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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different HT have been studied with the electron microscope and the findings compared to those in the literature. Five patients with thrombasthenia and three with Willebrand's diseases showed various disorders, usually anisocytosis and hypertrophic open canalicular system, in relation to regenerative states. Thirteen young children with 21-trisomy (2 with leukemia) and 13/15 trisomy (1 case) had enlarged platelets with abnormalities of membranes and vacuoles indicating some metabolic disorders and necrotic lesions. One child with Cooley's anemia showed a few granules and necrotic lesions. All these symptoms were related to regenerative or primitive megakaryocytopathias. The lesion of these latter cell appears in other HT: aberrations of membranes in giant platelets syndroms (J. Bernard and J. P. Soulier syndrome), disorders in membranes and/or granules in thrombopenic thrombopathias, the short platelet life span in May-Hegglin anomaly, storage pool disease in Hermansky-Pudlak syndrome. Finally the ultrastructural abnormalities of the platelets mainly help to distinguish several diseases of megakaryocytes.
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PMID:[Megakaryocytes and platelets in congenital thrombopathies]. 13 24

There is an increased incidence of acute leukemia in patients with Down's syndrome patients have a trisomy-21 chromosomal pattern, and chromosomal abnormalities can be seen in acute leukemia. It is possible that the increased incidence of acute leukemia in Down's syndrome persons may be due in part to their chromosomal abnormalities. Such abnormalities, some appearing in a stepwise clonal evolution, were found in five Down's syndrome patients, four with acute leukemia and one with abnormal regulation of leukopoiesis. Morphological abnormal chromosomes were also found in three patients. These chromosomal abnormalities are similar to those seen in non-Down's syndrome leukemic patients. There is suggestive evidence for clonal evolution hypothesis of luekemogenesis in non-Down's syndrome patients. The abnormal chromosomal pattern reported in our Down's syndrome patients could be the result of nondisjunction in mitosis, and leukemia may be the phenotypical expression of this nondisjunction.
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PMID:Down's syndrome and leukemia: mechanism of additional chromosomal abnormalities. 14 44

An experimental system was developed that permitted nonrandom chromosome changes that occur in radiation leukemia virus (RadLV)-induced lymphomas to be followed during tumor progression. RadLV variant-induced preleukemia and leukemia cells originating from female inbred C57BL/6 mice were injected into male animals of the same strain. Since all donors were females and all recipients were males, the sex chromosome complements (XX and XY) were used to distinguish the preleukemia and leukemia cells from those of host origin. The G-banding analysis revealed that more than 50% of animals that were inoculated with preleukemia cells and that developed leukemia possessed tumor stem-lines of 41 chromosomes with a tristomy of chromosome #15. In animals inoculated with overt leukemia cells and in which tumor progression occurred, the G-banding an additional trisomy of chromosome #17. The cytogenic data strongly suggested that the trisomy of chromosome #15 was the first specific tumor-associated chromosome change that occurred in the process of conversion of RadLV-induced preleukemia cells to fully autonomous tumor cells.
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PMID:Chromosome changes (trisomies #15 and 17) associated with tumor progression in leukemias induced by radiation leukemia virus. 20 3

In a 3 6/12 year old boy, with the juvenile type of chronic myelogeneous leukemia cytogenetic examination of bone marrow and blood, performed two months before onset of the acute blastic crisis, showed two cell lines: the first one with a normal karyotype 46, XY and the second one with a trisomic karyotype 47, XY, +21. This finding of a mosaic trisomy 21 in a patient without symptoms of Down's syndrome allow to assume the trisomy cells to be malignant, and the type of mosaicism to be proliferative. This karyologic finding could be taken for an early prognostic, unfavourable sign of the disease. The significance of karyologic examination with exact classification of atypical leukemias is stressed.
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PMID:[Juvenile type of chronic myelogenous leukemia in a 3 6/12 year old boy with trisomy 21 mosaicism but no symptoms of Down's syndrome (author's transl)]. 26 87

Marrow cells from an untreated man with preleukaemia were found to have trisomy for the long arm of chromosome 1 which was translocated to the end of the long arm of number 11, i.e., 46,XY, -11,+t (1:11) (q11 or q12; q25). The same abnormality was found in metaphases from 8 individual granulocytic colonies. With development of acute myelomonocytic leukaemia, in addition to the basic chromosome abnormality, trisomy of chromosome 8 and an extra chromosome number 19 with partial deletion were found. Fibroblasts grown from marrow biopsy material showed a normal diploid complement, 46,XY.
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PMID:Trisomy of 1q in preleukaemia with progression to acute leukaemia. 27 85

Two cases of Ph1-positive chronic granulocytic leukaemia with hitherto undescribed translocations are presented. In case 1 the deleted part of chromosome number 22q- was translocated to the short arm of the X chromosome, t(X;22)(p22;q11). Pronounced basophilia, trisomy 19 in the majority of metaphases, and a partial cytogenetic normalization of the bone marrow during busulphan induced remission were additional remarkable features of this case. In case 2 a translocation t(15;22)(q26;q11) was found. In this case the disease was characterized by an increase of unusually small megakaryocytes, thrombocytosis, and an accelerated course.
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PMID:New translocations in chronic granulocytic leukaemia: t(X;22)(p22;q11) and t(15;22)(q26;q11). 28 90

Karyotypes of two transplantable murine ascites leukemias, LBN/a2 and LBN/b3, were studied with the use of the trypsin-Giemsa technique. The original tumors arose in adult female mice of strains BN/a and BN/b after prolonged antilymphocyte globulin administration. The karyotypes of both leukemias showed similar patterns. Both were hyperdiploid with modal chromosome numbers of 41 and 42 in LBN/a2 and LBN/b3, respectively. The cells consisted of an average of 37 normal chromosomes and 4--5 abnormal chromosomes. The most consistent karyotype deviation was monosomy of the X-chromosome and of several autosomes: no. 9, 14, and 7 in the LBN/a2 line and no. 7, 12, 14, and 9 in the LBN/b3 line. In most LBN/b3 cells and in a lower proportion of LBN/a2 cells, trisomy of chromosome no. 15 was found. With regard to the occurrence of abnormal marker chromosomes, both tumors exhibited great cell-to-cell variation. Two of the markers were common to both leukemia lines.
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PMID:Chromosome studies of two transplantable leukemias of BN mice. 28 78

Cytogenetic studies have been done on a group of childhood patients over a period of 3 1/2 years in which time Giemsa trypsin banding was applied to all specimens. Fifteen of the 107 patients (14%) were diagnosed as having acute nonlymphoblastic leukemia (ANLL). Twelve of the 15 had chromosomal abnormalities. The most common was an involvement of the No. 7 chromosome which occurred in five patients. Three patients had trisomy 19. No correlation could be found between the disease subgroup and the karyotypic aberration in patients with anomalies involving a common chromosome.
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PMID:Acute nonlymphoblastic leukemia in childhood. 28 49

A patient with chronic myelocytic leukaemia (CML) had the Philadelphia chromosome from the standard 9/22 translocation, a partial trisomy 1 secondary to an unbalanced 1/17 translocation, and a more recent clone with the addition of trisomy 22. This is the third case of partial trisomy 1 associated with the Philadelphia chromosome. Trisomy 1 in haematological disorders is discussed with reference to its clinical significance in CML, the segment of chromosome no. 1 involved, and the mechanism of origin of the partial trisomies. Anomalies of chromosome 1, although not specific to any of them, seem to be important in the development of myeloproliferative disorders and of neoplasms in general.
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PMID:Partial trisomy 1 due to 1/17 translocation in Ph'-positive chronic myelocytic leukemia. 28 25

Trypsin-Giemsa banding studies on T cell leukemias induced in Robertsonian translocation mice by dimethylbenz[a]anthracene and Moloney leukemia virus show a trisomy of chromosome 15 even in cases in which chromosome 15 has undergone centromeric fusion with chromosomes 1, 5, or 6. These results suggest that the duplication of gene(s) located on chromosome 15 is of critical importance for murine T cell leukemia development.
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PMID:Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice. 31 45


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