Trisomy 12 is the most frequently reported chromosome abnormality in patients with B-cell chronic lymphocytic leukemia, but only normal karyotypes are found in one third of patients with that disorder. Moreover, samples from patients with trisomy 12 also have many normal metaphases. To identify immunologically the cells in which both the trisomy 12 and the normal karyotypes occur, we studied two patients with B-cell chronic lymphocytic leukemia--one whose neoplastic cells demonstrated lambda light-chain clonality and one whose cells had kappa light-chain clonality. We used a recently developed cytogenetic method that allows simultaneous analysis of cell morphology, immunologic phenotype, and karyotype in the same mitotic cell. In cultures of blood cells stimulated with pokeweed mitogen and tetradecanoylphorbol acetate, all the mitotic cells with either the lambda or the kappa immunoglobulin had trisomy 12, whereas all the cells that lacked these light chains or that had T-cell markers (OKT8 or OKT4) had normal karyotypes. These results show that trisomy 12 in B-cell chronic lymphocytic leukemia occurs in the neoplastic B cells, but not in the T cells, and they thus provide an explanation for the common finding of mitoses with normal karyotypes in patients with B-cell chronic lymphocytic leukemia.
We have studied neoplastic lymph nodes from six patients histologically, immunologically and cytogenetically. Histologically all the cases were classified as peripheral T-cell lymphomas. These were subclassified as T-zone lymphomas in three, large cell 'pale cell' variant in one, large cell immunoblastic in one, and small cell, mycosis fungoides in one. Two had features of angioimmunoblastic lymphadenopathy (AILD). Immunologically all cases expressed CD2 (OKT11) and CD4 (T4). All six cases had clonal chromosome abnormalities, although in four cases the majority of cells were chromosomally normal. Chromosome 3 was most often involved in abnormalities, occurring in five patients. The most common single chromosome abnormality, trisomy 3, was seen in all three cases classified as T-zone lymphoma and in no other cases. In the two cases with features of AILD only numerical abnormalities were seen, whereas in the other cases complicated structural rearrangements were present. Recurring structural abnormalities involved bands 1p12or13, 1q32, 3p25 and 14q11. Our data suggest that cytogenetic analysis may assist in diagnosis and classification of the peripheral T-cell lymphomas.
of skin and rectum biopsies in bone marrow transplant recipients. APMIS 100: 11 15-1122, 1992. We have studied histological and immunohistological specimens of 39 skin biopsies from 21, and 30 rectal biopsies from 17 bone marrow transplant recipients. The biopsies were taken before transplantation, during acute and chronic graft-versus-host disease (GVHD), and at times with no GVHD. In biopsies taken during cutaneous aGVHD grade I to 111, epithelial changes were seen in 16/23 biopsies. The cutaneous infiltrates during aGVHD consisted of CD2-, CD4-, CD8-and FMC-33-positive cells both in the epithelium and in the dermis. CD57-positive NK cells were also detected in most biopsies. During chronic GVHD the cutaneous cellular infiltrates were similar to those seen in moderate aGVHD, i.e. both CD4-and CD8-positive lymphoid cells were present. When the biopsy was taken after the beginning of corticosteroid treatment for aGVHD, or at times when the patient did not have GVHD symptoms, the cellular infiltrates were considerably smaller in the dermis. During clinical intestinal aGVHD mucosal epithelial changes were relatively uncommon; instead, increased numbers of both CD4-and CD8-positive lymphocytes in the lamina propria (LP) were seen in 1 1 / 13 samples. During chronic GVHD the number of CD4-positive cells exceeded that of CDS-positive cells in the LP, and the large lymphoid infiltrates also reached the muscularis mucosae. In rectal biopsies the differences were not so prominent because most of the pretransplant biopsies showed CD2-, CD4-, CD8-and CD57-positive lymphocytes both in the lamina propria and epithelium.
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