[The expression of mutation p53 gene from circulating cancer cells of peripheral blood and the clinical significance in detecting the patients with colorectal cancer].

OBJECTIVE: To study the clinical significance of detecting p53 gene mutation expression in colorectal cancer cells of peripheral blood. METHODS: Flow cytometry (FCM) was used to detect p53 gene mutation expression in peripheral blood cancer cells of 128 patients with colorectal cancer. Experimental data were analyzed by SPSS (v.11.0) software. RESULTS: The lymph node metastasis showed the significant difference statistically (P<0.01) between p53 positive and negative expression in the colorectal cancer patients. The mutation p53 expression associated with existing histological differentiation (r=0.8476, P<0.05). A lymph node metastasis difference was observed between left and right colorectal cancers of mutation p53 positive expression. CONCLUSION: Detecting the mutation p53 expression in cancer cells of peripheral blood might be helpful to the early diagnosis of colorectal cancer.

[Epigenetics promotes a new round of the genetic development].

Scientific development is pregnant with a breakthrough, epigenetic studies are pushing the genetics forward. Epigenetics is the study of heritable changes in gene expression that occurs without a change in DNA sequence. Epigenetics not only has practical significance for medicine and agriculture, but also provides new views on understanding heredity and evolution. Human genome contains information in two forms: the genetic information provides the blueprint for the manufacture of all the proteins necessary to create a living thing while the epigenetic information provides instructions on how, where, and when the genetic information should be used. The interrelationship of genetics and epigenetics is like a yin-yan, they are different from each other, and cooperatively take part in regulation of a variety of living activities. In this paper concept of gene and problems of evolution has been also discussed according to epigenetic viewpoints.

[Study of in vivo micronucleus formation in lymphocytes from the patients and its relation to malignant degrees of colorectal cancer].

OBJECTIVE: To investigate the association of the micronucleus (MN) formation in lymphocytes from patients with the malignant degrees of colorectal cancer. METHODS: The MN test in capillary blood lymphocytes was conducted in 112 patients randomly selected from in-hospital patients before therapy. Experimental data were analyzed by SPSS (v.10.1) software. RESULTS: The differences in the frequency of MN between 7 pathological types of colorectal cancers and controls were statistically significant (P<0.01). The frequency of MN increased with the decrease of the histological differentiation in colorectal cancer, and the statistically significant differences were seen between low differentiation group and the other differentiation groups in colorectal cancers. CONCLUSION: There is a significant correlation between MN formation and the malignant degrees of colorectal cancer, and MN formation will be a useful biomarker for the identification of malignant degrees of colorectal cancer before operation or for the screening of high risk subgroup.

[Molecular genetic and epigenetic mechanisms of hepatocarcinogenesis].

Hepatocellular carcinoma (HCC) is a major type of primary liver cancer and one of the most frequent human malignant neoplasms. Common risk factors of human HCC include chronic hepatitis virus (HBV and HCV) infection, dietary aflatoxin B1 (AFB1) ingestion, chronic alcohol abuse, and cirrhosis associated with genetic liver diseases. Hepatocarcinogenesis is the result of interaction between hereditary and environmental factors. Inheritance determines individual susceptibility to cancer; environment determines which susceptible individuals express cancer. Studies of genetic and epigenetic mechanisms of hepatocarcinogenesis showed that HCC development is a complex polygene and multipathway process; the activation of proto-oncogenes and the inactivation of tumor suppressor genes induced by genetic and epigenetic alterations are core biological processes of hepatocarcinogenesis; RB1, p53, and Wnt pathways are commonly affected in HCCs of different etiologies, which may reflect common pathologic sequence of HCC: chronic liver injury, cirrhosis, atypical hyperplastic nodules, and HCC of early stages. Hepatitis virus infection-associated HCCs have frequent alterations in RB1 pathway, including methylation of p16INK4a and RB1 genes and amplification of Cyclin D1. AFB1 exposure-associated HCCs have frequent alterations in p53 pathway; the G-->T mutation of p53 gene at codon 249 has been identified as a genetic hallmark of HCC caused by AFB1. Alcoholism-associated HCCs have frequent alterations in both RB1 and p53 pathways. The roles of some important genes related to cell apoptosis, DNA repair, drug metabolism, and tumor metastasis in hepatocarcinogenesis had been discussed.