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Host acid sphingomyelinase regulates microvascular function not tumor immunity.

Monica Garcia-Barros¹, Daniel Lacorazza, Howard Petrie

¹Laboratory of Signal Transduction, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Cancer Research

|November 19, 2004

Summary

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Tumor growth and radiation resistance in acid sphingomyelinase (asmase)-deficient mice are not due to immune response differences. These patterns are linked to the tumor endothelium's ability to undergo ASMase-mediated apoptosis.

Area of Science:

Oncology
Immunology
Biochemistry

Background:

Previous studies suggested acid sphingomyelinase (asmase) deficiency impacts tumor growth and radiation response.
Hypotheses included differences in host antitumor immunity or tumor microvascular endothelium apoptosis.

Purpose of the Study:

To investigate whether immune responses or tumor endothelial cell apoptosis mediate observed differences in tumor growth and radioresponsiveness in asmase-deficient mice.
To definitively link tumor growth and radiation response patterns to specific mechanisms.

Main Methods:

Tumor implantation (MCA/129 fibrosarcoma, B16 melanoma) into asmase-deficient and wild-type mice.
Assessment of tumor immunogenicity via infiltrates.
Tumor growth and radioresponsiveness evaluation in immune-deficient mouse models (Rag-/-, MEF(-/-)).

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Analysis of immune cell populations (B, T, NK) in asmase-deficient mice.

Main Results:

Tumor-host combinations lacked criteria for immunogenic tumors, showing minimal infiltrates.
No significant differences in tumor growth or radioresponsiveness were observed in immune-deficient mouse models.
Immune cell populations in asmase-deficient mice were normal and comparable to wild-type littermates.
MCA/129 fibrosarcomas and B16F1 melanomas did not elicit a host immune response in wild-type mice.

Conclusions:

The observed differences in tumor growth and radiation response are not attributable to a deficient host antitumor immune response in asmase-deficient mice.
The asmase(-/-) phenotype does not exhibit a deficiency in antitumor immunity.
Tumor growth and radiation response are conditionally linked to the tumor endothelium's capacity for acid sphingomyelinase-mediated apoptosis.