Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chromosome abnormalities were demonstrated in 50-100% of Giemsa-banded metaphases from nine cases of B-cell prolymphocytic leukemia (B-PLL). Mitoses were obtained with pokeweed mitogen following pretreatment of peripheral blood (PB) prolymphocytes with neuraminidase-galactose oxidase. Chromosome 14 was abnormal in eight of the nine cases: a marker 14q+, with breakpoint at band q32 in seven and trisomy 14 in one. In four cases the abnormal No. 14 was one of several primary abnormalities and in four others it was seen in secondary clones. The origin of the translocated material was unknown in three cases, in two it resulted from t(11;14), later becoming t(11;14;21) in one of them, t(1;14) in another, progressing later to t(1;14;17); in yet another patient, the 14q+ was the result of a complex rearrangement t(6;14;17). Abnormalities of chromosome 6 were seen in six cases: 6q- as the primary abnormality in three; trisomy 6 was part of secondary changes in one case. Structural abnormalities of chromosome 1 were seen in six cases: 1q- in four (in one as the only abnormality), 1q+ in one case, and 1p- in another, both in the main clone. Trisomy 12 was demonstrated in three cases but not as the primary change. Spleen cells in two patients showed a higher frequency of abnormalities than in the PB, supporting the concept of the spleen being the organ primarily involved in B-PLL. Evidence of karyotypic evolution was demonstrated in six patients, in some clearly associated with clinical progression of the disease. The type and frequency of the abnormalities observed in B-PLL resemble those seen in non-Hodgkin's lymphomas and suggest major differences from B-CLL, although a relationship with the latter can not be completely ruled out at present.
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PMID:Chromosome abnormalities in B-cell prolymphocytic leukemia: a study of nine cases. 660 59

The molecular lesions of human familial and common B-CLL remain unknown. As an approach to this problem, aged NZB mice with a B cell lymphoproliferative disorder were chosen as a murine model. Three groups of NZB mice (2 months, 6 months and > 18 months) for a total of nineteen were studied. A complete autopsy including a CBC was performed on each mouse. Spleen cells were immunophenotyped and cell cycle analysis was performed. Spleen weight, peritoneal cell counts and absolute lymphocytes counts were all elevated in the oldest group. All mice showed evidence of extramedulary hematopoiesis and the older group showed lymphocytic infiltrates in the lacrymal glands, kidneys, liver and lungs. Two of the seven aged mice had a malignant lymphoma. One was a marginal zone lymphoma and the other a lymphocytic lymphoma. Splenic immunophenotyping showed a loss of T cells with an increase in B cells as the mice age. Cell cycle analysis revealed hyperdiploidy in all of the aged mice with a decrease in the percentage G0G1 cells. This disease appears to involve an absolute lymphocytosis of the peritoneum and the peripheral blood compartment. This is associated with splenic aneuploidy. The infiltration of the spleen by malignant cells of varying morphology is a late event. The aged NZB mouse continues to be a model for human B-CLL.
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PMID:The natural history of a lymphoproliferative disorder in aged NZB mice. 789 86