Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Molecular characterization of eight gastric cancer cell lines established in Japan are summarized according to the genetic and epigenetic alterations and growth factor status. TMK-1 poorly differentiated adenocarcinoma cell line harbors mutant p53 tumor suppressor gene and rearrangement of p15MTS2. MKN-1 adenosquamous carcinoma line with mutant p53 reveals silencing of E-cadherin by promoter CpG hypermethylation. MKN-7 well-differentiated adenocarcinoma cell line has amplification of c-erbB2 oncogene and cyclin E gene. MKN-28 well-differentiated adenocarcinoma cell line reveals mutations in p53 and APC tumor suppressor genes and silencing of CD44. The MKN-45 poorly differentiated adenocarcinoma cell line with wild-type p53 is characterized by homozygous deletion of p16CDKN2/MTS1/INK4A and p15MTS2, amplification of c-met oncogene and promoter mutation of E-cadherin. MKN-74 derived from moderately differentiated tubular adenocarcinoma has wild-type p53. KATO-III signet ring cell carcinoma line has genomic deletion of p53, amplification of K-sam and c-met oncogene and mutation of E-cadherin. HSC-39 signet ring cell carcinoma cell line harboring p53 missense mutation has homozygous deletion of p16CDKN2/MTS1/INK4A and p15MTS2, amplifications of c-myc, c-met, K-sam and CD44 gene and mutation in beta-catenin gene.
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PMID:Molecular characteristics of eight gastric cancer cell lines established in Japan. 1110 48

Somatic mutations of the APC gene in eight cancer cell lines, twelve adenomas and sixteen intestinal metaplasias of the stomach were examined. The expression of the APC mRNA and protein in eight cancer cell lines was also investigated. PCR-SSCP analysis detected mutations of the APC gene in 25% (2 out of 8) of cancer cell lines, 42% (5 out of 12) of gastric adenomas, 6% (1 out of 16) of intestinal metaplasia mucosae. Direct sequencing analysis confirmed nonsense mutations in one cancer cell line, one adenoma and one intestinal metaplasia mucosa resulted in truncation of the product, frameshift mutations in one adenoma and silent mutations in one cancer cell line and three adenomas. In addition, the KATO-III cell line, which was established from signet ring cell carcinoma, expressed very low level of APC mRNA and its APC protein could not be detected. On the other hand, the expression level of variant APC mRNA transcript which lacks exon 7 was relatively high in KATO-III. It is supposed that the variant APC mRNA transcript might contribute to the inactivation of the APC gene. These data overall provide strong evidence that changes in the APC gene play an important role in the early event of stomach carcinogenesis, especially in intestinal type gastric cancer.
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PMID:Alterations of the apc gene in carcinoma cell-lines and precancerous lesions of the stomach. 2155 77