PMID- 7539284
OWN - NLM
STAT- MEDLINE
DCOM- 19950706
LR  - 20191023
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 12
IP  - 4
DP  - 1995 Apr
TI  - Visualization of INT2 and HST1 amplification in oral squamous cell carcinomas.
PG  - 288-95
AB  - Oral squamous cell carcinoma (OSCC) develops along a multistep genetic pathway 
      including loss of tumor suppressor genes and alteration of oncogenes. We 
      characterized seven OSCC cell lines by classical and molecular cytogenetic 
      analysis and fresh tumor and adjacent oral mucosa corresponding to three of the 
      cell lines by molecular cytogenetics. We observed homogeneously staining regions 
      (hsrs) in four of the seven cell lines, at 11q13 in three and at 11q23 and in an 
      unidentified marker chromosome in the fourth. Amplification of band 11q13 occurs 
      in 30-60% of head and neck squamous cell carcinomas. To determine whether INT2 
      and HST1, both located in band 11q13, are amplified in the tissues and cell lines 
      and to confirm the chromosomal location(s) of the amplification, we used 
      dual-color fluorescence in situ hybridization (FISH) with DNA probes for these 
      genes and the chromosome 11 centromere. We report chromosomal localization of 
      INT2/HST1 amplification in OSCC. Coamplification of INT2 and HST1 was detected in 
      the hsrs in cultured tumor cells from the four hsr-containing tumors and in 
      directly harvested tumor cells, which were available from only two of these 
      tumors. Amplification was not present in tumors lacking hsrs or adjacent oral 
      mucosa corresponding to any of the seven tumors. The observation of amplification 
      in fresh tumor cells suggests that the amplification was present in the patients, 
      may play a key role in the development and/or progression of OSCC, and is not due 
      to karyotypic evolution in vitro. The absence of amplification in the adjacent 
      mucosa suggests that 11q13 amplification is a relatively late event in OSCC 
      tumorigenesis.
FAU - Lese, C M
AU  - Lese CM
AD  - Department of Human Genetics, University of Pittsburgh, Pennsylvania, USA.
FAU - Rossie, K M
AU  - Rossie KM
FAU - Appel, B N
AU  - Appel BN
FAU - Reddy, J K
AU  - Reddy JK
FAU - Johnson, J T
AU  - Johnson JT
FAU - Myers, E N
AU  - Myers EN
FAU - Gollin, S M
AU  - Gollin SM
LA  - eng
GR  - DE10513/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (FGF3 protein, human)
RN  - 0 (FGF4 protein, human)
RN  - 0 (Fibroblast Growth Factor 3)
RN  - 0 (Fibroblast Growth Factor 4)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 62031-54-3 (Fibroblast Growth Factors)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
SB  - IM
GS  - HST1
GS  - INT2
MH  - Biopsy
MH  - Carcinoma, Squamous Cell/*genetics/pathology
MH  - Cell Line
MH  - Chromosome Aberrations
MH  - Chromosome Mapping
MH  - *Chromosomes, Human, Pair 11
MH  - Fibroblast Growth Factor 3
MH  - Fibroblast Growth Factor 4
MH  - Fibroblast Growth Factors/biosynthesis/*genetics
MH  - Gene Amplification
MH  - Head and Neck Neoplasms/genetics
MH  - Humans
MH  - Karyotyping
MH  - Mouth Mucosa/pathology
MH  - Mouth Neoplasms/*genetics/pathology
MH  - Protein-Tyrosine Kinases/genetics
MH  - Proto-Oncogene Proteins/biosynthesis/*genetics
EDAT- 1995/04/01 00:00
MHDA- 1995/04/01 00:01
CRDT- 1995/04/01 00:00
PHST- 1995/04/01 00:00 [pubmed]
PHST- 1995/04/01 00:01 [medline]
PHST- 1995/04/01 00:00 [entrez]
AID - 10.1002/gcc.2870120409 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1995 Apr;12(4):288-95. doi: 10.1002/gcc.2870120409.