Ethel Cesarman

Kaposi's sarcoma-associated herpesvirus and human herpesvirus 8 (KSHV/HHV8)-associated lymphoma of the bowel. Report of two cases in HIV-positive men with secondary effusion lymphomas.

This report describes two cases of Kaposis sarcoma-associated herpesvirus/human herpesvirus-8 (KSHV/HHV8)-associated lymphomas that primarily involved the large bowel and that secondarily caused malignant effusions. Involvement of the gastrointestinal tract is of interest because epidemiologic evidence suggests that KSHV/HHV-8 may be transmitted via the fecal-oral route, and KSHV/HHV8 DNA has been detected in rectal samples from HIV-positive patients. This report describes two HIV-positive men who developed primary KSHV/ HHV8-associated lymphomas of the bowel. Despite similar morphology and immunophenotype, these cases differ from most KSHV/HHV8-associated primary effusion lymphomas, which present with malignant effusions in the absence of a solid tumor mass. The spectrum of KSHV/HHV8-associated lymphomas is expanded to include a subset of primary bowel lymphomas in individuals infected with human immunodeficiency virus.

Kaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus†

Kaposis sarcoma‐associated herpesvirus (KSHV) DNA sequences have been identified in approximately 95% of Kaposis sarcoma (KS) lesions and primary effusion lymphomas (PELs), suggesting a pathogenetic role for this virus in these lesions. However, KSHV has also been identified in a variety of specimens, including lymph nodes, peripheral blood B cells, semen, and prostate tissue, with varying frequencies. This suggests that KSHV, like Epstein‐Barr virus, may be ubiquitously distributed. To evaluate further the clinical spectrum of KSHV infection and define better the prevalence of this virus in lymphoid tissues in the general population, the authors examined a wide spectrum of benign lymphoid proliferations occurring in human immunodeficiency virus (HIV)‐negative individuals.

Molecular genetic analysis demonstrates that multiple posttransplantation lymphoproliferative disorders occurring in one anatomic site in a single patient represent distinct primary lymphoid neoplasms

Background. Posttransplantation lymphoproliferative disorders (PT‐LPDs) are a clinicopathologically heterogeneous group of lymphoid proliferations of varied clonal composition, the majority of which are associated with Epstein‐Barr virus (EBV) infection. The clonal content and clonal relatedness of 24 separate PT‐LPD lesions occurring synchronously in one organ in a single patient were investigated.

Modified dose intensive R- CODOX-M/IVAC for HIV-associated burkitt (BL) (AMC 048) shows efficacy and tolerability, and predictive potential of IRF4/MUM1 expression

Methods Modifications of the US NCI regimen include rituximab (R), cyclophosphamide reduction [800 mg/m2 x 2 days], vincristine 2 mg cap, methotrexate (mtx) 3000 mg/m2, dual chemotherapy lumbar punctures and IVAC infusion (high risk pts). Antibiotic prophylaxis & growth factor support specified, 100% grade IV hematopoietic toxicities in the original regimen. HAART therapy at the discretion of the local MD. Pathology review included CD20, CD10, BCL2, BCL6, p53, Ki67, BLIMP1, IRF4/ MUM1 and EBV EBER. (Table 1)