In healthy adults, eosinophils usually make up between 0.3% and 5% of circulating white blood cells, corresponding to an absolute eosinophil count (AEC) of 0.05–0.5 × 10⁹/L. Any value above 0.5 × 10⁹/L is termed eosinophilia, while levels at or above 1.5 × 10⁹/L are considered hypereosinophilia. These thresholds are widely recognized in clinical practice. However, these numbers alone are not enough to diagnose cancer, since many other conditions such as asthma, eczema, autoimmune diseases, and parasitic infections can also drive eosinophilia. The key is to place the count in its proper medical context.
Some of the strongest and most statistically significant associations between eosinophils and cancer come from hematologic malignancies. In large-scale studies, individuals with severe eosinophilia (≥1.0 × 10⁹/L) were found to have a sharply increased risk of Hodgkin lymphoma, chronic lymphocytic leukemia, and chronic myeloproliferative neoplasms. Importantly, these risks rose in a dose-dependent manner: the higher the eosinophil count, the stronger the association with blood cancers. This indicates that when eosinophilia is persistent and unexplained, especially at severe levels, it should raise suspicion of hematologic malignancy.
Recent advances in genetics further support this relationship. Certain blood cancers, now formally categorized as myeloid or lymphoid neoplasms with eosinophilia, are driven by mutations involving tyrosine kinase gene fusions. For these patients, the elevated eosinophil count is not just a bystander effect but part of the malignant process itself. Identifying such cases is crucial because they open the door to targeted therapies that directly improve survival.
When it comes to solid tumors, the story is more complex. Population studies show that mild eosinophilia (0.5–1.0 × 10⁹/L) may sometimes signal cancer risk, but the association is highly dependent on the tumor type. For example, patients with mild eosinophilia were found to have an increased risk of bladder cancer, while paradoxically, the same patients had a lower risk of breast cancer. No significant links were identified with most other solid tumors. This suggests that eosinophils may play different roles depending on the type of tissue and cancer biology involved.
In colorectal cancer, eosinophils appear to infiltrate tumors and interact with the cancer microenvironment. Multiple clinical studies show that patients whose tumors contain higher numbers of eosinophils often experience fewer metastases and better survival outcomes. In this setting, eosinophils may act as allies of the immune system, helping to slow disease progression rather than marking aggressive disease.
In cancers of the mouth and throat, the situation is more diagnostic than prognostic. Pathologists have found that high eosinophil counts within tumors can serve as a marker of invasive disease. In particular, thresholds such as more than 10 eosinophils per high-power microscopic field in laryngeal cancer tissue strongly predict tumor invasion into surrounding stroma. Here, eosinophils serve less as indicators of overall prognosis and more as a histological clue for identifying aggressive local behavior.
Perhaps the most striking role for eosinophils in modern oncology is as a marker of response to immunotherapy. In metastatic melanoma, patients who develop eosinophilia during treatment with immune checkpoint inhibitors such as ipilimumab and pembrolizumab consistently show better outcomes. Counts above 5–10% of total white blood cells during therapy predict longer survival, and very high levels above 20% are linked with survival times more than double those of patients without eosinophilia.
The pattern repeats in lung cancer. In patients with non-small cell lung cancer treated with checkpoint inhibitors, both higher baseline eosinophil counts and rising eosinophil counts after treatment began correlated with longer survival. These findings highlight eosinophils as dynamic biomarkers of treatment success, reflecting immune system engagement against the tumor.
Cancer vaccines provide a similar story. In clinical trials where patients with advanced solid tumors received dendritic cell vaccines made from their own tumor RNA, many experienced sharp rises in eosinophil counts. Those who reached very high levels, at or above 20% of their circulating white blood cells, tended to survive far longer than those without eosinophilia. This finding reinforces the idea that eosinophils can act as real-time indicators of effective antitumor immune activity.
Evidence in breast cancer is less extensive but still noteworthy. Several studies suggest that patients with higher relative eosinophil counts at diagnosis have better survival and longer treatment response. In some cases, higher eosinophil counts were also associated with better responses to chemotherapy in aggressive subtypes such as triple-negative breast cancer. Though more research is needed, eosinophils may represent an affordable and accessible biomarker in this setting.
The answer depends heavily on the type of cancer and the clinical context. Persistent severe eosinophilia, at or above 1.0 × 10⁹/L, is strongly associated with hematologic malignancies and should always prompt careful investigation. In solid tumors, modest eosinophilia does not consistently predict cancer risk but often signals more favorable prognosis when it occurs within tumors or during treatment.
In the end, eosinophils are not a single number that points to cancer. They are storytellers, reflecting the interplay between the immune system and disease. Their value lies not in one fixed cutoff but in the context in which they rise, whether it be malignant clonal expansion or immune surveillance.