Related Experiment Videos
Host endocrine responses during tumor growth.
H Besedovsky1, A del Rey, S J Normann
1Schweizerisches Forschungsinstitut, Medizinische Abteilung, Davos, Switzerland.
Progress in Clinical and Biological Research
|January 1, 1989
Summary
Tumor transplantation in mice triggers early and late endocrine changes, including elevated corticosterone and reduced insulin. This response, mediated by T cells and linked to anti-inflammation, is crucial for understanding tumor-host interactions.
Area of Science:
- Immunology
- Endocrinology
- Oncology
Background:
- Tumor transplantation induces significant endocrine alterations.
- Early and late hormonal changes include biphasic corticosterone and insulin level shifts, decreased prolactin, and thyroxine deficiency.
Purpose of the Study:
- Investigate the mechanisms behind early endocrine changes post-tumor transplantation.
- Determine the role of corticosterone in tumor-associated anti-inflammation.
Main Methods:
- EL-4 lymphoma and mammary tumor virus (MTV) adenocarcinoma transplantation in syngeneic mice.
- Measurement of serum hormone levels (corticosterone, insulin, prolactin, thyroxine).
- Adrenalectomy to assess corticosterone's role in anti-inflammation.
Main Results:
- Tumor transplantation caused biphasic increases in corticosterone and decreases in insulin.
- Corticosterone elevation was T cell-dependent, MHC-restricted, and specific to immunogenic tumors.
- Elevated corticosterone correlated with tumor-associated anti-inflammation, which was abolished by adrenalectomy.
Conclusions:
- Early corticosterone response to tumor transplantation involves T cell recognition of tumor antigens.
- Corticosterone mediates the anti-inflammatory effects observed after tumor transplantation.
- Further research is needed to explore corticosterone's broader impact on host anti-tumor responses.