PMID- 12594387
OWN - NLM
STAT- MEDLINE
DCOM- 20030325
LR  - 20181130
IS  - 0242-6498 (Print)
IS  - 0242-6498 (Linking)
VI  - 22
IP  - 6
DP  - 2002 Dec
TI  - [Inflammatory myofibroblastic tumors].
PG  - 453-60
AB  - Inflammatory myofibroblastic tumors (IMT) are mesenchymal solid tumors that occur 
      preferentially in children and young adults. They present as myofibroblastic cell 
      proliferations accompanied by plasmocytes and lymphocytes. Recent cytogenetic and 
      molecular observations showed non-random abnormalities of chromosomal band 2p23 
      resulting in a rearrangement of the ALK gene. This finding of a specific gene 
      alteration suggests a neoplastic rather than a reactive inflammatory process for 
      IMT tumorigenesis. ALK is a tyrosine kinase oncogene initially found to be 
      rearranged in anaplastic large-cell lymphomas (ALCL). Of note, the breakpoints 
      within ALK, and also within some of the ALK fusion gene partners, such as TPM3 or 
      CLTC, are similar in IMT and ALCL. The consistent involvement of ALK, together 
      with the diversity of partner genes, underlines the central role of ALK 
      constitutive activation in IMT development, as well as the importance of 
      homodimerization mechanisms of the chimeric fusion proteins in this activation. 
      Immunohistochemical analyses performed on paraffin embedded tissue sections have 
      shown positive ALK expression with cytoplasmic localization in half of the IMT 
      cases containing the molecular ALK rearrangement. In conclusion, these novel 
      molecular data have defined a group of IMT of neoplastic origin characterized by 
      the presence of ALK alterations. The description of ALK gene rearrangements in 
      IMT and ALCL is the second example, after the observation of ETV6-NTRK3 in 
      congenital fibrosarcoma and in a case of chronic myeloid leukemia, of identical 
      gene fusions occurring in two different cell lines: hematopoietic and 
      mesenchymal. The search for rearrangement of ALK by fluorescence in situ 
      hybridization (FISH) is a useful complementary tool for IMT diagnosis.
FAU - Sirvent, Nicolas
AU  - Sirvent N
AD  - Service de Pediatrie, Hopital de l'Archet, CHU de Nice, 06202 Nice Cedex 3.
FAU - Coindre, Jean-Michel
AU  - Coindre JM
FAU - Pedeutour, Florence
AU  - Pedeutour F
LA  - fre
PT  - Journal Article
PT  - Review
TT  - Tumeurs myofibroblastiques inflammatoires.
PL  - France
TA  - Ann Pathol
JT  - Annales de pathologie
JID - 8106337
RN  - EC 2.7.10.1 (ALK protein, human)
RN  - EC 2.7.10.1 (Anaplastic Lymphoma Kinase)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Anaplastic Lymphoma Kinase
MH  - Cell Transformation, Neoplastic
MH  - Humans
MH  - Inflammation
MH  - Karyotyping
MH  - Neoplasms, Muscle Tissue/*genetics/*pathology/physiopathology
MH  - Protein-Tyrosine Kinases/*genetics
MH  - Receptor Protein-Tyrosine Kinases
RF  - 38
EDAT- 2003/02/21 04:00
MHDA- 2003/03/26 05:00
CRDT- 2003/02/21 04:00
PHST- 2003/02/21 04:00 [pubmed]
PHST- 2003/03/26 05:00 [medline]
PHST- 2003/02/21 04:00 [entrez]
AID - MDOI-AP-12-2002-22-6-0242-6498-101019-ART3 [pii]
PST - ppublish
SO  - Ann Pathol. 2002 Dec;22(6):453-60.