Characterization of a t(I0; II) (pI3‐I4; qI4‐2I) in the monoblastic cell line U937

Shipley, Janet; Williams, Sarah; O'Byrne, A; Kearney, Lyndal; Jones, Tania; Young, Bryan D.; Dyer, Martin J. S.; Catovsky, Daniel; Sheer, Denise; Gusterson, Barry A.

doi:10.1002/gcc.2870130211

Cited by 9 publications

(11 citation statements)

References 28 publications

(34 reference statements)

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“…However, two YACs that contained BMII (815c7 and 936g7) clearly mapped proximal to the translocation breakpoint. This observation is consistent with the results of Shipley et al (3) who used a phage insert containing the BMII gene for FISH analysis in U937. Fig.…”

Section: Resultssupporting

confidence: 83%

“…Its karyotype is complex and the true identity of many rearrangements has not yet been resolved. We and others have shown by fluorescence in situ hybridization (FISH) that one of these rearrangements is a reciprocal (10;11)(p13;q14) translocation (3,4). We now report that this translocation leads to the fusion of AFIO at 1Opl3 to a novel gene, CALM, at 11q14.…”

mentioning

confidence: 79%

“…The mouse, rat, and the fragments of the bovine ap-3 gene are highly homologous to each other with more than 97% identical amino acids. The human homolog ofap- 3 has not yet been cloned. We considered the possibility that CALM might be the human homolog of ap-3.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, we and others have shown by molecular cytogenetic techniques that the U937 cell line, which was derived from a diffuse histiocytic lymphoma (2), has a t(10;11)(p13;q14) translocation (3,4). This translocation is distinct from the t(10;11)(pll-13;q23) found in acute myeloid leukemia (5) which results in the fusion of the MLL gene at 1 1q23 (6)(7)(8)(9) to the recently clonedAFJO gene at 10p12 (10,11).…”

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confidence: 99%

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The t(10;11)(p13;q14) in the U937 cell line results in the fusion of the AF10 gene and CALM, encoding a new member of the AP-3 clathrin assembly protein family.

Dreyling

Martínez-Climent

Zheng

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

285

290

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The translocation t(10;11)(p13;q14) is a recurring chromosomal abnormality that has been observed in patients with acute lymphoblastic leukemia as well as acute myeloid leukemia. We have recently reported that the monocytic cell line U937 has a t(10;11)(pl3;ql4) translocation. Using a combination of positional cloning and candidate gene approach, we cloned the breakpoint and were able to show that AF1O is fused to a novel gene that we named CALM (Clathrin Assembly Lymphoid Myeloid leukemia gene) located at 11ql4. AFIO, a putative transcription factor, had recently been cloned as one of the fusion partners of MLL. CALM has a very high homology in its N-terminal third to the murine ap-3 gene which is one of the clathrin assembly proteins. The N-terminal region of ap-3 has been shown to bind to clathrin and to have a high-affinity binding site for phosphoinositols. The identification of the CALM/AFIO fusion gene in the widely used U937 cell line will contribute to our understanding of the malignant phenotype of this line.

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Section: Resultssupporting

confidence: 83%

mentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

The t(10;11)(p13;q14) in the U937 cell line results in the fusion of the AF10 gene and CALM, encoding a new member of the AP-3 clathrin assembly protein family.

Dreyling

Martínez-Climent

Zheng

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

285

290

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“…9 The presence of a reciprocal translocation between chromosomes 10 and 11, a t(10;11)(p13-14; q14-21) in the U937 cell line was confirmed and subsequently refined by cytogenetic analysis. 10,11 Using positional cloning techniques to narrow the chromosome 10 breakpoint to a 3 cM region, AF10 was identified as a candidate gene on chromosome 10 potentially involved in this translocation. Subsequent studies showed that the AF10 gene was indeed disrupted by the t(10;11) translocation, and identified CALM as the AF10 fusion partner in this recurrent translocation.…”

Section: Introductionmentioning

confidence: 99%

The role of CALM–AF10 gene fusion in acute leukemia

Caudell

Aplan

2007

Leukemia

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Chromosomal translocations are important genetic perturbations frequently associated with hematologic malignancies; characterization of these events has been a rich source of insights into the mechanisms that lead to malignant transformation. The t(10;11)(p13;q14-21) results in a recently identified rare but recurring chromosomal translocation seen in patients with ALL as well as AML, and results in the production of a CALM-AF10 fusion gene. Although the details by which the CALM-AF10 fusion protein exerts its leukemogenic effect remain unclear, emerging data suggests that the CALM-AF10 fusion impairs differentiation of hematopoietic cells, at least in part via an upregulation of HOXA cluster genes. This review discusses the normal structure and function of CALM and AF10, describes the spectrum of clinical findings seen in patients with CALM-AF10 fusions, summarizes recently published CALM-AF10 mouse models and highlights the role of HOXA cluster gene activation in CALM-AF10 leukemia.

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Hematologic malignancies with the t(10;11)(p13;q21) have the same molecular event and a variety of morphologic or immunologic phenotypes

Kobayashi

Hosoda²,

Maseki

et al. 1997

Genes Chromosom. Cancer

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Previous studies described the t(10;11)(p13‐14;q14‐21) as a recurring translocation associated with T‐cell acute lymphoblastic leukemia (ALL). This translocation has also been reported in monocytic leukemia or ALL with a very early pre‐B phenotype. However, whether these cytogenetically similar translocations involve the same molecular breakpoint is unknown. Using fluorescence in situ hybridization (FISH) with a series of probes on 11q, we mapped the 11q breakpoint of the U937 cell line, which was derived from a patient with diffuse histiocytic lymphoma and was shown by FISH to have the t(10;11)(p13‐14;q14‐21). Subsequently, we identified a yeast artificial chromosome (YAC) clone, y960g8, that included the breakpoint on 11q. From this YAC, we isolated a P1 clone, P91B1, that was split by the 10;11 translocation. We studied four patients with a t(10;11), one of whom had acute monocytic leukemia (AMoL), one had acute lymphoblastic leukemia (ALL), one had lymphoblastic lymphoma (LBL), and one had granulocytic sarcoma, by using FISH with y960g8 and P91B1. Y960g8 and P91B1 were split by the translocation in each patient. We showed that P91B1 included a recently identified gene, CALM (Clathrin Assembly Lymphoid Myeloid leukemia gene), and that AF10 was also rearranged in each patient by FISH when we used y807b3, which contains the AF10 gene. These findings indicate that hematologic malignant diseases with fusion of AF10 and CALM show various morphologic and immunologic phenotypes, suggesting that this fusion occurs in multipotential or very early precursor cells. Genes Chromosomes Cancer 20:253–259, 1997. © 1997 Wiley‐Liss, Inc.

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Characterization of a t(I0; II) (pI3‐I4; qI4‐2I) in the monoblastic cell line U937

Cited by 9 publications

References 28 publications

The t(10;11)(p13;q14) in the U937 cell line results in the fusion of the AF10 gene and CALM, encoding a new member of the AP-3 clathrin assembly protein family.

The t(10;11)(p13;q14) in the U937 cell line results in the fusion of the AF10 gene and CALM, encoding a new member of the AP-3 clathrin assembly protein family.

The role of CALM–AF10 gene fusion in acute leukemia

Hematologic malignancies with the t(10;11)(p13;q21) have the same molecular event and a variety of morphologic or immunologic phenotypes

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