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Genetics Faculty


Mitchell Drumm
Professor
Ph.D. Training Faculty
Department of Genetics
School of Medicine
Case Western Reserve University
Biomedical Research Building 733
2109 Adelbert Road
Cleveland, Ohio 44106-4955
Tel: (216) 368-6893
Fax: (216) 368-3432
E-mail: mitchell.drumm@case.edu


About Mitchell Drumm

Dr. Drumm is a native of Ohio, originally from New Philadelphia and a graduate of the Ohio State University where he received his B.S. in Genetics in 1983. His graduate work was carried out at the University of Michigan in the Department of Human Genetics where he worked under Francis Collins, M.D., Ph.D. After obtaining his Ph.D. in 1990, Dr. Drumm continued to work with Dr. Collins until moving to Cleveland and joining the Departments of Pediatrics and Genetics at Case Western Reserve University in 1992.


Research

Dr. Drumm's research focuses on the genetics of cystic fibrosis (CF), specifically with the goal of identifying therapeutic targets for the treatment of CF. His interest in CF began with his thesis work to develop a technique, termed "chromosome jumping" to rapidly move from one position in the genome to another on the same chromosome. The project evolved into identifying the location of the gene causing CF, and culminated in the discovery and cloning of the CFTR gene. Since that time, he has worked to understand how CFTR works at the cellular and tissue level, and more currently how the various tissues and organs interact to create the spectrum of traits associated with the disease. At the molecular level, his lab has investigating the promoter of the CFTR gene, as its regulation may be tied to the regulation of other genes, which may in turn contribute to the disease.

His lab has also returned to more classic genetic approaches to take advantage of the substantial variation in the course of disease between CF patients. Currently, Dr. Drumm and collaborators are examining genetic determinants of this variation. The rationale for these studies is that understanding the source of variation should suggest therapeutic targets for the disorder. To accomplish these goals, the Drumm lab is employing human and mouse genetics as complementing approaches. Using CF mice as a model, his laboratory is examining the heritability of traits believed to be involved in the pathophysiology of CF, such as epithelial ion transport and changes in the growth axis. Mouse genetics provide a powerful tool for identifying loci of interest, but clearly mice are a limited model of CF-relevant traits. Therefore, CF patients are also being studied by the Drumm laboratory and collaborators at the University of North Carolina, the Johns Hopkins University and the University of Toronto in which they are investigating the role of common genetic variants across the genome to identify genes involved in the pathophysiology of the disease.


Selected Publications

The Hypothesis-Driven GWAS identifies 'missing heritability' in modifiers of disease phenotypes: Application to Meconium Ileus in Cystic Fibrosis.
Sun, J.M. Rommens, H. Corvol, W. Li, X. Li, T. Chiang, F. Lin, R. Dorfman, P-F Busson, R.V. Parekh, D. Zelenika, S. Blackman, M. Corey, V. Doshi, L. Henderson, K. Naughton, W. K. O'Neal, R. G. Pace, J. R. Stonebraker, S. D. Wood, F. A. Wright, J. Zielenski, A. Clement, M. L. Drumm, P-Y Boëlle, G. R. Cutting, M. R. Knowles, P. R. Durie and L.J. Strug.
(2012);(In Press)

Characterization of Tissue-Specific and Developmentally Regulated Alternative Splicing of Exon 64 in the COL5A1 Gene.
Mitchell AL, Judis LM, Schwarze U, Vaynshtok PM, Drumm ML, Byers PH
Connect Tissue Res (2011);:
See PubMed abstract

Lack of cystic fibrosis transmembrane conductance regulator in CD3+ lymphocytes leads to aberrant cytokine secretion and hyperinflammatory adaptive immune responses.
Mueller C, Braag SA, Keeler A, Hodges C, Drumm M, Flotte TR
Am J Respir Cell Mol Biol (2011);44(6):922-9
See PubMed abstract

Genome-wide association and linkage identify modifier loci of lung disease severity in cystic fibrosis at 11p13 and 20q13.2.
Wright FA, Strug LJ, Doshi VK, Commander CW, Blackman SM, Sun L, Berthiaume Y, Cutler D, Cojocaru A, Collaco JM, Corey M, Dorfman R, Goddard K, Green D, Kent JW, Lange EM, Lee S, Li W, Luo J, Mayhew GM, Naughton KM, Pace RG, Paré P, Rommens JM, Sandford A, Stonebraker JR, Sun W, Taylor C, Vanscoy LL, Zou F, Blangero J, Zielenski J, O'Neal WK, Drumm ML, Durie PR, Knowles MR, Cutting GR
Nat Genet (2011);43(6):539-46
See PubMed abstract

Phospholipase C-β3 is a key modulator of IL-8 expression in cystic fibrosis bronchial epithelial cells.
Bezzerri V, d'Adamo P, Rimessi A, Lanzara C, Crovella S, Nicolis E, Tamanini A, Athanasakis E, Tebon M, Bisoffi G, Drumm ML, Knowles MR, Pinton P, Gasparini P, Berton G, Cabrini G
J Immunol (2011);186(8):4946-58
See PubMed abstract

EDNRA variants associate with smooth muscle mRNA levels, cell proliferation rates, and cystic fibrosis pulmonary disease severity.
Darrah R, McKone E, O'Connor C, Rodgers C, Genatossio A, McNamara S, Gibson R, Stuart Elborn J, Ennis M, Gallagher CG, Kalsheker N, Aitken M, Wiese D, Dunn J, Smith P, Pace R, Londono D, Goddard KA, Knowles MR, Drumm ML
Physiol Genomics (2010);41(1):71-7
See PubMed abstract

A susceptibility gene for type 2 diabetes confers substantial risk for diabetes complicating cystic fibrosis.
Blackman SM, Hsu S, Ritter SE, Naughton KM, Wright FA, Drumm ML, Knowles MR, Cutting GR
Diabetologia (2009);52(9):1858-65
See PubMed abstract

Loss of CFTR results in reduction of histone deacetylase 2 in airway epithelial cells.
Bartling TR, Drumm ML
Am J Physiol Lung Cell Mol Physiol (2009);297(1):L35-43
See PubMed abstract