Del cell line: A “malignant histiocytosis” CD30 + T(5;6)(Q35;P21) cell line

Barbey, S; Gogusev, Jean; Mouly, Hélène; Pelletier, Odile Le; Smith, W J; Richard, Stéphane; Soulie, Joëlle; Nézelof, C

doi:10.1002/ijc.2910450329

Cited by 18 publications

(11 citation statements)

References 42 publications

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“…A few ALCL cell lines have been established so far from ALCL or 'malignant histiocytosis', most of them being ALK þ . [24][25][26][27][28][29][30] Only the FE-PD cell line has been reported as an ALK-negative ALCL cell line. 31 The first cell line reported in the literature was the SU-DHL-1 cell line, established from a pleural effusion of a patient, 24 who presented with a 'diffuse histiocytic lymphoma', but was subsequently reclassified as ALCL according to the REAL classification.…”

Section: Discussionmentioning

confidence: 99%

“…25 However, the morphological features of the tumors from which the other cell lines are derived have not always been specified, and on occasion are referred to as 'malignant histiocytosis'. [26][27][28]32 Regarding the phenotype of these cell lines, they all express classical activation markers such as CD30, CD25, CD71 and HLA-DR, but their lymphoid lineage is not always clear, with some of them expressing B-or T-cell markers, both T-and B-lineage markers or none. Our cell line could be considered to be of null phenotype since it does not express specific T-cell specific antigens.…”

Section: Discussionmentioning

confidence: 99%

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Establishment of a novel anaplastic large-cell lymphoma-cell line (COST) from a ‘small-cell variant’ of ALCL

et al. 2004

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Anaplastic large-cell lymphoma (ALCL) is a distinct biological and cytogenetic entity with a broad spectrum of morphological features (common type, small-cell variant and lymphohistiocytic variant). Few cell lines of ALCL are available and they all originate from primary tumors demonstrating the common type morphology (ie large-sized lymphoma cells). We established a new ALCL cell line (COST) from the peripheral blood of a patient with a small-cell variant of ALCL, at diagnosis. Cells growing in vitro and in SCID mice consisted of two populations, that is, small-and large-sized cells as seen in the patient's tumor. Both large and small malignant cells were positive for CD43/MT1 T-cell associated antigen, perforin, granzyme B and TIA-1, but negative for CD2, CD3, CD5, CD7, CD4 and CD8 antigens. Standard cytogenetic studies as well as multiplex FISH confirmed the presence of the canonical t(2;5)(p23;q35) translocation, but also revealed additional numerical and structural abnormalities. The COST cell line is the first ALCL small-cell variant cell line, and thus provides a potentially useful tool for further functional and molecular studies that should improve our understanding of the small-cell variant of ALCL, which is more frequently complicated by a leukemic phase.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Establishment of a novel anaplastic large-cell lymphoma-cell line (COST) from a ‘small-cell variant’ of ALCL

et al. 2004

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“…However, only a small number of such human cell lines currently exist (Barbey et al, 1990;Dirks et al 1996;Drexler and Minowada, 1992;Drexler, 1993). Only four in vivo models of ALCL have been reported so far (Kinney et al, 1993;Kuefer et al, 1997;Pasqualucci et al, 1995;Terenzi et al, 1996).…”

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confidence: 99%

An Animal Model for Anaplastic Large Cell Lymphoma in the Immunocompetent Syngeneic C57Bl/6 Mouse

Bittner

Feller

Renauld

et al. 2000

Laboratory Investigation

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SUMMARY:We report on the analysis of a murine anaplastic lymphoid cell line TS1G6, established recently by interleukin (IL)-9 transfection. TS1G6 revealed a highly characteristic pattern of large anaplastic cells with mononuclear, binuclear, or multinuclear cells resembling Hodgkin (H) or Sternberg-Reed (SR) cells. This cell line is tumorigenous after injection of as few as 10 4 lymphoma cells into nude or immunocompetent C57Bl/6 mice and leads to death from progressive disease of all treated animals within a few weeks. The histological analysis of these tumors revealed a diffuse large cell malignant lymphoma that is morphologically almost identical to human anaplastic large cell lymphoma (ALCL). The lymphoma cells did not show overexpression of the anaplastic lymphoma kinase (ALK) gene, which is found in about 50% of the cases of human ALCL. Thus, this model may be an animal model for an important subset of human ALCL. The cytokine profile, which is of the T helper 2 type, showed strong parallels to the human lymphoma counterpart. Mice suffering from such lymphomas could not be cured with a regimen using high dose cyclophosphamide similar to many ALCL patients. Such an animal model for ALCL has not yet been recognized, but may provide the basis for investigating new antitumor immunotherapies in a fully immunocompetent host . (Lab Invest 2000, 80:1523-1531.

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“…The cell origin of ALCL remains unsettled because of similar frequency of either T-cell [5,8,9,11] or null-cell mide, vincristine, prednisone, doxorubicin) was the most commonly used (1 5 out of 19). In more recent cases, the duration of systemic therapy was shortened and the intensity increased, but strategy did not change whatever the initial diagnosis was (MH or ALCL).…”

Section: Nosology Pathology and Lmmunophenotypementioning

confidence: 91%

Childhood anaplastic large cell lymphoma Ki‐1/CD30: Clinicopathologic features of 19 cases

Rubie¹,

Gladieff²,

Robert³

et al. 1994

Med. Pediatr. Oncol.

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The authors report their cumulative experience of 19 children with what was previously called malignant histiocytosis (MH) but is now considered a true lymphoma and termed anaplastic large cell lymphoma (ALCL). The median age at diagnosis was 10 years and 6 months (range 2 y, 11 m, to 15 y). There were 13 males and 6 females. Most cases presented with fever, wasting and enlarged, often tender, lymph nodes. Other features were: fleeting cutaneous rashes in 7 cases; spontaneous regression of lymph nodes and skin lesions were seen in 5 patients. Bone marrow involvement was present in 3 cases, pulmonary infiltrate in 5, kidneys in 2, and central nervous system in none. The morphology of lymph node involvement was consistent with so-called MH, a description originally applied to sinusoïdal infiltration by large "histiocytic" cells. The coexpression of lymphoid activation antigens Ki-1/CD 30 (18/19), epithelial membrane antigen EMA (18/19) and interleukin-2 receptor/CD 25 (10/10) was the unifying immunopathologic feature of the neoplasm. Lineage antigens were not identifiable in 8/19 instances (null phenotype), while 10/19 expressed a T-cell phenotype. None of the tumors expressed histiocytic markers. After variable, but intensive, combination chemotherapy, 15 children out of 18 evaluable achieved complete remission (CR). Among all patients, thirteen are still alive in CR (ten in first CR) with a median follow-up of 5 years. This evaluation in the pediatric age group reinforces that so-called MH is a lymphoid neoplasm, a conceptual change that could lead to improved understanding and therapy.

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Del cell line: A “malignant histiocytosis” CD30 + T(5;6)(Q35;P21) cell line

Cited by 18 publications

References 42 publications

Establishment of a novel anaplastic large-cell lymphoma-cell line (COST) from a ‘small-cell variant’ of ALCL

Establishment of a novel anaplastic large-cell lymphoma-cell line (COST) from a ‘small-cell variant’ of ALCL

An Animal Model for Anaplastic Large Cell Lymphoma in the Immunocompetent Syngeneic C57Bl/6 Mouse

Childhood anaplastic large cell lymphoma Ki‐1/CD30: Clinicopathologic features of 19 cases

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