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William Brian Dalton, M.D., Ph.D.

Photo of Dr. William Brian Dalton, M.D., Ph.D.
  • Assistant Professor of Oncology


Internal Medicine, Oncology


The Bunting Blaustein Cancer Research Building

1650 Orleans St.
Suite 288
Baltimore, MD 21231 map


As a physician-scientist in the Division of Hematologic Malignancies at the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, I have a clinical specialty in myeloid leukemias and a research laboratory that focuses on the study of DNA mutations that drive those leukemias. In particular, we are working to better understand DNA mutations in something called the spliceosome, which occur in many patients with MDS and AML and are currently difficult to treat. We use bone marrow and blood samples generously donated by patients, together with cell ‘models’ that we genetically engineer in the lab, to understand what these DNA mutations do and how we might target them with new treatments. Our work has led to identification of vulnerabilities in cells containing these mutations that we aim to translate into novel therapeutic approaches in MDS and AML. more


  • Assistant Professor of Oncology

Departments / Divisions



  • MD, Emory University School of Medicine (2010)


  • Johns Hopkins University School of Medicine / Internal Medicine (2013)


  • Johns Hopkins University School of Medicine / Medical Oncology (2016)

Board Certifications

  • American Board of Internal Medicine / Internal Medicine (2013)
  • American Board of Internal Medicine / Medical Oncology (2016)

Research & Publications

Clinical Trial Keywords

Myelodysplastic Syndromes, Acute Myeloid Leukemia, Myeloproliferative Neoplasms, Acute Lymphoblastic Leukemia

Selected Publications

View all on Pubmed

Dalton WB, Helmenstine E, Pieterse L, Li B, Gocke CD, Donaldson J, Xiao Z, Gondek LP, Ghiaur G, Gojo I, Smith BD, Levis MJ, DeZern AE. The K666N mutation in SF3B1 is associated with increased progression of MDS and distinct RNA splicing. Blood Adv. 2020 Apr 14;4(7):1192-1196. PMID: 32211880 PMCID: PMC7160262 DOI: 10.1182/bloodadvances.2019001127

Dalton WB, Helmenstine E, Walsh N, Gondek LP, Kelkar DS, Read A, Natrajan R, Christenson ES, Roman B, Das S, Zhao L, Leone RD, Shinn D, Groginski T, Madugundu AK, Patil A, Zabransky DJ, Medford A, Lee J, Cole AJ, Rosen M, Thakar M, Ambinder A, Donaldson J, DeZern AE, Cravero K, Chu D, Madero-Marroquin R, Pandey A, Hurley PJ, Lauring J, Park BH. Hotspot SF3B1 mutations induce metabolic reprogramming and vulnerability to serine deprivation. J Clin Invest. 2019 Aug 8;130:4708-4723. doi: 10.1172/JCI125022.

Dalton WB, Forde PM, Kang H, Connolly RM, Stearns V, Gocke CD, Eshleman JR, Axilbund J, Petry D, Geoghegan C, Wolff AC, Loeb DM, Pratilas CA, Meyer CF, Christenson ES, Slater SA, Ensminger J, Parsons HA, Park BH, Lauring J. Personalized Medicine in the Oncology Clinic: Implementation and Outcomes of the Johns Hopkins Molecular Tumor Board. JCO Precis Oncol. 2017;2017. doi: 10.1200/PO.16.00046. Epub 2017 May 31.

Dalton WB, Yu B, Yang VW. p53 suppresses structural chromosome instability after mitotic arrest in human cells. Oncogene. 2010 Apr 1;29(13):1929-40. doi: 10.1038/onc.2009.477. Epub 2010 Jan 11.

Dalton WB, Nandan MO, Moore RT, Yang VW. Human cancer cells commonly acquire DNA damage during mitotic arrest. Cancer Res. 2007 Dec 15;67(24):11487-92.

Activities & Honors


  • American Society of Hematology, 2017
  • American Society of Clinical Oncology, 2013

Patient Ratings & Comments

The Patient Rating score is an average of all responses to physician related questions on the national CG-CAHPS Medical Practice patient experience survey through Press Ganey. Responses are measured on a scale of 1 to 5, with 5 being the best score. Comments are also gathered from our CG-CAHPS Medical Practice Survey through Press Ganey and displayed in their entirety. Patients are de-identified for confidentiality and patient privacy.

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