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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sequential lymph node biopsies taken from a non-Hodgkin lymphoma patient revealed two karyotype abnormalities peculiar to B cell neoplasias: trisomy 12 and t(2;8)(p12;q24) translocation. The first was documented in all cells analyzed, while the second was present in 20% of the metaphases from the first biopsy and in 100% from the second. This suggests that the t(2;8) translocation arose as a secondary karyotypic change. In addition, although immunological characterization of the neoplastic cells disclosed a monoclonal B cell population that expressed immunoglobulin kappa light chains, as usually found in Burkitt's lymphoma with t(2;8) translocation, Southern blot analysis provided evidence of rearrangement in only one kappa chain allele.
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PMID:Immunological and molecular studies in a case of follicular lymphoma with an extra chromosome 12 and t(2;8) translocation. 333 3

Non-random chromosome abnormalities have been found in all types of malignant lymphomas. It is obvious that some cytogenetic abnormalities are associated with certain morphological types. Thus, among the Burkitt's lymphomas the 2;8-, 8;14- and 8;22-translocations are found in the great majority of cases; t(14;18) is associated with follicular lymphomas; +12 and t(11;14) with well differentiated lymphomas; and rearrangements of 14q11 and trisomy 3 with T-cell lymphomas. The molecular changes involving the c-myc oncogene and the immunoglobulin loci in Burkitt's lymphoma have been intensively studied. Among other non-Hodgkin's lymphomas the molecular mechanisms behind t(11;14) and t(14;18) in B-cell lymphomas and 14q11 rearrangements in T-cell lymphomas are starting to be unravelled. A number of other aberrations, such as +3, 6q-, and +12, have been associated with non-Hodgkin's lymphoma although the molecular mechanisms behind these rearrangements are still unknown. Very little is known about clinicocytogenetic correlations, but some observations clearly indicate that the karyotypic pattern is an important prognostic factor in non-Hodgkin's lymphoma. Contrary to non-Hodgkin's lymphoma, very little is known about the cytogenetic findings in Hodgkin's disease. The sparse results, however, indicate that there are similarities to those in non-Hodgkin's lymphoma.
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PMID:What's new in lymphoma cytogenetics? 336 47

Cytogenetic studies were carried out in peripheral blood lymphocytes of 31 children with cancer (12 retinoblastomas, 9 non-Hodgkin's lymphomas, 7 neuroblastomas and 3 Wilms' tumors) with the purpose of investigating the prevalence and persistence of chromosomal aberrations before onset of antineoplastic treatment and at different intervals thereafter. The number of treated patients with chromosomal anomalies was significantly higher (p less than 0.01) and so was the percent of cells with aberrations, as compared to untreated patients or healthy controls. The most frequent aberrations were of chromatid type. One patient had a number five trisomy in the third posttreatment study and another presented abnormal aneuploid cells in the third and fourth posttreatment studies. Congenital chromosomal anomalies were not observed, nor anomalies described for some of these tumors. There was no regularity in the effected chromosomes. We conclude that the observed chromosomal aberrations were due to treatment. We consider a prolonged and stringent cytogenetic follow up of such patients necessary to detect the induced aberrations.
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PMID:Chromosomal anomalies in children treated for cancer. 378 70

The development of B-cell chronic lymphatic leukemia in two patients who had previously been treated for Hodgkin's disease is described. In both cases aneuploidy and multiple chromosome aberrations of hemopoietic cells were evident. In one patient these changes included a clonal 14q + abnormality in association with other complex rearrangements, interpreted as translocation abnormalities involving t(6;14), 5(1;15), and t(17;19). Although the chromosome abnormalities in the other patient were nonclonal, a 14q abnormality also was detected, namely t(14q+;18q-). Other chromosome abnormalities (all nonclonal) in the two patients included translocations involving chromosome 5 and deletion of 7q in one patient and trisomy of chromosome 8 in the other. Although these abnormalities have been associated with the presence or development of non-Hodgkin's lymphoma, acute nonlymphoblastic anemia, or myelodysplastic disorders, the findings in these patients suggest that the detection of clones and potential clones with these abnormalities may be only one stage in the development of secondary malignancy.
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PMID:B-cell chronic lymphatic leukemia in Hodgkin's disease. A report of two patients with unusual chromosome features. 380 34

There are very few chromosome studies using banding techniques of lymph nodes in Hodgkin's disease (HD), and determinations of immunologic phenotypes are scarce. We have performed both cytogenetic and immunologic studies in 12 of 22 lymph node biopsies of different histologic types obtained from 20 HD patients (no mitotic cells were found in the remaining ten lymph nodes). A near-diploid modal number was obtained in 80% of the cases, and 20% showed a bimodal distribution. Clones were observed in 50% of HD lymph nodes, with chromosome markers in 60% of them. Markers 15q+, 5p-, and der(X) and a trisomy of chromosome #21 were observed in our cases. Seventy-one percent of the lymph nodes studied showed a predominance of T lymphocytes. Within the lymph nodes, where the karyotype was determined, 4/12 lymph nodes presented a predominance of B lymphocytes, and they were all included in the group with structural chromosome abnormalities.
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PMID:Cytogenetic and immunologic phenotype findings in Hodgkin's disease. 387 58

Biclonal trisomy 3 in a case of epithelioid cellular lymphogranulomatosis (Lennert's lymphoma) was demonstrated by Q-banding polymorphisms of chromosome #3. Seventeen of 19 mitoses with trisomy 3 showed duplication of 1 of the homologous chromosomes and the remaining 2 showed duplication of the other chromosome. It is assumed that both chromosomes #3 independently underwent nondisjunction and that this led to the development of the two abnormal clones. Moreover, there appeared to be a qualitative difference between the two clones, because one of them made up a major proportion and the other a minor proportion of the cells in both of the two samples studied at different times.
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PMID:Biclonal trisomy 3 in a case of epithelioid cellular lymphogranulomatosis (Lennert's lymphoma). 650 31

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

Banding studies were done on tissues from tumors excised from 22 Japanese patients with non-Hodgkin's lymphomas. All tumors were found to be associated with aneuploidy. The chromosome abnormalities were diverse, with each chromosome type being involved in these abnormalities. Terminal deletions, derivative chromosomes as a result of unbalanced or nonreciprocal translocations, and markers of totally or partially unknown origin accounted for the majority of the structural abnormalities. Balanced reciprocal translocations were seen only occasionally. The 14q+, 6q-, partial trisomy of 1q, 11q+, 18q+, and 19q+ abnormalities were seen in more than two patients. The incidence of a missing sex chromosome was significantly higher than that of autosomes, but no particular other karyotypic abnormality seemed to be associated with the event. All six patients whose chromosomes could be totally characterized were in complete remission. Patients with one or more markers of unknown either totally or partially origin, had a median survival of only 8 months (p less than 0.01). Five of the former six patients showed a nodular histology. Fifteen of the latter 16 patients had a diffuse histology, with 13 of the 15 having diffuse histiocytic lymphoma. The median survival of 9.5 months for the 14 with only abnormal metaphases in the lymphatic tissues (AA-group) was shorter than the 26+ months for the seven patients with both normal and abnormal metaphases (AN-group). Thus certain aspects of chromosomal changes appear to correlate with histology and/or prognosis in non-Hodgkin's lymphomas.
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PMID:An analysis of chromosome findings in non-Hodgkin's lymphomas. 703 15

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.
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PMID:Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms. 752 Feb 72

We have carried out chromosome analysis in a series of 16 non-Hodgkin Lymphoma (NHL) cases in leukemic phase. The diagnoses in these patients based on histology and immunologic markers were as follows: follicular lymphoma (FL), 3 cases; mantle cell lymphoma (Mc), 4 cases; lymphoplasmacytic lymphoma (LPL), 8 cases, and large cell lymphoma, 1 case. We have shown that the t(14;18), t(11;14), and trisomy 12 retained their subtype association with FL, Mc, and LPL, respectively, as in their nonleukemic counterparts with one case of FL showing t(1;19)(q23;p13). Among the four LPL cases without trisomy 12, one case each showed t(12;14)(q13;q32), trisomy 14, t(1;3)(p34;q21), and del(3)(q21). The t(1;19) and t(12;14) may represent rare events in FL and LPL, respectively, and may be uniquely associated with the leukemic phase. The breakpoint 14q32 was the most common single breakpoint involved, sometimes involving both chromosome 14 homologues depicting its association with primary and secondary genetic events in the disease progression. In addition to the main abnormalities, we have shown additional complex abnormalities in 14 of 16 cases. Among these, chromosome 3 was the most commonly involved, affecting the short or long arm or the whole chromosome; 5 of the 16 cases involved breakpoint 3q21. The high incidence of additional abnormalities in these NHL in leukemic phase suggest an association with the development of leukemia and progression of the disease.
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PMID:Cytogenetic abnormalities in the leukemic phase of non-Hodgkin lymphoma. 765 98


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