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Alessandro Carrer, professor in the Department of Biology at the University of Padua, has been awarded a €570,000 grant to advance his research, which to date has revealed a link between high fructose consumption and a possible association with pancreatic cancer. The funding was issued by Wereld Kanker Onderzoek Fonds (WKOF), a member of the World Cancer Research Fund (WCRF) network and administered by WCRF International, whose scientific programme supports research exploring the relationship between lifestyle and cancer prevention.
His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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Alessandro Carrer, professor in the Department of Biology at the University of Padua, has been awarded a €570,000 grant to advance his research, which to date has revealed a link between high fructose consumption and a possible association with pancreatic cancer. The funding was issued by Wereld Kanker Onderzoek Fonds (WKOF), a member of the World Cancer Research Fund (WCRF) network and administered by WCRF International, whose scientific programme supports research exploring the relationship between lifestyle and cancer prevention.
His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
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His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
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“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
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Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
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“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
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Alessandro Carrer, professor in the Department of Biology at the University of Padua, has been awarded a €570,000 grant to advance his research, which to date has revealed a link between high fructose consumption and a possible association with pancreatic cancer. The funding was issued by Wereld Kanker Onderzoek Fonds (WKOF), a member of the World Cancer Research Fund (WCRF) network and administered by WCRF International, whose scientific programme supports research exploring the relationship between lifestyle and cancer prevention.
His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
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Alessandro Carrer, professor in the Department of Biology at the University of Padua, has been awarded a €570,000 grant to advance his research, which to date has revealed a link between high fructose consumption and a possible association with pancreatic cancer. The funding was issued by Wereld Kanker Onderzoek Fonds (WKOF), a member of the World Cancer Research Fund (WCRF) network and administered by WCRF International, whose scientific programme supports research exploring the relationship between lifestyle and cancer prevention.
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Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
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His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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Alessandro Carrer, professor in the Department of Biology at the University of Padua, has been awarded a €570,000 grant to advance his research, which to date has revealed a link between high fructose consumption and a possible association with pancreatic cancer. The funding was issued by Wereld Kanker Onderzoek Fonds (WKOF), a member of the World Cancer Research Fund (WCRF) network and administered by WCRF International, whose scientific programme supports research exploring the relationship between lifestyle and cancer prevention.
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Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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His studies have shown how fructose is metabolised in the intestine and how this process may lead to negative effects on human health, possibly including the development of pancreatic tumours. The mechanism is based on the production, by the gut microbiome, of a small lipid molecule called acetate.
Over recent decades, fructose intake has risen significantly, mainly due to the consumption of drinks and foods sweetened with high-fructose corn syrup. This global increase is generating considerable concern for several reasons, including a possible connection to rising cancer incidence. However, a causal relationship has not yet been proven, making it difficult to implement effective prevention policies.
Pancreatic cancer is one of the deadliest forms of cancer and is largely incurable. Reducing its incidence is therefore a major public health challenge. Several unhealthy lifestyle factors are associated with an increased risk of pancreatic cancer, but the role of diet remains unclear. In particular, the impact of dietary fructose has not been directly tested, despite growing epidemiological evidence.
“Preliminary data show that very high-fructose diets promote pancreatic carcinogenesis in mouse models,” explains Carrer. “Our hypothesis is that the intestinal flora converts excess fructose into acetate, a molecule that sends harmful signals to pancreatic cells. Our goal is to identify individuals at risk and guide them toward continuous monitoring by understanding the molecular alterations caused by increased acetate availability.”
“We will use murine models of pancreatic cancer development,” Carrer continues, “to systematically test the effect of ‘excessive’ fructose consumption—that is, fructose from industrially processed foods, not to be confused with the simple consumption of fruit. We will also examine structural and functional alterations in specific sites within the nuclei of tumour cells: the nucleoli. Preliminary studies indeed suggest that nucleoli act as cellular switches that detect acetate levels and coordinate the cellular response.”
Mice will receive a quantity of fructose equivalent to the daily consumption of a 350-ml can of sugary beverage in humans, administered over an extended period. The researchers will then evaluate tumour formation and progression. In a later phase, the findings will be validated in human patients. The study will be conducted in Professor Carrer’s laboratory, which includes students and researchers from the Department of Biology and the Veneto Institute of Molecular Medicine (VIMM), in collaboration with Professors Marchegiani and Cillo of the Hepato-biliary-pancreatic Surgery Unit at Padua Hospital, and with the GIGA Institute in Liège, Belgium.
Carrer’s research aims to assess whether dietary fructose can promote the onset or progression of pancreatic cancer while also investigating the specific molecular alterations responsible for tumour development. The findings will help refine current guidelines on fructose consumption and identify key factors underlying increased cancer risk.
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