Cancer is reshaping the architecture of our chromosomes so disease can set in and spread, researchers at the University of Virginia have found
This remodeling is important because the arrangement of components in our chromosomes actually affects how our genes work. With these renovations, cancer begins to make a comfortable home for itself inside our cells
Even when the genetic code of the DNA sequence can remain largely the same, the three-dimensional structure of chromosomes in cancer can be very different from our normal cells A better understanding of the structure of the cancer genome can help us provide ideas for developing new drugs to specifically target the Achilles heel of each cancer «
To make the desired changes inside our chromosomes, cancer relies on a protein called ‘CCCTC binding factor’, or CTCF for short CTCF occurs naturally in our cells In healthy cells it plays a role important role in maintaining chromosomal structure and turning genes on and off as needed But cancer, Zang discovered, turns CTCF up for its own purposes CTCF appears where it shouldn’t, and it doesn’t bind not where it should This changes the three-dimensional organization of our chromosomes and changes how genes work
To understand the role of CTCF in cancer, Zang and his team delved deep into genomic data collected from human tissue and cancer samples.They identified patterns of CTCF remodeling in six different cancers, including acute T-cell lymphoblastic leukemia, acute myeloid leukemia, breast cancer, colorectal cancer, lung cancer, and prostate cancer
“We have developed an innovative approach to data science to collect and integrate thousands of publicly available datasets in order to draw these conclusions,” said Zang “It’s exciting to see how many new discoveries scientists can only be done by analyzing the big data already available »
The researchers validated their findings by looking specifically at acute T-cell lymphoblastic leukemia, but they say further research into changes in CTCF binding will help scientists better understand the origins of other cancers as well. (A faulty CTCF binding has also been linked to developmental disorders and other conditions, so understanding it may offer important information about these diseases as well.)
“The abnormal CTCF binding patterns we found are likely a signature found in every type of cancer,” Zang said “These findings have taken us one step closer to fully discovering the molecular mechanism of cancer , an extremely complex disease »
The researchers published their results in the scientific journal Genome Biology The UVA research team consisted of Zhenjia Wang, Aakrosh Ratan and Zang The experimental work was carried out in collaboration with scientists from Northwestern University, the ‘University of Miami and the Mayo Clinic
Zang is a member of the Department of Public Health Sciences of the School of Medicine and the Department of Biochemistry and Molecular Genetics He is also a member of the UVA Cancer Center and the Department of Biomedical Engineering at UVA, a collaboration from the School of Medicine and the School of Engineering
Research at UVA was supported by National Institutes of Health (NIH) grants K22CA204439 and R35GM133712, as well as a Phi Beta Psi Sorority research grant
Tags: Acute lymphoblastic leukemia, Acute myeloid leukemia, Biochemistry, Breast cancer, Cancer, Cell, Chromosome, Colorectal, Colorectal cancer, DNA, Drugs, Genes, Genetics, Genetics, Genome, Genomics, Genomics, Leukemia, Cancer du lung, medical research, medicine, myeloid leukemia, prostate, prostate cancer, proteins, public health, research, T lymphocytes
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