Establishment and characterization of a megakaryoblast cell line with amplification of MLL

Allen, Robert J.; Smith, Stephen D.; Moldwin, Richard L.; Lu, Mu-Jie; Giordano, Lisa; Vignon, Christine; Suto, Yukio; Harden, Alanna M.; Tomek, Ronald J.; Veldman, Timothy; Ried, Thomas; Larson, Richard A.; Beau, Michelle M. Le; Rowley, Janet D.; Zeleznik‐Le, Nancy J.

doi:10.1038/sj.leu.2401002

Cited by 46 publications

(32 citation statements)

References 30 publications

(30 reference statements)

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“…[9][10][11][12] A brief summary of the 10 previously reported cases of MLL amplification is shown in Table 2. All 10 cases demonstrated amplification of the 11q23 region (including the MLL gene) using FISH probes containing MLL sequences.…”

Section: Discussionmentioning

confidence: 99%

“…7 While the gene most com-monly present in the amplicon is MYC (normally located at 8q24), 8 there have also been reports of amplification of MLL. [9][10][11][12] In a national collaborative study, we collected 12 cases demonstrating MLL amplification based upon FISH studies using the Oncor MLL probe. We compared their karyotypic and clinical features and investigated the integrity of the MLL gene using Southern blot analysis.…”

Section: Introductionmentioning

confidence: 99%

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MLL amplification in acute leukaemia: a United Kingdom Cancer Cytogenetics Group (UKCCG) study

et al. 2000

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The MLL gene, located at 11q23, is frequently rearranged in acute leukaemia as either chimaeric fusion genes or partial tandem duplications. We report a series of 12 acute leukaemia cases with apparent amplification of the MLL gene ascertained using fluorescence in situ hybridisation (FISH). Seven cases showed intrachromosomal amplification of MLL, four cases showed extrachromosomal amplification as double minute chromosomes (dmin) and one case had separate subclones with dmin and homogenously staining region (hsr). Southern blot analysis of the MLL gene showed MLL gene rearrangement in three of the 10 successful cases. These cases do not naturally fall into either of the two recognised categories of MLL rearrangement and may represent a third variety of MLL gene abnormalities.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MLL amplification in acute leukaemia: a United Kingdom Cancer Cytogenetics Group (UKCCG) study

et al. 2000

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“…The megakaryocytic cell line UoC-M1, established from a patient with AML M1, was shown to carry alternating segments of chromosomes 9 and 11 and four copies of the MLL gene against a near-diploid background. 57 Cell line SAML-2, derived from a patient with therapyinduced AML after radiation and chemotherapy for Hodgkin's disease, has two derivative chromosomes involving exchange and duplication of material between chromosomes 8 and 11, with amplification of MYC and MLL. 58 An MLL probe detected multiple signals on a der(5)t(5;11) chromosome and on a der(11) chromosome in cell line 2L1, which was established from a child with treatment-related AML postchemotherapy and radiation for neuroma and rhabdomyosarcoma.…”

Section: Mll Gene Amplificationsmentioning

confidence: 99%

Malignant hematopoietic cell lines: in vitro models for the study of MLL gene alterations

2003

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Human tumor cell lines are powerful tools for investigating basic and applied aspects of cell biology. Leukemia-lymphoma cell lines have been instrumental in the cytogenetic and molecular analysis of recurring chromosome rearrangements, notably translocations and inversions, thus illuminating the pathogenesis of hematological malignancy. Chromosomal translocations targeting the MLL gene at 11q23 have come to represent a paradigm in acute leukemias. These translocations result in the in-frame joining of the MLL gene with a partner gene to generate unique fusion proteins of putatively novel function. More than 30 partner genes that participate with MLL in the more than 60 known 11q23 translocations have been reported. Cell lines provide territory to both explore the detailed structures of 11q23 translocations and investigate the leukemogenic activities of MLL fusion proteins. We review here the leukemia cell lines that have been described to carry 11q23 translocations and MLL fusion genes. Except for the t(10;11)(p12;q23), each of the following relatively frequent 11q23/MLL translocations is represented by one or more cell lines: 16 cell lines with t(4;11)(q21;q23), two cell lines with t(6;11)(q27;q23), seven cell lines with t(9;11)(p22;q23), and eight cell lines with t(11;19)(q23;p13). For each of three rare translocations, one cell line has been reported: t(5;11)(q15;q23), t(11;16)(q23;p13), and t(X;11)(q13;q23). Of these 36 cell lines with 11q23 translocations, 17 have been made available to us; we confirmed the occurrence of the alterations reported in these cell lines at the chromosomal and/ or gene level. A second type of MLL gene alteration is the partial tandem duplication (PTD), which occurs in acute myeloid leukemia (AML). We found four AML cell lines with an MLL PTD; one acute lymphoblastic leukemia-derived cell line was reported to show a partial nontandem duplication. Finally, a third rearrangement involves intrachromosomal amplification of the unrearranged MLL gene leading to multiple copies of the gene and (presumably) increased expression. Three cell lines carrying such MLL amplifications have been described. The availability of these cell lines as model systems provides the opportunity to explore the altered expression or functions of MLL genes and their partners in oncogenesis.

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“…[1][2][3][4][5][6][7][8][9][10] Proliferation in some cytokine-dependent megakaryocytic leukemia cell lines is stimulated by TPO. [11][12][13] Expression of c-mpl is also observed in some megakaryocytic cell lines (eg M-07e and CMK).…”

Section: Introductionmentioning

confidence: 99%

Establishment and characterization of a new human megakaryoblastic cell line (SET-2) that spontaneously matures to megakaryocytes and produces platelet-like particles

et al. 2000

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A new factor-independent megakaryoblastic cell line, designated SET-2, was established from the peripheral blood of a patient with leukemic transformation of essential thrombocythemia (ET). SET-2 expressed CD 4, 7, 13, 33, 34, 36, 38, 41, 61, 71, 117, 126, 130 and c-mpl. In addition, it spontaneously produced numerous platelet-like particles in liquid culture. These particles were shown to be the same size as normal platelets, and to express CD 36, 38, 41, 61 and 71. Proliferation of SET-2 was not influenced by thrombopoietin (TPO) and other hemopoietic cytokines. SET-2 was found to express the platelet-specific proteins such as platelet factor 4 and ␤-thromboglobulin. The levels of expression were not altered by TPO. SET-2 also secreted interleukin-6 into the supernatants, as well as normal megakaryocytes. These results suggest that SET-2 spontaneously matures to megakaryocytes and produces platelet-like particles. These findings indicate that SET-2 may be useful for investigating the proliferation and differentiation mechanisms of leukemia cells and the role of c-mpl on megakaryoblasts, megakaryocytes, and platelets in ET. Leukemia (2000) 14, 142-152.

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Establishment and characterization of a megakaryoblast cell line with amplification of MLL

Cited by 46 publications

References 30 publications

MLL amplification in acute leukaemia: a United Kingdom Cancer Cytogenetics Group (UKCCG) study

MLL amplification in acute leukaemia: a United Kingdom Cancer Cytogenetics Group (UKCCG) study

Malignant hematopoietic cell lines: in vitro models for the study of MLL gene alterations

Establishment and characterization of a new human megakaryoblastic cell line (SET-2) that spontaneously matures to megakaryocytes and produces platelet-like particles

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