From Science Daily website (see original article).
Feb. 1, 2013 — Sugars are needed to provide us with energy and in moderate amounts contribute to our well-being. Sustained high levels of sugars, as is found in diabetics, damages our cells and now is shown that can also increase our chance to get cancer: "The dose makes the poison" as Paracelsus said.
It is well known that obesity is a leading cause of diabetes, a disease where the body fails to control blood sugar levels.
High blood sugar levels are characteristic in obesity and diabetes.
What is less well known is that diabetes and obesity are also linked to an increase in cancer risk.
That is, the diabetic population has up to double chances to suffer pancreatic or colon cancer among others, according to well sustained epidemiological studies.
With obesity in British and Spanish children reaching 16%, the highest in Europe, this epidemic has major health implications.
How obesity or diabetes increase cancer risk has been a major health issue.
Scientists led by Dr. Custodia Garcia-Jimenez at the University Rey Juan Carlos in Madrid have uncovered a key mechanism that links obesity and diabetes with cancer: high sugar levels, which increase activity of a gene widely implicated in cancer progression.
Dr Garcia Jimenez's laboratory was studying how cells in the intestine respond to sugars and signal to the pancreas to release insulin, the key hormone that controls blood sugar levels.
Sugars in the intestine trigger cells to release a hormone called GIP that enhances insulin release by the pancreas.
In a study published in Molecular Cell, Dr Garcia Jimenez's team showed that the ability of the intestinal cells to secrete GIP is controlled by a protein called β-catenin, and that the activity of β-catenin is strictly dependent on sugar levels.
Increased activity of β-catenin is known to be a major factor in the development of many cancers and can make normal cells immortal, a key step in early stages of cancer progression.
The study demonstrates that high (but not normal) sugar levels induce nuclear accumulation of β-catenin and leads to cell proliferation.
The changes induced on β-catenin, the molecules involved and the diversity of cancer cells susceptible to these changes are identified.
Dr. Custodia García said "We were surprised to realize that changes in our metabolism caused by dietary sugar impact on our cancer risk.
We are now investigating what other dietary components may influence our cancer risk. Changing diet is one of easiest prevention strategies that can potentially save a lot of suffering and money."
Colin Goding, Professor of Oncology at the University of Oxford, UK said 'Previously we were unsure about how increased blood sugar found in diabetes and obesity could increase cancer risk.
This study identifies a key molecular mechanism through which high blood glucose would predispose to cancer.
It opens the way for potential novel therapies aimed at reducing cancer risk in the obese and diabetic populations.'
Estimations published by the World Health Organisation (WHO): Obesity predisposes to diabetes and its prevalence is doubling every 20 years worldwide.
More than 1 in 10 adults worldwide (12%) are obese (BMI>30).
1 in 6 children in UK and Spain suffer obesity.
Diabetes caused 4.6 million deaths in 2011, more than 2 deaths per hour in Spain, more in USA. Worldwide, 1 in 10 adults (10%) suffered from diabetes in 2010 and more than one-third of individuals with diabetes are unaware they suffer from the disease.
The national cost of diabetes or cancer is in the order of billions of pounds or euros in Spain or England.
More than half (63%) of premature deaths worldwide are due to non communicable diseases (NCD) of which cancer and diabetes are among the 4 causes more frequent.
At least 1 in 3 of the main cancers (27-39%) can be prevented by improving diet, physical activity and body composition.
Visualizzazione post con etichetta glucose. Mostra tutti i post
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venerdì 8 febbraio 2013
lunedì 28 gennaio 2013
Tumor Cells Engineer Acidity to Drive Cell Invasion
From Science Daily website (see original article).
Jan. 25, 2013 — Researchers at Moffitt Cancer Center and colleagues at Wayne State University School of Medicine investigated the acidity in solid tumors to determine if pH levels play a role in cancer cell invasion in surrounding tissues. They found that an acidic microenvironment can drive cancer cells to spread and propose that neutralizing pH would inhibit further invasion, providing a therapeutic opportunity to slow the progression of cancers.
Their study appeared in the Jan. 3 online release of Cancer Research, a publication of the American Association for Cancer Research.
According to the study's corresponding author, Robert J. Gillies, Ph.D., chair of the Department of Cancer Imaging & Metabolism at Moffitt, acidity in solid tumors is the result of an increased fermentative metabolism combined with poor delivery of blood to tissues.
In this study, tumor invasion and pH were monitored in immunodeficient laboratory mice hosting a variety of tumors. "We monitored the test animals over time using microscopy and found that the highest regions of tumor invasion corresponded to areas with the lowest pH," Gillies explained. "Tumor invasion did not occur in regions with normal or near normal pH levels. Furthermore, when we neutralized the acidity with oral sodium bicarbonate, the invasion was halted."
Researchers proposed that the acidic pH of the tumor microenvironment represents a "niche engineering" strategy on the part of tumor cells, promoting invasion and growth of malignant tumors into surrounding tissue. Niche engineering is a concept in ecology describes how plants and animals alter their environment to in ways that promote their own growth and survival over their competitors. "We have long regarded cancers cells as an invading species," said study co-author Robert Gatenby, M.D., chair of the Diagnostic Imaging Services and Integrated Mathematical Oncology departments at Moffitt.
A key to this process of adaptation and invasion is increased glucose metabolism in the tumor. "The vast majority of malignant tumors metabolize glucose at high rates," Gillies said. "We have proposed that there is a direct, causative link between increased glucose metabolism and the ability of cancer cells to invade and metastasize."
According to the research, elevated glucose metabolism is the cause of increased acidity in the tumor microenvironment. Most tumors develop an abnormal vascular network that tends to be poorly organized and leaky, disrupting blood flow and hampering the delivery of oxygen.
"This poorly organized vascular system has a two-fold effect on tumor acidity," explained Gatenby. "First, it subjects tumor regions to poor perfusion, which restricts oxygen and increases the rate of glucose fermentation. Second, the poor perfusion hampers the ability to eliminate the resulting acids, resulting in very low pH in surrounding tissues."
As tumor cells adapt to increasing acidity, niche engineering through normal cell death and new blood vessel formation occurs in the tumor and the immune response is suppressed.
"Tumor cells perform niche engineering by creating an acidic environment that is not toxic to the malignant cells but, through its negative effects on normal cells and tissues, promotes local invasion of malignant cells," Gatenby said.
The researchers suggested that targeting this activity with buffers and other mechanisms aimed at increasing pH levels will likely provide a valuable alternative to traditional therapies focused entirely on killing tumor cells.
Jan. 25, 2013 — Researchers at Moffitt Cancer Center and colleagues at Wayne State University School of Medicine investigated the acidity in solid tumors to determine if pH levels play a role in cancer cell invasion in surrounding tissues. They found that an acidic microenvironment can drive cancer cells to spread and propose that neutralizing pH would inhibit further invasion, providing a therapeutic opportunity to slow the progression of cancers.
Their study appeared in the Jan. 3 online release of Cancer Research, a publication of the American Association for Cancer Research.
According to the study's corresponding author, Robert J. Gillies, Ph.D., chair of the Department of Cancer Imaging & Metabolism at Moffitt, acidity in solid tumors is the result of an increased fermentative metabolism combined with poor delivery of blood to tissues.
In this study, tumor invasion and pH were monitored in immunodeficient laboratory mice hosting a variety of tumors. "We monitored the test animals over time using microscopy and found that the highest regions of tumor invasion corresponded to areas with the lowest pH," Gillies explained. "Tumor invasion did not occur in regions with normal or near normal pH levels. Furthermore, when we neutralized the acidity with oral sodium bicarbonate, the invasion was halted."
Researchers proposed that the acidic pH of the tumor microenvironment represents a "niche engineering" strategy on the part of tumor cells, promoting invasion and growth of malignant tumors into surrounding tissue. Niche engineering is a concept in ecology describes how plants and animals alter their environment to in ways that promote their own growth and survival over their competitors. "We have long regarded cancers cells as an invading species," said study co-author Robert Gatenby, M.D., chair of the Diagnostic Imaging Services and Integrated Mathematical Oncology departments at Moffitt.
A key to this process of adaptation and invasion is increased glucose metabolism in the tumor. "The vast majority of malignant tumors metabolize glucose at high rates," Gillies said. "We have proposed that there is a direct, causative link between increased glucose metabolism and the ability of cancer cells to invade and metastasize."
According to the research, elevated glucose metabolism is the cause of increased acidity in the tumor microenvironment. Most tumors develop an abnormal vascular network that tends to be poorly organized and leaky, disrupting blood flow and hampering the delivery of oxygen.
"This poorly organized vascular system has a two-fold effect on tumor acidity," explained Gatenby. "First, it subjects tumor regions to poor perfusion, which restricts oxygen and increases the rate of glucose fermentation. Second, the poor perfusion hampers the ability to eliminate the resulting acids, resulting in very low pH in surrounding tissues."
As tumor cells adapt to increasing acidity, niche engineering through normal cell death and new blood vessel formation occurs in the tumor and the immune response is suppressed.
"Tumor cells perform niche engineering by creating an acidic environment that is not toxic to the malignant cells but, through its negative effects on normal cells and tissues, promotes local invasion of malignant cells," Gatenby said.
The researchers suggested that targeting this activity with buffers and other mechanisms aimed at increasing pH levels will likely provide a valuable alternative to traditional therapies focused entirely on killing tumor cells.
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