Immunotherapy - the enlisting of the immune system to fight cancer - is an exciting new field that has already led to early trials of new treatments. However, these often fail because promising results seen in petri dishes are not translating into successful attacks on real tumors.

cancer immunotherapy cells 206x136Now, a new study from the Massachusetts Institute of Technology (MIT) suggests that one reason immunotherapy treatments appear to fail when they leave the lab may be because they are only enlisting one arm of the immune system. So far, immunotherapy developers have focused either on attacking tumors with antibodies, which enlists the innate immune response, or approaches like adoptive T cell therapy to boost numbers of T cells, which form the backbone of the adaptive immune response.

In a report on their work in the journal Cancer Cell, senior author Dane Wittrup, a professor in chemical engineering, and colleagues describe how a combination of the two approaches successfully halted a very aggressive type of melanoma in mice. Their idea began as they were investigating how to improve the immune response of an antibody-based therapy using IL-2, a signaling molecule. Making IL-2 hang around longer boosts anti-tumor antibody therapy.

Using brain tumor samples collected from children in the United States and Europe, an international team of scientists found that the drug panobinostat and similar gene regulating drugs may be effective at treating diffuse intrinsic pontine gliomas (DIPG), an aggressive and lethal form of pediatric cancer.

pediatriccancerThe study, published inNature Medicine, was partially funded by the National Institutes of Health, the Department of Defense, and more than 25 nonprofit foundations devoted to finding cures for childhood brain cancer.

“Our results provide a glimmer of hope for treating this heartbreaking disease,” said Michelle Monje, M.D., Ph.D., assistant professor of neurology and neurological sciences, Stanford University School of Medicine, California, a senior author of the study and a specialist in DIPG. “Caring for DIPG patients drives me to find new ways to treat them.”

DIPG typically attacks children 4 to 9 years of age. Children progressively lose muscle control as the tumor rapidly attacks the pons, a region deep inside the brain that connects the brain to the spinal cord, and is difficult to reach and surgically remove. Despite radiation treatment, children usually survive for about nine months, and less than 1 percent survive longer than five years.

Stimulating both major branches of the immune system halts tumor growth more effectively.

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The human immune system is poised to spring into action at the first sign of a foreign invader, but it often fails to eliminate tumors that arise from the body’s own cells. Cancer biologists hope to harness that untapped power using an approach known as cancer immunotherapy.

Orchestrating a successful immune attack against tumors has proven difficult so far, but a new study from MIT suggests that such therapies could be improved by simultaneously activating both arms of the immune system. Until now, most researchers have focused on one of two strategies: attacking tumors with antibodies, which activate the innate immune system, or stimulating T cells, which form the backbone of the adaptive immune system.

By combining these approaches, the MIT team was able to halt the growth of a very aggressive form of melanoma in mice.

Powerful drugs known as BRAF-inhibitors have been crucial for melanoma patients, saving lives through their ability to turn off the BRAF protein’s power to spur cancer cell growth.

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Yet they often work for only a year or less. Scientists know some of the DNA mutations that cause the drug resistance, but scientists have not been able to determine the underlying cause of the resistance in as many as a third of these patients. As a result, identifying genomic-based follow-up therapies for these patients has been a challenge.

Researchers at The University of Texas MD Anderson Cancer Center may have found a way to more accurately predict which patients will likely respond to genomic-based follow-up therapies, by looking at unique “protein patterns” in melanoma patients.

“There are patients whose DNA does not reveal how their melanomas became resistant to BRAF inhibitors,” saidLawrence Kwong, Ph.D., instructor in  Genomic Medicine at MD Anderson.  “So we looked at patterns of changes in 150 proteins which can give clues to the causes of resistance, even when DNA sequencing data is uninformative.”

When battling a chronic infection, killer T cells must take a break so they can continue to fight off infection. New research shows this decline in activity is actually an essential coping mechanism for T cells.

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Killer T cells are one of the body's main lines of defense against pathogens. Their job is to kill infected cells so that the viruses inside cannot replicate and spread. But often the force of their attack wanes during a chronic infection, as they become less effective at finding and destroying their targets – a state known as T cell exhaustion. T cells that target cancer cells for destruction become exhausted too, weakening the body's fight against a tumor. Howard Hughes Medical Institute scientists have discovered that this decline in activity is an essential coping mechanism that actually allows the T cells to persist in the face of a chronic infection.

Understanding the triggers and consequences of T cell exhaustion could help scientists fine tune therapies that aim to treat chronic infection or cancer by reactivating an immune response, says Susan Kaech, an HHMI Early Career Scientist at Yale University who led the study. Kaech and her colleagues found that in mice with chronic viral infections, T cells specialized against that virus died when they could not enter an exhausted state. They reported their findings in the November 13, 2014, issue of the journal Immunity.

Timing of inflammation determines whether potentially cancerous mutations may arise.

new study from MIT reveals one reason why people who suffer from chronic inflammatory diseases such as colitis have a higher risk of mutations that cause cancer. The researchers also found that exposure to DNA-damaging chemicals after a bout of inflammation boosts these mutations even more, further increasing cancer risk. The findings confirm a longstanding theory about why inflammation and cancer are linked, and offer possible ways to help prevent and treat cancer, says Bevin Engelward, an MIT professor of biological engineering and senior author of a Jan. 15 PLoS Genetics paper describing the findings. 


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This news service is provided by Good Samaritan Institute, located in Santa Rosa Beach, Florida.

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