No abstract available.
Chemoprevention ; Tuberculosis

No abstract available.
Chemoprevention* ; Head and Neck Neoplasms* ; Head*

One of the best approaches against cancer is prevention. Inactivation of the p53 or p16INK4a genes has been extensively reported in most human cancer cells. Both p53 and p16INK4a function as tumor suppressors. Therefore, functional restoration of these molecules is considered to be one of the most useful methods for cancer prevention and therapy. We have proposed a concept termed ‘gene-regulating chemoprevention and chemotherapy’ regarding the above pathway. This concept assumes that transcriptional regulation by drugs on tumor-suppressor genes, downstream target genes or functionally similar genes (for example, family genes) of the tumor-suppressor genes would contribute to the prevention of human malignancies. Histone deacetylase (HDAC) inhibitors have been shown to be potent inducers of growth arrest, differentiation and apoptotic cell death. Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21WAF1/Cip1, a downstream target gene of p53, in a p53-independent manner. Furthermore, we have recently shown that HDAC inhibitors activate Gadd45, another downstream target gene of p53, and p19INK4d, a gene functionally similar to p16INK4a. Our results, taken together with previous findings, suggest that HDAC inhibitors may be one of the most attractive and promising agents for ‘gene-regulating chemoprevention’ and ‘molecular-targeting prevention’ of cancer.
Prevention ; Malignant Neoplasms ; Chemoprevention ; inhibitors ; Genes

No abstract available.
*Chemoprevention ; Colorectal Neoplasms/*prevention & control ; *Diet ; Humans

Metformin is a first-line anti-diabetic drug that has been widely used in patients with type 2 diabetes. Many population-based epidemiologic studies have shown that metformin treatment is associated with decreased risk for various cancers. Recent epidemiologic studies showed that the use of metformin was associated with a reduction in gastric cancer risk, especially in patients with type 2 diabetes who used metformin for long periods of time (>2~3 years). Currently, there are no registered clinical trials investigating the anti-cancer effect of metformin in gastric cancer; hence, further well-designed clinical trials are required. Herein, we review the literature regarding the use of metformin for the prevention of gastric cancer.
Chemoprevention* ; Epidemiologic Studies ; Humans ; Metformin* ; Stomach Neoplasms*

Background: Administration of chemotherapy to prevent postmolar gestational trophoblastic neoplasia was first implemented in the 1960’s. However, its use has remained controversial. Objectives: This study aimed to describe the effect of chemoprophylaxis in preventing progression of hydatidiform mole to gestational trophoblastic neoplasia among patients managed in a tertiary hospital in Davao City from 2011 to 2015. Materials & Method: This retrospective cross-sectional study evaluated 123 cases of hydatidiform mole who were managed at a tertiary hospital in Davao City from the years 2011 to 2015. The patients’ charts were retrieved to get the clinicodemographic profile, progression to gestational trophoblastic neoplasia, and occurrence of adverse effects secondary to chemoprophylaxis. Patients with rising or plateauing beta human chorionic gonadotropin titer were identified within the 3-year period from molar evacuation. Collected data were analyzed using frequency and percentage distribution. Results: The mean age of the patients was 30.5 years, 24% of whom were noted in women more than 40 years of age. The average age of gestation on admission was 14.89 weeks. All patients had a histopathologic diagnosis of complete mole and at least one risk factor for developing postmolar gestational trophoblastic neoplasia. Patients did not experience any significant side effect to chemoprophylaxis. None of the patients developed gestational trophoblastic neoplasia within the 3-year period of monitoring. Conclusion The administration of chemoprophylaxis to patients diagnosed with hydatidiform mole may be effective against the development of postmolar gestational trophoblastic neoplasia.
Pregnancy ; Female ; Gestational Trophoblastic Disease ; Hydatidiform Mole ; Neoplasms ; Chemoprevention

A number of naturally-occurring or synthetic chemicals have been reported to exhibit prostate chemopreventive effects. Synthetic 5alpha-reductase (5-AR) inhibitors, e.g. finasteride and durasteride, gained special interests as possible prostate chemopreventive agents. Indeed, two large-scale epidemiological studies have demonstrated that finasteride or durasteride significantly reduced the incidence of prostate cancer formation in men. However, these studies have raised an unexpected concern; finasteride and durasteride increased the occurrence of aggressive prostate tumor formation. In the present study, we have observed that treatment of finasteride did not affect the growth of androgen-refractory PC-3 prostate cancer cells. Finasteride also failed to induce apoptosis or affect the expression of proto-oncogenes in PC-3 cells. Interestingly, we found that treatment of finasteride induced the expression of Nrf2 and HO-1 proteins in PC-3 cells. In particular, basal level of Nrf2 protein was higher in androgen-refractory prostate cancer cells, e.g. DU-145 and PC-3 cells, compared with androgen-responsive prostate cancer cells, e.g. LNCaP cells. Also, treatment of finasteride resulted in a selective induction of Nrf2 protein in DU-145 and PC-3 cells, but not in LNCaP cells. In view of the fact that upregulation of Nrf2-mediated phase II cytoprotective enzymes contribute to attenuating tumor promotion in normal cells, but, on the other hand, confers a selective advantage for cancer cells to proliferate and survive against chemical carcinogenesis and other forms of toxicity, we propose that finasteride-mediated induction of Nrf2 protein might be responsible, at least in part, for an increased risk of high-grade prostate tumor formation in men.
Apoptosis ; Carcinogenesis ; Chemoprevention ; Finasteride* ; Hand ; Humans ; Incidence ; Male ; Prostate* ; Prostatic Neoplasms ; Proto-Oncogenes ; Up-Regulation

The retinoic acid, one of the most popular agents for chemoprevention can inhibit the proliferation of many cancer cells including neuroblastoma and glioblastoma but there is increasing demand reaccessing its in vitro inhibitory effect on the tumor proliferation because of poor responsiveness from recent clinical trial for malignant brain tumor with retinoic acid. If was known to effect on tumor cells by diffferentiation and apoptosis so that its effect was expected greater in pediatric brain tumor than in adult brain tumor, but there is no report on the effect of retinoic acid in medulloblastoma cell proliferation except all-trans and 13-cis retinoic acid. Therefore, we compared the effects of all-trans, 13-cis, and 9-cis retinoic acid and N-(4-hydroxyphenyl) retinamide to inhibit proliferation of medulloblastoma tumor cells. Medulloblastoma cells were derived from primary culture of patient's specimen. We estimated the rate of growth inhibition of each tumor cells using MTT assay in the concentration from 10-12 M to 10-5 M of all-trans, 13-cis, and 9-cis retinoic acid and N-(4-hydroxyphenyl) retinamide. Medulloblastoma cells showed more than 30% growth inhibition by all-trans, 12% by 13-cis, 20% by 9-cis retinoic acid and 7% by N-(4-hydroxyphenyl) retinamide at 14 days culture on the concentration of 10-6M. In conclusion, significanty and dramatic effect by, especially, all-trans retinoic acid, moderate response by 13-cis retinoic acid and variable or poor response by 9-cis retinoic acid and N-(4-hydroxyphenyl) retinamide.
Adult ; Apoptosis ; Brain Neoplasms ; Cell Culture Techniques* ; Cell Proliferation ; Chemoprevention ; Glioblastoma ; Humans ; Medulloblastoma* ; Neuroblastoma ; Retinoids* ; Tretinoin

When a Korean child is living in close contact with a person with active pulmonary tuberculosis, the risk of his acquiring the disease is great. In seeking an effective means of reducing this risk to the chi1d, isoniazid was given as secondary chemoprophylaxis to 233 tuberculin-positive children under 5 years of age who were clinically free of disease but were living in close contact with a household member with active tuberculosis. The condition of these children after 9 to 12 months of chemoprophylaxis was compared with a similar control group of 216 children living under exact1y comparable circumstances. An analysis of tile results of this study indicates that secondary chemoprophylaxis with isoniazid is effective and worthwhile for children under 4 years of age who are under constant exposure to tuberculosis. That there was such a protection is indicated by the fact that (1) isoniazid markedly reduced the size of the tuberculin reaction and that (2) only 2 children receiving isoniazid developed active tuberculosis (0.8%) as against the 8 controls who did (3.70%). The faithful cooperation of parents in administering prophylactic isoniazid to small children is often difficult to obtain. This difficulty is suggested by the fact that in the case of the 2 children in the isoniazid test group who developed active tuberculosis, the actual drug intake had been irregularly given and amounted to less than half the prescribed dose.
Chemoprevention ; Child ; Family Characteristics* ; Humans ; Isoniazid ; Parents ; Tuberculin ; Tuberculosis ; Tuberculosis, Pulmonary*

Cancer prevention is a challenging project both in the basic and clinical medicine. In particular, prevention of liver cancer is the most urgent task in countries where the incidence of hepatitis virus-related liver cancer is rising. As reviewed in this article, liver cancer is going to be the first cancer that will be actually prevented by primary and secondary interventions. Even the improvement of absolute survival of the patients can be expected by successful prevention, as already demonstrated in a few clinical trials. Thus, prevention of liver cancer is promising to provide not only cost-effectiveness by morbidity reduction but also cost-benefit by mortality improvement.
Animals ; Chemoprevention ; Hepatitis B/complications/drug therapy ; Human ; Liver Neoplasms/etiology/*prevention & control ; Retinoids/*therapeutic use