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Results for “Leukemia, Lymphoid”

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At least 19 recordsLinked to original sources
PubMed1990

Transformation of bilineal hybrid acute leukemia to acute lymphoid leukemia: a case report with serial analyses of cytogenetics and gene rearrangement.

A 17-year-old male with bilineal hybrid acute leukemia is described. Two-color flow cytometric analysis of blast surface phenotype revealed that there were two groups of blasts which showed either CD 10+ CD 19+ CD 13- CD 33- or CD 10- CD 19- CD 13+ CD 33+, but not both. He developed a complete remission by treatment with vincristine, prednisolone, adriamycin, and L-asparaginase. After 8 months, however, leukemia relapsed and lymphoid blasts were dominant. Cytogenetic analysis at presentation showed 46,XY,t(3;9)(p21;p22), and at relapse it showed 46,XY,t(1;3;9)(1pter----1q32::3p25----3pter;3 qter----3p21::9p22----9pter; 9qter----9p22::3p21----3p25::1q32----1q ter),t(2;19)(p21;q13). Analysis of the heavy chain joining region at diagnosis showed three hybridizing bands, all rearranged, but at relapse only one rearranged band. Analysis of the constant region for the beta T-cell receptor gene (TCR beta) both at diagnosis and at relapse showed one rearranged and one germline band, suggesting that rearrangement of one allele of TCR beta of not only lymphoid but also myeloid blasts occurred. It is considered that the target cell of lymphoid leukemia cells and that of myeloid leukemia cells at diagnosis were the same, which differentiated to two lineages, and the clone which evolved from lymphoid lineage proliferated at relapse.

Adolescent↗
PubMed1985

Lymphoid leukemia in the dog. Acute lymphoblastic leukemia and chronic lymphocytic leukemia.

True lymphoid leukemia of bone-marrow origin may present as two distinct clinical forms in the dog. Acute lymphoblastic leukemia is a rapidly progressive disease associated with proliferation of malignant, undifferentiated lymphoblasts. Chronic lymphocytic leukemia is a more insidious form of malignancy associated with abnormal proliferation of small lymphocytes. Recognition of these clinically distinct forms of leukemia and their differentiation from lymphosarcoma are important in considering prognosis and approach to therapy.

Animals↗
PubMed1987

[Morphometric characteristics of argentaffin nucleolar structures in peripheral blood lymphoid cells from patients with non-Hodgkin's lymphomas and chronic lymphoid leukemias].

Interphase lymphoid nucleoli of Ag-NOR stained site areas were measured on the TAS system in peripheral blood lymphoid cells with the known immunologic phenotype of 19 patients with lymphoid neoplasia (non-Hidgkin's lymphoma, CLL, hair-cell leukemia) and 10 healthy donors. The area of Ag-granules in neoplastic cells is much greater than in normal lymphocytes and does not correlate with a proliferation of cells but correlates with a malignancy grade of the disease. These data are discussed in terms of rDNA transcription patterns in malignant cells.

Adolescent↗
PubMed1989

Secondary acute myeloid leukemia in children treated for acute lymphoid leukemia.

We studied the risk of the development of acute myeloid leukemia (AML) during initial remission in 733 consecutive children with acute lymphoid leukemia (ALL) who were treated with intensive chemotherapy. This complication was identified according to standard morphologic and cytochemical criteria in 13 patients 1.2 to 6 years (median, 3.0) after the diagnosis of ALL. At three years of follow-up, the cumulative risk of secondary AML during the first bone marrow remission was 1.6 percent (95 percent confidence limits, 0.7 and 3.5 percent); at six years, it was 4.7 percent (2 and 10 percent). The development of secondary AML was much more likely among patients with a T-cell than a non-T-cell immunophenotype (cumulative risk, 19.1 percent [6 and 47 percent] at six years). Sequential cytogenetic studies in 10 patients revealed entirely different karyotypes in 9, suggesting the induction of a second neoplasm. In eight of these patients, the blast cells had abnormalities of the 11q23 chromosomal region, which has been associated with malignant transformation of a pluripotential stem cell. There was no evidence of loss of DNA from chromosome 5 or 7, a karyotypic change commonly observed in cases of AML secondary to treatment with alkylating agents, irradiation, or both. We conclude that there is a substantial risk of AML in patients who receive intensive treatment for ALL, especially in those with a T-cell immunophenotype, and that 11q23 chromosomal abnormalities may be important in the pathogenesis of this complication.

Adolescent↗
PubMed1992

[Clinical analysis of 10 patients with chronic lymphoid leukemia].

Ten patients with chronic lymphoid leukemia were analyzed for clinical characteristics, morphology and phenotype of leukemic cells. There were 3 patients with T-chronic lymphocytic leukemia (CLL), 2 with T-prolymphocytic leukemia (PLL), 2 with B-CLL, 1 with B-PLL, 1 with non-T-non-B-CLL and 1 with Waldenström's macroglobulinemia. Although chronic lymphoid leukemia is usually characterized by proliferation of B-lymphocytes, our study revealed that 5 of 10 patients had T-cell phenotype. A peripheral blood specimen of T-CLL showed small lymphocytes with a mature appearance and an irregular nuclear margin. Most of the cells lacked large azurophilic granules in the cytoplasm and nucleoli were also inconspicuous in the nucleus by light and electron microscopic examinations. In PLL, a majority of the cells were large lymphocytes with a prominent nucleolus and abundant basophilic cytoplasm which were more clearly observed by transmitted electron microscopic examination. The patients were treated with cyclophosphamide and prednisolone, but response to treatment was transient. The median survival time was 7 months for all patients, while that of T-cell lineage cases was only 1 month. Therefore, new modalities of treatment must be investigated in the future.

Aged↗
PubMed1986

Hand mirror cell lymphoid leukemia in adults. A distinct clinicopathologic syndrome. Case report and literature review.

Hand mirror cell (HMC) lymphoid leukemia is an unusual variant of acute lymphocytic leukemia (ALL) in which the bone marrow lymphoblasts manifest distinctive hand mirror morphologic features. Reported here is a 66-year-old woman with HMC lymphoid leukemia whose clinical course was characterized by 12 months of initial disease stability while she was receiving no chemotherapy; a prompt response to cyclophosphamide, vincristine, and prednisone therapy once instituted; and a hyperleukocytic episode (leukocyte count 607,000/mm3), which resulted in her death after 22 months of disease. This patient and 13 other reported adults (15 years and older) with HMC lymphoid leukemia (greater than 40% bone marrow HMC) are reviewed. HMC lymphoid leukemia appears to differ from typical adult ALL in that it has a female predominance, a relatively indolent early clinical course that lasts 1 year or longer, and it manifests the possibility of survival for 1 or 2 years despite the failure to achieve a complete remission with chemotherapy. Phenotypically, the HMC leukemic cells from all adults evaluated were null cells, Ia-positive, TdT-positive, and stained positively with acid phosphates, which suggests that HMC lymphoid leukemia is a variant of non-T, non-B-ALL. HMC lymphoid leukemia in adults appears to be a distinctive clinicopathologic entity.

Aged↗
PubMed1976

[Chronic lymphoid leukemia and multiple myeloma].

The authors report a case of multiple kappa myeloma comboned with chronic lymphoid leukemia. The chronic lymphoid leukemia had evolved over a 13-year period in the classical manner, without serum or urnary monoclonal immunoglobulins. The multiple myeloma with blood and urinary kappa chains appeared suddenly with a typical clinical and radiological picture accompanied by renal insufficiency. Thd diagnosis was confirmed by the demonstration of both lymphocyte and plasmocyte cell proliferation and a study of the ultrastructure which showed the sarcomatous and secretory character of the plasmocytes. A study of plasmocyte subpopulation showed the proliferation of B lymphocytes. A combination of chronic lymphoid leukemia and multiple myeloma is exceptional. The physiopathological interpretation (mono or biclonal proliferation) is discussed in the light of current nosological conceptions concerning lymphoproliferative disorders.

B-Lymphocytes↗