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Identification of novel fusion partners of ALK, the anaplastic lymphoma kinase, in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor.
Genes Chromosomes Cancer 2002; 34(4):354-62GC

Abstract

ALK-positive anaplastic large-cell lymphoma (ALCL) has been recognized as a distinct type of lymphoma in the heterogeneous group of T/Null-ALCL. While most of the ALK-positive ALCL (ALKomas) are characterized by the presence of the NPM-ALK fusion protein, the product of the t(2;5)(p23;q35), 10-20% of ALKomas contain variant ALK fusions, including ATIC-ALK, TFG-ALK, CLTC-ALK (previously designated CLTCL-ALK), TMP3-ALK, and MSN-ALK. TMP3-ALK and TMP4-ALK fusions also have been detected in inflammatory myofibroblastic tumors (IMTs), making clear that aberrations of the ALK gene are not associated exclusively with the pathogenesis of ALK-positive ALCL. Here we report results of molecular studies on two lymphoma cases and one IMT case with variant rearrangements of ALK. Our study led to the detection of the CLTC-ALK fusion in an ALCL case and to the identification of two novel fusion partners of ALK: ALO17 (KIAA1618), a gene with unknown function, which was fused to ALK in an ALCL case with a t(2;17)(p23;q25), and CARS, encoding the cysteinyl-tRNA synthetase, which was fused to ALK in an IMT case with a t(2;11;2)(p23;p15;q31). These results confirm the recurrent involvement of ALK in IMT and further demonstrate the diversity of ALK fusion partners, with the ability to homodimerize as a common characteristic.

Authors+Show Affiliations

Center for Human Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), University of Leuven, Campus Gasthuisberg O&N 06, Herestraat 49, B-3000 Leuven, Belgium.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Case Reports
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12112524

Citation

Cools, Jan, et al. "Identification of Novel Fusion Partners of ALK, the Anaplastic Lymphoma Kinase, in Anaplastic Large-cell Lymphoma and Inflammatory Myofibroblastic Tumor." Genes, Chromosomes & Cancer, vol. 34, no. 4, 2002, pp. 354-62.
Cools J, Wlodarska I, Somers R, et al. Identification of novel fusion partners of ALK, the anaplastic lymphoma kinase, in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor. Genes Chromosomes Cancer. 2002;34(4):354-62.
Cools, J., Wlodarska, I., Somers, R., Mentens, N., Pedeutour, F., Maes, B., ... Marynen, P. (2002). Identification of novel fusion partners of ALK, the anaplastic lymphoma kinase, in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor. Genes, Chromosomes & Cancer, 34(4), pp. 354-62.
Cools J, et al. Identification of Novel Fusion Partners of ALK, the Anaplastic Lymphoma Kinase, in Anaplastic Large-cell Lymphoma and Inflammatory Myofibroblastic Tumor. Genes Chromosomes Cancer. 2002;34(4):354-62. PubMed PMID: 12112524.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Identification of novel fusion partners of ALK, the anaplastic lymphoma kinase, in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor. AU - Cools,Jan, AU - Wlodarska,Iwona, AU - Somers,Riet, AU - Mentens,Nicole, AU - Pedeutour,Florence, AU - Maes,Brigitte, AU - De Wolf-Peeters,Christiane, AU - Pauwels,Patrick, AU - Hagemeijer,Anne, AU - Marynen,Peter, PY - 2002/7/12/pubmed PY - 2002/8/14/medline PY - 2002/7/12/entrez SP - 354 EP - 62 JF - Genes, chromosomes & cancer JO - Genes Chromosomes Cancer VL - 34 IS - 4 N2 - ALK-positive anaplastic large-cell lymphoma (ALCL) has been recognized as a distinct type of lymphoma in the heterogeneous group of T/Null-ALCL. While most of the ALK-positive ALCL (ALKomas) are characterized by the presence of the NPM-ALK fusion protein, the product of the t(2;5)(p23;q35), 10-20% of ALKomas contain variant ALK fusions, including ATIC-ALK, TFG-ALK, CLTC-ALK (previously designated CLTCL-ALK), TMP3-ALK, and MSN-ALK. TMP3-ALK and TMP4-ALK fusions also have been detected in inflammatory myofibroblastic tumors (IMTs), making clear that aberrations of the ALK gene are not associated exclusively with the pathogenesis of ALK-positive ALCL. Here we report results of molecular studies on two lymphoma cases and one IMT case with variant rearrangements of ALK. Our study led to the detection of the CLTC-ALK fusion in an ALCL case and to the identification of two novel fusion partners of ALK: ALO17 (KIAA1618), a gene with unknown function, which was fused to ALK in an ALCL case with a t(2;17)(p23;q25), and CARS, encoding the cysteinyl-tRNA synthetase, which was fused to ALK in an IMT case with a t(2;11;2)(p23;p15;q31). These results confirm the recurrent involvement of ALK in IMT and further demonstrate the diversity of ALK fusion partners, with the ability to homodimerize as a common characteristic. SN - 1045-2257 UR - https://www.unboundmedicine.com/medline/citation/12112524/Identification_of_novel_fusion_partners_of_ALK_the_anaplastic_lymphoma_kinase_in_anaplastic_large_cell_lymphoma_and_inflammatory_myofibroblastic_tumor_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1045-2257&date=2002&volume=34&issue=4&spage=354 DB - PRIME DP - Unbound Medicine ER -