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E Jaffe

Publications and source records attributed to E Jaffe.

48 records · Page 3Linked to original sources
PubMed1978

Myeloproliferative syndromes: a unique presentation of chronic myelogenous leukemia (CML) as a primary tumor of bone.

A 45-yr-old female presented with a rapidly enlarging bony tumor that was eventually identified as a Philadelphia chromosome (Ph1)-positive myeloproliferative disorder with extramedullary blastic transformation. This transformation occurred in the absence of demonstrable chronic or acute leukemic phase. She had no history of a chronic or prodromal illness in spite of a bone marrow biopsy showing myelofibrosis and liver biopsy documenting extramedullary hematopoiesis. This case represents a unique constellation of features of the myeloproliferative syndrome in which the diagnosis was obscure until special stains of the bony tumor and cytogenetic studies were performed.

Bone Neoplasms↗
PubMed1977

Amyloid AA protein. Cellular distribution and appearance.

To investigate the cellular distribution and possibly the cellular origin of the AA protein associated primarily with the fibrils of secondary amyloid deposits, a variety of human tissues was studied by indirect immunofluorescence using a specific anti-AA immunoglobulin and FITC-goat anti-rabbit IgG. Positive cells were most frequently identified in reactive lymphoid tissues. They were most numerous in tonsils and, to a lesser extent, frequent in spleens. Both cellular appearance and distribution of the positive cells suggested a plasmacytic nature. Double staining with rhodamine-labeled anti-IgG demonstrated IgG within some of these cells. The data suggest that the AA protein may be an immunoprotein. In the absence of kinetic data, however, it is not possible definitively to assign the origin of the AA protein to the plasma cell.

Amyloid↗
PubMed1977

Gastrointestinal involvement in the Sézary syndrome.

A case of documented Sézary syndrome, a cutaneous T-cell lymphoma, with gastrointestinal lymphocytic infiltration is presented. The symptom of diarrhea waxed and waned with the course of the disease process. Radiographic studies were normal, and no evidence of malabsorption was elicited. The diagnosis was established by endoscopic and biopsy techniques, with light and electron microscopy of colonic and small bowel biopsies demonstrating extensive infiltration with typical Sézary cells. To our knowledge this is the first reported case of gastrointestinal involvement in the Sézary syndrome.

Dermatitis, Exfoliative↗
PubMedDate not supplied

Clustering of breakpoints on chromosome 11 in human B-cell neoplasms with the t(11;14) chromosome translocation.

The t(11;14) (q13;q32) chromosome translocation has been reported in diffuse small and large cell lymphomas and in chronic lymphocytic leukaemia (B-CLL) and multiple myeloma. Because chromosome band 14q32 is involved in this translocation, as well as in the t(8;14) (q24;q32) translocation of the Burkitt tumour, interruption of the immunoglobulin heavy-chain locus was postulated for this rearrangement. We have cloned the chromosomal joinings between chromosomes 11 and 14 and also between chromosomes 14 and 18, in B-cell tumours carrying translocations involving these chromosomes, and suggested the existence of two translocated loci, bcl-1 and bcl-2, normally located on chromosomes 11 (band q13) and 18 (band q21) respectively, involved in the pathogenesis of human B-cell neoplasms. The results indicate that in the leukaemic cells from two different cases of CLL, the breakpoints on chromosome 11 are within 8 nucleotides of each other and on chromosome 14 involve the J4-DNA segment. Because we detected a 7mer-9mer signal-like sequence with a 12-base-long spacer on the normal chromosome 11, close to the breakpoint, we speculate that the t(11;14) chromosome translocation in CLL may be sequence specific and may involve the recombination system for immunoglobulin gene segment (V-D-J) joining.

B-Lymphocytes↗
PubMedDate not supplied

Regression and clonally distinct recurrence of human immunodeficiency virus related Burkitt-like lymphoma during antiretroviral therapy.

An increased incidence of intermediate to high-grade Non Hodgkin's Lymphoma is found in individuals with AIDS. Although immune function in AIDS patients can be improved through the use of antiretroviral therapy, the contribution of these drugs to lymphoma regression is not known. Here we describe the complete regression and subsequent recurrence of high grade, Burkitt-like lymphoma during antiretroviral therapy in a patient with AIDS. Antiretroviral therapy resulted in diminished viral load and modest improvement in CD4+ T cell counts. Lymphoma regressed initially, but relapsed 3 months later. Tissue taken from the initial and recurrent tumor demonstrated different clonal rearrangements. The recurrent lymphoma did not respond to continued antiretroviral therapy. In Conclusion, antiretroviral therapy may contribute to lymphoma regression in AIDS lymphoma. Clinically recurrent disease may be clonally distinct.

Adult↗