Fusion of the SEC31L1 and ALK genes in an inflammatory myofibroblastic tumor.
(2006) In International Journal of Cancer 118(5). p.1181-1186- Abstract
- Inflammatory myofibroblastic tumor (IMT) is a neoplasm composed of myofibroblastic spindle cells and infiltrating inflammatory cells. Cytogenetic analyses have revealed that a subgroup of IMT, in particular among children and young adults, harbors clonal chromosomal rearrangements involving chromosome band 2p23. Further, molecular genetic studies have shown that these rearrangements target the ALK gene, serving as the 3'-partner in fusion genes with various translocation partners. In the present study, we describe the finding of a novel SEC31L1/ALK fusion gene in an intraabdominal IMT of a young man. G-band analysis revealed a translocation t(2;4)(p23;q21) and subsequent fluorescence in situ hybridization with locus-specific probes... (More)
- Inflammatory myofibroblastic tumor (IMT) is a neoplasm composed of myofibroblastic spindle cells and infiltrating inflammatory cells. Cytogenetic analyses have revealed that a subgroup of IMT, in particular among children and young adults, harbors clonal chromosomal rearrangements involving chromosome band 2p23. Further, molecular genetic studies have shown that these rearrangements target the ALK gene, serving as the 3'-partner in fusion genes with various translocation partners. In the present study, we describe the finding of a novel SEC31L1/ALK fusion gene in an intraabdominal IMT of a young man. G-band analysis revealed a translocation t(2;4)(p23;q21) and subsequent fluorescence in situ hybridization with locus-specific probes strongly indicated disruption of the ALK locus on, chromosome 2. Immunostaining with monoclonal mouse anti-human CD246 ALK Protein showed diffuse cytoplasmic positivity. Using reverse primers for the ALK-gene, we could, by 5'-RACE methodology, amplify a single 1.2 kb fragment. Sequence analysis showed that the fragment was a hybrid cDNA product in which nt 3012 of SEC31L1 (NM 016211), located in band 4q21, was fused in-frame to nt 4080 of A (L) over barK (NM 004304). RT-PCR with two sets of primer pairs specific for SE (C) over bar 31L1 and ALK amplified two transcripts, which at sequencing corresponded to two types of chimeric SEC31L1/ALK transcripts. In the long, type I, transcript nt 3012 of SEC31L1 (NM 016211) was fused in-frame to nt 4080 of ALK. In the short, type II, transcript nt 2670 of SEC31L1 was fused in-frame to nt 4080 of ALK. Genomic PCR and subsequent sequencing showed that the breakpoints were located in intron 23 of SEC31L1 and intron 20 of ALK. (c) 2005 Wiley-Liss, Inc. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/143681
- author
- Panagopoulos, Ioannis LU ; Nilsson, Therese LU ; Domanski, Henryk LU ; Isaksson, Margareth LU ; Lindblom, Pia LU ; Mertens, Fredrik LU and Mandahl, Nils LU
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- ALK gene fusion, SEC31L1, myofibroblastic tumor
- in
- International Journal of Cancer
- volume
- 118
- issue
- 5
- pages
- 1181 - 1186
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000235056100014
- pmid:16161041
- scopus:31844448139
- ISSN
- 0020-7136
- DOI
- 10.1002/ijc.21490
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Surgery (Lund) (013009000), Pathology, (Lund) (013030000), Division of Clinical Genetics (013022003)
- id
- 2f1bf75c-3b9d-415a-a0a6-906b748b772b (old id 143681)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16161041&dopt=Abstract
- date added to LUP
- 2016-04-01 11:44:40
- date last changed
- 2022-01-26 17:34:27
@article{2f1bf75c-3b9d-415a-a0a6-906b748b772b, abstract = {{Inflammatory myofibroblastic tumor (IMT) is a neoplasm composed of myofibroblastic spindle cells and infiltrating inflammatory cells. Cytogenetic analyses have revealed that a subgroup of IMT, in particular among children and young adults, harbors clonal chromosomal rearrangements involving chromosome band 2p23. Further, molecular genetic studies have shown that these rearrangements target the ALK gene, serving as the 3'-partner in fusion genes with various translocation partners. In the present study, we describe the finding of a novel SEC31L1/ALK fusion gene in an intraabdominal IMT of a young man. G-band analysis revealed a translocation t(2;4)(p23;q21) and subsequent fluorescence in situ hybridization with locus-specific probes strongly indicated disruption of the ALK locus on, chromosome 2. Immunostaining with monoclonal mouse anti-human CD246 ALK Protein showed diffuse cytoplasmic positivity. Using reverse primers for the ALK-gene, we could, by 5'-RACE methodology, amplify a single 1.2 kb fragment. Sequence analysis showed that the fragment was a hybrid cDNA product in which nt 3012 of SEC31L1 (NM 016211), located in band 4q21, was fused in-frame to nt 4080 of A (L) over barK (NM 004304). RT-PCR with two sets of primer pairs specific for SE (C) over bar 31L1 and ALK amplified two transcripts, which at sequencing corresponded to two types of chimeric SEC31L1/ALK transcripts. In the long, type I, transcript nt 3012 of SEC31L1 (NM 016211) was fused in-frame to nt 4080 of ALK. In the short, type II, transcript nt 2670 of SEC31L1 was fused in-frame to nt 4080 of ALK. Genomic PCR and subsequent sequencing showed that the breakpoints were located in intron 23 of SEC31L1 and intron 20 of ALK. (c) 2005 Wiley-Liss, Inc.}}, author = {{Panagopoulos, Ioannis and Nilsson, Therese and Domanski, Henryk and Isaksson, Margareth and Lindblom, Pia and Mertens, Fredrik and Mandahl, Nils}}, issn = {{0020-7136}}, keywords = {{ALK gene fusion; SEC31L1; myofibroblastic tumor}}, language = {{eng}}, number = {{5}}, pages = {{1181--1186}}, publisher = {{John Wiley & Sons Inc.}}, series = {{International Journal of Cancer}}, title = {{Fusion of the SEC31L1 and ALK genes in an inflammatory myofibroblastic tumor.}}, url = {{http://dx.doi.org/10.1002/ijc.21490}}, doi = {{10.1002/ijc.21490}}, volume = {{118}}, year = {{2006}}, }