PMID- 10049065
OWN - NLM
STAT- MEDLINE
DCOM- 19990225
LR  - 20190915
IS  - 0887-6924 (Print)
IS  - 0887-6924 (Linking)
VI  - 13
IP  - 1
DP  - 1999 Jan
TI  - Allelic loss of 11q13 as detected by MEN1-FISH is not associated with mutation of 
      the MEN1 gene in lymphoid neoplasms.
PG  - 85-91
AB  - Deletions and rearrangements involving the long arm of chromosome 11 are not 
      infrequent occurrences in the non-Hodgkin's lymphomas. Recently, a tumor 
      suppressor gene, the multiple endocrine neoplasia type 1 gene (MEN1) was cloned 
      and mapped to chromosome 11q13. To assess the potential involvement of this gene 
      in lymphomagenesis, we examined 94 primary cases of lymphoma and 12 cell lines by 
      a combination of fluorescent in situ hybridization and PCR-SSCP analysis. In our 
      initial analysis of 41 primary B or T lymphomas, MEN1 FISH analysis revealed 
      allelic deletions in 15 cases (three of four B cell chronic lymphocytic 
      leukemias, six of 15 follicular lymphomas, three of nine diffuse large B cell 
      lymphomas, two of five mantle cell lymphomas, one of four Burkitt's lymphoma). To 
      discern whether the MEN1 gene was in fact the target of the deletions, we 
      assessed 20 of these 41 cases and an additional 74 primary lymphomas and 12 cell 
      lines for MEN1 gene mutations using PCR-SSCP analysis. Abnormal SSCP patterns 
      were found in exon 2 in two of the primary lymphoma cases and in one of the cell 
      lines, but not in any of the original cases that showed MEN1 deletions by FISH. 
      Furthermore, sequencing analysis revealed that the abnormal SSCP patterns in exon 
      2 were the result of a previously described genetic polymorphism (S145S: AGC --> 
      ACT), and in one sample, the result of this S145S polymorphism associated with a 
      second nucleotide substitution at position 498 which left the encoded amino acid 
      unchanged. Our study indicates that the 11q13 locus is a frequent target of 
      deletion in lymphoid neoplasms, but that there are no associated mutations of the 
      MEN1 gene. This suggests that the 11q deletions either target another gene in 
      lymphomas, or that the MEN1 gene is inactivated through means other than 
      mutation.
FAU - Thieblemont, C
AU  - Thieblemont C
AD  - Laboratory of Pathology, National Cancer Institute, National Institutes of 
      Health, Bethesda, MD 20892, USA.
FAU - Pack, S
AU  - Pack S
FAU - Sakai, A
AU  - Sakai A
FAU - Beaty, M
AU  - Beaty M
FAU - Pak, E
AU  - Pak E
FAU - Vortmeyer, A O
AU  - Vortmeyer AO
FAU - Wellmann, A
AU  - Wellmann A
FAU - Zhuang, Z
AU  - Zhuang Z
FAU - Jaffe, E S
AU  - Jaffe ES
FAU - Raffeld, M
AU  - Raffeld M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Leukemia
JT  - Leukemia
JID - 8704895
RN  - 0 (MEN1 protein, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Amino Acid Substitution
MH  - Burkitt Lymphoma/genetics
MH  - Chromosome Mapping
MH  - *Chromosomes, Human, Pair 11
MH  - Exons
MH  - *Gene Deletion
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/*genetics/pathology
MH  - Lymph Nodes/pathology
MH  - Lymphoma/blood/*genetics/pathology
MH  - Lymphoma, B-Cell/genetics
MH  - Lymphoma, T-Cell/genetics
MH  - Multiple Endocrine Neoplasia Type 1/genetics
MH  - Neoplasm Proteins/*genetics
MH  - Point Mutation
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Genetic
MH  - Polymorphism, Single-Stranded Conformational
MH  - *Proto-Oncogene Proteins
MH  - Tumor Cells, Cultured
EDAT- 1999/02/12 00:00
MHDA- 1999/02/12 00:01
CRDT- 1999/02/12 00:00
PHST- 1999/02/12 00:00 [pubmed]
PHST- 1999/02/12 00:01 [medline]
PHST- 1999/02/12 00:00 [entrez]
AID - 10.1038/sj.leu.2401216 [doi]
PST - ppublish
SO  - Leukemia. 1999 Jan;13(1):85-91. doi: 10.1038/sj.leu.2401216.