematically explored. Here we analyze whole genome sequences of 170 pediatric high-grade gliomas and find that truncating mutations in PPM1D that increase the stability of its phosphatase are clonal driver events in 11% of Diffuse Midline Gliomas (DMGs) and are enriched in primary pontine tumors. Through the development of DMG mouse models, we show that PPM1D mutations potentiate gliomagenesis and that PPM1D phosphatase activity is required for in vivo oncogenesis. Finally, we apply integrative phosphoproteomic and functional genomics assays and find that oncogenic effects of PPM1D truncation converge on regulators of cell cycle, DNA damage response, and p53 pathways, revealing therapeutic vulnerabilities including MDM2 inhibition.
Authors
Khadka, P; Reitman, ZJ; Lu, S; Buchan, G; Gionet, G; Dubois, F; Carvalho, DM; Shih, J; Zhang, S; Greenwald, NF; Zack, T; Shapira, O; Pelton, K; Hartley, R; Bear, H; Georgis, Y; Jarmale, S; Melanson, R; Bonanno, K; Schoolcraft, K; Miller, PG; Condurat, AL; Gonzalez, EM; Qian, K; Morin, E; Langhnoja, J; Lupien, LE; Rendo, V; Digiacomo, J; Wang, D; Zhou, K; Kumbhani, R; Guerra Garcia, ME; Sinai, CE; Becker, S; Schneider, R; Vogelzang, J; Krug, K; Goodale, A; Abid, T; Kalani, Z; Piccioni, F; Beroukhim, R; Persky, NS; Root, DE; Carcaboso, AM; Ebert, BL; Fuller, C; Babur, O; Kieran, MW; Jones, C; Keshishian, H; Ligon, KL; Carr, SA; Phoenix, TN; Bandopadhayay, P
MLA Citation
Khadka, Prasidda, et al. “PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation.Nat Commun, vol. 13, no. 1, Feb. 2022, p. 604. Pubmed, doi:10.1038/s41467-022-28198-8.
URI
https://scholars.duke.edu/individual/pub1509601
PMID
35105861
Source
pubmed
Published In
Nature Communications
Volume
13
Published Date
Start Page
604
DOI
10.1038/s41467-022-28198-8

Combining Laser Interstitial Thermal Therapy With SRS Improves Time to Progression for Recurrent SRS-Treated Brain Metastases.

<h4>Purpose/objective(s)</h4>Improved survival for patients with brain metastases (BM) has been accompanied by a rise in tumor recurrence after stereotactic radiosurgery (SRS). Laser interstitial thermal therapy (LITT) has evolved as an effective treatment for SRS failures and an alternative to open resection or repeat SRS. We aimed to evaluate the efficacy of LITT followed by SRS (LITT+SRS) in recurrent SRS-treated BM, and to compare outcomes to LITT alone vs. repeat SRS alone.<h4>Materials/methods</h4>A multicenter, retrospective study was performed of patients who underwent treatment for biopsy-proven BM recurrence after SRS. Patients were stratified by planned LITT+SRS vs. LITT alone vs. repeat SRS alone. Index lesion progression was determined by RANO criteria.<h4>Results</h4>Forty-five patients met inclusion criteria, with a median follow-up of 7.3 months (range:1.1-30.5), age of 60 (range:37-86), KPS of 80 (range:60-100), and pre-procedure contrasted tumor volume (preCTV) of 6.1cc (range:1.4-19.4). Primary diagnoses included NSCLC (44%), breast cancer (24%), SCLC, melanoma, colon cancer, and oroesophageal cancer (< 10% each). 27% of patients underwent LITT+SRS, 56% LITT alone, and 18% SRS alone. Median time to index lesion progression (> 23, 7.5, and 3.6 months, respectively [P = 0.018]) and overall survival (23.7, 5.9, and 7.0 months, respectively [P = 0.023]) were significantly improved with LITT+SRS compared to LITT or repeat SRS alone. On univariate analysis, age, sex, primary histology, preCTV, and treatment strategy predicted tumor progression. Blue thermal dose threshold (TDT) line ablation coverage predicted progression with LITT alone, but not with LITT+SRS. In a univariate model, patients not treated with LITT+SRS were more likely to have index lesion progression (P = 0.016). When controlling for tumor histology and preCTV in a multivariate analysis, patients not treated with LITT+SRS remained significantly more likely to have index lesion progression (P = 0.001). All patients undergoing LITT+SRS who experienced subsequent radiographic progression were diagnosed with recurrent tumor, whereas patients treated with SRS alone had a 25% incidence of radiation necrosis.<h4>Conclusion</h4>These data suggest that LITT+SRS is superior to LITT or repeat SRS alone for treatment of biopsy-proven BM recurrence after SRS failure, even after controlling for variables known to predict progression. Prospective trials are warranted to validate the efficacy of using combination LITT+SRS for treatment of recurrent BM previously treated with SRS.<h4>Author disclosure</h4>E.J. Vaios: None. M. Grabowski: None. E. Srinivasan: None. D. Huie: None. E. Sankey: None. B. Otvos: None. M. Olufawo: None. A. Scott: None. A.H. Kim: None. E.C. Leuthardt: None. G.H. Barnett: Consultant; Monteris Medical, Inc. A.M. Mohammadi: None. Z. Reitman: None. S.R. Floyd: Instructor in a company-sponsored training course designed for new users of the CyberKnife system; Accuray Incorporated. J.P. Kirkpatrick: None. P. Fecci: None.
Authors
Vaios, EJ; Grabowski, M; Srinivasan, E; Huie, D; Sankey, E; Otvos, B; Olufawo, M; Scott, A; Kim, AH; Leuthardt, EC; Barnett, GH; Mohammadi, AM; Reitman, Z; Floyd, SR; Kirkpatrick, JP; Fecci, P
MLA Citation
Vaios, E. J., et al. “Combining Laser Interstitial Thermal Therapy With SRS Improves Time to Progression for Recurrent SRS-Treated Brain Metastases.International Journal of Radiation Oncology, Biology, Physics, vol. 111, no. 3S, 2021, pp. e583–84. Epmc, doi:10.1016/j.ijrobp.2021.07.1565.
URI
https://scholars.duke.edu/individual/pub1502889
PMID
34701802
Source
epmc
Published In
International Journal of Radiation Oncology, Biology, Physics
Volume
111
Published Date
Start Page
e583
End Page
e584
DOI
10.1016/j.ijrobp.2021.07.1565

Research Areas:

Cancer
Ganglioglioma
Genomics
Glioma
Molecular Biology
Molecular radiobiology
Muser Mentor
Radiotherapy
Single Cell Biology