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Prevention of Obesity-related Cancers: Setting up of a Multi-Cancer Education and Prevention Program in Hong Kong

ABSTRACT: Obesity could increase the risk of many chronic diseases, including hypertension, cardiovascular diseases, high lipid level, diabetes, stroke, endometrial cancer and certain types of cancer which could benefit by secondary prevention through screening programs. The World Cancer Research Fund of the American Institute for Cancer Research has reviewed all the studies about the link between obesity and cancer. Studies shown that obesity is an independent risk factor for colorectal, breast and prostate cancer. These three cancers (will be named as "obesity-related cancers" thereafter) demonstrate a rapidly increasing trend of incidence in Asia in the past decade. Among Chinese adults of Hong Kong in 2014, 39% were overweight or obese (compared with 20.9% reported in European adults in the same year) and up to 69.7% reported that they did not perform any measures to achieve optimal weight control. Men (49.6%) had a higher proportion of overweight or obesity than females (29.5%). Adults who are aged 45-54 had the highest rate (50.5%) of overweight or obesity than other age groups. In addition, there were 62.5% whose physical activity level did not meet the recommendations from the World Health Organization (WHO). Only 18.7% consumed at least 5 portions of fruit and vegetables per day; yet about 30% were alcoholic drinkers; and more than 10% were daily or occasional smoker. These figures imply that the incidence of obesity and obesity-related cancers will further escalate - and urgent actions at the community level are needed to combat the rising incidence and mortality of these conditions. According to Hong Kong Cancer Registry, the discrepancy between the number of new cases (incidence) and number of deaths (mortality) is much higher for colorectal, breast and prostate cancer as compared to other cancers. It is well recognized that screening could effectively reduce mortality for these three obesity-related cancers when they are detected at an earlier stage. The concept of a one-stop approach to screen for multiple cancers was found to be feasible, with an ability to detect a wide range of neoplastic lesions at an early stage. In the recent decade, there are also emerging centres that have been established as multi-cancer screening clinics worldwide. Nevertheless, there is a scarcity of studies that have highlighted the outcomes of these multi-cancer screening programs.

DISEASE(S): Obesity,Prostatic Neoplasms,Colorectal Cancer,Colorectal Neoplasms,Prostate Cancer,Breast Cancer

PROVIDER: 2312081 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related mortality among adults in developed countries. The discovery of the most common genetic alterations as well as the development of organoids models of pancreatic cancer have provided insight into the fundamental pathways driving the progression from normal cell, to non-invasive precursor lesion, to widely metastatic disease, offering new opportunities for the discovery of key activated pathways along cancer progression. Obesity is one of the most serious public health challenges of the 21st century. Several epidemiological studies have shown the positive association between obesity and cancer-related morbidity/mortality, as well as poor prognosis and poorer treatment outcome. Despite strong evidence indicates a link between obesity and cancer incidence, the molecular basis of the initiating events remains largely elusive. This is mainly due to the lack of an accurate and reliable model of pancreatic carcinogenesis that mimics human obesity-associated PDAC, making data interpretation difficult and often confusing. Here we propose, to our knowledge, the best suitable and manageable preclinical tool, based on next-generation cell culture models, to study the effects of obesity on pancreatic carcinogenesis. Therefore we tracked the effects of obesity on the natural evolution of PDAC in a genetically-defined transplantable model of syngeneic murine pancreatic preneoplastic lesion (mP) and tumor (mT) derived organoids that recapitulates the progression of human disease from early preinvasive lesions to metastatic disease. Our models indicated that both genetic- and diet-induced obesity promoted incidence engraftment rate and growth of both preneoplastic and neoplastic organoids, favoring pancreatic cancer progression and distant metastases dissemination. Our obesity models of carcinogenesis mimic the evolution of human pancreatic cancer pathology, promoting carcinogenesis and concomitant accumulation of a myeloid infiltrate. These changes in cancer immune infiltrate were also associated to a specific pattern of anti-inflammatory Th2 signature. Moreover, gene expression profile analysis revealed a change in gene expression programs that addresses cells to different pancreatic subtypes and stromal conditions. Our results suggest that organoid-derived transplants in obese mice represent a suitable system to study early step of carcinogenesis and support the hypothesis that inflammation induced by obesity stimulates tumor progression and metastatization during pancreatic carcinogenesis.

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Prevention of Obesity-related Cancers: Setting up of a Multi-Cancer Education and Prevention Program in Hong Kong

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