Posts Tagged ‘cancer research’

Cancer Leaves a Common Fingerprint on DNA

 :: Posted by American Biotechnologist on 08-26-2014

Regardless of their stage or type, cancers appear to share a telltale signature of widespread changes to the so-called epigenome, according to a team of researchers. In a study published online in Genome Medicine on Aug. 26, the investigators say they have found widespread and distinctive changes in a broad variety of cancers to chemical marks known as methyl groups attached to DNA, which help govern whether genes are turned “on” or “off,” and ultimately how the cell behaves. Such reversible chemical marks on DNA are known as epigenetic, and together they make up the epigenome.

“Regardless of the type of solid tumor, the pattern of methylation is much different on the genomes of cancerous cells than in healthy cells,” says Andrew Feinberg, M.D., M.P.H., a professor of medicine, molecular biology and genetics, oncology, and biostatistics at the Johns Hopkins University School of Medicine. Feinberg led the new study along with Rafael Irizarry, Ph.D., a professor of biostatics at Harvard University and the Dana-Farber Cancer Institute. “These changes happen very early in tumor formation, and we think they enable tumor cells to adapt to changes in their environment and thrive by quickly turning their genes on or off,” Feinberg says.

Feinberg, along with Johns Hopkins University School of Medicine oncology professor Bert Vogelstein, M.D., first identified abnormal methylation in some cancers in 1983. Since then, Feinberg’s and other research groups have found other cancer-associated changes in epigenetic marks. But only recently, says Feinberg, did researchers gain the tools needed to find out just how widespread these changes are.

For their study, the research team took DNA samples from breast, colon, lung, thyroid and pancreas tumors, and from healthy tissue, and analyzed methylation patterns on the DNA. “All of the tumors had big blocks of DNA where the methylation was randomized in cancer, leading to loss of methylation over big chunks and gain of methylation in smaller regions,” says Winston Timp, Ph.D., an assistant professor of biomedical engineering at Johns Hopkins. “The changes arise early in cancer development, suggesting that they could conspire with genetic mutations to aid cancer development,” he says.

The overall effect, Feinberg says, appears to be that cancers can easily turn genes “on” or “off” as needed. For example, they often switch off genes that cause dangerous cells to self-destruct while switching on genes that are normally only used very early in development and that enable cancers to spread and invade healthy tissue. “They have a toolbox that their healthy neighbors lack, and that gives them a competitive advantage,” Feinberg says.

“These insights into the cancer epigenome could provide a foundation for development of early screening or preventive treatment for cancer,” Timp says, suggesting that the distinctive methylation “fingerprint” could potentially be used to tell early-stage cancers apart from other, harmless growths. Even better, he says, would be to find a way to prevent the transition to a cancerous fingerprint from happening at all.

Thanks to Johns Hopkins Medicine for contributing this story.

New Discovery in Living Cell Signaling

 :: Posted by American Biotechnologist on 07-04-2014

A breakthrough discovery into how living cells process and respond to chemical information could help advance the development of treatments for a large number of cancers and other cellular disorders that have been resistant to therapy. An international collaboration of researchers, led by scientists with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley, have unlocked the secret behind the activation of the Ras family of proteins, one of the most important components of cellular signaling networks in biology and major drivers of cancers that are among the most difficult to treat.

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Pied Piper Approach to Killing Cancer

 :: Posted by American Biotechnologist on 02-17-2014

One factor that makes glioblastoma cancers so difficult to treat is that malignant cells from the tumors spread throughout the brain by following nerve fibers and blood vessels to invade new locations. Now, researchers have learned to hijack this migratory mechanism, turning it against the cancer by using a film of nanofibers thinner than human hair to lure tumor cells away.

Instead of invading new areas, the migrating cells latch onto the specially-designed nanofibers and follow them to a location – potentially outside the brain – where they can be captured and killed. Using this technique, researchers can partially move tumors from inoperable locations to more accessible ones. Though it won’t eliminate the cancer, the new technique reduced the size of brain tumors in animal models, suggesting that this form of brain cancer might one day be treated more like a chronic disease.

“We have designed a polymer thin film nanofiber that mimics the structure of nerves and blood vessels that brain tumor cells normally use to invade other parts of the brain,” explained Ravi Bellamkonda, lead investigator and chair of the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. “The cancer cells normally latch onto these natural structures and ride them like a monorail to other parts of the brain. By providing an attractive alternative fiber, we can efficiently move the tumors along a different path to a destination that we choose.”

Details of the technique were reported February 16 in the journal Nature Materials. The research was supported by the National Cancer Institute (NCI), part of the National Institutes of Health; by Atlanta-based Ian’s Friends Foundation, and by the Georgia Research Alliance. In addition to the Coulter Department of Biomedical Engineering, the research team included Children’s Healthcare of Atlanta and Emory University.

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Alternative Splicing Thought to be an Important Target for Cancer Therapy

 :: Posted by American Biotechnologist on 04-19-2013

Researchers at UT Southwestern Medical Center have found that alternative splicing – a process that allows a single gene to code for multiple proteins – appears to be a new potential target for anti-telomerase cancer therapy.

The enzyme telomerase is overexpressed in almost all cancer cells, and previous research efforts have failed to identify good telomerase inhibitors. The study by Dr. Woodring Wright and UT Southwestern colleagues in the April 4 issue of Cell Reports identifies a new approach for inhibiting telomerase, which is an enzyme that drives uncontrolled division and replication of cancer cells.

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New Molecule Targets Proteins Inside Cancer Cells

 :: Posted by American Biotechnologist on 03-14-2013

Researchers have discovered a unique monoclonal antibody that can effectively reach inside a cancer cell, a key goal for these important anticancer agents, since most proteins that cause cancer or are associated with cancer are buried inside cancer cells. Scientists from Memorial Sloan-Kettering Cancer Center and Eureka Therapeutics have collaborated to create the new human monoclonal antibody, which targets a protein associated with many types of cancer and is of great interest to cancer researchers.

Unlike other human therapeutic monoclonal antibodies, which can target only proteins that remain on the outside of cancer cells, the new monoclonal antibody, called ESK1, targets a protein that resides on the inside of the cell.

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