However, according to Dr Kutikov, the authors of the current study presented “an entirely novel biological pathway that leads to castration-resistant disease and, more importantly, offers a viable therapeutic mechanism for its blockade.”

“This is the first step toward conceptually identifying a viable target in prostate cancer,” said Sumanta Kumar Pal, MD, of the City of Hope in Duarte, California, whose team has also worked on the roles of MDSCs in the progression of prostate cancer.2 “I think it remains to be seen whether or not this will pan out as a clinical strategy,” Dr Pal said. “This might potentially be a salvage treatment, but if this is truly a driver of prostate tumor progression along the androgen signaling axis, perhaps this could be used earlier in the treatment algorithm.”

The findings bolster the case for research targeting MDSCs, agreed Guocan Wang, MD, PhD, assistant professor of genitourinary medical oncology at the University of Texas MD Anderson Cancer Center in Houston.

“It is not surprising to me that MDSCs, an immature myeloid population that expanded and accumulated in tumors, promote castration resistance in prostate cancer,” Dr Wang said. “The stromal cells present in the tumor microenvironment have been implicated in therapeutic resistance in multiple cancer types.”

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Blocking MDSC IL-23 is “a promising way to overcome castration resistance and can be potentially translated into clinical practice,” Dr Wang said. “However, more work needs to be done in preclinical models.”

The Pten-knockout mouse model used in the European study is considered to be a less-aggressive model of prostate cancer than others, Dr Wang  noted.

“It remains to be determined whether this approach works in preclinical models of aggressive prostate cancer,” he said. “[I]t will be critical to determine whether this approach works in preclinical models [featuring] more aggressive prostate cancer, [such as] metastasis to distant organs.”