ScienceDiscovery Sheds New Light on How Cancer Cells Infect Healthy Tissue
Tiffany Kaiser - December 13, 2010 5:53 PM
Tiffany Kaiser - December 13, 2010 5:53 PM
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Researchers at the Montreal Neurological Institute and Hospital at McGill University have discovered how tumor cells infect healthy tissue, which is a breakthrough that can help prevent cancer cells from spreading.
Dr. Deborah Maret, lead author of the study and research associate at the Montreal Neurological Institute and Hospital of McGill University, along with Dr. David Colman, co-author of the study and director at the Montreal Neurological Institute, and Dr. Rolando Del Maestro, co-author of the study and director of The Brain Tumour Research Centre, have found that a certain protein which "glues" cells together has a non-adhesive version of itself that exists on tumor cells, allowing cancer cells to break apart and spread to healthy tissue.
These certain proteins are called cadherins, and they reside on the surface of cells. They bind cells together, kind of like glue, in order to hold tissue structures together properly. Prior to this study, it was not clear what happened to cells and the adhesive cadherins in tumor growth and metastases.
"We were concerned that previous research showed that N-cadherin, an adhesive molecule, was important for both normal tissue organization, as well as tumor metastases," said Colman. "We therefore decided to further investigate this apparent paradox."
What they found was a non-adhesive version of N-cadherin, which is called proNcad. It exists only on tumor cells, but is seen in much higher numbers on the more aggressive melanoma, brain tumor cells, breast cancer and prostate tumor cells.
"It appears that although total N-cadherin levels remain constant, the higher levels of the non-adhesive proNcad promote detachment, tumor cell migration and invasion," said Maret. "This supports an overall conclusion that non-adhesive [proNcad] and adhesive [Ncad] forms of cadherins co-exist on tumor cell surfaces, but it is the ratio between these functionally opposite molecules that directly dictates the invasion potential of tumor cells."
N-cadherin is not a new discovery, but because the differences between Ncad and proNcad are so minuscule, previous studies on the matter just assumed all Ncad's on tumor cell surfaces were adhesive. This latest study from the researchers at the Montreal Neurological Institute and Hospital is unique because it has recognized that there are non-adhesive cadherins as well, which allows tumor cells to detach from other cells and infect healthy tissue.
The next step in this research is to measure the ratios of proNcad and Ncad on cell surfaces, which could help researchers develop diagnostic tools that can help prevent cancer cells from spreading.
"As a brain tumor surgeon, I know that stopping cancer cells from migrating is critical for patient survival," said Del Maestro. "We are determined to improve treatment options for patients. We have already introduced new neurosurgical methods and technologies that are unique in North America and are spearheading multidisciplinary initiatives to advance brain tumor research."
This study was published in the journal Neoplasia.
(dailtech.com)
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Scientists discover new way in which HPV
triggers cancer
University of Manchester scientists have discovered for the first time an important new way in which the human papilloma virus (HPV) triggers cancer in what could lead to new treatments for cervical and mouth cancer.
HPV infection is known to increase the risk of developing cancers of the cervix and mouth with the two high-risk forms of the virus accounting for approximately 70% of all cervical cancer cases.
Vaccinations against these high-risk forms of HPV should reduce the incidence of cervical cancer but the frequency of mouth cancer actually increased in the UK by about 50% between 1989 and 2007, a trend that seems to be accelerating.
If the current vaccines prove effective at preventing oral HPV infection, the authors claim their findings provide additional justification for the current programme of vaccinating young girls and may also lend support to extending the programme to young boys too.
"Scientists have known for some years about the link between HPV and certain cancers but the biological processes involved are not fully understood," said Dr Ian Hampson, who with wife Dr Lynne Hampson headed the research. "Our latest results shed new light on this.
"Our study has shown that a protein in cells called Cdc42, which is already known to be implicated in a number of cancers as well as in tumour spread, is inappropriately activated by the human papilloma virus.
"The findings are important since it is essential to increase our understanding of how the virus causes the disease if we are to design new approaches for the prevention or treatment of HPV-related cancers. Mouth cancer, in particular, is notoriously difficult to treat and often leads to long-term disability.
"If the vaccination programme is shown to reduce the incidence of oral HPV infection then this study would appear to support its continued use as a way to prevent HPV-related mouth cancer and perhaps consideration should be given to extending the programme to boys."
The research, published in the British Journal of Cancer, was carried out in the Gynaecological Oncology Laboratories at St Mary's Hospital, Manchester, by one of the Hampsons' PhD students, Dr Anthony Oliver.
Dr Oliver said: "There are literally hundreds of publications describing the potential role of Cdc42 in malignant disease but our work is the first to show that HPV can activate this protein.
"There is already a drive towards developing drugs that target activated Cdc42 and our findings now indicate that these agents may be useful for the treatment of HPV-related cancers too."
SOURCE University of Manchester
Vaccinations against these high-risk forms of HPV should reduce the incidence of cervical cancer but the frequency of mouth cancer actually increased in the UK by about 50% between 1989 and 2007, a trend that seems to be accelerating.
If the current vaccines prove effective at preventing oral HPV infection, the authors claim their findings provide additional justification for the current programme of vaccinating young girls and may also lend support to extending the programme to young boys too.
"Scientists have known for some years about the link between HPV and certain cancers but the biological processes involved are not fully understood," said Dr Ian Hampson, who with wife Dr Lynne Hampson headed the research. "Our latest results shed new light on this.
"Our study has shown that a protein in cells called Cdc42, which is already known to be implicated in a number of cancers as well as in tumour spread, is inappropriately activated by the human papilloma virus.
"The findings are important since it is essential to increase our understanding of how the virus causes the disease if we are to design new approaches for the prevention or treatment of HPV-related cancers. Mouth cancer, in particular, is notoriously difficult to treat and often leads to long-term disability.
"If the vaccination programme is shown to reduce the incidence of oral HPV infection then this study would appear to support its continued use as a way to prevent HPV-related mouth cancer and perhaps consideration should be given to extending the programme to boys."
The research, published in the British Journal of Cancer, was carried out in the Gynaecological Oncology Laboratories at St Mary's Hospital, Manchester, by one of the Hampsons' PhD students, Dr Anthony Oliver.
Dr Oliver said: "There are literally hundreds of publications describing the potential role of Cdc42 in malignant disease but our work is the first to show that HPV can activate this protein.
"There is already a drive towards developing drugs that target activated Cdc42 and our findings now indicate that these agents may be useful for the treatment of HPV-related cancers too."
SOURCE University of Manchester
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Main Category: Breast Cancer
Also Included In: Cancer / Oncology; Genetics
Article Date: 14 Dec 2010 - 4:00 PST
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Cancer Research UK scientists have discovered that a single gene controls the oestrogen-fuelled growth ofbreast cancer cells, according to research published in Nature Genetics.
And, crucially, they have shown that the gene determines whether breast cancer cells respond to hormone treatments, like tamoxifen.
Tamoxifen works by blocking oestrogen receptors found in some, but not all, breast cancer cells. These receptors would normally switch on genes that lead to cell growth.
It remains one of the most effective breast cancer treatments for so-called 'oestrogen receptor (ER) positive' breast cancers.
But about a third of women who take the drug will either fail to respond initially or develop resistance to it over time.
Now researchers based at Cancer Research UK's Cambridge Research Institute have discovered that a single gene - known as FOXA1 - appears to be the key that allows oestrogen receptors to interact with the DNA inside breast cancer cells, switching on genes that trigger unchecked cell growth.
They believe that developing drugs to block FOXA1 could help women who are resistant to tamoxifen.
Lead author, Dr Jason Carroll said: "We discovered that almost none of the genes normally switched on by oestrogen receptors interacting with the DNA were activated in breast cancer cells lacking FOXA1. Instead the oestrogen receptor was just left floating around in the cell, unable to make contact with the DNA and kick start cell growth.
"We also found that the FOXA1 protein forms an essential part of tamoxifen response in breast cancer cells, since like oestrogen, it also uses FOXA1 to interact with the DNA. This is exciting because it suggests that developing drugs to block FOXA1 could provide an effective treatment for women with ER positive breast cancers who have become resistant to standard hormone treatments, like tamoxifen."
The researchers used a technique known as ChIP-sequencing to look at how the FOXA1 protein interacted with the DNA. This revealed that FOXA1 attached to the DNA at almost all the same points as the oestrogen receptors did and that it was essential for them to be able to make contact with the DNA.
Breast cancer is the most common cancer in the UK. Almost 45,700 women are diagnosed with the disease each year, of which about 30,000 women have hormone-sensitive breast cancers.
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "We know that some women with breast cancer stop responding to tamoxifen, making them more prone to relapsing. This important discovery could one day lead to new drugs that help improve the outcome for these patients.
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