PMID- 8204884
OWN - NLM
STAT- MEDLINE
DCOM- 19940712
LR  - 20211203
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 83
IP  - 12
DP  - 1994 Jun 15
TI  - Molecular characterization of CD30+ anaplastic large-cell lymphoma: high 
      frequency of c-myc proto-oncogene activation.
PG  - 3581-90
AB  - Anaplastic large-cell lymphoma (ALCL) represents a morphologically distinct type 
      of non-Hodgkin's lymphoma (NHL) characterized phenotypically by the expression of 
      the CD30 antigen, a new member of the nerve growth factor gene family. The 
      lymphoid origin of ALCL has been documented using immunohistochemical and 
      molecular genetic analyses. However, very little is known so far regarding the 
      precise pathogenetic mechanisms involved in its development and progression. 
      Therefore, we investigated bcl-2, p53, and retinoblastoma gene (Rb) expression 
      immunohistochemically; the occurrence of bcl-2, c-myc, and Rb gene rearrangements 
      using Southern blotting; and the presence of ras and p53 gene somatic mutations 
      by single-strand conformation polymorphism assay in a panel of 18 
      well-characterized ALCLs. In addition, the presence of Epstein-Barr (EBV) and 
      human T-cell lymphotropic virus type I (HTLV-I) genomes were investigated using 
      polymerase chain reaction. We identified abnormal c-myc gene products in 6 of 18 
      cases (33%) of ALCL. On the other hand, the bcl-2 and Rb genes were not 
      rearranged and K-, N-, and H-ras gene somatic mutations were not found. 
      Significant levels of p53 protein expression were found in more than 60% of 
      ALCLs, but only a single ALCL carried a p53 gene mutation (exon 5). Only 3 ALCL 
      cases, all occurring in human immunodeficiency virus-infected patients, were 
      positive for EBV genomes. On the other hand, contrary to previous findings, no 
      HTLV-I products could be identified. Despite the fact that the c-myc 
      proto-oncogene appears to be frequently altered in ALCL, no pathognomonic 
      abnormality could be identified and therefore additional studies and new 
      strategies should be designed to identify the pathogenetic mechanisms involved in 
      the development of ALCL.
FAU - Inghirami, G
AU  - Inghirami G
AD  - Division of Surgical Pathology, College of Physicians and Surgeons of Columbia 
      University, New York, NY.
FAU - Macri, L
AU  - Macri L
FAU - Cesarman, E
AU  - Cesarman E
FAU - Chadburn, A
AU  - Chadburn A
FAU - Zhong, J
AU  - Zhong J
FAU - Knowles, D M
AU  - Knowles DM
LA  - eng
GR  - CA42836/CA/NCI NIH HHS/United States
GR  - EY06337/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
SB  - IM
GS  - c-myc
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Base Sequence
MH  - Female
MH  - *Gene Expression Regulation
MH  - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor
MH  - Genes, Retinoblastoma
MH  - *Genes, myc
MH  - Genes, p53
MH  - Herpesvirus 4, Human/genetics
MH  - Human T-lymphotropic virus 1/genetics
MH  - Humans
MH  - Immunophenotyping
MH  - Lymphoma, Large-Cell, Anaplastic/*genetics
MH  - Male
MH  - Middle Aged
MH  - Molecular Sequence Data
MH  - Proto-Oncogene Mas
EDAT- 1994/06/15 00:00
MHDA- 1994/06/15 00:01
CRDT- 1994/06/15 00:00
PHST- 1994/06/15 00:00 [pubmed]
PHST- 1994/06/15 00:01 [medline]
PHST- 1994/06/15 00:00 [entrez]
AID - S0006-4971(20)78855-5 [pii]
PST - ppublish
SO  - Blood. 1994 Jun 15;83(12):3581-90.