Table 2

Frameshift mutations in MMP+ endometrial tumors and cell lines

hMLH1a methylationhMSH3b (A)8hMSH6b (C)8BAXb (G)8IGFIIRb (G)8caspase-5b (A)10TGFβRIIb (A)10
MMP+ endometrial tumor cell linesc
 AN3CA++d+d
 RL95-2+d+u+d+d
 SK-UT-1+u+u+d
 SK-UT-1B+u+u+d
 HEC-1A++d,d++u,uu
 HEC-1B++d,d++u,uu
MMP+ endometrial tumorsd
 ET9+d
 ET24+d+d
 ET39+d+d
 ET45+d
 ET46+d+d+d
 ET67++d
 ET68+d
 ET69++d+d
 ET70+
 ET83+++d,d+d
 ET86+d
 ET100++d,d
 ET106+d
 ET132+d
 ET153+u
 ET156+d
 ET162+++d,d+d
 ET167++d
  • a −, not methylated; +, methylated.

  • b −, wild type; +, mutant; +u, 1-bp insertion; ++u,uu, homozygous insertions of 1 and 2 bp; +d, 1-bp deletion; ++d,d, homozygous deletion of 1 bp.

  • c Hypermethylation was absent in three MMP− endometrial (Hs34.T, Hs248.T, and Hs825.T) and colon SW620 cell lines and in MMP+ colon carcinoma (LoVo, LS411N, DLD-1, LS174, LS180, and HCT116) and prostate carcinoma DU-145 cell lines. The three MMP− endometrial cell lines were negative for mutations in all the target genes. Additional MMP− cell lines were also negative for mutations, including: 16 from colon (SW620, SW403, SK-CO-1, NCI-H747, NCI-H508, Caco-2, HT-29, BM314, CHC-Y1, COLO201, RCM-1, SW837, SW1417, WiDr, and COCO320DM); 9 from pancreas (MiAPaCa-2, Capan-1, Capan-2, PANC-1, AsPC-1, HPAF, Hs766T, BxPC3, and Hs578T); 7 from stomach (AZ521, JRST, KATOIII, MKN 1, MKN28, MKN 45, and MKN74); 2 from lung (A549 and SK-LU-1); and 1 each from small intestine (HuTu80), ovary (PA-1), and breast (MDA-MB-468).