Escalating burden of breast cancer in southern Thailand: Analysis of 1990–2010 incidence and prediction of future trends

BackgroundThailand is undergoing an epidemiologic transition, with decreasing incidence of infectious diseases and increasing rates of chronic conditions, including cancer. Breast cancer has the highest incidence rates among females both in the southern region Thailand and throughout Thailand. However, there is a lack of research on the epidemiology of this and other cancers.MethodsHere we use cancer incidence data from the Songkhla Cancer Registry to characterize and analyze the incidence of breast cancer in Southern Thailand. We use joinpoint analysis, age-period-cohort models and nordpred analysis to investigate the incidence of breast cancer in Southern Thailand from 1990 to 2010 and project future trends from 2010 to 2029.ResultsWe found that age-adjusted breast cancer incidence rates in Southern Thailand increased by almost 300% from 1990 to 2010 going from 10.0 to 27.8 cases per 100,000 person-years. Both period and cohort effects played a role in shaping the increase in incidence. Three distinct incidence projection methods consistently suggested that incidence rates will continue to increase in the future with incidence for women age 50 and above increasing at a higher rate than for women below 50.ConclusionsTo date, this is the first study to examine Thai breast cancer incidence from a regional registry. This study provides a basis for future planning strategies in breast cancer prevention and to guide hypotheses for population-based epidemiologic research in Thailand.     

The number distribution for involved lymph nodes in cancer

The number of involved lymph nodes exhibits considerable heterogeneity within populations. Here, the implications of population heterogeneity are explored with respect to the kinematics of nodal metastases. Data from the National Cancer Institute's Surveillance, Epidemiology, and End Results program for 224656 breast, 12404 gastric, 18015 rectal, 4117 cervical and 2443 laryngeal cancers as well as 9118 melanomas were used to construct frequency distributions for the number of involved nodes which were then fitted to the negative binomial distribution. The negative binomial distribution described the heterogeneity in nodal involvement well. The patterns of nodal involvement can be explained by either of two models: one where involved nodes could seed further nodal metastases, the other where the number of nodal metastases in any individual was randomly distributed, with the deviations between patients accounted for by population heterogeneity. Since the number of sampled nodes similarly approximated a negative binomial distribution, random involvement with superimposed population heterogeneity would more credibly explain both sets of observations.     

Modeling Exposure Intensity and Susceptibility-Latency Effect from Retrospective Cohort Data - Application to Lung Cancer Mortality in Blackfoot Disease Endemic Area in Taiwan

It is challenge in epidemiology to characterize the temperol aspect of exposure-disease association. The authors propose a stochastic model to deal with exposures that are time-dependent and exhibit susceptibility and latency effects. The model is applied to a retrospective cohort data on lung cancer mortality in the blackfoot disease endemic area in Taiwan. The authors compare the proposed model with the multistage model, the back-calculation model, the catalytic model, and the age-period-cohort models.     

Forecasting with the age-period-cohort model and the extended chain-ladder model

We consider forecasting from age-period-cohort models, as wellas from the extended chain-ladder model. The parameters of thesemodels are known only to be identified up to linear trends.Forecasts from such models may therefore depend on arbitrarylinear trends. A condition for invariant forecasts is proposed.A number of standard forecast models are analysed.     

The future burden of cancer in Canada: Long-term cancer incidence projections 2013–2042

BackgroundCancer is the leading cause of death in Canada and the estimated annual spending associated with cancer is approximately $7.5 billion. Projecting the future burden of cancer in Canada is essential for health planning and evaluation. We aimed to estimate the future incidence of cancer in Canada to 2042.MethodsAge-sex-region-specific cancer incidence data were obtained for the years 1983-2012 and cancer incidence was projected from 2013 to 2042 for the top five cancer sites. The modelling algorithm combined a mixture of cancer projection methods to select the best-fitted model. When the chosen model produced by the modelling algorithm resulted in estimates that were not consistent with expert opinion, an alternate model was selected that took into consideration historical changes in policy, screening and lifestyle behaviours. Incidence projections were made for Canada and its provinces.ResultsLung cancer incidence is estimated to rise to 14,866 cases in men and 19,162 in women in 2042. Colorectal cancer incidence is estimated to rise to 28,146 in men and 21,102 in women. Cases of bladder cancer are projected to rise to 10,708 and 3,364 in men and women, respectively. Breast cancer incidence is predicted to rise to 40,712 and prostate cancer incidence is projected to rise to 92,949.ConclusionThese cancer incidence projections up to 2042 can be used for planning cancer control strategies and prevention programs. Given the ongoing changes in the prevalence of risk factors and in cancer prevention policies, these estimates should be interpreted with caution.     

Trends in socioeconomic inequalities in cervical,breast, and colorectal cancer screening participation among women in Japan, 2010–2019

BackgroundIt is known that socioeconomic status (SES) influences the outcome of cancer treatment and this could partly be explained by decreased use of cancer screening services by people of lower SES. Many studies have indicated that low SES, including low educational attainment or unstable employment, was related to nonparticipation in cancer screening. However, studies investigating trends in SES inequalities within cancer screening participation are limited. Our objective was to examine trends in SES inequalities in cervical, breast, and colorectal cancer screening participation among women in Japan between 2010 and 2019.MethodsWe analyzed 189,442, 168,571, 163,341, and 150,828 women in 2010, 2013, 2016, and 2019 respectively, using nationally representative cross-sectional surveys. The main outcome variables are participation in each cancer screening. We used educational attainment and employment status as measures for SES. Multivariable logistic regression analysis, adjusted for age, marital status, educational attainment, and employment status was performed to evaluate the associations between SES and nonparticipation in each cancer screening.ResultsOverall participation rates in each cancer screening increased between 2010 and 2019. Low educational attainment and non-permanent employment status were related to nonparticipation in each cancer screening and inequality according to employment status increased within each screening participation during the study period. For example, dispatched workers were more likely to not participate in cervical cancer screening than permanent workers: in 2010, [aOR 1.11 95 %CI: 1.01 –1.21], and in 2019, [aOR 1.46 95 %CI: 1.34–1.60]. The inequality was greatest in colorectal cancer screening nonparticipation, followed by breast and cervical screening.ConclusionsAlthough the participation rates in each cancer screening have increased, inequality in participation in terms of employment status widened among women in Japan between 2010 and 2019. Reducing inequalities in cancer screening participation is essential for cancer screening intervention policies.     

Animal models for breast cancer

Rodent mammary tumors induced by chemical carcinogens have proven to be very useful in the genetic analysis of initiation, promotion and progression of mammary carcinogenesis. We are studying rat mammary carcinomas induced by the chemical carcinogen, N-nitroso-N-methylurea. The earliest genetic event observed in the mammary gland is the activation of Ha-ras oncogenes, which is followed by promotion of the initiated cells by hormones involved in puberty. Preferential amplification of the mutated Ha-ras allele, of PRAD-1 and IGF2, loss of expression of the mitogenic growth factor gene, MK, and mutation in the tumor suppressor gene, p53, are seen in the mammary tumors during tumor progression.     

Evolutionary dynamics of BRCA1 alterations in breast tumorigenesis

Cancer results from the accumulation of alterations in oncogenes and tumor suppressor genes. Tumor suppressors are classically defined as genes which contribute to tumorigenesis if their function is lost. Genetic or epigenetic alterations inactivating such genes may arise during somatic cell divisions or alternatively may be inherited from a parent. One notable exception to this rule is the BRCA1 tumor suppressor that predisposes to hereditary breast cancer when lost. Genetic alterations of this gene are hardly ever observed in sporadic breast cancer, while individuals harboring a germline mutation readily accumulate a second alteration inactivating the remaining allele—a finding which represents a conundrum in cancer genetics. In this paper, we present a novel mathematical framework of sporadic and hereditary breast tumorigenesis. We study the dynamics of genetic alterations driving breast tumorigenesis and explore those scenarios which can explain the absence of somatic BRCA1 alterations while replicating all other disease statistics. Our results support the existence of a heterozygous phenotype of BRCA1 and suggest that the loss of one BRCA1 allele may suppress the fitness advantage caused by the inactivation of other tumor suppressor genes. This paper contributes to the mathematical investigation of breast tumorigenesis.     

Murine model of hepatic breast cancer

Background and aimsBreast cancer is the most common cancer in women and the second leading cause of cancer-related deaths in this population. Breast cancer related deaths have declined due to screening and adjuvant therapies, yet a driving clinical need exists to better understand the cause of the deadliest aspect of breast cancer, metastatic disease. Breast cancer metastasizes to several distant organs, the liver being the third most common site. To date, very few murine models of hepatic breast cancer exist.MethodsIn this study, a novel murine model of liver breast cancer using the MDA-MB-231 cell line is introduced as an experimental (preclinical) model.ResultsHistological typing revealed consistent hepatic breast cancer tumor foci. Common features of the murine model were vascular invasion, lung metastasis and peritoneal seeding.ConclusionsThe novel murine model of hepatic breast cancer established in this study provides a tool to be used to investigate mechanisms of hepatic metastasis and to test potential therapeutic interventions.     

人乳头瘤病毒的致瘤性及机制

高危型人乳头瘤病毒(HPV)可能引发多种癌症,公认的如宫颈癌和宫颈上皮内瘤变.近年来的研究表明,HPV还与头颈部鳞癌、食管癌及乳房癌等的发生密切相关.HPV引起头颈部鳞癌的机制在某种程度上与宫颈癌相似,但又有所不同.因此,阐明HPV的致癌机制对于HPV相关肿瘤的治疗具有重要意义.     

Secular trends in incidence and mortality of bladder cancer in China, 1990–2017: A joinpoint and age-period-cohort analysis

BackgroundBladder cancer is closely related to occupational carcinogens, and China is undergoing a rapid industrialization. However, trend of bladder cancer incidence and mortality remains unknown in China.MethodsIncidence and mortality rates of bladder cancer (1990–2017) were collected for each 5-year age group stratified by gender (males/females) from the Global Burden of Disease (GBD) 2017 study. The average annual percentage change (AAPC) of rates were analyzed by joinpoint regression analysis; age, period and cohort effects on incidence and mortality were simultaneously estimated by age-period-cohort model.ResultsThrough 1990–2017, age-standardized incidence rates significantly rose in men (AAPC = 0.72%, 95% CI: 0.5%, 0.9%) while decreased in women (-1.25%: -1.6%, -0.9%); age-standardized mortality rates decreased in both men (-1.09%: -1.2%, -0.9%) and women (-2.48%: -2.8%, -2.2%). The joinpoint regression analysis showed the mortality almost decreased in all age groups; while the incidence increased in men for older age groups (from 45 to 49 to 80–84). Moreover, age effect showed the incidence and mortality increased with age; the incidence and mortality increased with time period, while in women period effect stop decreasing and began to increase since 2007; cohort effect showed them decreased with birth cohorts.ConclusionsThe incidence of bladder cancer is increasing in men but mortality decreases in both sexes. Both the incidence and mortality in men substantially increase with age and period, while the rates in women increased with period since 2007. The period effect may indicate the increased risks to bladder cancer in Chinese men. Etiological studies are needed to identify the factors driving these trends of bladder cancer.     

Mouse models for breast cancer metastasis

Metastasis of cancer cells is the main cause of death in most breast cancer patients. Although markers for early diagnosis and drugs that limit the spread of cancer to other organs have been developed, it is difficult to prevent the relapse of breast cancer. Recent research has highlighted the importance of tumor environment in which communication between tumor cells and the body system occurs. Emerging data have suggested that animal models are a good system to investigate this communication. Therefore, studies with mouse models have been developed as a reasonable method for a systemic approach to understand breast cancer metastasis. In this review, we summarize mouse models of breast cancer and their applications to the study of human breast cancers, and discuss limitation of model system and advanced techniques to overcome it.     

乳腺癌体外骨转移瘤3D模型的建立

目的:构建乳腺癌体外骨转移瘤3D模型。方法:新生CD-1小鼠的颅骨单独孵育为正常组,新生CD-1小鼠的颅骨与MDA-MB-231细胞低氧共孵育四天为模型组。通过扫描电镜(SEM)鉴定骨转移瘤模型,中性红染色法鉴定骨组织中的破骨细胞,硝酸银复染法观察骨的溶解,结晶紫染色法观察骨转移瘤模型中肿瘤细胞的生长。结果:正常组骨表面光滑完整;模型组骨组织表面黏附大量肿瘤细胞,破骨细胞活性增强,产生严重的溶骨,表面出现骨陷窝,骨纤维发生断裂。结论:成功建立了乳腺癌骨转移瘤体外3D模型,该模型能够模拟体内骨转移瘤微环境。