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Male
Expertise: Pathology
Research Interests: Molecular diagnosis of cancer; Genetic instability; Pancreatic cancer genetics and chemosensitivity
600 N. Wolfe Street
David H. Koch Cancer Research Building, Suite 344
Baltimore, MD 21287
map
Phone: 410-955-9790
Fax: 410-614-0671
Dr. James Eshleman is a professor of pathology and oncology at the Johns Hopkins University School of Medicine and a member of its Kimmel Cancer Center. His areas of clinical expertise includes molecular diagnosis. Dr. Eshleman serves as the associate director of the Molecular Diagnostics Laboratory at the Johns Hopkins School of Medicine.
Dr. Eshleman earned his M.D. and Ph.D. from the University of Pennsylvania School of Medicine. He completed a residency in clinical pathology and a fellowship in blood banking and transfusion medicine at the Hospital of the University of Pennsylvania.
His research interests include studying the genetics of hereditary and sporadic pancreatic cancers; using genetics to develop personalized chemotherapy regimens and other treatments for pancreatic cancer patients; finding new ways to enable rapid drug screening for pancreatic cancer; and developing new molecular pathology tools.
Pancreatic cancers: genetics of sporadic and familial pancreatic cancer. In collaboration with the Vogelstein/Kinzler lab, in 2008 we reported exome sequencing for 24 pancreatic cancers, where we confirmed identified genes in another 92 cancers. In Jones 2009, we identified that the partner and localizer of BRCA2 (PALB2) was a familial pancreatic cancer predisposition gene. Using gene mutations in primary cancers and their metastases, we clocked the progression of pancreatic cancer to demonstrate that metastasis is a late event, occurring after 17 years of growth in the primary site. Finally, in Norris et al, we reported a new method of mutagenesis in pancreatic cancer.
Chemotherapy of pancreatic cancer. In Cui et al, we correlated the genetics of pancreatic cancer with responses to various classes of chemotherapy. In Kamiyama, we developed mice that are both immunodeficient and biochemically selectable. After growth of human cancers in these mice, pure cancer cells can be routinely obtained for drug screening.
Novel molecular pathology tools. We wrote software to simulate pyrosequencing (Chen et al), and developed a method (haplotype counting) to overcome the error rate of next-generation sequencing (Debeljak et al).
The Pathology Molecular Diagnostics Laboratory offers state-of-the-art clinical molecular testing for leukemia, lymphoma, solid tumors, cancer predisposition and a number of hematologic mutations associated with disease. Their tests are based on the latest research-based knowledge and provide initial diagnostic information, detection of residual disease following therapy, and assessment of disease risk for inherited conditions.
The Pathology Cytogenetics Laboratory offers the most advanced clinical cytogenetics testing available for leukemia, lymphoma and solid tumors. The tests provide initial diagnostic information and minimal risidual disease detection following therapy or transplant. Expert results, interpretation and consultation services from these laboratories aid referring physicians, including oncologists, hematologists, pathologists, obstetricians and geneticists, in the appropriate diagnosis and management of their patients.
Core Facility: Molecular Pathology & Cytogenetics
Shi C, Fukushima N, Abe T, Bian Y, Hua L, Wendelburg BJ, Yeo CJ, Hruban RH, Goggins MG, and Eshleman JR. "Sensitive and quantitative detection of KRAS2 gene mutations in pancreatic duct juice differentiates patients with pancreatic cancer from chronic pancreatitis, potential for early detection." Cancer Biol Ther, 3/2008; 7:260-7.
Shi C, Eshleman SH, Jones D, Fukushima N, Hua L, Parker AR, Yeo CJ, Hruban RH, Goggins MG, and Eshleman JR. LigAmp for Sensitive Detection of Single Nucleotide Differences. Nature Methods, 1: 141-147, November, 2004.
Shi C, Parker AR, Hua L, Morrell CN, Lee SC, Bandaru W, Wu TC and Eshleman JR. Anti-gene padlocks kill bacterial cells based on their genotype. Submitted.
Jones S, Zhang X, Parsons DW, Lin JC, Leary RJ, Angenendt P, Mankoo P, Carter H, Kamiyama H, Jimeno A, Hong SM, Fu B, Lin MT, Calhoun ES, Kamiyama M, Walter K, Nikolskaya T, Nikolsky Y, Hartigan J, Smith DR, Hidalgo M, Leach SD, Klein AP, Jaffee EM, Goggins M, Maitra A, Iacobuzio-Donahue C, Eshleman JR, Kern SE, Hruban RH, Karchin R, Papadopoulos N, Parmigiani G, Vogelstein B, Velculescu VE, and Kinzler KW. "Core signaling pathways in human pancreatic cancers revealed by global genomic analyses." Science. 9/2008; 321:1801-6.
Shi C, Hong SM, Lim P, Kamiyama H, Khan M, Anders RA, Goggins M, Hruban RH, and Eshleman JR. "KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: Implications for the human pancreatic cancer cell of origin." Mol Cancer Res, 2/2009; 7:230-6 [NIHMS #89589].
Jones S, Hruban RH, Kamiyama M, Borges M, Zhang X, Parsons DW, Cheng-Ho Lin J, Palmisano E, Brune K, Jaffee EM, Iacobuzio-Donahue CA, Maitra A, Parmigini G, Kern SE, Velculescu VE, Kinzler KW, Vogelstein B, Eshleman JR, Goggins M, and Klein AP. "Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene." Science. 4/2009; 324:217.
Shi C, Chandrasekharan A, Thuluvath PJ, Karikari C, Argani P, Goggins M, Maitra A, and Eshleman JR. "Ultrasensitive detection of KRAS2 mutations in bile and serum from patients with biliary tract carcinoma using LigAmp technology." J Molec Diagnostics. 2009 Nov;11(6):583-9.
Pathobiology, Cellular and Molecular Medicine
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