Monosomy 7 and multipotential stem cell transformation

Li, Chan; Sheer, Denise; Drysdale, H. C.; Bevan, David; Greaves, Melvyn F.

doi:10.1111/j.1365-2141.1985.tb02858.x

Cited by 38 publications

(7 citation statements)

References 28 publications

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“…The genetic data raise the possibility that Knudson's 2-hit model of tumorigenesis [Knudson, 19861 may be the pathogenetic mechanism underlying MLSM7. Such an explanation has been postulated by others in MLSM7 [Chan et al, 1985;Carroll et al, 1985;Look et al, 19881. However, a prediction of the allelic 2-hit model is that the remaining chromosome 7 carrying the abnormal allele should be demonstrably the same in the bone marrow of sibs with monosomy 7 due to MLSM7. This has recently been shown not to be so by DNA marker analysis in 2 of 3 affected sib pairs [Shannon et al, 19891. The geneis) responsible for the genetic predisposition to MLSM7 seems not to be located on chromosome 7, or at least not exclusively so.…”

Section: Genetics Of Mlsm7supporting

confidence: 55%

Myelodysplasia and leukemia syndrome with monosomy 7: A genetic perspective

Gilchrist

Friedman²,

Rogers

et al. 1990

Am. J. Med. Genet.

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Acquired monosomy 7 is a frequent finding in myelodysplastic syndromes, including acute myelogenous leukemia. A subset of these patients has been described with an apparently distinct condition: myelodysplasia and leukemia syndrome with monosomy 7 (MLSM7). We report 2 brothers, 3 and 5 years of age, with MLSM7 and review other reports of familial occurrence. Genetic factors appear to be important in the cause of MLSM7, but the reported families do not fit neatly into any monogenic pattern. Recognition of the frequently familial nature of this condition requires hematological evaluation and genetic counseling for the families of patients with MLSM7.

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Section: Genetics Of Mlsm7supporting

confidence: 55%

Myelodysplasia and leukemia syndrome with monosomy 7: A genetic perspective

Gilchrist

Friedman²,

Rogers

et al. 1990

Am. J. Med. Genet.

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“…In addition, with decreases in basophils and eosinophils, the clone with monosomy 7 disappeared. It has been speculated that monosomy 7 represents abnormalities at the stem cell level [11,12]. In this patient, basophils and eosinophils seemed to have been derived from the same clone at the stem cell level.…”

Section: Discussionmentioning

confidence: 94%

A Patient with Basophilic-Eosinophilic Myeloproliferative Disorder Showing Monosomy 7 and Hyperhistaminemia

Takimoto¹,

Imanaka²,

Hayashi

et al. 1997

Acta Haematol

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We encountered a male patient with marked basophilia and eosinophilia complicated by anemia, thrombocytopenia, myelofibrosis, and hyperhistaminemia. Since morphological abnormalities were unclear and since chromosome analysis showed 45, XY,-7, a diagnosis of basophilic-eosinophilic myeloproliferative disorder was made. After administration of prednisolone and cytarabine ocfosfate, basophil and eosinophil levels decreased, but blasts transiently appeared in the peripheral blood. Chromosome analysis performed at the time of appearance of blasts showed a clone with 45, XY,-7, del(16)(q22). Subsequently, pancytopenia developed, after which white blood cell count and its classification were normal, as were chromosome findings. In this patient, monosomy 7 seemed to have induced myeloproliferative disorder with basophilia and eosinophilia, and del(16)(q22) may have enhanced the eosinophilia.

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“…There have also been two reports of mixed leukaemia (Chan et a/. 1985, Sanz et al 1986), and two of ALL (Chan et al 1985, Stricker eta/. 1983.…”

Section: Discussionmentioning

confidence: 99%

“…One patient had a history of radiation exposure to the Hiroshima bomb (Stricker & Linker 1983). The other presented as a spontaneous common ALL, but there was a myeloid phenotype at relapse (Chan et al 1985). Both survived less than 6 months despite intensive chemotherapy.…”

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confidence: 99%

Monosomy 7, leukaemia and immunoglobulin heavy chain gene rearrangement

Barnett

Wodzinski²,

Watmore³

1990

Clinical &Amp; Laboratory Haematology

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We describe the haematological findings and clinical course of. a IS-year-old male who presented with a spontaneous acute lymphoblastic leukaemia. The lymphoid origin of the leukaemia was supported by cell surface antigen studies and immunoglobulin heavy chain gene analysis. Bone marrow karyotype was simple monosomy 7 and the lymphoblasts expressing the myeloid associated antigen CD 33. Both of these features have been previously shown to indicate a poor prognosis. The findings in this patient support a previous hypothesis that monosomy 7 can arise at the stem cell level.

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Monosomy 7 and multipotential stem cell transformation

Cited by 38 publications

References 28 publications

Myelodysplasia and leukemia syndrome with monosomy 7: A genetic perspective

Myelodysplasia and leukemia syndrome with monosomy 7: A genetic perspective

A Patient with Basophilic-Eosinophilic Myeloproliferative Disorder Showing Monosomy 7 and Hyperhistaminemia

Monosomy 7, leukaemia and immunoglobulin heavy chain gene rearrangement

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