Chemopreventive effect of Panax ginseng.

Asian ginseng (Panax ginseng C. A. Meyer) has been used in Chinese medicine for two thousand years. The root of ginseng contains several saponins (ginsenosides) which are biologically active compounds. Individual ginsenosides suppress tumor cell growth, induce cell differentiation, regulate apoptosis and inhibit metastasis formation. The aim of this study was to evaluate its chemo-preventive effects in an animal test model, through its regulatory effects on apoptosis and the cell cycle.The expression of genes (Bcl-2, Bcl-x and Cyclin D1) which affect apoptosis were examined, in different organs of animals which had consumed a ginseng-containing diet in the presence of a known carcinogen (DMBA). The pattern of gene expression was determined by Q-RT-PCR. The increase of antiapoptotic gene expression after carcinogenic exposure was suppressed by consumption of ginseng which promoted apoptosis.The population is exposed to numerous physical and chemical insults in the modern environment and these include compounds which are known carcinogens. Research has shown that it is possible to interfere with the multi-step process of carcinogenesis through the use of compounds with chemo-preventive effects, such as the inhibition of the activation of antiapoptotic genes.These results support the efficacy of ginseng-containing diets and dietary supplements in the prevention of cancerous diseases.

Early effects of transplatin on oncogene activation in vivo.

The aim of the study was to investigate the early effect of Transplatin (the stereo-isomer of Cisplatin) on oncogenes in inbred CBA/Ca mice. Cisplatin is commonly used for the treatment of squamous cell carcinomas of the head and neck. Cisplatin has a strong oncogene activation effect compared to the structural analogue Transplatin. Body weight equivalent amounts of a human dose of Transplatin were administered intra-peritoneally to 6- to 8-week-old, inbred, female CBA/Ca mice. Twenty-four, 48 and 72 hours after the treatment, RNA was isolated from the target organs and the expressions of c-myc, Ha-ras and p53 genes were examined. Investigation of early changes showed no significant overexpression compared to Cisplatin, which had a significant effect on oncogene expression in the "short-term" in vivo test system.

Early effects of different cytostatic protocols for head and neck cancer on oncogene activation in animal experiments.

In vivo investigations on oncogenes and onco-suppressor genes may provide new findings on the potential carcinogenic effects of various cytostatic protocols inducing secondary tumours of the head and neck. Further surgeries are often necessary due to regional recurrence after the Cisplatin-supplemented BVM (Bleomycin, Vincristine, Methotrexate) protocol in the treatment of human head and neck tumours. Our earlier studies have illustrated the carcinogenic and mutagenic potential of Cisplatin. The effect of Cisplatin on the alteration of different onco- and suppressor genes has also been proven. Our present study aimed at investigating the early effects of the BVM and the CFu (Cisplatin, 5-Fluorouracil) protocols on early oncogene and tumour suppressor gene expressions in mice. Body weight equivalent amounts of cytostatics were administered intraperitoneally to 6- to 8-week-old, inbred, female CBA/Ca mice. Twenty-four, 48 and 72 hours after the treatment, RNA was isolated from the target organs and the quantitative expression of c-myc, Ha-ras and p53 genes were examined. The protocols caused detectable changes. A "short-term" in vivo test, the 24-hour examination of gene expression, is suitable for detecting early effects of carcinogen exposure. The alterations of gene expression, caused by the Cisplatin-containing protocol, draw attention to the probable role of Cisplatin in the development of regional recurrence and to the possibility of prevention.

Long-term effects of 1-nitropyrene on oncogene and tumor suppressor gene expression.

Late changes in the expression of oncogenes and tumor suppressor genes following carcinogenic exposure were examined in lung, liver and kidney. 1-Nitropyrene (1-NP), which is a high-risk exposure factor in urban and industrial zones, was used as a carcinogenic agent. c-myc, Ha-ras and p53 gene expression was investigated after administration of a single dose of 1-NP to sensitive CBA/Ca mice in lung, liver and kidney for one year. One week after a single dose 1-NP administration, the expression of p53 was elevated in the liver, but, decreased in the lung and kidney. There was no increase in the expression of c-myc or Ha-ras genes at that time. One month after the administration of the 1-NP, the expression of p53 was increased in the kidney while the expression of Ha-ras and p53 was elevated in the liver. There was no significant difference in gene expression between the treated and control animal groups at any of the investigated periods except for the above-mentioned organs and at the end point of the investigation. According to the literature, 1-NP and its metabolites remain at high concentrations in the kidney, liver and lung. The concentration of the carcinogenic agent and the expression of the studied genes did not seem to correlate with each other in this experiment.

[Diagnosis of Prader-Willi syndrome by reverse transcriptase polymerase chain reaction]. / Prader-Willi-szindróma diagnózisa reverz transzkripciós polimeráz láncreakcióval.

To approve Prader-Willi syndrome by molecular diagnostic assay, polymerase chain reaction of reverse-transcribed RNA was introduced by which indirect information can be gained on all known forms of the mutation. In this pilot study, 4 patients and 16 healthy control individuals were examined. Although the different mutation forms can not directly by identified by this approach, it is a useful and reliable test to confirm the clinical diagnosis of the Prader-Willi syndrome, and to screen for the syndrome in patients who present with only a few typical features.

[Mutation analysis in the CTG-base multiplication in a family with myotonic dystrophy in three generations]. / Mutációanalízis a CTG-bázishármas megsokszorozódásának vizsgálatával egy háromgenerációs myotoniás dystrophiás családban.

A PCR-based method with a novel silver staining detection was developed for the determination of CTG repeat number in the 3' untranslated region of the MD-PK gene responsible for myotonic dystrophy. Through the investigation of a family with affected members in three generations the application of the method is presented. According to the results, healthy individuals were verified easily, and the repeat number in patients with mild features or with premutation could be determined accurately. In severe clinical forms, e.g. congenital myopathy, the expansion can be deduced only from the lack of amplification, however, this is also helpful if the segregation of familial alleles is known.

[Molecular biologic screening test (PCR) for fragile X syndrome]. / Fragilis X szindróma szürésére alkalmas molekuláris biológiai (PCR) eljárás.

Fragile X syndrome is the most common inherited from of familial mental retardation. It is caused by an expanded CGG repeat in the first exon of the fragile X mental retardation gene. A polymerase chain reaction based technique was used for the identification of full mutations among men. According to our conditions full mutations failed to amplify. An internal control was used at a CG rich region 147 bp upstream of the polymorphic region. The bands were visualised on silver stained polyacrylamide gels. From the 57 individuals studied molecular analysis was performed on 38 males and 16 females. From the 26 males with suspected fragile X syndrome 9 males resulted in no amplification of the 500 kb product, all having a positive cytogenetic result for fragile X syndrome. One cytogeneticly positive male had normal results by molecular studies suggesting a different mutation. All control males had normal results. The results on the 16 females studied were inconclusive. We suggest that our method is highly sensitive and specific for screening males for fragile X syndrome.