PMID- 14511407
OWN - NLM
STAT- MEDLINE
DCOM- 20040430
LR  - 20220310
IS  - 1522-8002 (Print)
IS  - 1476-5586 (Electronic)
IS  - 1476-5586 (Linking)
VI  - 5
IP  - 4
DP  - 2003 Jul-Aug
TI  - RASSF1A promoter methylation and Kras2 mutations in non small cell lung cancer.
PG  - 362-6
LID - S1476-5586(03)80029-5 [pii]
LID - 10.1016/S1476-5586(03)80029-5 [doi]
AB  - In the present studies, we investigated the correlation between RASSF1A promoter 
      methylation status and Kras2 mutations in 65 primary non small cell lung cancer 
      (NSCLC) including 33 adenocarcinomas, 12 large cell carcinomas, and 20 squamous 
      cell carcinomas. Mutational analysis of Kras2 showed: 30% (10 of 33) of 
      adenocarcinomas, 25% (3 of 12) of large cell carcinomas, and only 5% (1 of 20) of 
      squamous cell carcinomas contained activated Kras2 mutation at codon 12 or 13. 
      RASSF1A promoter region CpG island methylation was detected in adenocarcinomas 
      (55%), large cell carcinomas (25%), and squamous cell carcinomas (25%). 
      Interestingly, combined RASSF1A methylation and Kras2 mutation data show that 
      only - 7% adenocarcinomas/large cell carcinomas exhibited both KRASSF1A promoter 
      methylation and Kras2 mutation, whereas 24% adenocarcinomas, 50% large cell 
      carcinomas, and 70% squamous cell carcinomas showed neither Kras2 mutation nor 
      RASSF1A promoter methylation. These results showed that the majority of the 
      primary NSCLCs with Kras2 mutations lack RASSF1A inactivation, and both RASSF1A 
      inactivation and Kras2 mutation events occur frequently in adenocarcinomas and 
      large cell carcinomas. Our results indicate a trend of inverse relationship 
      between Kras2 activation and RASSF1A promoter methylation in the majority of 
      human lung adenocarcinomas and large cell carcinomas.
FAU - Li, Jie
AU  - Li J
AD  - Department of Surgery, Washington University School of Medicine, St. Louis, MO, 
      USA.
FAU - Zhang, Zhongqiu
AU  - Zhang Z
FAU - Dai, Zunyan
AU  - Dai Z
FAU - Popkie, Anthony P
AU  - Popkie AP
FAU - Plass, Christoph
AU  - Plass C
FAU - Morrison, Carl
AU  - Morrison C
FAU - Wang, Yian
AU  - Wang Y
FAU - You, Ming
AU  - You M
LA  - eng
GR  - R01 CA058554/CA/NCI NIH HHS/United States
GR  - R01CA58554/CA/NCI NIH HHS/United States
GR  - R01CA78797/CA/NCI NIH HHS/United States
GR  - R41CA093204/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Neoplasia
JT  - Neoplasia (New York, N.Y.)
JID - 100886622
RN  - 0 (KRAS protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RASSF1 protein, human)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 9007-49-2 (DNA)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Adenocarcinoma/genetics
MH  - Carcinoma, Large Cell/genetics
MH  - Carcinoma, Non-Small-Cell Lung/*genetics
MH  - Carcinoma, Squamous Cell/genetics
MH  - Cell Line, Tumor
MH  - Colonic Neoplasms/genetics
MH  - DNA/metabolism
MH  - *DNA Methylation
MH  - Humans
MH  - Lung Neoplasms/*genetics
MH  - Mutation
MH  - Polymerase Chain Reaction
MH  - *Promoter Regions, Genetic
MH  - Proto-Oncogene Proteins/*genetics
MH  - Proto-Oncogene Proteins p21(ras)
MH  - Sequence Analysis, DNA
MH  - Signal Transduction
MH  - Tumor Suppressor Proteins/*genetics
MH  - ras Proteins
PMC - PMC1550336
EDAT- 2003/09/27 05:00
MHDA- 2004/05/01 05:00
PMCR- 2003/07/01
CRDT- 2003/09/27 05:00
PHST- 2003/09/27 05:00 [pubmed]
PHST- 2004/05/01 05:00 [medline]
PHST- 2003/09/27 05:00 [entrez]
PHST- 2003/07/01 00:00 [pmc-release]
AID - S1476-5586(03)80029-5 [pii]
AID - 03157 [pii]
AID - 10.1016/S1476-5586(03)80029-5 [doi]
PST - ppublish
SO  - Neoplasia. 2003 Jul-Aug;5(4):362-6. doi: 10.1016/S1476-5586(03)80029-5.