A missing group C chromosome in the bone marrow cells of three children with myeloproliferative disease

Teasdale, J.; Worth, Ann; Corey, M J

doi:10.1002/1097-0142(197006)25:6<1468::aid-cncr2820250627>3.0.co;2-f

Cited by 57 publications

(9 citation statements)

References 15 publications

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“…(Petit et al, 1973;Kaufmann et al, 1974;Macdougall et al, 1974;Secker Walker & Sandler, 1978). Seven other similar observations of childhood MPD eventually terminating in acute leukaemia and with absence of a group C chromosome were also reported before the use of banding techniques, precluding the exact identification of the C-chromosome involved (Teasdale et al, 1970;Humbert et al, 1971;Kamiyama et al, 1973;McClure et al, 1975). Two small groups of children with ANLL and BM karyotype abnormalities have been reported (Morse et al, 1978;Hagemeijer et al, 1979); absence or deletion of chromosome 7 were observed in five out of 12 and three out of nine children, respectively.…”

Section: Discussionmentioning

confidence: 63%

C‐Group Chromosome Abnormalities in Bone Marrow Cells of Three Children with Dyshaematopoiesis of Unknown Origin

et al. 1980

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Clinical and cytogenetic findings in three children with dyshaematopoiesis and bone marrow aneuploidy are described. Monosomy 7 was found in immature cells of one 10-year-old boy with myelofibrosis following a 3 years evolution of severe thrombocytopenia and anaemia. Trisomy 8 was found in 80% of the bone marrow metaphases of a 5 1/2-year-old girl with aplastic anaemia and Australia antigen positivity. During a 3 year observation period the number of cells with trisomy 8 regressed and eventually disappeared. Improvement of her clinical condition is present but still limited. Trisomy 8 was also found in all bone marrow cells of an 8-year-old girl with an undefined myeloproliferative disorder. Her disease was apparently related to collagen-vascular disorders like periarteritis or other necrotizing angiitis and presented with periods of exacerbation and periods of chronic evolution. Periods of exacerbation were accompanied by excessive myeloid proliferation. Repeated bone marrow cytogenetic analysis during the acute and chronic phases showed trisomy 8 in all the metaphases analysed. During the last episode of acute illness, further clonal evolution was observed, characterized by a translocation (8;17).

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Section: Discussionmentioning

confidence: 63%

C‐Group Chromosome Abnormalities in Bone Marrow Cells of Three Children with Dyshaematopoiesis of Unknown Origin

et al. 1980

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“…Chronic myeloproliferative disorders have been noted in children and adults with a missing No. 7 or C chromosome; AML may develop in these patients (Teasdale et al, 1970;Sieff et al, 1981). A hypoplastic phase preceding ALL has been described in 2 per cent of children with ALL (Breatnach et al,198 1).…”

Section: Discussionmentioning

confidence: 95%

Acute leukemias of childhood: Pathologic features

Swerdlow

Glick

Cousar

et al. 1985

Hematological Oncology

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Major advances have been made in the diagnosis and therapy of childhood leukemia over the last two decades (Zuelzer and Flatz, 1960; Miller, 1980; Steinhorn and Myers, 1981; Kobrinsky et al., 1980). Sophisticated phenotypic analysis of these leukemias has partially revealed their complexity; there are at least three to five distinct clinical pathological entities in the childhood leukemia groups. Improved therapy has resulted in marked increases in survival and cures. Less attention has been given to the pathology of childhood leukemia, although the frequency and complexity of tissue examinations have greatly increased. In particular, the pathologic manifestation of relapses, detection of focal leukemia after treatment and the pathology of complications have not been systematically reviewed. Our goal was to look at all of the pathologic manifestations of leukemia and to relate these manifestations to homogeneous patient populations grouped by their type of leukemia. Therefore all of the cytologic, hematologic, histopathologic, ultrastructural and immunologic materials on a consecutive group of leukemic children seen at Vanderbilt from 1970 to 1981 were reviewed; pathologic manifestations of leukemia were then analysed in relationship to diagnostic categories.

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“…Unlike the patient reported here, normal-to-increased megakary- ocytes were noted despite peripheral thrombocytopenia. The preleukemia phase ranged from four weeks to two years in the three patients reported by Teasdale et a1 [3]. In one of these patients the response to chemotherapy was poor.…”

Section: I Scussl Onmentioning

confidence: 85%

Trisomy 21 in bone marrow cells of a patient with a prolonged preleukemic phase

Sikand

Taysi

Strandjord

et al. 1980

Med. Pediatr. Oncol.

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The clinical, hematologic, and cytogenetic findings are described in a patient who developed clinical and hematologic features of acute myelogenous leukemia (AML) after a three-year period of observation with unexplained thrombocytopenia. Five months before the diagnosis of AML she developed hepatosplenomegaly and a lupus-like syndrome. At this time she was also found to have trisomy 21 in all bone marrow cells studied, in addition to trisomy 8 in a few cells. The finding of trisomy 21 in all of the bone marrow cells examined could reflect a nonrandom alteration in the leukemic stem line or it might indicate that mosaic patients with trisomy 21 cells in their bone marrow share the increased risk of AML that has been documented for trisomy 21 patients.

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A missing group C chromosome in the bone marrow cells of three children with myeloproliferative disease

Cited by 57 publications

References 15 publications

C‐Group Chromosome Abnormalities in Bone Marrow Cells of Three Children with Dyshaematopoiesis of Unknown Origin

C‐Group Chromosome Abnormalities in Bone Marrow Cells of Three Children with Dyshaematopoiesis of Unknown Origin

Acute leukemias of childhood: Pathologic features

Trisomy 21 in bone marrow cells of a patient with a prolonged preleukemic phase

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