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Risk factors for anal cancer: results of a population-based case – control study
Cancer Causes & Control
source: http://www.kluweronline.com/article.asp?PIPS=5146198&PDF=1
An International Journal of Studies of Cancer in Human Populations
Cancer Causes and Control
14 (9): 837-846, November 2003
Copyright © 2003 Kluwer Academic Publishers
All rights reserved
Risk factors for anal cancer: results of a population-based case – control study
Hung-Fu Tseng
Hal Morgenstern
Department of Epidemiology, UCLA School of Public Health, Los Angeles, CA, USA
Thomas M. Mack
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
Ruth K. Peters
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
Abstract
Objective : Although the incidence of anal cancer is higher in women than in men, the reasons for this gender difference are not clear. The purpose of this study was to identify risk factors for anal cancer in both men and women. Methods : We conducted in-person interviews with 102 males and 106 females with squamous or transitional cell carcinoma of the anus and 208 individually matched controls. Results : Compared with persons who had never experienced receptive anal intercourse, those who had experienced it more than 130 times were 18 times as likely to develop anal cancer (adjusted odds ratio [OR] = 17.6 (95% confidence interval [CI] = 1.3 – 234). This elevated risk occurred primarily among males. The adjusted OR for males having more than 10% of their sexual experiences with other men was 5.6 (95% CI = 1.4 – 22.0). A history of other anogenital or endometrial cancers increased the risk in women but not men.
A history of anal warts, syphilis, severe hemorrhoids, physical inactivity, multiple sexual partners who smoked, and current smoking were also associated with increased risk. Conclusions : The results of this study suggest that both sexual and non-sexual factors are important in the etiology of anal cancer.
Molecular Link Discovered Between Inflammation And Cancer
A team led by biochemists at the University of California, San Diego has found what could be a long-elusive mechanism through which inflammation can promote cancer. The findings may provide a new approach for developing cancer therapies.
The study, published in the January 26 issue of the journal
Cell, shows that what scientists thought were two distinct processes in cells - the cells' normal development and the cells' response to dangers such as invading organisms - are actually linked. The researchers, who were also from the Salk Institute for Biological Studies and the La Jolla Institute for Allergy and Immunology, say that the linkage of these two processes may explain why cancer, which is normal growth and development gone awry, can result from chronic inflammation, which is an out-of-control response to danger.
"Although there is plenty of evidence that chronic inflammation can promote cancer, the cause of this relationship is not understood," said Alexander Hoffmann, an assistant professor of chemistry and biochemistry at U.C. San Diego, who led the study. "We have identified a basic cellular mechanism that we think may be linking chronic inflammation and cancer."
Cellular defense is a rapid process compared to cellular development, just as a state's response to terrorist threats is swifter than the construction of new infrastructure. However, in both settings, safeguarding against threats and building structures have certain steps in common and require similar types of workers, or molecules.
Hoffmann referred to the parallel sets of steps in cellular defense and development as "mirror image pathways." His team showed that these pathways are not distinct from one another because they are linked by a protein called p100. They found that inflammation leads to an increase in p100, but that p100 is also used in certain steps in development. Therefore p100 allows communication between inflammation and development.
A small amount of dialogue between inflammation and development is beneficial, say the researchers, akin to how information from anti-terrorism efforts could be useful to crews building the state's infrastructure. On the other hand, the constant influence of defense processes on development is detrimental.
"Studies with animals have shown that a little inflammation is necessary for the normal development of the immune system and other organ systems," explained Hoffmann. "We discovered that the protein p100 provides the cell with a way in which inflammation can influence development. But there can be too much of a good thing. In the case of chronic inflammation, the presence of too much p100 may overactivate the developmental pathway, resulting in cancer."
In the paper, the researchers propose that thinking of the processes of defense and development as part of a single large system "represents an opportunity for therapeutic intervention." For example, it might be easier to break the link between inflammation and cancer by targeting the developmental pathway, rather than the inflammation pathway.
"Many of the developmental signals that cells use are sent outside the cell, so they should be easier to block with drugs than inflammation signals, which tend to be confined within cells," said Hoffmann. "It's more challenging to design drugs that will enter cells."
Because the molecules that play a role in the inflammation and development pathways have been extensively studied for many years, the researchers say that it is surprising to find a new molecule that significantly revises scientists' understanding about the interactions between inflammation and development. They credit their discovery to an approach that combines biochemical techniques and computation.
"Our mathematical model of inflammation and development includes 98 biochemical reactions," said Soumen Basak, a postdoctoral fellow working with Hoffmann. " When we ran the model, it predicted that p100 levels would be elevated for a significant period of time when the inflammation pathway was stimulated. We confirmed the prediction using biochemical techniques with cells in the laboratory."
" The finding is exciting because it means that p100 provides cells with a memory to inflammatory exposure," added Basak, who was the first author on the paper.
Also contributing to the study were Hana Kim, Jeffrey D. Kearns, Ellen O'Dea, Shannon L. Werner and Gourisankar Ghosh from U.C. San Diego, Vinay Tergaonkar and Inder M. Verma from the Salk Institute for Biological Studies, and Chris A. Benedict and Carl F. Ware from the La Jolla Institute for Allergy and Immunology.
The study was supported by the National Institutes of Health, the Leukemia and Lymphoma Society of America and the American Heart Association.
Contact: Sherry Seethaler
University of California - San Diego
Scientists Reveal Cells' 'Energy Factories' Linked To Cancer
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University of Glasgow scientists have discovered how mitochondria - the energy factories in our cells - can sustain a cancer, reporting their findings in a new study published in Cancer Cell.
Mitochondria are complex structures that exist in cells to generate energy for growth and activity.
The Cancer Research UK researchers based at the University of Glasgow's Beatson Institute for Cancer Research in Glasgow have found out how the excessive build-up of a simple metabolic molecule in mitochondria can trigger a sequence of events that leads to tumour growth.
The discovery increases our understanding of the molecular basis of several types of cancer, which is crucial for the development of new ways to prevent, diagnose and treat the disease.
Scientists know that a number of genes that code for the mitochondria's energy generating machinery are tumour suppressors and that defects in these genes can lead to cancer. But, until now, it was unclear as to how mutations in these genes resulted in the disease.
The team looked at one of the known tumour suppressor genes called SDH, which codes for a molecule called succinate dehydrogenase. When the SDH gene is damaged, a metabolic product called succinic acid accumulates in cells. This then causes the levels of a protein called HIF-1to rise. The HIF-1 protein is normally only activated in response to certain types of crisis in the cell, such as a lack of oxygen. Under these conditions it encourages the growth of blood vessels to help cells get more oxygen.
The researchers have found the missing pieces in this puzzle. They show how the high levels of succinic acid in the cell that result from SDH mutations block the cell's usual method of ridding the cell of HIF-1. HIF-1 levels can then build up, resulting in inappropriate growth of blood vessels, which can feed a tumour.
Dr. Eyal Gottlieb, from the University of Glasgow's Beatson Institute, said: "We found that damage to the SDH gene boosts the levels of succinic acid in a cell and this, in turn, prevents the degradation of HIF-1. HIF-1 is then free to increase the expression of genes that facilitate blood vessel growth, tumour development and cancer spread.
Dr. Lesley Walker, Director of Cancer Information at Cancer Research UK, says: "Mutations in SDH can predispose a person to cancer of the kidney, adrenal gland and thyroid gland.
Changes in SDH activity may also be associated with stomach and bowel cancer.
"This study is exciting because it is the first to find a molecular mechanism that links mitochondrial mutations to tumour formation. Increasing our understanding of the molecular basis of cancer is crucial if we are to find new ways of preventing, diagnosing and treating the disease in the future."
"Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-a prolyl hydroxylase", is published in Cancer Cell 2005 7: 77-85.
Editor's Note: The original news release can be found here.
