Table 1

Somatic mutations of LKB1/STK11 in primary LADs and in lung cancer cell linesa

Sample IdentificationCodon locationDNA changePredicted effectK-rasp53p16b
1012-LAD37cag-tagQ-Termtcmtwt
758-LAD44aag-tagK-Terwtmtwt
898-LAD210tgc-tgaC-Terwtwtwt
946-LAD223gag-tagE-Terwtmtwt
1122-LAD2791C deletionStop codon 286mtwtwt
997-LADPromoterPHNo proteinwtmtwt
A549d37cag-tagQ-Termtwtmt
H23332tgg-tgaW-Termtmtwt
  • a Primary tumors were selected for loss of heterozygosity at chromosome 19p.

  • b Six of 14 primary adenocarcinomas without LKB1/STK11 alterations harbored p16/INK4A inactivation. Kras, p53, and p16 genes mutational status of primary tumors was reported previously (32 , 33) .

  • c PH, promoter hypermethylation; mt, mutant; wt, wild type.

  • d Mutations in cell lines were homozygous. Lung tumors analyzed for LKB1/STK11 alterations: 20 primary LADs; 12 primary squamous cell carcinomas; and nine lung cancer cell lines (nonadenocarcinomas, H209, H1155, H1299, H1618, H1770, and adenocarcinomas H522, H23, A549, H358).