Erythroid and granulocyte‐macrophage colony formation in myelodysplastic syndromes

Ruutu, Tapani; Partanen, Seppo; Lintula, R.; Teerenhovi, Lasse; Knuutila, Sakari

doi:10.1111/j.1600-0609.1984.tb00695.x

Cited by 72 publications

(8 citation statements)

References 25 publications

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“…A similar correlation between the growth pattern and FAB class was seen in the granulocytemacrophage lineage in the present study as well as in our previous study (1). Normal granulocytemacrophage colony formation was mainly seen in patients with RA or RARS, with few exceptions.…”

Section: Discussionsupporting

confidence: 91%

“…No correlation between any specific karyotype abnormality and the megakaryocyte growth pattern was found. Normal granulocyte-macrophage colony formation together with diminished erythroid growth has been previously reported in many patients with 5q-chromosome (1,14).…”

Section: Discussionmentioning

confidence: 72%

“…One manifestation of the disturbed bone marrow function is the abnormal behaviour of haematopoietic progenitor cells in in vitro cultures. In some patients with MDS the formation of colonies and clusters by granulocyte-macrophage progenitors is defective and similar to the growth pattern seen in patients with acute myeloid leukaemia, while some of the patients show normal granulocyte-macrophage colony growth (1)(2)(3). Erythroid colony formation has been shown to be markedly decreased in a great majority of patients ( 1 , 2, 4).…”

mentioning

confidence: 71%

“…This correlation has not, however, been clearly evident in all studies (2,3). Erythroid colony formation has been defective in a great majority of patients and no study has demonstrated any clear correlation between the colony growth and morphological subtype (1,2,4).…”

Section: Discussionmentioning

confidence: 94%

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Colony formation by megakaryocyte progenitors in myelodysplatic syndromes

Juvonen

Partanen

Knuutila

et al. 1989

European J of Haematology

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In vitro megakaryocytic colony formation by progenitors from the bone marrow was studied in 40 myelodysplastic syndrome patients. Megakaryocytic colonies were decreased in number or absent in 30 patients; only 10 showed normal colony growth. The growth correlated to some extent with the FAB‐class. Patients with normal colony formation had either RA or RARS, but also in these two FAB‐types half of the patients showed reduced megakaryocytic colony formation. Only 1 out of 15 patients with RAEB or RAEBt had normal megakaryocyte growth. The patients with CMML did not show any megakaryocytic colonies. The growth of erythroid colonies was normal in 3 patients and reduced or absent in the others. All 3 with normal erythroid colony formation also showed normal megakaryocyte growth, and all patients with normal megakaryocyte colony formation also had normal granulocyte‐macrophage colony growth. Granulocyte‐macrophage colony and cluster formation was normal in 17 patients. Defective formation of megakaryocytic, erythroid, and granulocyte‐macrophage colonies was seen in 22 patients, compatible with a defect in a pluripotent stem cell. Megakaryocytic colony formation had no obvious correlation with any specific chromosome abnormality, and the distribution of the growth patterns was almost similar in patients with a normal and those with an abnormal karyotype.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 72%

mentioning

confidence: 71%

Section: Discussionmentioning

confidence: 94%

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Colony formation by megakaryocyte progenitors in myelodysplatic syndromes

Juvonen

Partanen

Knuutila

et al. 1989

European J of Haematology

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“…In addition to increased cell death or apoptosis, failure of differentiation contributes to the lack of terminally differentiated blood cells in patients with MDS (6). In vitro colony assays demonstrate abnormal colony formation by granulocyte-macrophage (CFU-GM), erythroid (BFU-E, CFU-E) and megakaryocyte (CFU-Meg) progenitors in many patients with MDS (7-9). …”

Section: Introductionmentioning

confidence: 99%

Impaired differentiation and apoptosis of hematopoietic precursors in a mouse model of myelodysplastic syndrome

Choi¹,

Chung²,

Slape³

et al. 2008

Haematologica

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Expression of a NUP98-HOXD13 (NHD13) fusion gene, initially identified in a patient with myelodysplastic syndrome, leads to a highly penetrant myelodysplastic syndrome in mice that recapitulates all of the key features of the human disease. Expansion of undifferentiated lineage negative (lin neg ) hematopoietic precursors that express NHD13 was markedly inhibited (30-fold) in vitro. Decreased expansion was accompanied by decreased production of terminally differentiated cells, indicating impaired differentiation of NHD13 precursors. Rather than differentiate, the majority (80%) of NHD13 lin neg precursors underwent apoptotic cell death when induced to differentiate. These findings demonstrate that NHD13 lin neg cells provide a tractable in vitro system for studies of myelodysplastic syndrome.

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Interstitial deletion of chromosome 5, del(5q), in a newborn with down syndrome and an unusual hematologic disorder

Adams¹,

Lemons²,

Thangavelu³

et al. 1989

American J Hematol

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A newborn with Down syndrome was noted on the 1st day of life to have an elevated white blood cell count of 79,900/mm3 with 62% lymphoblasts and a platelet count of 61,000/mm3, consistent with either transient myeloproliferative disorder of Down syndrome (TMD) or acute leukemia. Karyotype analysis of a bone marrow aspirate revealed that 20% of the cells had a 47,XY, +21 karyotype, and 80% had a 47,XY, +21, del(5)(q13q31) complement. Cytochemical and immunophenotyping of the peripheral blasts were consistent with the presence of an acute undifferentiated precursor blast clone. Results of clonogenic assays of hematopoietic progenitors from this patient's bone marrow were similar to those of patients with TMD. This patient's hematologic abnormalities resolved spontaneously without treatment by week 10 of life. This is the first report of an interstitial deletion of 5q associated with a hematologic abnormality present in an infant at birth.

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Erythroid and granulocyte‐macrophage colony formation in myelodysplastic syndromes

Cited by 72 publications

References 25 publications

Colony formation by megakaryocyte progenitors in myelodysplatic syndromes

Colony formation by megakaryocyte progenitors in myelodysplatic syndromes

Impaired differentiation and apoptosis of hematopoietic precursors in a mouse model of myelodysplastic syndrome

Interstitial deletion of chromosome 5, del(5q), in a newborn with down syndrome and an unusual hematologic disorder

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