[1505] Tumor-Associated Inflammatory Cells in Post-Transplant, Relapsed Classical Hodgkin Lymphoma May Be Recruited by Hodgkin/Reed-Sternberg Cells

Mark A Samols, Laura A Morsberger, Michele L Thiess, Denise Batista, Michael J Borowitz, Christopher D Gocke, Richard F Ambinder, Amy S Duffield. Johns Hopkins Hospital, Baltimore, MD

Background: Tumor-associated inflammatory cells in Classical Hodgkin Lymphoma (CHL) typically outnumber the neoplastic Hodgkin and Reed-Sternberg (HRS) cells. Several studies have demonstrated that the composition of the inflammatory infiltrate influences the clinical behavior of the tumor; however, the relationship between the neoplastic cells and the inflammatory cells has not been fully characterized. We examined whether the inflammatory cells are an intrinsic component of CHL or if they are recruited to the tumor by the HRS cells.
Design: We identified patients with CHL who had received an allogenic bone marrow transplant (BMT), and then relapsed post-BMT. Formalin fixed paraffin embedded (FFPE) tissue that was involved by CHL was identified, and molecular chimerism studies and XY fluorescence in situ hybridization (FISH) studies were performed. Additionally, immunohistochemical (IHC) stains for HRS cells (CD30), histiocytes (CD68), B-cells (CD20) and T-cells (CD3, CD4, CD8) were performed to examine the composition of the inflammatory infiltrate.
Results: Three patients were identified who satisfied the above criteria and had available post-BMT FFPE that contained neoplastic tissue. Two of these patients had opposite-sex donors. XY FISH studies for these two patients demonstrated that while the HRS cells were derived from the patient, the inflammatory cells were derived from the donor. These findings were confirmed with molecular chimerism studies, which showed that the DNA content in the post-BMT recurrent CHL was predominantly derived from the donor. The molecular chimerism studies also demonstrated that the inflammatory cells in the third patient with a same sex donor were derived from the donor. Both pre- and post-BMT FFPE tissue involved by CHL was available for two of the three patients. IHC studies of these tumors showed that the composition of the inflammatory cells pre- and post-BMT revealed no significant differences in the number of histiocytes or CD8+ T lymphocytes. Interestingly, both showed increased numbers of CD20+ B lymphocytes in the post-BMT tumor.
Conclusions: The tumor-associated inflammatory cells in relapsed CHL post-BMT are derived from the donor marrow. Additionally, the composition of the inflammatory infiltrate is largely unchanged from the original tumor, indicating patients did not change risk stratification groups in regards to percentages of CD68+ histiocytes or CD8+ T cells. These findings suggest that the inflammatory infiltrate may be recruited to the tumor by the HRS cells.
Category: Hematopathology

Monday, March 4, 2013 9:30 AM

Poster Session I Stowell-Orbison/Surgical Pathology/Autopsy Awards Poster Session # 232, Monday Morning

 

Close Window