Tulane Cancer Center Members: E
Faculty Membership Application and Membership Definitions

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Edmunds, Ehrlich, El-Dahr, Engel

J. Ollie Edmunds, Jr., M.D.
Professor of Orthopaedics
Director of Hand and Upper Extremity Service
Chief of Orthopaedic Surgery at Charity Hospital
TCC Associate Member
ollie@deltapac.com
(504) 988-5479, (504) 988-3517 fax
1430 Tulane Ave., Box SL-32, New Orleans, LA 70112-2699
Homepage on the Orthopaedics website:
http://www.som.tulane.edu/departments/orthopaedics/edmunds.htm

Selected Publications:

• Cook SD, Barrack RL, Salkeld SL, Prewett AB, Edmunds JO Jr. Bone ingrowth into a porous-coated total shoulder component retrieved postmortem. J Arthroplasty Apr 8(2):189-94 (1993 )

Melanie Ehrlich, Ph.D.
Professor of Biochemistry and Genetics
TCC Program Member
Founder of the DNA Methylation Society
ehrlich@tulane.edu
Homepages:
http://www.tulane.edu/~biochem/faculty/ehrlich.htm
http://www.som.tulane.edu/departments/human_genetics/ehrlich
(504) 988-2449, (504) 988-2739 fax
1430 Tulane Ave., Box SL-31, New Orleans, LA 70112-2699

Biographical Narrative:
Dr. Ehrlich is a graduate of Columbia University and the State University of New York at Stony Brook. She did her postdoctoral research at the Albert Einstein School of Medicine. She has been a faculty member at Tulane University Health Sciences Center since 1971 and is a member of the Molecular Genetics Program of the Louisiana Cancer Research Consortium. Dr. Ehrlich is founder, for nine years was president, and is currently a vice-president of the DNA Methylation Society, an international scientific society open to all those interested in aspects of biological methylation. Dr. Ehrlich is studying the role of mammalian DNA methylation (naturally occurring 5-methylcytosine) and chromatin structure in chromosomal stability, birth defects, cancer, differentiation, and transcription control. This research includes developing basic insights into human DNA methylation to apply to understanding the role of alterations in methylation of the human genome in carcinogenesis and the formation of birth defects. Dr. Ehrlich is also studying the mechanisms of chromosome rearrangement in cancer and in genetic syndromes and relationships between chromatin structure, gene expression, and chromosome rearrangements. Her ongoing research involves analysis of colony formation and DNA methylation in bone marrow samples from patients with chronic myeloid leukemia and work on various human cell lines. The cell lines are from patients with the ICF syndrome (immunodeficiency, centromeric region instability, and facial anomalies), a rare DNA methylation deficiency disease; cell lines and muscle biopsy samples from patients with FSHD (fascioscapular humeral muscular dystrophy), the third most frequent cause of muscular dystrophy, which is autosomal dominant and involves a very unusual type of deletion of a repeated DNA sequence; ovarian epithelial tumors; Wilms tumors; and studies of chorionic villus and amniocyte cultures

Selected Publications:

• Ehrlich M, Tsien F, Herrera D, Blackman V, Roggenbuck J, Tuck-Muller C. High frequencies of ICF syndrome-like pericentromeric heterochromatin decondensation and breakage in chromosome 1 seen in a chorionic villus sample, J Med Gen 38: 882-884 (2001).
• Tsien F, Sun B., Hopkins N., Vedanarayanan V, Figlewicz F, Winokur S, Ehrlich M. Methylation of the FSHD syndrome-linked subtelomeric repeat in normal and FSHD cells cultures and tissues. Molec Gen Metab 74: 1-10 (2001).
• Sun B, Jiang G, Zaydin M, LaRussa V, Safah H, Ehrlich M. ABL1 promoter methylation can exist independently of BCR-ABL transcription in chronic myeloid leukemia hematopoietic progenitors. Cancer Res 61: 6931-6937 (2001).
• Ehrlich M, Buchanan K, Tsien F, Jiang G, Sun B, Uicker W, Weemaes C, Smeets D, Sperling K, Belohradsky B, Tommerup N, Misek D, Kuick R, Hanash S. DNA methyltransferase 3B mutations linked to the ICF Syndrome cause dysregulation of lymphocyte migration, activation, and survival genes. Hum Molec Gen 10: 2917-2931 (2001).
• Ehrlich M. DNA hypomethylation, cancer, the ICF syndrome, and chromosomal rearrangements, J Nutrition 132: 24424S- 2429S (2002). 95. Ehrlich, M. DNA methylation in cancer: too much, but also too little. Oncogene 21: 5400-5413 (2002).
• Ehrlich M, Jiang G, Fiala E, Dome J, Yu M, Long T, Youn B., Sohn O, Widschwendter M, Tomlinson G, Chintagumpala M, Champagne M, Parham D, Liang G, Malik K, Laird P. Hypomethylation and hypermethylation of DNA in Wilms tumors, Oncogene 21: 6694-6702 (2002).
• Ehrlich M, Hopkins N, Jiang G, Dome J, Yu M, Woods C, Tomlinson G, Chintagumpala M, Champagne M, Diller L, Parham D, Sawyer J. Satellite DNA hypomethylation in karyotyped Wilms tumors. Cancer Genet Cytogen, in press (2003).
• Tsien F, Youn B, Fiala E, Laird P, Long T, Weissbecker K, Ehrlich M. Prolonged culture of chorionic villus cells yields ICF syndrome-like chromatin decondensation and rearrangements. Cytogen Genome Res, in press (2003).
• Ehrlich M. Expression of various genes is controlled by DNA methylation during mammalian development, J Cell Biochem, in press (2003).
• Jiang G, Fan Y, Li M, Weissbecker K, Price S, Kim KC, LaRussa V, Safah H, Ehrlich M. In vitro treatment with imatinib (STI571) of hematopoietic precursors shows only limited selectivity for CML cells and may be compromised by silent BCR-ABL genes. Cancer Biol Ther, in press (2003).

Samir S. El-Dahr, M.D.
Professor of Pediatric Nephrology
Vice Chairman for Research
TCC Program Member
seldahr@tulane.edu
(504) 988-5377, (504) 988-1771 fax
1430 Tulane Ave., Box SL-37, New Orleans, LA 70112-2699

Biographical Narrative:
Dr. El-Dahr's research efforts are centered on the molecular mechanisms of renal cell differentiation. In particular, he is interested in defining the transcription factors involved in terminal renal epithelial cell differentiation. Recently, he identified the p53 transcription factor as an important regulator upstream of several renal function genes. Mutations in the p53-binding site of the human bradykinin B2 receptor promoter are associated with hypertension and end-stage-renal disease. Thus, p53 may link renal cell differentiation and functional maturation. These findings also suggest a possible novel link between cancer susceptibility and the development of renal disease and hypertension. Another aspect of his work is to define the cellular and molecular pathways leading to renal dysplasia in a mouse model of renal dysgenesis in mice lacking a GPCR, the bradykinin B2 receptor. Of particular interest is the aberrant activity of EGF-R function in this model of renal dysgenesis, thus mimicking human cystic renal dysplasia. Dr. El-Dahr has generated a mouse model of an important human renal disease that accounts for about 30% of all childhood chronic renal failure.

Selected Publications:

• El-Dahr SS, Dipp S, Meleg-Smith S, Pinna-Parpaglia P Madeddu P. Fetal ontogeny and role of metanephric bradykinin B2 receptors. Pediatr Nephrol 14:288-296 (2000)
• Saifudeen Z, Du H, Dipp S, El-Dahr SS. The bradykinin type 2 receptor is a target for p53-mediated transcriptional activation. J Biol Chem 275: 15557-155562 (2000)
• El-Dahr SS, Harrison-Bernard LM, Dipp S, Yosypiv IV, Meleg-Smith S. Bradykinin B2 null mice are prone to renal dysplasia: gene-environment interactions in kidney development. Physiol Genomics 3: 121-131 (2000)
• Prieto M, Dipp S, Meleg-Smith S, El-Dahr SS. Ureteric bud derivatives express angiotensinogen and AT1 receptors. Physiol Genomics 6: 29-37 (2001)
• Yosipiv IV, Dipp S, El-Dahr SS. Targeted disruption of the bradykinin B2 receptor gene in mice alters the ontogeny of the renin-angiotensin system. Am J Physiol (Renal Physiol) 281: F795-F801 (2001)
• Saifudeen Z., Marks J, Du H, El-Dahr SS. Spatial repression of PCNA by p53 during kidney development. Am J Physiol (Renal Physiol) 283: F727-F733 (2002)
• Saifudeen Z, Dipp, S. El-Dahr SS. A role for p53 in terminal epithelial cell differentiation. J Clin Invest 109: 1021-1030 (2002)
• Marks J, Saifudeen Z, Dipp S, El-Dahr SS. Two functionally divergent p53-responsive elements in the rat bradykinin B2 receptor promoter. J Biol Chem 278: 34158-34166 (2003)

Astrid M. Engel, Ph.D.
Research Assistant Professor of Epidemiology
TCC Program Member
aengel@tulane.edu
(504) 988-6316, (504) 988-5516 fax
1430 Tulane Ave., Box SL-66, New Orleans, LA 70112-2699
Faculty listing on the Epidemiology website:
http://www.epidemiology.tulane.edu/epi_pages/faculty/engel.html

Biographical Narrative:
Dr. Engel was born in San Jose, Costa Rica, where she obtained her microbiology degree (Licenciatura) at the University of Costa Rica. She obtained her doctoral degree from the Department of Microbiology, Immunology and Parasitology at the Louisiana State University Health Sciences Center in New Orleans. She did her postdoctoral research at Tulane University with Dr. Prescott Deininger. She has been a faculty member at Tulane University Health Sciences Center in the Department of Epidemiology since 2004 and is a member of the Molecular Genetics Program of the Louisiana Cancer Research Consortium. Dr. Engel is studying the role of environmental exposure on human retroelement activation and their contribution to cancer. This research includes the understanding of the basic mechanism of retroelement amplification and their regulation.

Selected Publications:

• Kale SP, Carmichael MC, Harris K, Roy-Engel AM. The L1 retrotranspositional stimulation by particulate and soluble cadmium exposure is independent of the generation of DNA breaks. Int J Env Res Public Health, 3:121-128, 2006.
• El-Sawy M, Kale S, Dugan C, Nguyen TQ, Belancio V, Bruch H, Roy-Engel AM, Deininger PL. Nickel stimulates L1 retrotransposition through a post-transcriptional mechanism. J. Mol Biol, 354:201, 2005.
• Kale SP, Moore L, Deininger PL, Roy-Engel AM. Heavy metals stimulate human LINE-1 retrotransposition. Int J Env Res Public Health, 2:84-90, 2005.
• Roy-Engel AM, El-Sawy M, Farooq L, Odom GL, Perepelitsa-Belancio V, Bruch H, Oyeniran OO, Deininger PL. Human retroelements may introduce intragenic polyadenylation signals. Cytogenetic and Genome Res, 110: 365-371, 2005.
• Johanning K, Aleman Stevenson C, Oyeniran OO, Gozal YM, Roy-Engel AM, Jurka J, Deininger PL. Potential for retroposition by old Alu subfamilies. J Mol Evol, 56: 658-664, 2003.
• Roy-Engel AM, Salem AHM, Oyeniran OO, Deininger L, Hedges DJ, Kilroy GE, Batzer MA, Deininger PL. Active Alu element "A-tails": size does matter. Genome Res, 12: 1333-1344, 2002.

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