David J. Araten, MD

  • Specialties: Hematology, Leukemia & Lymphoma, Oncology
  • Language: English
  • Phone: 212-731-5186

Credentials

Positions
  • Assistant Professor, Department of Medicine
Board Certifications
  • American Board of Internal Medicine (Medical Oncology), 1998
  • American Board of Internal Medicine (Hematology), 1998
Education and Training
  • Fellowship, Memorial Sloan-Kettering Cancer Center, Hematology Oncology, 1999
  • Residency, Columbia-Presbyterian Medical Center, Internal Medicine, 1994
  • MD from Harvard Medical School, 1991
Departments

Locations and Appointments

64 Insurance Plans Accepted
  • Aetna HMO
  • Aetna Indemnity
  • Aetna Medicare
  • Aetna POS
  • Aetna PPO/EPO
  • Affinity
  • Affinity Exchange- Essential
  • Cigna EPO/POS
  • Cigna PPO
  • ElderPlan
  • Empire Blue Cross Blue Shield EPO
  • Empire Blue Cross Blue Shield HMO
  • Empire Blue Cross Blue Shield Indemnity
  • Empire Blue Cross Blue Shield MediBlue
  • Empire Blue Cross Blue Shield POS
  • Empire Blue Cross Blue Shield PPO
  • Empire Blue Cross Blue Shield Pathways, Enhanced
  • Fidelis Child Health
  • Fidelis Exchange
  • Fidelis Family Health
  • Fidelis Medicaid
  • Fidelis Medicare
  • GHI CBP
  • HIP Access I
  • HIP Access II
  • HIP Child Health
  • HIP EPO/PPO
  • HIP Family Health
  • HIP HMO
  • HIP Medicaid
  • HIP Medicare
  • HIP POS
  • HealthPlus Child Health (Amerigroup)
  • HealthPlus Family Health (Amerigroup)
  • HealthPlus Medicaid (Amerigroup)
  • HealthRepublic
  • HealthSmart (WTC)
  • Humana Medicare
  • Local 1199 PPO
  • MagnaCare PPO
  • Medicare
  • MetroPlus Child Health
  • MetroPlus Exchange Plans
  • MetroPlus Family Health
  • MetroPlus Medicaid
  • MultiPlan/PHCS PPO
  • NY Medicaid
  • NYS Empire Plan
  • Oscar
  • Oxford Exchange
  • Oxford Freedom
  • Oxford Liberty
  • Oxford Medicare
  • Tricare
  • UPN Elite
  • United Exchange- Compass
  • UnitedHealthcare Community & State Plan
  • UnitedHealthcare EPO
  • UnitedHealthcare HMO
  • UnitedHealthcare Medicare
  • UnitedHealthcare POS
  • UnitedHealthcare PPO
  • UnitedHealthcare Top Tier
  • Visiting Nurse Service (VNS) Medicare
*Insurance listed above may not be accepted at all office locations. Please confirm prior to each visit. The information presented here may not be complete or may have been changed.
NYU Hematology Associates

240 East 38th Street
New York, NY 10016

Contact

Phone: 212-731-5186

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My Research

Acquired inactivating somatic mutations are likely to be critical in the development of malignancies, and yet they are extremely difficult to detect in populations of normal human cells. This is because mutations are rare, and most mutations will either not produce a phenotype, or conversely, will interfere with the survival of the cell. Furthermore, because of the diploid nature of the human genome, the effect of inactivating mutations would tend to be complemented by the wild type allele on the homologous chromosome. One way around this problem is to study genes that are on the X-chromosome, which is present in only one copy in cells from males and which is present in only one functional copy in cells from females, due to Lyonization. Historically, the identification of rare mutants has been possible for the X-linked HPRT gene; inactivating mutations in this gene allow for the cell to grow in the presence of 6-thioguanine. It has been known for some time that normal individuals harbor circulating 6-thioguanine-resistant lymphocytes that arise due to acquired HPRT mutations, and these can be enumerated by limiting dilution cloning. Our laboratory uses two different X-linked genes, PIG-A and XK, as sentinels for spontaneous somatic mutations. These genes have the advantage that the mutant phenotype affects surface proteins, so that the mutants can be picked up by flow cytometry using monoclonal antibodies, which can rapidly screen for rare mutants within a population of over a million cells within minutes. PIG-A is the gene that is mutated in the condition Paroxysmal Nocturnal Hemoglobinuria (PNH) and it is known that a broad spectrum of mutations can confer the PIG-A null phenotype. It is thought that apart from the very special case of PNH, PIG-A mutants have neither a growth advantage or disadvantage. PIG-A encodes an enzyme that is essential in the biosynthesis of the structure glycosylphosphatidylinositol (GPI). A subset of proteins lack transmembrane domains and require the GPI structure for their association with the cell surface. Because of the central role of PIG-A in the synthesis of GPI, when this gene is mutated, the expression of all GPI-linked proteins is affected, and antibodies specific for more than one GPI-linked protein can be used simultaneously to increase the specificity of the assay. Similarly, the FLAER reagent binds to GPI directly and can be used for the same purpose. The expression of transmembrane proteins is not affected by the mutation in PIG-A, and antibodies recognizing a lineage specific marker that does not depend upon GPI is useful to identify intact cells.

Publications

  • Selective splenic artery embolization for the treatment of thrombocytopenia and hypersplenism in paroxysmal nocturnal hemoglobinuria

    Araten, David J; Iori, Anna Paola; Brown, Karen; Torelli, Giovanni Fernando; Barberi, Walter; Natalino, Fiammetta; De Propris, Maria Stefania; Girmenia, Corrado; Salvatori, Filippo Maria; Zelig, Orly; Foa, Robin; Luzzatto, Lucio
    Journal of hematology & oncology. 2014. 7: 27-27

  • No evidence of hypermutability in red cells from patients with paroxysmal nocturnal hemoglobinuria using the XK gene

    Araten, David J; Zamechek, Leah; Halverson, Gregory
    Haematologica (Roma). 2014 May. e142-e144

  • Leukemic blasts with the PNH phenotype: Correlation with cytogenetics in ALL [Meeting Abstract]

    Araten, D J; Loh, M L; Devidas, M; Carroll, A J; Heerema, N A; Hunger, S P; Amro, C; Zamechek, L
    Blood. 2013 21 Oct. 122 (21):

Read All Publications (40)