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Supportive tissue in tumors hinders, rather than helps, pancreatic cancer
Date:5/22/2014

"But it's not just a negative study, because it suggests what might work for these patients."

And what might work hinges on immune checkpoint blockade.

The immune system connection

To understand the cause of the swift progression, the team conducted gene expression profiling and RNA sequence analysis comparing control tumors to myofibroblast-depleted tumors.

Genes associated with tumor immunity were suppressed and fewer T cells and B cells infiltrated the myofibroblast-depleted tumors. The proportion of regulatory T cells, which suppress immune response, increased. They found greater expression of the immune checkpoint CTLA-4, which shuts down immune response.

The researchers then set up a new experiment using ipilimumab, a drug developed by co-author Jim Allison, Ph.D., chair of Immunology, that blocks CTLA-4, freeing T cells to attack tumors.

Mice with depleted myofibroblasts who were treated with ipilimumab to stifle CTLA-4 had an average survival increase of 60% compared to untreated control mice and those with either depleted myofibroblasts or treated with ipilimumab alone.

These findings suggest that ipilimumab might work for patients with low levels of fibrosis in their tumors, Kalluri noted. Combining ipilimumab with a hedgehog inhibitor is likely to work better for those with high-fibrosis. The Kalluri laboratory is exploring these issues.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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