David J. Araten, MD

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



  • Assistant Professor, Department of Medicine

Board Certifications

  • American Board of Internal Medicine (Medical Oncology)
  • American Board of Internal Medicine (Hematology)

Education and Training

  • 1999
  • Fellowship, Memorial Sloan-Kettering Cancer Center, Hematology Oncology
  • 1994
  • Residency, Columbia-Presbyterian Medical Center, Internal Medicine
  • 1991
  • MD from Harvard Medical School


Locations and Appointments

61 Insurance Plans Accepted
  • Aetna HMO
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  • Fidelis Child Health
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  • Fidelis Medicaid
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  • HIP Access I
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  • HealthPlus Child Health (Amerigroup)
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*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


Phone: 212-731-5186

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My Research

We have found that using flow cytometry to detect the GPI-negative phenotype, it is possible to measure the frequency of spontaneous mutants within populations of hematopoietic cells of different lineages from normal individuals, without the requirement for cell growth. For cells that do grow well, we have also found that it is possible to eliminate pre-existing mutants from a population by sorting, allowing us to expand a purified GPI (+) population in vitro, so that we can calculate the rate of new mutations as they occur prospectively in a dividing population. This value, the mutation rate, is otherwise very difficult to measure in human cells, though it was first calculated by Luria and Delbruck for bacteria in the 1940's. We have been able to calculate the mutation rate in B-lymphoblastoid cell lines (BLCLs) from normal individuals, in BLCLs from patients with various genetic diseases, in expanding T cell cultures from normal individuals, in cord blood-derived CD34 cells growing under the influence of myeloid-inducing cytokines and fusion oncoproteins, as well as in cell lines derived from human hematopoietic malignancies. The XK gene is centromeric to PIG-A on the short arm of the X-chromosome and is also known to us through clinical Hematology, this being the gene that, when mutated, is responsible for the McLeod syndrome. This disorder is characterized by a great reduction in the level of Kell proteins on the surface of the red cell, probably because the XK gene product is normally covalently linked to the Kell protein through a disulfide bond. Like PIG-A, a broad spectrum of mutations are known to inactivate the gene. Obligate female heterozygotes have two populations of red cells, due to inactivation of the X-chromosome carrying either the wild type or the mutant allele. In collaboration with investigators at the New York Blood Center, we have found that normal individuals also harbor small populations of spontaneously arising Kell-low red cells that appear similar to Kell-low red cells are due to inherited mutations of XK. The laboratory is interested in using these techniques for the quantitation of rare mutations in order to predict cancer risk, to screen for compounds that might decrease the mutation rate, to study the pathophysiology of genetic cancer predisposition and premature ageing syndromes, to investigate the relationship between cancer and normal ageing, and to investigate whether an increase in the mutation rate is a requirement for carcinogenesis (as has been proposed by others). Our recent work has shown that there are two subgroups of samples of acute lymphoblastic leukemia--those with a low frequency and those with an elevation in the frequency of mutants, and we are interested in investigating the clinical significance of this phenotype. Addresses of published articles and abstracts (copy and paste into browser window): http://www.ncbi.nlm.nih.gov/pubmed/19909712?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=2 http://www.pnas.org/content/96/9/5209.full?sid=8c8f4f16-3b23-42b1-b362-ed267a8de540 http://cancerres.aacrjournals.org/cgi/content/abstract/65/18/8111 http://bloodjournal.hematologylibrary.org/cgi/content/full/108/2/734 http://ash.confex.com/ash/2008/webprogram/Paper7892.html http://www.abstracts2view.com/hem07/view.php?nu=HEM07L1_2675&terms

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.


  • 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 2014; 27-27, Journal of hematology & oncology — id: 881852, year: 2014, page: 27, stat: Journal Article
  • No evidence of hypermutability in red cells from patients with paroxysmal nocturnal hemoglobinuria using the XK gene

    Araten, David J; Zamechek, Leah; Halverson, Gregory 2014 May; e142-e144, Haematologica (Roma) — id: 977462, year: 2014, page: e142, stat: JOURNAL ARTICLE
  • Leukemic blasts with the PNH phenotype: Correlation with cytogenetics in ALL

    Araten, D J; Loh, M L; Devidas, M; Carroll, A J; Heerema, N A; Hunger, S P; Amro, C; Zamechek, L 2013 21 Oct; -, Blood — id: 713042, year: 2013
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