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On the 25th of March, 2001, a ceremony was held at the Training Centre of the Asian Pacific Organization for CancerPrevention (APOCP) to commemorate its official opening. Attended by the Chairman, Secretary-general and Treasurer ofthe the APOCP, as well as the Director of the National Cancer Institute of Thailand and individuals from Chulalongkornand Mahidol Universities, and the Japanese International Cooperation Association Office in Thaiiland, the occasion featuredaddresses from Kazuo Tajima and a representative of JICA, with whom Aichi Cancer Centre is collaborating in developingone of the types of course which it is hoped will now be able to be offered in a central location in Bangkok, right at the hubof the Asian Pacific region.
This symposium was the first projected for general population to provide comprehensive information on research subjectsin the Study Area of Cancer Epidemiology (SACE) newly established in the Special Priority Area (C) sponsored by theJapanese Ministry of Education, Science, Culture, Sports and Technology. This (SACE) consists of five research branchesfunctionally divided into: 1) Ethnoepidemiology; 2) Cohort studies; 3) Case-control studies; 4) Molecular epidemiology;and 5) Clinical epidemiology.In this symposium eight scientists selected on the basis of these five different research branches presented work in foursections: 1) Ethnoepidemiologic topics regarding the cancer pattern in the world and Japan; 2) Cancer risk factors in generallifestyles analyzed by case-control and cohort studies in Japan; 3) Viruses and cancer with special reference to the originalrelationship between human evolution and virus infection; 4) New strategies of prevention and treatment taking into accountindividual characteristics.The final goal of epidemiological research is to establish a prevention strategy after clarifying risk and protective factorsfor human cancer by long-term observation of large populations. In general, the pattern of human cancers varies withchange in actual exposure to specific carcinogenic agents, e.g., quality and quantity of environmental factors, over time andspace. On the other hand, the biological risk of cancer related to a specific agent varies with genetic background amongdifferent ethnic groups in the world, and even among individuals in the same ethnic group.We human beings have established our own cultures adapting to the given environment in each area in the world.Unfortunately, in some cases, this has had a negative outcome in generating culture-specific diseases. Now we need innovative,comprehensive and multidisciplinary ideas to build up new prevention strategies to fight against cancer. In this symposiumwe presented general information on cancer epidemiology as clearly and succinctly as possible to promote discussion withaudience about goals in the 21st century.
Cancer research has a long and distinguished history and as we continue our work in ever expanding new fields, molecularor otherwise, it is perhaps worthwhile to take time out occasionally to ponder what lessons we can learn from the past. Manyof the paradigms which are presently accorded respect in fact were hinted at by very early work and it is fitting that we takea look at how previous developments knit with the present status of cancer research in different areas of the world. For thispurpose the present review focuses on Japan and the United States, in the hope of gleaning advantage from past experiencein planning future programs.
Preneoplastic lesions have been described for most major sites of human tumour development. They appear to be sharecharacteristics like monoclonality, induction by all classes of carcinogens and some quantitative relationship to actualtumours. Extensive studies of preneoplasia in the liver of the rat has indicated that a directed shift in phenotype occurs,commensurate with greater physiological emphasis on growth potential. One characteristic change is increase in the keyenzyme of the pentose phosphate pathway, glucose 6 phosphatase dehydrogenase as well as elevation in glycolysis, reductionof gluconeogenesis. In general, the changes observed in preneoplastic liver lesions appear reminiscent of the effects ofinsulin or other hormones on hepatocytes, pointing to possible application of specific inhibitors for cancer chemoprevention.
The anticarcinogenic effect of tomato juice, a natural source of antioxidants and other chemopreventive /antimutagenic agents, was studied in a skin carcinogenesis model in mice. The possible mode of action was alsoinvestigated. Oral administration of tomato juice afforded protection from development of skin tumour and increasedlife expectancy which may be attributed to the combined action of a number of chemical compounds with cancerchemopreventive properties present in tomato. The protective role may be associated with a decreased level of lipidperoxides noted in the tomato treated group and modulation of host detoxification enzymes. Exposure to the carcinogenresulted in a depression of the liver enzymes- glutathione-S-transferase (GST), glutathione peroxidase (GPx) andsuperoxide dismutase (SOD). Oral administration of tomato juice resulted in significant activation of all these enzymes(p<0.001). These results suggest a preventive role of tomato juice during carcinogenesis which is mediated possiblyby their modulatory effects on biotransformation enzymes and the detoxification system of the host.
Few studies have been performed to evaluate the effect of skin surveillance on melanoma risk. This populationbasedcase-control study was carried out to confirm the association of phenotype with melanoma and to investigatethe effect of surveillance by skin examination on the risk of melanoma in New Zealand. Cases were patients with afirst diagnosis of in-situ or invasive cutaneous malignant melanoma from three regions of New Zealand. Controlswere selected at random from the electoral rolls and frequency-matched by age. Participants included men andwomen of European origin aged between 20 and 79 years. A strong association was found between host phenotypicfactors (red hair, fair skin, many freckles on the face, and numbers of moles) and melanoma risk. These effects werelargely independent of each other.The relative risk of melanoma was significantly reduced after skin examination byone’s self, partner or a health professional; this reduction in risk remained after adjustment for phenotype, molecounts, skin reaction to sun, and exposure to sun. People who attended a ‘skin check clinic’ had a non-significantincrease in risk of melanoma.
Cyclooxygenase 2 (COX2) is an inducible enzyme synthesizing prostaglandins from arachidonic acid, which isthought to play an important role in colorectal carcinogenesis. Since the COX2 polymorphisms, if functional, maymodify the carcinogenesis pathway, the associations between the reported polymorphisms and colorectal cancer riskwere examined in a hospital-based case-control study. Six polymorphisms of the gene encoding COX2 were genotypedfor 241 non-cancer individuals (controls) and 148 colorectal cancer patients (74 colon cancer, 73 rectal cancer, and 1colorectal cancer date, 22 polymorphisms including the above six have been reported for COX2. The otherpolymorphisms remain to be examined.
Epidemiological studies, especially cohort studies have many limitations in countries like India. The presentpopulation based molecular epidemiolohgical cohort study was planned to address the prevalence, risk factors andnatural history of uterine cervical HPV infection in women in an area of suburban dwellings in South India.Epidemiological data, blood samples and cervical scrape smears were collected from women after obtaining aninformed consent. A compliance rate of 38% for the first round of screening was noted. More than 70% of womendemonstrated evidence of inflammation in their smears.
The present experiment was conducted to assess the influence of vitamin E, given in the diet at 0.5 or 1%, oninduction of lesions in the Syrian hamster liver by long term combined administration of sodium nitrite andaminopyrine in the drinking water. Inhibition of both cholangiofibrosis and cholangiocarcinoma development, aswell as a reduction in hepatocellular nodules was the result. The underlying mechanisms presumably involve alterationof endogenous dimethylnitrosamine formation by the vitamin, with clear implications for prevention in the humanenvironment.
Considerable increase in cancer deaths has been observed since 1995, after when the tenth version of the internationalclassification of disease (ICD) was introduced in Japan according with the revision of a death certificate form at thesame time. We assessed the contributing factors for this unnatural fluctuation, using a population-based cancerregistry data as a model. All deaths of the prefectural residents are collated with the cancer registry database in theregistration process. For all Japanese deaths of Aichi Prefecture in 1994 (n=41,111) and in 1995 (n=42,944), thedescription of the death certificates were compared with the ICD classified as the cause of death. It was ascertainedthat 97-99% of cancer and 97-98% of non-cancer deaths classified by ICD were proper. Among those classified ascancer as the cause of death and stated as other than the direct cause of death (n=92 in 1994, n=428 in 1995), only22% (1994) and 8% (1995) were considered to be classifiable to both cancer and non-cancer as the cause of death.Among those who were classified as non-cancer as the cause of death in spite of including cancer in the originalstatement (n=770 in 1994, n=638 in 1995), 24% (1994) 10% (1995) were considered to be non-cancer as the cause ofdeath, and the rest were considered classifiable into both cancer and non-cancer. Even if all cancer deaths classifiableto non-cancer were classified as non-cancer deaths, change in the number of cancer deaths was inconsiderable inboth years. Therefore, it is suggested that the increase of cancer deaths after introduction of the new ICD was causednot by the artifact such as change in selection rule of disease when classify the cause of death, but by the improvementof the description of death certificate by physicians as a result of revision of death certificate form.
Extensive studies have so far been principally made using hydrophobic carcinogens in the field of chemicalcarcinogenesis. However, the species of glutathione S-transferases (GSTP1-1) linked to neoplasia of rat and humanwere recently shown to be selective for hydrophilic carcinogens such as acrolein and hydroxyalkenals (Satoh, 1998;Satoh et al., 1999) in accord with the finding of a water-network in the active site of the human GSTP1-1 by X-rayanalysis (Hu et al.; Ji et al., 1997). These results indicate that water-soluble carcinogens may be more significant thantheir hydrophobic counterparts in vivo. Of note, half-times for excretion of hydrophilic compounds are as short asseveral hrs, while those for hydrophobic ones are as long as several months or years. These available enzymologicaldata suggest on importance of consuming water to prevent cancer.
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