Messenger RNA differential display was used to study liver‐gene expression in paired tumor and non‐tumor tissues from hepatocellular carcinoma (HCC) patients. mRNA differential display and Northern‐blot analyses showed that a 0.8‐kb cDNA fragment was diminished or absent from the tumorous tissues of 7 HCC patients. The cDNA fragment was sequenced and found to have 98.7% nucleotide sequence homology with human glycine‐N‐methyltransferase cDNA (GNMT). In addition, there was no detectable level of GNMT expression in 4 human HCC cell lines, SK‐Hep1, Hep 3B, HuH‐7 and HA22T, examined by Northern‐blot assay. A full‐length GNMT cDNA clone‐9‐1‐2 was obtained by screening a Taiwanese liver cDNA library. In comparison with the GNMT cDNA sequence reported elsewhere, clone 9‐1‐2 had 4 nucleotide differences resulting in 1 amino‐acid change. Immunohistochemical staining with rabbit anti‐recombinant GNMT serum showed that GNMT protein almost completely disappeared in liver‐cancer cells, while it was abundant in the non‐tumorous liver cells. Down‐regulation of GNMT gene expression may be involved in the pathogenesis of liver cancer. Int. J. Cancer 75:787–793, 1998.© 1998 Wiley‐Liss, Inc.

Gastric carcinoma is a common malignancy worldwide. Advanced stages of the disease may result in metastases to many other organs of the body. However, colonic metastases are rare. We report a case of gastric carcinoma with symptoms of abdominal fullness and weight loss. The serum carcinoembryonic antigen level was elevated. Esophagogastroduodenoscopy revealed giant folds occupying the whole gastric body and poor expansion of the stomach. Histologic examination of biopsy specimens from the giant fold demonstrated poorly differentiated adenocarcinoma with signet ring-cell differentiation. Total colonoscopy revealed five or six discrete flat elevated lesions in the distal transverse, descending, and sigmoid colons. These lesions were characterized by a clear margin of 3-5 mm in diameter and erosions on the tips. Polypectomy specimens demonstrated signet ring-cell carcinoma, which was histologically similar to the specimens taken from the gastric lesion. We conclude that this was a rare case in which gastric signet ring-cell carcinoma had metastasized to the colon in the form of flat elevated lesions, combined with rapid and wide lymphatic spread to the thorax and abdomen in a clinical course as short as 46 days.

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A rapid, simple, and nonradioactive method for diagnosing point mutations of c-K-ras oncogenes in gastroenterologic cancers is described. This method involved the selective amplification of DNA fragments from cancer tissues of surgical specimens with specific oligonucleotide primers, followed by digestion with restriction enzymes that recognized artificially created or naturally occurring restriction sites. To detect codon 12 mutations, an artificial Msp I site was created by introducing a single nucleotide mismatch into the 5' mutagenesis primer. Using a similar approach, an Hae III site was created to detect codon 13 mutations. Bal I and MBo II sites were used to detect codon 61 mutations. A total of 61 gastroenterologic cancer cases were studied. Of 35 cases of colorectal cancer, 7 showed mutations: 6 at codon 12 and 1 at codon 13. In 1 of 2 cases of cholangiocellular carcinoma, point mutation at codon 12 was found. One case of duodenal cancer showed point mutation at codon 12. No mutations were found in the cases of hepatocellular carcinoma (4), gastric cancer (12), esophageal cancer (3), or pancreatic cancer (2).