No abstract available.
Chemoprevention ; Tuberculosis

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

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*

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

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

No abstract available.
Antibiotic Prophylaxis

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

Cancer is the most dreaded disease in human and also major health problem worldwide. Despite its high occurrence, the exact molecular mechanisms of the development and progression are not fully understood. The existing cancer therapy based on allopathic medicine is expensive, exhibits side effects; and may also alter the normal functioning of genes. Thus, a non-toxic and effective mode of treatment is needed to control cancer development and progression. Some medicinal plants offer a safe, effective and affordable remedy to control the cancer progression. Nimbolide, a limnoid derived from the neem (Azadirachta indica) leaves and flowers of neem, is widely used in traditional medical practices for treating various human diseases. Nimbolide exhibits several pharmacological effects among which its anticancer activity is the most promising. The previous studies carried out over the decades have shown that nimbolide inhibits cell proliferation and metastasis of cancer cells. This review highlights the current knowledge on the molecular targets that contribute to the observed anticancer activity of nimbolide related to induction of apoptosis and cell cycle arrest; and inhibition of signaling pathways related to cancer progression.
Apoptosis ; Cell Cycle Checkpoints ; Cell Proliferation ; Chemoprevention ; Flowers ; Humans ; Neoplasm Metastasis ; Plants, Medicinal