Cytogentics of fibroblastic colonies in Ph1-positive chronic myelogenous leukemia

Greenberg, BR; Wilson, Floyd D.; Woo, Linda; Jenks, HM

doi:10.1182/blood.v51.6.1039.bloodjournal5161039

Cited by 16 publications

(8 citation statements)

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“…Cytogenetic findings were in support of the concept that in CMPD marrow fibrosis represents a reactive process with a non-neoplastic nature of the collagen-producing fibroblasts (Maniatis et al, 1969;Van Slyck et al, 1970;Greenberg et al, 1978;Castro-Malaspina et al, 1982). Pleomorphic appearance associated with abnormalities of maturation and bizarre and pyknotic forms (naked nuclei) were particularly conspicuous in megakaryocytes of patients with AMM (Buyssens and Bourgeois, 1977;Burkhardt et al, 1984Burkhardt et al, , 1986Georgii et al, 1984a,b;Frisch and Bartl, 1985;Wolf and Neiman, 1987).…”

Section: Histological Studiessupporting

confidence: 56%

Agnogenic myeloid metaplasia (AMM)—correlation of bone marrow lesions with laboratory data: A longitudinal clinicopathological study on 114 patients

Thiele¹,

Zankovich²,

Steinberg³

et al. 1989

Hematological Oncology

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A clinicopathological study was performed on 114 patients (46 male/68 female, median age 67 years) with the diagnosis of agnogenic myeloid metaplasia (AMM) respectively primary osteo-myelofibrosis which was not preceded by any other or allied subtype of chronic myeloproliferative disorders. On admission patients revealed a striking variability of laboratory data as well as different histopathological features of initial bone marrow biopsies. For this reason discrimination was done into two groups based on bone marrow findings: group I patients (n = 46, 19 male/27 female) showed a hypercellular marrow without or only borderline (n = 24) to slight (n = 22) reticulin fibrosis and group II cases (n = 68, 27 male/41 female) displayed coarse bundles of collagen fibres (n = 18) frequently accompanied by osteosclerosis (n = 50). Statistical analysis of the corresponding initial hematological findings resulted in significant differences. These differences concerned also the complications occurring during the lengthy course of disease, which included a higher incidence of pancytopenia and severe marrow failure with hemorrhage and blast crisis in group II patients. However, overall survival time was not different in both groups. This may be related to the similarity of age distribution (64 resp. 65 years) and its significant association with arteriosclerotic vascular lesions. Consequently acute myocardial infarction and congestive heart failure were frequent causes of death in addition to infections due to marrow failure and blast crisis. Repeated bone marrow biopsies in 24 patients revealed an insidious transition from hypercellular lesions (group I) into advanced fibro-osteosclerotic changes (group II) concurring with laboratory data. Therefore our discrimination into two groups of patients represents variable stages or static histological and corresponding hematologic features in the evolution of a dynamic disease process in AMM.

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Section: Histological Studiessupporting

confidence: 56%

Agnogenic myeloid metaplasia (AMM)—correlation of bone marrow lesions with laboratory data: A longitudinal clinicopathological study on 114 patients

Thiele¹,

Zankovich²,

Steinberg³

et al. 1989

Hematological Oncology

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“…To determine the origin of the bone marrow fibroblasts in man, we studied three bone marrow transplant recipients conditioned with high doses of drugs and 300-1000 rads total body irradiation. 300 rads is in the range of LDww for total body irradiation in man and 1000 rads is clearly a supralethal dose (Hall, 1973). Post-transplant cytogenetic studies showed that these patients were all completely reconstituted with haematopoietic cells of donor origin .…”

Section: W Colde Et A1mentioning

confidence: 95%

Origin of Human Bone Marrow Fibroblasts

et al. 1980

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We investigated the origin of bone marrow fibroblasts in three bone marrow transplant recipients with aplastic anaemia and leukaemia who received grafts from HLA-identical siblings of opposite sex. The patients were conditioned for transplantation with high doses of cytotoxic drugs and 300--1000 rads total body irradiation. After transplantation, bone marrow cells were cultured in T flasks for 3 weeks and the adherent cells were then trypsinized and passaged weekly. After several passages the cells had the typical morphology and growth pattern of fibroblasts. Metaphases from these cells were all of recipient sex type. In contrast, haematopoietic cells and lymphocytes obtained at the same time were of donor sex type. Our findings indicate that the human bone marrow fibroblast is not derived from a precursor common to haemotopoietic cells or lymphocytes. The bone marrow fibroblast appears to be a mesenchymal cell, unrelated to haematopoietic stem cells, which is capable of in vitro proliferation after as much as 1000 rads of total body irradiation.

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“…Origin and development of fibres must be analysed when studying MMS particularly in regard t o their relationship with the neoplastic haematopoiesis, their extent throughout the bone marrow space and finally the suggested time of generation. Evolution of reticulin and collagen fibres is considered to represent a rather nonspecific response (26), since fibroblasts/-cytes d o not take part in the process of malignant transformation (27,28), as was shown by chromosomal (27)(28)(29)(30)(31)(32) and enzymatic studies (33,34). Novel findings point towards a major role of immune complexes in the pathogenesis of marrow fibrosis particularly in agnogenic myeloid metaplasia with accompanying fibrosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Malignant (acute) myelosclerosis ‐ a clinical and pathological study in 6 patients

Thiele

Krech

Vykoupil

et al. 1984

Scandinavian Journal of Haematology

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Clinical and morphological findings are described in 6 patients with malignant (acute) myelosclerosis/fibrosis (MMS). Haematological data are characterized by severe anaemia and thrombocytopenia, frequently accompanied by a leucopenia with an increase in myeloblasts and promyelocytes in the peripheral blood count. There is an absence of, or a minimal hepatosplenomegaly and the survival times after onset of clinical symptoms to death range from 4–12 months. The histopathology of the bone marrow shows a conspicuous proliferation of blasts (myeloblasts, promyelocytes and megakaryoblasts) in a variable amount, besides a fibrosclerosis consisting of reticulin and collagen fibrils. A comparison of MMS with ordinary myelofibrosis/osteomyelosclerosis (MF/OMS) of a chronic course implicates two important facts: (a) evolution of fibrosclerosis takes a considerable period of time for manifestation, which ranges between 20–30 months; (b) the histopathology of MMS is identical with those features observable in the rare event of a terminal stage, i.e. blastic transformation of chronic MF/OMS. Consequently MMS should be designated as an accelerated variant of MF/OMS with a rather early occurrence of a blastic crisis. The insidious onset with the dominant clinical finding of anaemia is probably responsible for the relatively late appearance of symptoms, while the progressive course prevents an overt myeloid metaplasia with a massive hepatosplenomegaly.

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Cytogentics of fibroblastic colonies in Ph1-positive chronic myelogenous leukemia

Cited by 16 publications

References 0 publications

Agnogenic myeloid metaplasia (AMM)—correlation of bone marrow lesions with laboratory data: A longitudinal clinicopathological study on 114 patients

Agnogenic myeloid metaplasia (AMM)—correlation of bone marrow lesions with laboratory data: A longitudinal clinicopathological study on 114 patients

Origin of Human Bone Marrow Fibroblasts

Malignant (acute) myelosclerosis ‐ a clinical and pathological study in 6 patients

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