by John R. Fischer
, Senior Reporter | April 26, 2019
The reasons behind this act of inhibition are explored in the third study, in which ephrinB2 inhibition was applied in models of pancreatic cancer. Such an approach with ephrinB2 has traditionally resulted in poor prognoses, but through collaboration with multiple partners, it was found that ephrinB2 inhibition reduces "fibrosis" in tumors by packing them less tightly with cross-linked collagen fibers.
As these fibers are known to make pancreatic tumors less permeable to anti-cancer drugs, less vulnerable to the immune system, and more likely to metastasize, their decrease reduces resistance and allows for an immune system, stimulated by radiotherapy, to be better able to attack and destroy cancer cells.
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“By understanding how the Tregs enter the tumor, how T cells that are normally destined to become effector T cells are converted to Tregs, what the Tregs use to stay alive, and what attracts Tregs to the tumor, we hope to develop new generation Treg targets that can potentially synergize with radiation,” said Karam. “Equally important in solving this puzzle is understanding why certain tumors do not have Tregs while others do. Capitalizing on the diverse biological heterogeneity will not only be key to identifying new targets, but might give us a glimpse into identifying biomarkers of response to certain therapies.”
The findings of the first study were published in the Journal of the National Cancer Institute
, while those of the second and third were published in Cancer Research
and Clinical Cancer Research
, respectively. Back to HCB News