C-Monosomy myeloproliferative syndrome: A case of 7-monosomy

Macdougall, Lorna G.; Brown, J. Anne; Cohen, Maimon M.; Judisch, Janifer M.

doi:10.1016/s0022-3476(74)80616-5

Cited by 52 publications

(17 citation statements)

References 8 publications

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“…Accurate karyotypes determined with banding techniques, either quinacrine or Giemsa, were available for an additional 29 patients who had some hematologic disorder and a C group aberration. Results for 23 of these patients from 13 laboratories were obtained from published reports (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24); results for six patients came from personal communications by H. Van den Berghe, A. de la Chapelle, S. F. Pan, and C. C. Lin. These 29 patients included three with CML in the acute phase (9, 10), one with Ph' negative CML (11), 12 with AL (12)(13)(14)(15)(16)(17)(18), four with PV (11,19), and nine with other disorders such as refractory anemia (with or without ring sideroblasts) (17,20), neutropenia (21), and myelofibrosis (22)(23)(24).…”

Section: Methodsmentioning

confidence: 99%

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Nonrandom chromosomal abnormalities in hematologic disorders of man.

Rowley¹

1975

Proc. Natl. Acad. Sci. U.S.A.

127

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A nonrandom pattern of chromosomal abnormalities occurs in bone marrow cells obtained from patients with hematologic disorders who have an abnormal karyotype involving a C group chromosome. An additional number 8 chromosome is the most common abnormality, found in more than one-half of the patients studies. An additional number 9 chromosome and the loss of all or part of a number 7 are abnormalities that occur more often than might be expected by chance. It is proposed that specific human chromosomal abnormalities may be related to different specific etiologic agents.

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Section: Methodsmentioning

confidence: 99%

“…When chromosomal losses were present, four individuals had lost all or part of no. 7 (12)(13)(14)24), and one had lost a no. 9 (16).…”

Section: Methodsmentioning

confidence: 99%

Nonrandom chromosomal abnormalities in hematologic disorders of man.

Rowley¹

1975

Proc. Natl. Acad. Sci. U.S.A.

127

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“…It was found in four children with acute leukaemia following a long history (up to 5 years) of MPD, characterized by anaemia, thrombocytopenia, splenomegaly, etc. (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).…”

Section: Discussionmentioning

confidence: 99%

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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“…Other family members have a number of findings that previously have been noted in those with preleukemic states, suggesting that these individuals may represent members of a "leukemia-prone'' family. The simultaneous occur- No. 5 FATAL MYELOPROLIFERATIVE SYNDROME Luddy et al.…”

Section: Discussionmentioning

confidence: 99%

A fatal myeloproliferative syndrome in a family with thrombocytopenia and platelet dysfunction

Luddy

Champion

Schwartz

1978

Cancer

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Three siblings with a lifelong history of a bleeding disorder and thrombocytopenia died from a myeloproliferative disease. In 2, the terminal event resembled juvenile chronic myelogenous leukemia, and in the third, the diagnosis was acute monocytic leukemia. A family study revealed that the mother and 5 other siblings had a variety of hematologic abnormalities. These included chronic thrombocytopenia, abnormal platelet function, elevated concentrations of HgbF or serum vitamin B12, and low leukocyte alkaline phosphatase (LAP) scores either singly or in combination. At the time of study, none had evidence of malignancy. Members of this family have a myeloproliferative disorder that has the potential for terminating in nonlymphocytic leukemia, a combination of events which appears not to have been reported previously.

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C-Monosomy myeloproliferative syndrome: A case of 7-monosomy

Cited by 52 publications

References 8 publications

Nonrandom chromosomal abnormalities in hematologic disorders of man.

Nonrandom chromosomal abnormalities in hematologic disorders of man.

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

A fatal myeloproliferative syndrome in a family with thrombocytopenia and platelet dysfunction

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