Article - How a gene that usually protects against
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Posted On: 11/09/2017 8:03:12 PM
Article - How a gene that usually protects against cancer becomes the disease’s aggressor
Video - Patient-Centered Care in the 21st Century - 2017 UCSF Cancer Showcase
A study led by a University of California San Diego researcher has found an explanation for one of the biggest causes of cancer, mutations in a gene that normally guards against cancer.
Mutations in the gene, called p53, can lead to inflammation, stimulating an immune response that fuels cancer, the study found. The effect was seen in common human tumors such as colon and breast cancers, said Shannon Lauberth, the study’s senior author.
In these cancers, inflammation can help the cancers grow and spread, the study said.
A better understanding of just how the mutations trigger inflammation could result in better therapies, Lauberth said.
The study was published Oct. 23 in Nature Communications. It can be found at j.mp/p53cancer. Coauthors include UCSD colleagues Hanbin Lu, Sascha Duttke, Christopher Benner and Christopher Glass.
Human tumor samples were provided by the UCSD Moores Cancer Center, she said. These were compared with normal tissues from the same patient to find differences in p53.
The mutations act in concert with an inflammatory substance called NFkB. They trigger changes throughout the genome, activating regions that are normally silent. These are believed to help promote cancer, Lauberth said.
Geneticist Inder Verma of the Salk Institute said the study underscores the paradoxical role of inflammation in cancer.
“Inflammation is a double-edged sword; in some cancers it inflames the tumor growth and in others it dampens the tumor development,” Verma said by email. “It is thus important to know the status of the inflammatory genes in treatment with immunotherapy.”
The relationship between mutant p53, which is altered in more than half of all cancers, and NFkB is “elegantly dissected,” Verma said, “which should help in planning treatments of various cancers.”
The research was funded by the Sidney Kimmel Foundation for Cancer Research and a CRI-Irvington Fellowship.
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Video - Patient-Centered Care in the 21st Century - 2017 UCSF Cancer Showcase
A study led by a University of California San Diego researcher has found an explanation for one of the biggest causes of cancer, mutations in a gene that normally guards against cancer.
Mutations in the gene, called p53, can lead to inflammation, stimulating an immune response that fuels cancer, the study found. The effect was seen in common human tumors such as colon and breast cancers, said Shannon Lauberth, the study’s senior author.
In these cancers, inflammation can help the cancers grow and spread, the study said.
A better understanding of just how the mutations trigger inflammation could result in better therapies, Lauberth said.
The study was published Oct. 23 in Nature Communications. It can be found at j.mp/p53cancer. Coauthors include UCSD colleagues Hanbin Lu, Sascha Duttke, Christopher Benner and Christopher Glass.
Human tumor samples were provided by the UCSD Moores Cancer Center, she said. These were compared with normal tissues from the same patient to find differences in p53.
The mutations act in concert with an inflammatory substance called NFkB. They trigger changes throughout the genome, activating regions that are normally silent. These are believed to help promote cancer, Lauberth said.
Geneticist Inder Verma of the Salk Institute said the study underscores the paradoxical role of inflammation in cancer.
“Inflammation is a double-edged sword; in some cancers it inflames the tumor growth and in others it dampens the tumor development,” Verma said by email. “It is thus important to know the status of the inflammatory genes in treatment with immunotherapy.”
The relationship between mutant p53, which is altered in more than half of all cancers, and NFkB is “elegantly dissected,” Verma said, “which should help in planning treatments of various cancers.”
The research was funded by the Sidney Kimmel Foundation for Cancer Research and a CRI-Irvington Fellowship.
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