The use of fluorescent in situ hybridization for detection of the t(2;5)(p23;q35) translocation in anaplastic large-cell lymphoma

Johnson, Peter; Leek, J.P.; Swinbank, K.; Angus, Brian; Roberts, Patrick; Markham, AF; Selby, Peter J.; MacLennan, KA

doi:10.1093/annonc/8.suppl_2.s65

Cited by 12 publications

(7 citation statements)

References 26 publications

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“…Our results suggest that in the particular cases of Burkitt lymphoma and lymphoblastic lymphoma, tumor touch imprints and cell preparations of easily accessible malignant effusions such as ascites and pleural fluids appear to provide an excellent reservoir of cells for cytomorphologic analyses. Together with flow cytometric immunophenotyping and FISH analyses on cells from the lymphomatous body fluids or cell suspensions from solid biopsy material the established diagnoses were sufficiently safe and rapidly available for an early start of treatment [15][16][17][18].…”

Section: Discussionmentioning

confidence: 99%

EARLY AND RELIABLE DIAGNOSIS OF NON-HODGKIN LYMPHOMA in CHILDHOOD AND ADOLESCENCE: Contribution of Cytomorphology and Flow Cytometric Immunophenotyping

Mann

Attarbaschi

Steiner

et al. 2006

Pediatric Hematology and Oncology

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Non-Hodgkin lymphoma (NHL) represents one of the most rapidly growing malignancies in childhood and adolescence. About 80% of patients now are cured with adequate treatment. Serious complications at presentation due to tumor lysis syndrome or local tumor effects are commonly observed. Thus, a rapid diagnosis with the least invasive procedure enabling the initiation of early and specific therapy is necessary to diminish early fatality or persistent impairment. In 56 centrally registered patients with NHL, cytomorphologic analyses (FAB criteria) of May-Grünwald-Giemsa-stained touch imprints or malignant effusions and flow cytometric immunophenotyping (EGIL criteria) of fresh cell suspensions with a standardized panel of monoclonal antibodies were performed. The authors identified 23 patients with Burkitt lymphoma by the combination of FAB L3 morphology and a mature B-cell phenotype and 22 patients with lymphoblastic lymphoma by FAB L1/L2 morphology and a T-/B-cell precursor phenotype. They also found 11 patients with large cell lymphomas, 3 of them with anaplastic large cell lymphoma (T-cell phenotype; NPM/ALK-positive). In the remaining 8 patients diffuse large B-cell lymphoma was suspected by the combined use of cytologic and immunophenotypic findings (mature B-cell phenotype). In all cases with available solid tumor material (n = 42/56) the preliminary diagnosis was confirmed by histopathology. Burkitt lymphoma, lymphoblastic lymphoma, and, in a few cases, some large cell lymphomas could be classified reliably by cytomorphology and immunophenotyping of freshly obtained tumor cell material, enabling an early start of specific lymphoma treatment.

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Section: Discussionmentioning

confidence: 99%

EARLY AND RELIABLE DIAGNOSIS OF NON-HODGKIN LYMPHOMA in CHILDHOOD AND ADOLESCENCE: Contribution of Cytomorphology and Flow Cytometric Immunophenotyping

Mann

Attarbaschi

Steiner

et al. 2006

Pediatric Hematology and Oncology

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“…The cloning of the NPM-ALK fusion generated by the t(2;5)(p23;q35) chromosomal rearrangement has permitted the facile diagnosis of NPM-ALKexpressing ALCLs using methodologies such as fluorescence in-situ hybridisation (FISH) and reverse transcriptase chain reaction (RT-PCR). [144][145][146][147][148][149][150] In addition, given that normal hematopoietic cells do not express detectable levels of the normal, full-length ALK protein, the development of ALK-specific antibodies has further revolutionized the diagnosis of ALCL (due to the anaplastic, often bizarre and heterogeneous morphology of ALCLs, these lymphomas had formerly often been quite difficult for pathologists to make an unequivocal diagnosis). Using immunostaining methods, 60-80% of ALCLs have been found to be ALK-positive.…”

Section: B Alk Fusion Protein Expression In Hematopoietic Tumorsmentioning

confidence: 99%

Development of anaplastic lymphoma kinase (ALK) small‐molecule inhibitors for cancer therapy

Morris

2007

Medicinal Research Reviews

119

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Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) involved in the genesis of several human cancers; indeed, ALK was initially identified in constitutively activated and oncogenic fusion forms--the most common being nucleophosmin (NPM)-ALK--in a non-Hodgkin's lymphoma (NHL) known as anaplastic large-cell lymphoma (ALCL) and subsequent studies identified ALK fusions in the human sarcomas called inflammatory myofibroblastic tumors (IMTs). In addition, two recent reports have suggested that the ALK fusion, TPM4-ALK, may be involved in the genesis of a subset of esophageal squamous cell carcinomas. While the cause-effect relationship between ALK fusions and malignancies such as ALCL and IMT is very well established, more circumstantial links implicate the involvement of the full-length, normal ALK receptor in the genesis of additional malignancies including glioblastoma, neuroblastoma, breast cancer, and others; in these instances, ALK is believed to foster tumorigenesis following activation by autocrine and/or paracrine growth loops involving the reported ALK ligands, pleiotrophin (PTN) and midkine (MK). There are no currently available ALK small-molecule inhibitors approved for clinical cancer therapy; however, recognition of the variety of malignancies in which ALK may play a causative role has recently begun to prompt developmental efforts in this area. This review provides a succinct summary of normal ALK biology, the confirmed and putative roles of ALK fusions and the full-length ALK receptor in the development of human cancers, and efforts to target ALK using small-molecule kinase inhibitors.

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“…The identification of the genes involved in the t(2;5) as those encoding ALK and NPM has meant that rapid progress has been possible in the study of ALCL using molecular biological methodologies, such as fluorescence in‐situ hybridisation (FISH) and reverse transcriptase polymerase chain reaction (RT‐PCR) (Bullrich et al, 1994; Elmberger et al, 1995; Mathew et al, 1995; Waggott et al, 1995; Wellmann et al, 1995; Simonitsch et al, 1996; Johnson et al, 1997; Mathew et al, 1997). Since normal hematopoietic cells do not express detectable levels of the full‐length ALK protein, the advent of antibody reagents specific for ALK has further revolutionised the diagnosis of ALCL.…”

Section: Alk Fusion Proteinsmentioning

confidence: 99%

Anaplastic lymphoma kinase proteins in growth control and cancer

Pulford

Morris

Turturro

2004

Journal Cellular Physiology

207

181

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The normal functions of full-length anaplastic lymphoma kinase (ALK) remain to be completely elucidated. Although considered to be important in neural development, recent studies in Drosophila also highlight a role for ALK in gut muscle differentiation. Indeed, the Drosophila model offers a future arena for the study of ALK, its ligands and signalling cascades. The discovery of activated fusion forms of the ALK tyrosine kinase in anaplastic large cell lymphoma (ALCL) has dramatically improved our understanding of the pathogenesis of these lymphomas and enhanced the pathological diagnosis of this subtype of non-Hodgkin's lymphoma (NHL). Likewise, the realisation that a high percentage of inflammatory myofibroblastic tumours express activated-ALK fusion proteins has clarified the causation of these mesenchymal neoplasms and provided for their easier discrimination from other mesenchymal-derived inflammatory myofibroblastic tumour (IMT) mimics. Recent reports of ALK expression in a range of carcinoma-derived cell lines together with its apparent role as a receptor for PTN and MK, both of which have been implicated in tumourigenesis, raise the possibility that ALK-mediated signalling could play a role in the development and/or progression of a number of common solid tumours. The therapeutic targeting of ALK may prove to have efficacy in the treatment of many of these neoplasms.

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The use of fluorescent in situ hybridization for detection of the t(2;5)(p23;q35) translocation in anaplastic large-cell lymphoma

Cited by 12 publications

References 26 publications

EARLY AND RELIABLE DIAGNOSIS OF NON-HODGKIN LYMPHOMA in CHILDHOOD AND ADOLESCENCE: Contribution of Cytomorphology and Flow Cytometric Immunophenotyping

EARLY AND RELIABLE DIAGNOSIS OF NON-HODGKIN LYMPHOMA in CHILDHOOD AND ADOLESCENCE: Contribution of Cytomorphology and Flow Cytometric Immunophenotyping

Development of anaplastic lymphoma kinase (ALK) small‐molecule inhibitors for cancer therapy

Anaplastic lymphoma kinase proteins in growth control and cancer

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