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British-based researchers said a gene called UTX, found in the X gender chromosome, played the role of ringmaster in 10 percent of cases of multiple myeloma and one in 12 cancers of the oesophagus.
UTX controls an enzyme that contributes to the structure of DNA in our cells. The enzyme also acts as a switch, turning other genes on and off.
In a massive genetic trawl through tissue samples from patients with a form of kidney cancer, the scientists found a rare but telling signature among a mutated form of UTX.
By expanding the search to other cancer types, they also found the variant gene played a part in multiple myeloma -- cancer of the immune cells -- and in throat tumours.
"It influences some of the most fundamental mechanisms controlling gene activity in our cells," said Andy Futreal, co-leader of the Cancer Genome Project at Britain's Wellcome Trust Sanger Institute, which led the study.
"Unlike many cancer genes, UTX does not appear to be directly involved in cell division or cell death but in basic regulation, and shows the depths to which cancers will plumb in order to get themselves ready to go."
Separately, investigators in the United States and Britain identified several new genetic regions pointing to an enhanced risk for breast cancer.
Breast cancer is linked to lifestyle and environmental factors, such as exposure to tobacco smoke, but also has a strong genetic component.
Around half a dozen mutated genes are already closely linked to vulnerability to breast cancer, most famously the variants of the BRCA-1 and BRCA-2 genes, for which genetic tests are available.
But scientists say the list of culprits is far from complete, given the complex protein machinery involved in cancer.
Researchers from the US National Institutes of Health (NIH), meanwhile, said they had uncovered new insights into melanoma, the deadliest form of skin cancer.
They found that an enzyme gene called MMP-8 is designed to suppress tumour growth and variants in the gene help cancers to proliferate out of control.
The finding is important, because MMP-8 was previously considered to be a different category of gene -- an oncogene, which sends signals to promote cancer growth as opposed to suppressing it.
This could explain why drugs designed to inhibit members of the MMP family have often failed to work.
"In the estimated six percent of melanoma patients whose tumours harbour a mutated MMP-8 gene or related tumour suppressor, it may not be wise to block all MMPs," the NIH said in a press release.
"The study suggests that a better approach may be to look for drugs that restore or increase MMP-8 function or for drugs that block only those MMPs that are truly oncogenes."
The studies are the latest in a widening series of investigations that use genomics -- comparative scanning of individual genetic codes -- to spot tiny defects in genes that contribute to the molecular ballet of cancer.
Knowledge derived from this can be used to make better diagnostic tools and help drug designers in their search for treatments to stop or reverse the cancer-causing process.
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UTX controls an enzyme that contributes to the structure of DNA in our cells. The enzyme also acts as a switch, turning other genes on and off.
In a massive genetic trawl through tissue samples from patients with a form of kidney cancer, the scientists found a rare but telling signature among a mutated form of UTX.
By expanding the search to other cancer types, they also found the variant gene played a part in multiple myeloma -- cancer of the immune cells -- and in throat tumours.
"It influences some of the most fundamental mechanisms controlling gene activity in our cells," said Andy Futreal, co-leader of the Cancer Genome Project at Britain's Wellcome Trust Sanger Institute, which led the study.
"Unlike many cancer genes, UTX does not appear to be directly involved in cell division or cell death but in basic regulation, and shows the depths to which cancers will plumb in order to get themselves ready to go."
Separately, investigators in the United States and Britain identified several new genetic regions pointing to an enhanced risk for breast cancer.
Breast cancer is linked to lifestyle and environmental factors, such as exposure to tobacco smoke, but also has a strong genetic component.
Around half a dozen mutated genes are already closely linked to vulnerability to breast cancer, most famously the variants of the BRCA-1 and BRCA-2 genes, for which genetic tests are available.
But scientists say the list of culprits is far from complete, given the complex protein machinery involved in cancer.
Researchers from the US National Institutes of Health (NIH), meanwhile, said they had uncovered new insights into melanoma, the deadliest form of skin cancer.
They found that an enzyme gene called MMP-8 is designed to suppress tumour growth and variants in the gene help cancers to proliferate out of control.
The finding is important, because MMP-8 was previously considered to be a different category of gene -- an oncogene, which sends signals to promote cancer growth as opposed to suppressing it.
This could explain why drugs designed to inhibit members of the MMP family have often failed to work.
"In the estimated six percent of melanoma patients whose tumours harbour a mutated MMP-8 gene or related tumour suppressor, it may not be wise to block all MMPs," the NIH said in a press release.
"The study suggests that a better approach may be to look for drugs that restore or increase MMP-8 function or for drugs that block only those MMPs that are truly oncogenes."
The studies are the latest in a widening series of investigations that use genomics -- comparative scanning of individual genetic codes -- to spot tiny defects in genes that contribute to the molecular ballet of cancer.
Knowledge derived from this can be used to make better diagnostic tools and help drug designers in their search for treatments to stop or reverse the cancer-causing process.
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