Dr. Scott J. Rodig

	Department of Pathology
	Brigham and Women's Hospital
	A teaching Affliate of Harvard Medical School
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Name and Present Position:

SCOTT J. RODIG, Assistant Professor in Pathology

Address:

Brigham & Women's Hospital, 75 Francis Street, Boston, MA 02115

Medical School (including school name, date and degree awarded):

1998 MD, Washington University School of Medicine, St. Louis, MO

Graduate Medical Education (including dates and institution of internships, residencies, fellowships, etc.):

1998 PhD, Immunology, Washington University School of Medicine, St. Louis, MO
1998-2000 Resident in Anatomic Pathology, Brigham & Women's Hospital, Boston, MA
2000-2001 Fellow in Hematopathology, Brigham & Women's Hospital, Boston, MA
2000-2001 Chief Resident in Anatomic Pathology (April-June 2001), Brigham & Women's Hospital, Boston, MA.
2001-2003 Research Fellow in Pathology, Brigham & Women's Hospital, Boston, MA

Certification:

2002 American Board of Pathology (Anatomic Pathology and Hematology)

Current Academic Appointment:

Assistant Professor in Pathology, Harvard Medical School, Boston, MA

Current Medical Staff Appointment:

Associate Pathologist, Brigham & Women's Hospital, Boston, MA

Selected Bibliography:

Meraz MA, White JM, Sheehan KCF, Bach EA, Rodig, SJ, Dighe AS, Kaplan DH, Riley JK, Greenlund AC, Cambell D, Carver-Moore K, DuBois RN, Clark R, Aguet M, Schreiber RD. Targeted disruption of the STAT1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway. Cell 1996; 84: 431-442.
Rodig SJ, Meraz MA, White JM, Lampe PA, Riley JK, Arthur CA, King KL, Sheehan KCF, Yin L, Pennica D, Johnson EM, Schreiber RD. Disruption of the JAK1 gene demonstrates obligatory and nonredundant roles of the Jaks in cytokine-induced biologic responses. Cell 1998; 93: 373-383.
Migone TS, Rodig SJ, Cacalano NA, Berg M, Schreiber RD, Leonard WJ. Functional cooperation of the interleukin-2 receptor beta chain and Jak1 in phosphatidylinositol 3-kinase recruitment and phosphorylation. Mol Cell Bio. 1998; 18 (11): 6416-22.
Satoskar AR, Rodig S, Telford III SR, Satoskar AA, Ghosh SK, von Lichtenberg F, David JR. IL-12 gene-deficient C57BL/6 mice are susceptible to Leishmania donovani but have diminished hepatic immunopathology. Eur J Immun. 2000; 30:834-839.
Hu J, Roy SK, Shapiro PS, Rodig SR, Reddy SP, Platanias LC, Schreiber RD, Kalvakolanu DV. ERK1 and ERK2 activate CCAAAT/enhancer-binding protein-beta-dependent gene transcription in response to interferon-gamma. J Biol Chem, 2001;276(1):287-97.
Rodig SJ, Jones D, Shahsafaei A, Dorfman DM. CCR6 is a functional chemokine receptor that serves to identify select B-cell non-Hodgkin's lymphomas. Hum Path, 2002; 33(12):1227-33.
Rodig SJ, Savage KJ, Nguyen V, Pinkus GS, Shipp MA, Aster JC, Kutok JL. TRAF-1 expression and c-Rel activation distinguish classical Hodgkin lymphoma from other morphologically or immunophenotypically similar forms of malignant lymphoma. Am J Surg Path, 2005; 29(2):196-203.
Rodig SJ, Shahsafaei A, Dorfman DM. The CD45 isoform B220 identifies select subsets of human B cells and B cell lymphoproliferative disorders. Hum Path, 2005; 36(1):51-7.
Rodig SJ, Shahsafaei A, Li B, Mackay CR, Dorfman DM. BAFF-R, the major B cell activating factor receptor, is expressed on the majority of mature B cells and B cell lymphoproliferative disorders. Human Pathol, 2005; 36(10):1113-9.