PMID- 18618503
OWN - NLM
STAT- MEDLINE
DCOM- 20080829
LR  - 20240417
IS  - 1545-5017 (Electronic)
IS  - 1545-5009 (Print)
IS  - 1545-5009 (Linking)
VI  - 51
IP  - 4
DP  - 2008 Oct
TI  - Characterization of childhood precursor T-lymphoblastic lymphoma by 
      immunophenotyping and fluorescent in situ hybridization: a report from the 
      Children's Oncology Group.
PG  - 489-94
LID - 10.1002/pbc.21666 [doi]
AB  - BACKGROUND: T-lymphoblastic lymphoma (T-LBL) accounts for 25-30% of childhood 
      non-Hodgkin's lymphoma and is closely related to T-lymphoblastic leukemia 
      (T-ALL). Recently, we demonstrated distinct differences in gene expression 
      between childhood T-LBL and T-ALL, but molecular pathogenesis and relevant 
      protein expression patterns in T-LBL remain poorly understood. PROCEDURE: 
      Children with T-LBL with disseminated disease were registered and treated on COG 
      protocol 5971. Paraffin-embedded tumor tissue was obtained at diagnosis for 
      immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) studies. 
      We determined the pattern and intensity of staining for c-Myc, Skp2, Mib-1, p53, 
      TCL-1, bcl-2, and bcl-6 proteins by IHC and c-Myc, p53, bcl-2, bcl-6, and TCR 
      alpha/delta molecular alterations by FISH in 22 pediatric T-LBL cases. RESULTS: 
      The majority of T-LBL samples expressed Mib-1 (59%) and c-Myc (77%) proteins in 
      greater than 50% of the cells, but Skp2 (14%), p53 (14%), and bcl-2 (23%) 
      expression was less common. FISH studies demonstrated 18% gains and 10% losses in 
      c-Myc, 16% gains in p53, 12% gains and 6% losses in bcl-2, and 6% gains and 19% 
      losses in bcl-6 with little direct correlation between the IHC and FISH studies. 
      CONCLUSIONS: Childhood T-LBL is a highly proliferative tumor associated with 
      enhanced expression of c-Myc protein, but without detectable c-Myc molecular 
      alterations. FISH studies did not identify consistent etiologies of molecular 
      dysregulation, and future studies with other molecular approaches may be required 
      to elucidate the molecular pathogenesis of childhood T-LBL.
CI  - (c) 2008 Wiley-Liss, Inc.
FAU - Smock, Kristi J
AU  - Smock KJ
AD  - Department of Pathology, University of Utah Health Sciences Center, ARUP 
      Laboratories, Salt Lake City, Utah, USA.
FAU - Nelson, Marilu
AU  - Nelson M
FAU - Tripp, Sheryl R
AU  - Tripp SR
FAU - Sanger, Warren G
AU  - Sanger WG
FAU - Abromowitch, Minnie
AU  - Abromowitch M
FAU - Cairo, Mitchell S
AU  - Cairo MS
FAU - Perkins, Sherrie L
AU  - Perkins SL
CN  - Children's Oncology Group
LA  - eng
GR  - U10 CA098413-05/CA/NCI NIH HHS/United States
GR  - U10 CA098543/CA/NCI NIH HHS/United States
GR  - U10 CA098543-06/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Pediatr Blood Cancer
JT  - Pediatric blood & cancer
JID - 101186624
SB  - IM
MH  - Child
MH  - Humans
MH  - Immunohistochemistry
MH  - Immunophenotyping
MH  - In Situ Hybridization, Fluorescence
MH  - Medical Oncology
MH  - Precursor T-Cell Lymphoblastic 
      Leukemia-Lymphoma/*classification/immunology/metabolism/*pathology
PMC - PMC2712233
MID - NIHMS123020
EDAT- 2008/07/12 09:00
MHDA- 2008/08/30 09:00
PMCR- 2009/10/01
CRDT- 2008/07/12 09:00
PHST- 2008/07/12 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2008/07/12 09:00 [entrez]
PHST- 2009/10/01 00:00 [pmc-release]
AID - 10.1002/pbc.21666 [doi]
PST - ppublish
SO  - Pediatr Blood Cancer. 2008 Oct;51(4):489-94. doi: 10.1002/pbc.21666.