Platelets may play an unexpected role in glioblastoma progression
· Medical Xpressedited by Sadie Harley, reviewed by Robert Egan
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New Cleveland Clinic research published in Cancer Cell shows that people with glioblastoma have more active platelets, which are cells involved in blood clotting. Platelets also communicate with other cells and can influence immune activity. The overactive platelets in people with glioblastoma slow the activity of cancer-fighting T cells, which can contribute to tumor growth and cancer progression.
Researchers from the lab of Justin Lathia, Ph.D., continue to investigate the unknowns around sex differences associated with glioblastoma (GBM), including why it is more common in males and is associated with shorter survival in males than females. Led by postdoctoral fellow Anthony Sloan, Ph.D., the team found in preclinical models that blocking a specific receptor reverses the suppression of cancer-fighting T cells—but only in females.
From these early results, the researchers believe that overactive platelets likely drive disease progression and could be an overlooked target for improving the body's immune response to glioblastoma and other types of tumors. They also believe that hormones likely regulate these mechanisms.
Clotting risk complicates cancer care
People with cancers including GBM, lung, kidney and gastrointestinal cancers are known to be at increased risk for blood-clot conditions like pulmonary embolism (PE) and deep vein thrombosis (DVT). These thrombotic events are the second leading cause of death in cancer patients. Patients who develop these conditions have a lower chance of survival, but why is not yet understood.
"The development of events like PE, DVT, stroke and myocardial infarction affects patients directly and indirectly," says Alok Khorana, M.D., director of the Gastrointestinal Malignancies Program at Cleveland Clinic and contributor to the paper. "They may require urgent hospitalization and care, which could then interrupt or delay their cancer therapy."
To explore why these clotting events occur, Sloan and the team looked at activity in the environment around the tumor, which includes platelets and other types of cells.
Blocking PAR4 benefits females in models
The team identified platelet hyperactivity through a receptor called protease-activated receptor 4 (PAR4), which acts like a light switch for platelets. When the switch is "on" (active), platelets slow the activity of a type of T cell that normally kills cancer cells, which can increase cancer aggression. In preclinical models, the team found that blocking the PAR4 receptor reversed that suppression, but only in females.
"While both male and female preclinical models showed increased platelet reactivity, we were surprised to see that only females showed improved survival when targeting this platelet activation," Sloan says. "We believe it is related to hormones—particularly estrogen."
Sloan notes that the findings suggest a molecular bridge between the body's clotting system and its hormonal environment—two systems not previously linked in this context. This link may help explain sex differences in cancer response, as well as why females are more prone to clotting events in some situations.
A target for immunity and clotting
"In addition to telling us more about the role of platelets in our bodies, this research highlights PAR4 as a key for cancer biology and blood-clotting biology," Lathia says.
"For cancer biology, targeting the receptor may help the immune system fight glioblastoma, as well as guiding the development of new therapeutics. It may also explain why platelet and clotting risk differ between patients—including in relation to hormonal factors."
Publication details
Anthony R. Sloan et al., A sex-specific platelet switch controls anti-tumor immunity in glioblastoma, Cancer Cell (2026). DOI: 10.1016/j.ccell.2026.10.004
Journal information: Cancer Cell
Key medical concepts
Blood PlateletsGlioblastomaT-Lymphocytes
Clinical categories
OncologyNeurology Provided by Cleveland Clinic Who's behind this story?
Sadie Harley
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