Experimental treatment turns cancer cells back on after chemotherapy

Experimental cancer drug and treatment showed the potential to reverse part of the tumor’s resistance to standard treatments in lab mice, especially in mice bred to resist standard chemotherapy treatments. Researchers from the Johns…

Experimental treatment turns cancer cells back on after chemotherapy

Experimental cancer drug and treatment showed the potential to reverse part of the tumor’s resistance to standard treatments in lab mice, especially in mice bred to resist standard chemotherapy treatments.

Researchers from the Johns Hopkins Kimmel Cancer Center announced a “breakthrough” in cancer treatment in mice with the pharmaceutical anti-apoptosis agent NYX10460 after they were able to boost a drug’s ability to kill pancreatic cancer cells.

NYX10460 is a molecular inhibitor of programmed cell death gene (PDD) activator-like 2 (luteinizing hormone activator 2, or LAX2), a growth hormone receptor that assists cell growth and survival.

Mice lacking LAX2 were thought to be resistant to a type of chemotherapy called endocrine therapy. Endocrine therapy is a class of drugs that makes cancer cells stop growing by blocking female hormones like estrogen and progesterone.

Previous studies have shown that LAX2 can suppress or interfere with cell survival in genetically modified mice. The researchers used this study to show that an experimental drug, called NYX10460, can achieve its desired effect, particularly on mice with tumors that lack LAX2.

The research, published in Science Translational Medicine, is the first study to demonstrate the ability of this inhibitor to target an endocrine therapy.

“It is often assumed that only cisplatin works in advanced metastatic pancreatic cancer because it acts similarly to endocrine therapy,” said the study’s senior author Yi Jiao, Ph.D., an associate professor of cancer genetics and pathobiology at the Johns Hopkins Kimmel Cancer Center. “Our experiments show that in rare cases, a use of LAX2 as a human cancer drug could be a favorable alternative to cisplatin.”

NYX10460 can slow down the growth of pancreatic cancer tumor cells, but it also leads to an increase in the amount of glucose, a potentially dangerous side effect.

“NYX10460 causes some glucose damage in cells, which leads to rewiring, and the cells behave differently, leading to slower cancer growth,” Jiao said. “They have acquired the ability to make glucose. This distinction needs to be clarified so that we can optimize the therapeutic strategy in humans.”

NYX10460 has shown its ability to target cancer cells in about 25 percent of human pancreatic cancer tumors, according to Jiao.

Since New YorkX10460 is still in the early stages of testing and testing results will be needed to determine the levels of this drug that could work best for pancreatic cancer patients, Jiao hopes this study will spur further research into how to better treat pancreatic cancer.

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