Joan G. Clark, MD

Joshua O. Benditt, MD

Professor, Section Head
Division of Pulmonary and Critical Care Medicine

Contact Information

Fred Hutchinson Cancer Research Center
1100 Fairview Avenue N. (D3-190)
P.O. Box 19024
Seattle, WA 98109-1024

jclark@fhcrc.org
Academic Office: (206) 667-5073
Fax: (206) 667-5765

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Education and Training

B.A., University of Minnesota, Minneapolis, MN, 1970.

M.D., Washington University, St. Louis, MO, 1974.

Internship in Internal Medicine, Washington University, St. Louis, MO, 1975.

Residency in Internal Medicine, Washington University, St. Louis, MO, 1977.

Fellowship in Pulmonary Diseases, Washington University, St. Louis, MO, 1979.

Research Interests

Investigations of acute lung injury association with systemic immune responses involving both cellular and cytokine components.

The central hypothesis is that Th 1 cell activation initiates a multi-step sequence of signals that results in selective adherence of activated effector T cells in lung, amplification by selective recruitment of mononuclear cells, and accumulation of activated mononuclear cells and alveolar macrophages.

Representative Publications

Clark JG, Hansen JA, Hertz MI, Parkman R, Jensen L, Peavy HH. Idiopathic pneumonia syndrome following bone marrow transplantation. Am Rev Respir Dis 147:1601-1606, 1993.

Strandjord TP, Sage EH, Clark JG. SPARC participates in the branching morphogenesis of developing fetal lung. Am J Respir Cell Mol Biol 13:279-287, 1995.

Chesnutt AN, Matthay MA, Tibaya F, Clark JG. Early detection of type III procollagen peptide in acute lung injury: Pathogenetic and prognostic significance. Am J Respir Crit Care Med 156:840-847, 1997.

Weiss DJ, Liggit D, Clark JG. In situ histochemical detection of beta-galactosidase activity in lung: assessment of X-gal reagent in distinguishing Lac-Z gene expression and endogenous beta-galactosidase activity. Hum Gene Ther 8:1545-1554, 1997.

Clark JG, Hackman RC, Madtes DK, Chen W, Cheever MA, Martin PJ. Lung injury induced by alloreactive Th1 cells is characterized by host derived mononuclear cell inflammation and activation of alveolar macrophages. J Immunol 161:1913-1920, 1998.

 

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