When a new drug kills cancer, it’s a sign of a trend and not a sign that there’s a new paradigm in cancer treatment
Cancer patients and doctors are using technology and social media to fight cancer.
They’re asking: Is there a new way to treat cancer?
A growing body of research suggests yes.
A new study in Nature Methods finds that a drug that blocks the immune system’s ability to fight infections by disrupting a protein known as CXCL10 could effectively slow the progression of advanced melanoma.
A group of scientists at Columbia University and elsewhere tested CXCR4 inhibitors in mice and found that they slowed progression to advanced melanomas in mice by about 40 percent, and could slow progression in humans by 30 percent.
The new study, led by Dr. Mark Mathers of Columbia, was published online Feb. 15 in Nature.
It’s the first time scientists have found that the drug, known as a CX4 inhibitor, slows progression to melanoma by a significant margin in humans.
“I think it’s just a matter of time before we can look at therapies to reverse these tumors,” said Dr. Scott Stolz, an oncologist at Brigham and Women’s Hospital in Boston and one of the study’s authors.
“The hope is that it’s not a bad thing.”
The drug, called CX7, is a gene-editing tool designed to treat mutations in the gene that codes for a protein called CCL10.
The mutation in CCL9, which causes the disease, can cause tumors to form.
Researchers are currently trying to figure out how the CCL11 mutation in patients can slow cancer’s progression.
One way to make CXC7 inhibitors is to genetically alter them.
A few studies have shown that this can be done, but so far, no one has successfully created CX10 inhibitors.
“It’s a little hard to do,” said Mather.
“You want to make the gene itself that’s active.”
To make the CX3 inhibitors, researchers have been working on a drug called CCl3D2, which inhibits CCL5, the protein that codes a protein that makes CCL4.
The gene for CCL3D3 was sequenced and found to be active in humans, but not in mice.
“We’re really looking forward to seeing this gene-edited drug in human clinical trials,” said Andrew Biesecker, an associate professor of cancer genetics at the University of Pennsylvania and the first author of the Nature Methods study.
The CXCl10 inhibitor has been studied extensively.
Its effectiveness against melanoma in mice is thought to be about 50 percent.
The CXCT10 inhibitor, which blocks the enzyme CCL7, has also been studied and found effective against advanced melanocytes.
But neither has been shown to work as well in humans as CCL6, the enzyme that controls the progression to tumors.CXCT7 is also used to treat a few cancers.
The drug’s effectiveness against leukemia and other types of cancers is not known.”CXC-7 has been effective in humans for some time,” said Stolzz.
“We’re not sure what the clinical impact of that is going to be in humans.”
In the new study and others, researchers used mice with a mutation in a gene known as Bcl-2, a protein involved in the production of antibodies that help fight infection.
This is a common mutation that can lead to a variety of cancers, including lung cancer.
The scientists then injected mice with the CCR5 inhibitor CX2B and the Ccl7 inhibitor CCL2C, which blocked the activity of CCL1, the proteins that make CCLs.
They then injected the mice with Bcl2B or Ccl2C or both.
Mice treated with CX-2B showed an increase in tumor growth in the lab, while mice treated with the other drugs did not.
In the lab tests, CXcl7 inhibitors reduced tumor growth by about 30 percent in the Bcl3L3 mice.
In humans, the drugs also reduced tumor formation in mice with CCL8, a mutation that causes cancer.
In this test, CCL-8-blocking drugs also increased the survival rate of the mice.
The researchers also showed that CCLC8-blockers also slowed tumor growth.CCl7 inhibitors are more effective than CXct7 inhibitors in people.
Mice treated by the CCl7 inhibitor treated with BCL2B had more tumor growth than the other mice, and the mice treated by CCLc8 treated with both drugs had less tumor growth as compared to mice treated only with Ccl6.
The study, “Drug-based inhibition of CX9-mediated inhibition of cell growth in mice,” was led by researchers from Columbia, the University at Albany and the University in London.
The work was supported by the National Institutes of Health.