Zhonghua Yi Xue Yi Chuan Xue Za Zhi

[The relationship between p53 mutation and esophageal cancer biological behavior]

He Y. Li M. Shang X.
Department of Biology, Nanjing Railway Medical College, Nanjing, 210009 P. R. China.
OBJECTIVE: To investigate the relationship between p53 mutation and esophageal cancer biological behavior as well as its prognostic role in esophageal cancer. METHOD: Mutations in exon 5-8 of p53 were screened in 30 sporadic esophageal cancers by a combination of PCR-SSCP and PCR-direct DNA silver sequencing. RESULTS: Mutations were found in 11 cases (36.7%). There were 9 point mutations, including 4 missense mutations, 2 nonsense mutations, 3 silent mutations. The other 2 cases were frameshift mutations due to base insertion and deletion. With statistical analysis, the p53 mutation rate was 56.3% in moderately and poorly-differentiated esophageal cancers, 14.3% in well-differentiated cases, with a highly significant difference between the two groups (P=0.025). The mutation rate of the cancers with all layers invaded (52.6%) was remarkably higher than that of the cancers without all layers invaded (9.1%)(P=0.024). A significantly higher rate of p53 mutation was also seen in cases with lymph nodes metastasis (61.5%) than in cases with no lymph nodes metastasis (17.6%) (P=0.024). CONCLUSION: The data suggest that there is a strong correlation between the presence of p53 mutation and the biological behavior of human esophageal cancer, such as histologic differentiation, invasion stage, and regional lymph nodes metastasis. Detection of p53 mutation can be helpful in identifying more progressive esophageal cancer and assessing prognosis. The study also discussed the dominant negative effect of p53 and the genetic effect of silent mutation.

[Molecular cytogenetic study on four human esophageal cancer cell lines]

Year 1998
Xiao F. Wang X. Wang M. Guan X. Wu M.
Nation Laboratory Molecular Oncology Cancer Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021 P. R. China.
OBJECTIVE: To investigate the possible involvement of chromosome abnormalities in pathogenesis of human esophageal cancer. METHODS: Four cell lines of human esophageal cancer (EC) established in our laboratory were analysed using interphase fluorescence in situ hybridization (FISH), chromosome painting technique and comparative genomic hybridization (CGH). RESULTS: Chromosome gain of 1,2,3,8,16, 17, and 20 was found in the four cell lines, and loss of chromosome Y in cell line EC8712, EC8733 and EC8501 was noted. Other frequent changes were partial deletion of 1p, translocation of 2q and amplification of 5p in all 4 cell lines, and amplification of 8q and 13q in EC8733 and deletion of 17p in EC8712. CONCLUSION: The data suggest that nonrandom chromosome aberrations may play an important role in the pathogenesis of human esophageal cancer.

[Studies of microsatellite instability in Chinese gastric cancer tissues]

Year 1998
Wang Y. Ke Y. Ning T. Feng L. Lu G. Liu W. E Z.
Department of Cancer Genetics, Beijing Institute for Cancer Research, Beijing Medical University, Beijing, 100034 P.R.China.
OBJECTIVE: To identify the microsatellite instability(MSI) rates in Chinese gastric cancer samples. METHODS: 29 microsatellite markers were selected to examine 42 paired gastric cancer tissues for MSI on all chromosomes except Y. RESULTS: The total frequency of MSI in all 42 gastric cancers was 33.9% with higher rates at loci of D3S1577, D3S1067,D8S279,D9S257, D1S248, D7S520 and D2S147,and the highest rate at D3S1577 and D3S1067(51.35%). MSI varied with different pathological types.The frequencies of MSI were signi- ficantly higher in poorly differentiated tumors and signet cell types, compared with well differentiated tumors(P=0.0026 and 0.0013 by chi-square test),and no difference was noted between poorly differentiated and signet cell types. CONCLUSION: MSI may play an important role in Chinese gastric cancer, particularly the poorly differentiated adenocarcinomas. The data presented here further support the previous hypothesis that pathologically distinct subtypes of gastric cancer undergo different genetic pathways during tumorigenesis.