PMID- 11807981
OWN - NLM
STAT- MEDLINE
DCOM- 20020301
LR  - 20191025
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 33
IP  - 3
DP  - 2002 Mar
TI  - Fluorescence in situ hybridization study of chromosome 7 aberrations in 
      hepatosplenic T-cell lymphoma: isochromosome 7q as a common abnormality 
      accumulating in forms with features of cytologic progression.
PG  - 243-51
AB  - Hepatosplenic gamma delta T-cell lymphoma (HS gamma delta TCL) is a rare and 
      aggressive subtype of peripheral T-cell lymphoma that has been associated 
      cytogenetically with the isochromosome 7q [i(7)(q10)]. The incidence of this 
      aberration and its relevance to pathogenesis of HS gamma delta TCL is still 
      unknown. We investigated the status of chromosome 7 in 12 HSTCL cases, including 
      nine with a typical gamma delta phenotype, one with a so-called T-cell receptor 
      (TCR)-silent phenotype, and two with the variant alpha beta phenotype. We 
      analyzed available fresh and archival material using a dual-color interphase 
      fluorescence in situ hybridization (FISH) approach with 7p and 7q probes. A 
      significant population of cells with predominance of 7q signals was detected in 
      10 cases (eight gamma delta, one alpha beta, and one TCR silent), and two 
      lymphomas did not show clonal 7p/7q signal imbalances. In four of 10 cases with 
      chromosome 7 aberrations, a hybridization pattern indicative of the presence of 
      one chromosome 7 and one i(7)(q10) was found. In four other cases, the 
      configuration of signals (2 x 7p/3 x 7q) suggested the presence of the i(7)(q10) 
      and additional structural aberrations involving the second chromosome 7. In two 
      cases, including one alpha beta phenotypic variant, a variety of FISH patterns 
      equivalent to two to five copies of i(7)(q10) or numerical and structural 
      aberrations of second chromosome 7 has been detected. These findings support 
      cytogenetic data pointing to a characteristic association of i(7)(q10) with 
      HSTCL, irrespective of the immunophenotype of malignant cells. An increased 
      number of 7q signals was found in three cases with cytologic features of 
      progression, indicating a tendency of HSTCL to multiply the i(7)(q10) chromosome 
      during evolution.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Wlodarska, Iwona
AU  - Wlodarska I
AD  - Center for Human Genetics, University of Leuven, Leuven, Belgium. 
      Iwona.Wlodarska@med.kuleuven.ac.be
FAU - Martin-Garcia, Nadine
AU  - Martin-Garcia N
FAU - Achten, Ruth
AU  - Achten R
FAU - De Wolf-Peeters, Chris
AU  - De Wolf-Peeters C
FAU - Pauwels, Patrick
AU  - Pauwels P
FAU - Tulliez, Micheline
AU  - Tulliez M
FAU - de Mascarel, Antoine
AU  - de Mascarel A
FAU - Briere, Josette
AU  - Briere J
FAU - Patey, Martine
AU  - Patey M
FAU - Hagemeijer, Anne
AU  - Hagemeijer A
FAU - Gaulard, Philippe
AU  - Gaulard P
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
MH  - Adult
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 7/*genetics
MH  - Disease Progression
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence/*methods
MH  - Interphase/genetics
MH  - Isochromosomes/*genetics
MH  - Liver Neoplasms/*genetics/pathology
MH  - Lymphoma, T-Cell/*genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - Splenic Neoplasms/*genetics/pathology
EDAT- 2002/01/25 10:00
MHDA- 2002/03/02 10:01
CRDT- 2002/01/25 10:00
PHST- 2002/01/25 10:00 [pubmed]
PHST- 2002/03/02 10:01 [medline]
PHST- 2002/01/25 10:00 [entrez]
AID - 10.1002/gcc.10021 [pii]
AID - 10.1002/gcc.10021 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2002 Mar;33(3):243-51. doi: 10.1002/gcc.10021.