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Testing Cancer Immunotherapeutics in a Humanized Mouse Model Bearing Human Tumors

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Immunomodulation and lymphoma in humans.

Rafael A Ponce¹, Thomas Gelzleichter, Helen G Haggerty

¹Amgen, Inc , Seattle, WA , USA .

Journal of Immunotoxicology

|June 11, 2013

Summary

Increased cancer risk is linked to immune deficiencies and inflammation. Chronic inflammation or immunosuppression uniquely elevates B-cell lymphoma risk, driven by DNA damage during immune responses, not solely Epstein-Barr virus (EBV).

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Area of Science:

Immunology
Oncology
Virology

Background:

Observational and clinical studies link immunodeficiencies, autoimmunity, and immunotherapies to increased cancer risks.
Existing models (immunosurveillance, inflammation) explain some immune-cancer links but not the heightened B-cell lymphoma risk in immunosuppressed or inflamed states.
Epstein-Barr virus (EBV) plays a variable role in lymphomagenesis across different patient populations.

Purpose of the Study:

To investigate the mechanisms underlying the disproportionate increase in B-cell lymphoma risk associated with chronic immunosuppression and inflammation.
To elucidate the role of B-cell specific vulnerabilities in oncogenic transformation.
To differentiate between disease- and treatment-related risks for lymphoma.

Main Methods:

Evaluation of Epstein-Barr virus (EBV) presence in lymphomas from diverse patient groups.
Analysis of DNA alterations in lymphomas.
Assessment of B-cell ontogeny and transformation pathways.

Main Results:

EBV's role in lymphomagenesis varies significantly across patient populations.
EBV-independent B-cell transformation is driven by chronic antigenic stimulation (from inflammation or unresolved infection).
Transformation results from DNA damage during genomic recombination and mutation (class switching, somatic hypermutation).

Conclusions:

A new model explains increased B-cell lymphoma risk via chronic antigenic stimulation leading to DNA damage during B-cell maturation.
This model accounts for heightened lymphoma risk in autoimmunity and immunosuppression, independent of EBV status.
Distinguishing disease- versus treatment-related lymphoma risks and understanding B-cell transformation etiology are crucial for risk assessment and immunotherapy regulation.