Trends in Mortality and Morbidity of Uterine Cervix, Female Breast, and Ovarian Cancer in Korea.

In Korea, leading causes of death have dramatically changed from infectious diseases to chronic degenerative illnesses, including malignant neoplasms since 1960. However, little is known about the long-term trends of female malignancies in Korea. This study was conducted to find epidemiological evidence of changes in mortality and morbidity of uterine cervix, female breast, and ovarian cancer through a long-term trends analysis with data representative of the Korean population. Age-standardized mortality rates of three female malignancies were markedly increasing throughout the observation period. Increment ratios in mortality were about two to five during the period 1981-1990. As a proxy estimate of incidence, age-standardized admission rates of female malignancies, as well as proportion index of admission due to each cancer to total admissions, showed a similar increasing trend from 1981 to 1990 in Korea. These results are highly suggestive of the view that both the mortality and morbidity for uterine cervix. female breast, and ovarian cancer must be increasing during the ten-year period since 1981 in Korea. Of the female malignancies, it is most likely that morbidity and mortality of uterine cervix cancer begin to decline after the end of the 19805 in Korea. Particularly noteworthy was a shift of the prevalent age for uterine cervix cancer to older women

Orbital Variations of Biogenic CaCO3 and Opal Abundance in the Western and Central Equatorial Pacific Ocean During the Late Quaternary

Biogenic CaCO3 and opal abundances were measured in two piston cores (PC313 and PC5101) collected, respectively, along the equator in the western and central Pacific Ocean. The age model for core PC313, which extends to about 750 ka, was developed by comparing the oxygen isotope stratigraphy of planktonic foraminifera (N. dutetrei) to the SPECMAP stack. The age model for core PC5101, which extends to about 600 ka, was developed by stratigraphic correlation of CaCO3 contents to those in the well-dated core RC11-210 (Chuey et al. 1987). Both cores distinctly exhibited a series of CaCO3 and opal variations, which are mainly controlled by the orbital eccentricity cycle of about 100-kyr. The orbital-scale cyclic variations of CaCO3 and opal contents appear to be contrasting in both cores such that high CaCO3 and low opal contents occurred during the glacial periods. In contrast, during the interglacial periods, low CaCO3 and high opal contents occurred. Mostly remarkable is the distinct occurrence of a mid-Bruhnes event (MBE) at around 350 ka. The CaCO3 content was higher in core PC5101 than in core PC313 before the MBE, whereas biogenic opal abundance became higher in core PC5101 after the MBE. Such a characteristic discrepancy of biogenic (CaCO3 and opal) production, i.e., a succession of primary producers from coccolithophore to diatom, between cores PC313 and PC5101 may be attributed to the prevailing dominant hydrographic conditions (i.e., the South Equatorial Current), in the path of which both cores are located. The intensity of westward propagation might have been an important factor in contrasting biogenic production centering around the MBE

Evaluation of the Satisfaction and Usefulness of a Web-Based Educational Program for Breast Cancer Patients

The purpose of this study was to evaluate the effectiveness of a web-based breast cancer educational program which consists of special features such as flash animations and online counseling as well as 7 different categories of information on breast cancer. The effectiveness of the program was analyzed in terms of its function and content. A total of 147 women with breast cancer who visited the website for at least 30 minutes and a minimum of 3 visits, participated in the survey

Overview of Players and Information in the Cancer Epidemiology and Control World in Asia

Cancer and related lifestyle diseases are on the increase across Asia and already account for over half the disease-associated mortality in the vast majority of the included countries. An understanding of the epidemiology is therefore of paramount importance. In addition, given the immensity of the problem, cooperation among all the interested parties is of the essence. The present series of reviews were complied with the aim of promoting better comprehension and interaction, focusing on cancer prevalence and the underlying risk and preventive factors in Asia. Data from Cancer Incidence in Five Continents and Globocan 2002, published by the International Agency for Research on Cancer, as well as various other cancer registry sources, were thus married with research information in the public domain, accessible through PubMed. It is hoped that the comprehensive approach adopted for the different regions will help bring together all of the Asian community of individuals involved in cancer epidemiology and control and contribute to establishment of Asian networks for collaborative research. The major players and the overall picture for cancer control are covered in the present overview. Further details are then provided in seven separate regional reviews: for North-Western and Central Asia; South-West Asia; South Asia; Mainland South-East Asia; Peninsular and Island South-East Asia, the Pacific; and North-East Asia. The final section covers possible organ-based strategies for cancer control and, lastly, an Appendix has been included listing research institutes and staff in Asia to facilitate contacts between interested individuals.MOORE MA, 2010, ASIAN PACIFIC J CA S, V11, P147SHIN HR, 2010, ASIAN PACIFIC J CA S, V11, P147Tanaka H, 2009, ASIAN PAC J CANCER P, V10, P1191Yoo KY, 2008, JPN J CLIN ONCOL, V38, P327, DOI 10.1093/jjco/hyn026Sobue T, 2008, INT J CLIN ONCOL, V13, P97, DOI 10.1007/s10147-008-0761-7Okamoto N, 2008, INT J CLIN ONCOL, V13, P90, DOI 10.1007/s10147-008-0759-1Park S, 2008, ASIAN PAC J CANCER P, V9, P371Moore MA, 2008, ASIAN PAC J CANCER P, V9, P815Akhtar F, 2007, ASIAN PAC J CANCER P, V8, P452Kawahara N, 2007, ASIAN PAC J CANCER P, V8, P464CURADO MP, 2007, IARC SCI PUBLICATION, V160WIANGNON S, 2007, ASIAN PAC J CANCER P, V8, P457AHN YO, 2007, J PREV MED PUB HLTH, V40, P265Deerasamee S, 2007, ASIAN PAC J CANCER P, V8, P547Tamakoshi A, 2007, ASIAN PAC J CANCER P, V8, P1Kawahara N, 2007, ASIAN PAC J CANCER P, V8, P146CHENG C, 2006, ASIAN PAC J CANCER P, V7, P350YOO KY, 2005, ASIAN PAC J CANCER P, V6, P238FERLAY J, 2004, GLOBOCAN 2002 CANC IBHURGRI Y, 2004, ASIAN PAC J CANCER P, V5, P77Coleman MP, 2003, CLIN MED, V3, P219Lim GCC, 2002, JPN J CLIN ONCOL, V32, pS37PARKIN DM, 2002, IARC SCI PUBLICATION, V155Tjindarbumi D, 2002, JPN J CLIN ONCOL, V32, pS17Hock LC, 2002, JPN J CLIN ONCOL, V32, pS62Vatanasapt V, 2002, JPN J CLIN ONCOL, V32, pS82Ngelangel CA, 2002, JPN J CLIN ONCOL, V32, pS52Anh PTH, 2002, JPN J CLIN ONCOL, V32, pS92YOO KY, 2002, ASIAN PAC J CANCER P, V3, P85Desai PB, 2002, JPN J CLIN ONCOL, V32, pS13ANH PHT, 2002, JPN J CLIN ONCOL, V32, pS82AHN YO, 2002, JPN J CLIN ONCOL S, V32, pS37YAMAGUCHI K, 2002, JPN J CLIN ONCOL S, V32, pS37TAJIMA K, 2002, ASIAN PAC J CANCER P, V3, P263ROSEMAWATI A, 2001, ASIAN PACIFIC J CA S, V2, P43Wang HE, 2001, ANN EMERG MED, V37, P38MOSAVIJARRAHI A, 2001, ASIAN PAC J CANCER P, V2, P25OSHIMA A, 2001, ASIAN PACIFIC J CA S, V2, P31PARKIN DM, 2001, ASIAN PAC J CANCER P, V2, pS1GAJALAKSHMI V, 2001, ASIAN PACIFIC J CA S, V2, P13SARJADI PT, 2001, ASIAN PACIFIC J CA S, V2, P21ESTEBAN DB, 2001, ASIAN PACIFIC J CA S, V2, P25QASEM BM, 2001, ASIAN PACIFIC J CA S, V2, P25AHN YO, 2001, ASIAN PACIFIC J CA S, V2, P39MUNKHTAIVAN A, 2001, ASIAN PACIFIC J CA S, V2, P47BHURGRI Y, 2001, ASIAN PACIFIC J CA S, V2, P51ALHAMDAN N, 2001, ASIAN PACIFIC J CA S, V2, P61ALLAWATI JA, 2001, ASIAN PACIFIC J CA S, V2, P71YOU SL, 2001, ASIAN PACIFIC J CA S, V2, P75DEERASAMEE S, 2001, ASIAN PACIFIC J CA S, V2, P79ANH PH, 2001, ASIAN PACIFIC J CA S, V2, P85FOO W, 2001, ASIAN PACIFIC J CA S, V2, P9PARKIN DM, 1997, IARC SCI PUBLICATION, V143PARKIN DM, 1992, IARC SCI PUBLICATION, V120MUIR CS, 1987, IARC SCI PUBLICATION, V88WATERHOUSE JAH, 1982, IARC SCI PUBLICATION, V42

S100a9 Knockdown Decreases the Memory Impairment and the Neuropathology in Tg2576 Mice, AD Animal Model

Inflammation, insoluble protein deposition and neuronal cell loss are important features in the Alzheimer's disease (AD) brain. To investigate the regulatory genes responsible for the neuropathology in AD, we performed microarray analysis with APPV717I-CT100 transgenic mice, an animal model of AD, and isolated the S100a9 gene, which encodes an inflammation-associated calcium binding protein. In another AD animal model, Tg2576 mouse brain, and in human AD brain, induction of S100a9 was confirmed. The endogenous expression of S100a9 was induced by treatment with Aβ or CT peptides in a microglia cell line, BV2 cells. In these cells, silencing study of S100a9 showed that the induction of S100a9 increased the intracellular calcium level and up-regulated the inflammatory cytokines (IL-1β and TNFα) and iNOS. S100a9 lentiviral short hairpin RNA (sh-S100a9) was injected into the hippocampus region of the brains of 13-month-old Tg2576 mice. At two months after injection, we found that knockdown of S100a9 expression had improved the cognition decline of Tg2576 mice in the water maze task, and had reduced amyloid plaque burden. These results suggest that S100a9 induced by Aβ or CT contributes to cause inflammation, which then affects the neuropathology including amyloid plaques burden and impairs cognitive function. Thus, the inhibition of S100a9 is a possible target for AD therapy

An Evaluation of the Weibull and the Logistic Models for Cox's Proportional Hazards Model

Cox's proportional hazards model has been widely used in medical researches to evaluate the relationship between prognostic factors of a disease and the occurrence of outcome event. On a theoretical basis, regression coefficient estimated from Cox's proportional hazards model could be approximated by using the Weibull and the logistic model. Breast cancer cases (n=86) diagnosed at the Seoul National University Hospital were selected to evaluate the possibility of some accelerated models as an approximate model to Cox's proportional hazards model. Age at operation, tumor size and lymph node metastasis were the variables concerned in this study. Parameter estimates of two variables from the Weibull model, which seemed not to violate the proportionality assumption of Cox's model, showed almost identical values to those from Cox's proportional hazards model. However, there was a substantial degree of discrepancy in the parameter estimate of another variable, which showed an apparent unproportionality. This study confirmed that both the Weibull and the logistic models could be used as approximate methods to the estimates from Cox's proportional hazards model. Particularly noteworthy was the fact that the PC-SAS system could be successfully applied to survival analysis when the parameters were going to be estimated using Cox's model

Ecologic correlation Study on Nutrients/Foods Intake and Mortal ity for Female Breast Cancer in Korea

In order to investigate the possible role of dieta-ry factors on the recent increase in mortality for female breast cancer in Korea, an ecologic correlation study between per capita intakes of nutrients and foods and the mortality for female breast cancer during the last 10 years was conducted. In spite of the possibility of an ecologic fallacy, the age-adjusted mortality rates for female breast cancer were positively correlated with protein from animal source, total lipid, total animal foods, animal foods to total intake, fresh fish and shellfish, milk and milk products, and meat and meat products. The rates were inversely associated with energy from cereal, total carbohydrate, vegetable foods to total intake, total vegetable foods, daily intake of cereals and grain products, and starch and starch roots. These results suggest that an increased intake of protein- and fat-rich foods rather than carbohydrate-rich foods or vegetables might be associated with the increase in mortality for breast cancer during the last 10 years in Korea

Biogenic CaCO3 and Opal Depositions and Their Latitudinal Comparison During the Past 600 ka in the Central Equatorial Pacific

The orbital-scale variations in biogenic CaCO3 and opal abundance in two piston cores collected in the central equatorial Pacific (core PC5101 from a southern site at _ and core PC5103 from a northern site at _ were compared to assess latitudinal differences. The correlation between the oxygen isotope stratigraphy of planktonic foraminifera (Globigerinoides sacculifer) of PC5103 with the LR04 stacks provides the age of PC5103 to be approximately 950 ka. The age of PC5103 was further refined by correlating the CaCO3 content with the well-dated core RC11-210. The age of PC5101 was also constrained by the same CaCO3 chronostratigraphic correlation with RC11-210, resulting in an age of approximately 650 ka. Distinct orbital-scale series of CaCO3 and opal variations appear to be parallel between the two cores during the past 600 ka, which are controlled mainly by eccentricity with an approximate periodicity of 100 ka. It is worth noting that the biogenic CaCO3 and opal deposition patterns in the two cores differ between interglacial and glacial periods. During interglacial periods the biogenic opal content is higher in the southern core than in the northern core, which corresponds with the present-day condition. In contrast the CaCO3 content is higher in the northern core, which is contradictory to the present-day northward decreasing CaCO3 deposition pattern from the Equator. The collection site of PC5101 is approximately 350 m deeper than that of PC5103, which significantly promotes CaCO3 dissolution and causes unexpectedly high CaCO3 content at the northern site in contrast to the biogenic opal content

Chfr is linked to tumour metastasis through the downregulation of HDAC1

Chfr is a ubiquitin ligase that functions in the mitotic checkpoint by delaying entry into metaphase in response to mitotic stress. It has been suggested that Chfr is a tumour suppressor as Chfr is frequently silenced in human cancers. To better understand how Chfr activity relates to cell-cycle progression and tumorigenesis, we sought to identify Chfr-interacting proteins using affinity purification combined with mass spectrometry. Histone deacetylase 1 (HDAC1), which represses transcription by deacetylating histones, was newly isolated as a Chfr-interacting protein. Chfr binds and downregulates HDAC1 by inducing its polyubiquitylation, both in vitro and in vivo. Ectopic expression of Chfr in cancer cells that normally do not express it results in downregulation of HDAC1, leading to upregulation of the Cdk inhibitor p21^(CIP1/WAF1) and the metastasis suppressors KAI1 and E-cadherin. Coincident with these changes, cells arrest in the G1 phase of the cell cycle and become less invasive. Collectively, our data suggest that Chfr functions as a tumour suppressor by regulating HDAC1