Onze observations d'un modèle précis d'évolution caryotypique au cours de la leucémie myéloïde chronique

Grouchy, J. de; Nava, C. De; Feingold, J; Bilski-Pasquier, G; Bousser, J

doi:10.1016/0014-2964(68)90004-2

Cited by 39 publications

(8 citation statements)

References 7 publications

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“…16 may replace one normal member of the group 17,18. This anomaly, which seems likely to be an isochromosome for the long arm of a 17,18 chromosome, has been observedinHodgkin's tissue (Ricci et al, 1962), reticulum cell sarcoma (Sasaki, Sofuni and Makino, 1965), in peripheral blood culture in chronic lymphocytic leukaemia (Fitzgerald and Adams, 1965), and in no less than 13 cases of chronic granulocytic leukaemia at the stage of metamorphosis (Engel et al, 1965;Stich et al, 1966;Engel, McKee and Bunting, 1967;de Grouchy et al, 1968). The anomaly has also been described in myelosclerosis after transformation to acute granulocytic leukaemia (Nowell and Hungerford, 1962), and in a myeloproliferative disorder characterized by anaemia, thrombocytopenia, and maturation arrest in the bone marrow (Engel McKee and Bunting, 1967).…”

Section: Experimental Evidencementioning

confidence: 83%

“…17 chromosome is a secondary phenomenon but relevant to the further evolution of the neoplasm. Thus, in the early stages of the disease, the Ph' chromosome is the only anomaly present, whilst after the occurrence of metamorphosis to a more anaplastic neoplasm, the isochromosome 17 is observed in a surprisingly high proportion of cases (de Grouchy et al, 1968). When a lymphoma cell apparently loses one No.…”

Section: Discussionmentioning

confidence: 99%

“…1), are quite often the dominant line in the tumours in which they occur (Spiers and Baikie, 1968a, b). Structural modifications also may confer a growth Authors Ricci et al, 1962Sasaki et al, 1965Spiers and Baikie, 1968Fitzgerald and Adams, 1965de Grouchy et al, 1968Engel et al, 1967Stich et al, 1966Nowell and Hungerford, 1962Engel et al, 1967Spiers and Baikie, 1968Spiers and Baikie, 1968Millard, 1968Kajii et al, 1968Miles et al, 1966Seif and Spriggs, 1967Spiers and Baikie, 1968Millard, 1968 Fig. 1), or by a long-arm isochromosome (B in Fig.…”

Section: Discussionmentioning

confidence: 99%

“…1) Consistent loss of a 17,18 chromosome from the tumour cells has been reported in 5 cases of Hodgkin's disease (Miles, Geller and O'Neill, 1966;Sinks and Clein, 1966), 3 cases of reticulum cell sarcoma (Spiers and Baikie, 1968a;Miles, Geller and O'Neill, 1966;Lawler, Pentycross and Reeves, 1968), and a case of lymphosarcoma (Spiers and Baikie, 1968a). A 17,18 monosomy has been described in at least 7 cases of chronic granulocytic leukaemia after metamorphosis (Court Brown and Tough, 1963;Pedersen, 1964;de Grouchy et al, 1966;Spiers and Baikie, 1968b). Pedersen (1967) finds that in chronic granulocytic leukaemia, Ph'-positive cells with monosomy in the group 17,18 occur more commonly in patients who have recently received treatment for their disease.…”

Section: Experimental Evidencementioning

confidence: 99%

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A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Spiers¹,

Baikie²

1970

Br J Cancer

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The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph 1 anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph 1 in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes. Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines.

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Section: Experimental Evidencementioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Experimental Evidencementioning

confidence: 99%

See 2 more Smart Citations

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Spiers¹,

Baikie²

1970

Br J Cancer

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“…This aberration has been described in some other cases of chronic granulocytic leukaemia, both in the chronic phase of the disease (Goh, Swisher and Troup, 1964) and after the occurrence of acute transformation (Levan, Nichols and Norden, 1963;Pedersen, 1964;de Grouchy et al, 1966;Duvall et al 1967 21,22 termed Philadelphia chromosomes, which may in fact display a very special liability to mitotic nondisjunction (Pedersen, 1967b). The new cell lines differ from those observed in acute leukaemia principally in their possession of the Ph1.…”

mentioning

confidence: 86%

Cytogenetic evolution and clonal proliferation in acute transformation of chronic granulocytic leukaemia

Spiers¹,

Baikie²

1968

Br J Cancer

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AMONGST the more important results of chromosome studies in human leukaemias is the occasional demonstration of increasing genetic variation as evidenced by the appearance of a range of cell lines of differing chromosomal constitution. The finding of a variety of cell lines which are not obviously related is common in cases of acute leukaemia and in chronic granulocytic leukaemia at the stage of acute transformation. Only rarely has it been possible by serial study to trace the development of increasing genetic variation and still more rarely to propose any scheme for the interrelationship of the various cell lines. Outstanding exceptions include a case of acute leukaemia studied by Ford and Clarke (1963), a case of chronic granulocytic leukaemia in acute transformation reported by Court Brown and Tough (1963), and a series of cases with chronic granulocytic leukaemia described by de Grouchy and his colleagues (1966).The importance of cases in which the cell lineage can be deduced is that these successive alterations of karyotype may indicate cytogenetic steps essential to the development of increasing malignancy and cellular autonomy. If a pattern can be discerned in these successive changes, it will have implications important for the study of neoplastic disease in general. We have recently studied two cases of chronic granulocytic leukaemia at the stage of acute transformation in which some possible relationships between a range of cell lines may be deduced. CASE REPORTSCase 1 A man, aged 46, presented with clinical and haematological features typical of chronic granulocytic leukaemia. Initial treatment by splenic irradiation was followed by a satisfactory remission which was, however, short-lived. The response to treatment with busulphan was unsatisfactory. Further splenic irradiation led to an incomplete and transient remission, and a second course of busulphan was without beneficial effect. At that time he had severe constitutional symptoms with rapidly progressive splenomegaly and increasing numbers of blast cells and basophils in the peripheral blood. Acute transformation of chronic granulocytic leukaemia was diagnosed 8 months after his initial presentation in the chronic phase of the disease. Treatment with 6-mercaptopurine was followed by a rapid fall in white cell count accompanied by some clinical improvement without

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Chromosomes and causation of human cancer and leukemia.VI. Blastic phase, cellular origin, and the Ph1 in CML

Sandberg

Hossfeld

Ezdinli

et al. 1971

Cancer

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The cytogenetic, histologic, and pertinent clinical data on 107 cases of CML from our laboratory and those from the literature on the incidence of Ph1‐negative cells in marrows of patients with Ph1‐positive CML have been collected and summarized. In addition, the distribution of multiple Ph1‐chromosomes in 5 cases of CML, with and without the blastic phase, has been described and discussed. The findings served as a basis for caution in utilizing the high incidence of Ph1‐positive cells in the marrows of the preponderant number of patients with CML as support for the unicellular stem cell origin of such cells. The occurrence of Ph1‐negative cells in significant percentages in some patients with chronic myelocytic leukemia indicates that several other hypotheses, including a multi‐stem cell origin of marrow cells, are compatible with the observations in CML.

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Onze observations d'un modèle précis d'évolution caryotypique au cours de la leucémie myéloïde chronique

Cited by 39 publications

References 7 publications

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

A Special Role of the Group 17,18 Chromosomes in Reticuloendothelial Neoplasia

Cytogenetic evolution and clonal proliferation in acute transformation of chronic granulocytic leukaemia

Chromosomes and causation of human cancer and leukemia.VI. Blastic phase, cellular origin, and the Ph1 in CML

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