PMID- 9575422
OWN - NLM
STAT- MEDLINE
DCOM- 19980611
LR  - 20071114
IS  - 0258-851X (Print)
IS  - 0258-851X (Linking)
VI  - 12
IP  - 1
DP  - 1998 Jan-Feb
TI  - Individuals at high risk for lung cancer have airway epithelial cells with 
      chromosome aberrations frequently found in lung tumor cells.
PG  - 23-6
AB  - Identification of individuals at greatest risk of developing lung cancer could 
      enhance the efficacy of intervention modalities, thereby greatly reducing 
      mortality from this disease. One strategy for identifying these people is to 
      establish molecular markers which reflect the severity of their cancerization 
      field. Thus, investigations were initiated to determine of cells with chromosome 
      aberrations frequently exhibited by lung tumor cells, i.e., trisomy 7, trisomy 
      20, and deletion of 9p23, are prevalent within the uninvolved airways of cancer 
      patients. As a result, cells containing these aberrations were consistently found 
      at significantly elevated levels by using fluorescence in situ hybridization 
      (FISH). In contrast, cells collected from non-smokers who had never smoked were 
      normal by this assay. The next objective was to determine of cells exhibiting 
      these alterations are also present in upper airways of exposed, but cancer-free 
      smokers and ex-uranium miners. The results showed that, although only a subset of 
      these people will develop lung cancer in their lifetimes, they universally harbor 
      increased numbers of abnormal cells within their airway epithelium. However, the 
      number of sites with multiple verities of abnormal cells tended to be fewer 
      compared with the cancer patients. Thus, quantifying cells with molecular 
      alterations within the cancerization field of a smoker may delineate those with a 
      lesser grade of damage, and these individuals may be at a lesser risk of 
      developing disease. However, differences in the extent of genetic damage afforded 
      by these assays may not clearly define individuals with pending disease, and 
      additional molecular assays must be devised.
FAU - Lechner, J F
AU  - Lechner JF
AD  - Lovelace Respiratory Research Institute, Albuquerque, NM 87185, USA. 
      jlechner@lrri.org
FAU - Neft, R E
AU  - Neft RE
FAU - Gilliland, F D
AU  - Gilliland FD
FAU - Crowell, R E
AU  - Crowell RE
FAU - Auckley, D H
AU  - Auckley DH
FAU - Temes, R T
AU  - Temes RT
FAU - Belinsky, S A
AU  - Belinsky SA
LA  - eng
GR  - 1-P50-CA58184/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Greece
TA  - In Vivo
JT  - In vivo (Athens, Greece)
JID - 8806809
SB  - IM
MH  - Bronchi/*pathology
MH  - Cells, Cultured
MH  - *Chromosome Aberrations
MH  - Epithelial Cells
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Lung Neoplasms/*genetics/pathology
MH  - Risk Factors
MH  - Trisomy
MH  - Tumor Cells, Cultured
EDAT- 1998/05/12 00:00
MHDA- 1998/05/12 00:01
CRDT- 1998/05/12 00:00
PHST- 1998/05/12 00:00 [pubmed]
PHST- 1998/05/12 00:01 [medline]
PHST- 1998/05/12 00:00 [entrez]
PST - ppublish
SO  - In Vivo. 1998 Jan-Feb;12(1):23-6.