Researchers at the Case Comprehensive Cancer Center have revealed a potentially important role for the protein-encoding gene MYO10 in tumorigenesis and immunotherapy responses.Their findings are today Science Advances..
A team led by Youwei Zhang, an associate professor of pharmacology at Case Western Reserve University School of Medicine, found breast cancers with high levels of MYO10 (including the most malignant triple-negative breast cancer) that respond favorably to immune checkpoint inhibition (ICB). Did. ) Treatment, supporting the use of this treatment to treat these types of tumors.
ICB is an innovative treatment that uses drugs known as immune checkpoint inhibitors. This is a drug that can help the body’s immune system recognize and attack. cancer cell..
The team’s findings also suggest that ICB use should be avoided in breast tumors with low MYO10, as these tumors actually grew after ICB treatment.
Studies show that high levels of MYO10 cause chronic inflammation in tumors and reduce major immune capacity. cellKnown as T cells for slowing tumor growth.
But at the same time, this inflammatory environment within the tumor increased the ability of immune cells to elicit an immune response.This was finally allowed Tumor cells Supports ICB therapy and improves outcomes.
Proteins called interferon and interleukin, and other factors that regulate their production, are part of the body’s natural defenses.When they sense bacteria or cancer cell In the body, they strengthen the immune system and trigger killer immune cells to fight these invaders.
In this study, researchers found that high levels of MYO10 increased the presence of interferon. Conversely, low levels of MYO10 correlated with decreased interferon production. The researchers explained that these findings at least partially explain why MYO10 hypotumors did not respond to ICB therapy.
Is consistent with Chronic inflammation Tumor environment with high levels of MYO10 leading to loss of T cell function, treatment with aspirin to reduce inflammation Breast tumor Overexpressing MYO10.
This is consistent with studies showing that long-term use of aspirin or non-steroidal anti-inflammatory drugs significantly reduced the tumor risk of esophageal, colorectal, and gastric cancers, as well as breast, lung, and prostate cancers. I have.
Team members have further elucidated how MYO10 promotes tumor growth. They say that MYO10 regulates genomic stability, cancer Growth by mediating the shape of the nucleus. They also found that the protein levels of MYO10 are important for this function.
They also showed how the protein recycling system tightly regulates MYO10 expression levels.These findings support tumor research and emphasize the importance of MYO10. Tumor development And the reaction of immunotherapy.
“This is the first study to correlate MYO10 with genomic instability and examine the role of MYO10. tumor Zhang, a member of the Molecular Oncology Program at the Center for Case Comprehensive Cancer, said, “Development and immunotherapy response,” “continuing these studies and how this knowledge has clinical implications for patient care. I would like to see if it gives, and I hope that these findings will be more effective. Treatment Elimination of options and ineffective treatments for breast cancer patients. “
The co-authors of the study are: Mark Jackson of Case General Cancer Center and Case Western Reserve Medical School. Franklin Meikapozo, Singlangen, Ilaria Tamano of Case Western Reserve Medical School. Ernest G. Heimsus and Richard Cheney at the University of North Carolina at Chapel Hill. John Hammer of the National Institute of Cardiopulmonary Blood.
MYO10 causes genomic instability and inflammation of cancer. Science Advances (2021). DOI: 10.1126 / sciadv.abg6908
Case Western Reserve University
Quote: The study linked the protein-encoding gene to tumorigenesis, activation of the body’s natural immune defenses against cancer (September 15, 2021), https://medicalxpress.com on September 15, 2021. Obtained from / news / 2021-09-links-protein-coding-. gene-tumor-body.html
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