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TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors.
Am J Pathol 2000; 157(2):377-84AJ

Abstract

Inflammatory myofibroblastic tumors (IMTs) are neoplastic mesenchymal proliferations featuring an inflammatory infiltrate composed primarily of lymphocytes and plasma cells. The myofibroblastic cells in some IMTs contain chromosomal rearrangements involving the ALK receptor tyrosine-kinase locus region (chromosome band 2p23). ALK-which is normally restricted in its expression to neural tissues-is expressed strikingly in the IMT cells with 2p23 rearrangements. We now report a recurrent oncogenic mechanism, in IMTs, in which tropomyosin (TPM) N-terminal coiled-coil domains are fused to the ALK C-terminal kinase domain. We have cloned two ALK fusion genes, TPM4-ALK and TPM3-ALK, which encode approximately 95-kd fusion oncoproteins characterized by constitutive kinase activity and tyrosylphosphorylation. Immunohistochemical and molecular correlations, in other IMTs, implicate non-TPM ALK oncoproteins that are predominantly cytoplasmic or pre- dominantly nuclear, presumably depending on the subcellular localization of the ALK fusion partner. Notably, a TPM3-ALK oncogene was reported recently in anaplastic lymphoma, and TPM3-ALK is thereby the first known fusion oncogene that transforms, in vivo, both mesenchymal and lymphoid human cell lineages.

Authors+Show Affiliations

Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA.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 availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10934142

Citation

Lawrence, B, et al. "TPM3-ALK and TPM4-ALK Oncogenes in Inflammatory Myofibroblastic Tumors." The American Journal of Pathology, vol. 157, no. 2, 2000, pp. 377-84.
Lawrence B, Perez-Atayde A, Hibbard MK, et al. TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors. Am J Pathol. 2000;157(2):377-84.
Lawrence, B., Perez-Atayde, A., Hibbard, M. K., Rubin, B. P., Dal Cin, P., Pinkus, J. L., ... Fletcher, J. A. (2000). TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors. The American Journal of Pathology, 157(2), pp. 377-84.
Lawrence B, et al. TPM3-ALK and TPM4-ALK Oncogenes in Inflammatory Myofibroblastic Tumors. Am J Pathol. 2000;157(2):377-84. PubMed PMID: 10934142.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors. AU - Lawrence,B, AU - Perez-Atayde,A, AU - Hibbard,M K, AU - Rubin,B P, AU - Dal Cin,P, AU - Pinkus,J L, AU - Pinkus,G S, AU - Xiao,S, AU - Yi,E S, AU - Fletcher,C D, AU - Fletcher,J A, PY - 2000/8/10/pubmed PY - 2000/8/29/medline PY - 2000/8/10/entrez SP - 377 EP - 84 JF - The American journal of pathology JO - Am. J. Pathol. VL - 157 IS - 2 N2 - Inflammatory myofibroblastic tumors (IMTs) are neoplastic mesenchymal proliferations featuring an inflammatory infiltrate composed primarily of lymphocytes and plasma cells. The myofibroblastic cells in some IMTs contain chromosomal rearrangements involving the ALK receptor tyrosine-kinase locus region (chromosome band 2p23). ALK-which is normally restricted in its expression to neural tissues-is expressed strikingly in the IMT cells with 2p23 rearrangements. We now report a recurrent oncogenic mechanism, in IMTs, in which tropomyosin (TPM) N-terminal coiled-coil domains are fused to the ALK C-terminal kinase domain. We have cloned two ALK fusion genes, TPM4-ALK and TPM3-ALK, which encode approximately 95-kd fusion oncoproteins characterized by constitutive kinase activity and tyrosylphosphorylation. Immunohistochemical and molecular correlations, in other IMTs, implicate non-TPM ALK oncoproteins that are predominantly cytoplasmic or pre- dominantly nuclear, presumably depending on the subcellular localization of the ALK fusion partner. Notably, a TPM3-ALK oncogene was reported recently in anaplastic lymphoma, and TPM3-ALK is thereby the first known fusion oncogene that transforms, in vivo, both mesenchymal and lymphoid human cell lineages. SN - 0002-9440 UR - https://www.unboundmedicine.com/medline/citation/10934142/TPM3_ALK_and_TPM4_ALK_oncogenes_in_inflammatory_myofibroblastic_tumors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9440(10)64550-6 DB - PRIME DP - Unbound Medicine ER -