Immune Complexes & Cancer: Stem Cell Protection
- New research from Weill Cornell Medicine suggests that immune proteins known as inflammasomes can play a key role in preventing blood stem cells from developing into cancer.
- The findings support the idea that the inflammasome has a dual role: while it can contribute to inflammation in later stages of cancer, it appears to actively prevent...
- Julie Magarian Blander, the Gladys and Roland Harriman Professor of Immunology in Medicine at Weill Cornell Medicine, emphasized the unexpected role of the innate immune system.
Discover the crucial role of immune proteins, specifically inflammasomes, in safeguarding blood stem cells from cancer. This groundbreaking research from Weill Cornell Medicine reveals how thes proteins function, inhibiting cancer gene activity and preventing early-stage malignancy. The dual role of inflammasomes, previously understood for their involvement in inflammation, has now been redefined. This new understanding could yield innovative therapies for cancer at its earliest stages. The study, published in nature Immunology, highlights the innate immune system’s unexpected role in maintaining tissue homeostasis. Explore how these findings may reshape cancer treatment approaches, possibly paving the way for more effective interventions. Stay informed with News Directory 3 for the latest updates. Discover what’s next in this exciting field of study.
Immune Proteins’ Role in Preventing Malignancy Discovered
New research from Weill Cornell Medicine suggests that immune proteins known as inflammasomes can play a key role in preventing blood stem cells from developing into cancer. The preclinical study, published Jan. 2 in Nature Immunology, indicates that these proteins work by removing specific receptors from cell surfaces and inhibiting cancer gene activity.
The findings support the idea that the inflammasome has a dual role: while it can contribute to inflammation in later stages of cancer, it appears to actively prevent cells from becoming cancerous in the early stages.this discovery could pave the way for therapies that target cancer at its earliest advancement.
Dr. Julie Magarian Blander, the Gladys and Roland Harriman Professor of Immunology in Medicine at Weill Cornell Medicine, emphasized the unexpected role of the innate immune system. “We found that it functions in maintaining homeostasis in the tissue, keeping an eye on whether stem cells are proliferating too much,” Blander said. “by doing so, it prevents cells from becoming cancerous, and this activity is autonomous of inflammation.”
The studyS co-first authors are Dr. Andrew Kent, an assistant professor of medicine-hematology at the University of Colorado School of Medicine, and Dr. Kristel Joy Yee Mon, a postdoctoral associate in Blander’s lab.
To investigate cancer’s origins, the researchers studied a mouse model of B-cell lymphoma with a mutation in the Myc oncogene. this model allowed them to observe the early stages of cancer development. They found that disrupting inflammasome activity accelerated stem cell proliferation and tumor development. Further, stem cells lacking the inflammasome also proliferated rapidly, suggesting the complex plays a vital role in healthy cells.
The team discovered that without the inflammasome, stem cells had high levels of the protein Ras, another oncogene product. The inflammasome’s normal function of controlling Ras delays tumorigenesis. The protective activity originated in the bone marrow stroma, which surrounds and supports the stem cells.
Blander noted that higher levels of soluble tumor necrosis factor (TNF) receptors were found in the stroma of control mice. ”We think that the inflammasome in the stroma is orchestrating something where it’s cleaving TNF receptors, shaving them off the stem cells,” Blander said.
What’s next
The research team plans to investigate the inflammasome’s protective effects in other tissues and identify the specific stromal cell types and molecules responsible for its activity.Their ultimate goal is to develop a therapeutic approach to prevent cancer by targeting the inflammasome’s inflammatory activity while preserving its beneficial function in delaying tumorigenesis.