A study published this week has found that when cancer cells are stressed, they produce a certain protein that helps the cancer to avoid detection by the immune system. This discovery opens an opportunity for developing therapies that target this particular protein in order to make immunotherapy more effective against cancer.
The study, which was conducted by a large team led by a group at New York University Langone Health, focused on pancreatic and lung cancer tumors. They studied the ISR (Integrated Stress Response) of the tumors. Tumor cells are constantly stressed because they multiply so fast and often lack all the nutrients they need to support their survival and further proliferation. As a result, the ISR of these cells is always turned on. It triggers ATF4 (Activating Transcription Factor 4), a protein which commands several genes to activate and help tumor cells survive.
The researchers also found that ATF4 initiates the production of LCN2 (lipocalin 2), a protein that makes it possible for tumor cells to avoid detection by the immune system. LCN2 prompts tumor cells to activate their immunosuppressive features, and this prevents immune cells from gaining access into the tumor.
Noticing that LCN2 circulates outside tumors, the research team saw an opportunity to target this protein in the fight against cancer. The idea was that if LCN2 could be deactivated, it would become a lot easier for immune cells that kill cancer to enter the tumor and suppress it from within. To this end, the team designed an antibody therapy that could bind to and block the action of LCN2.
Using engineered mice that had cancer and lacked the LCN2 protein as test subjects, the team found that the growth of the tumors slowed down significantly. It is notable that this suppressed growth only happened in mice whose immune systems were healthy. This showed that blocking LCN2 gave the immune system an opportunity to do its work, and also proved that LCN2 serves to prevent the immune system from attacking tumors.
To further test the validity of their findings, the researchers obtained tumor samples from 30 patients with pancreatic cancer and 100 patients with lung cancer. An analysis of those tumors revealed that patients who had low levels of LCN2 in the tumors tended to survive for longer when compared to patients whose tumors had high levels of this protein.
These results make a strong case for developing treatments targeting the LCN2 protein in lung cancer tumors, and for pancreatic cancer. The researchers are now planning to analyze tumors taken from patients with other forms of cancer in order to ascertain whether LCN2 plays a similar immune-suppression role.
Entities like Calidi Biotherapeutics Inc. (NYSE American: CLDI) working to develop immunotherapies with higher efficacy rates for more patients are likely to assess the clinical implications of pairing LCN2 blockers with existing immune therapies targeting cancer.
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