Accelerated tumor growth after stopping prednisolone?

Question

I have a pet rat who was taking prednisolone for allergies. I've read that prednisolone can slow or inhibit tumor growth. When he was taken off of the medication, he grew a grape-sized tumor over the course of one day. I'm sure the timing of him getting a tumor was a coincidence and not caused by the prednisolone or removal thereof, but is it possible that taking him off of the prednisolone caused the tumor to grow at an accelerated rate (i.e. faster than it would have if he was never on the medication in the first place)?

Answer 1

I am not a veterinary so I can't answer your question in particular. Though, maybe following points on the mechanisms of action of prednisolone might perhaps bring some clarifications:

Prednisolone is a synthetic glucocorticoid. The effects of prednisolones are multiple and the antitumor effect of glucocorticoid has been investigated in many studies (most of them were actually conducted in mice or rats). Possible mechanisms of action have been described among which inhibition of glucose transport, phosphorylation, or induction of cell death in immature lymphocytes.

Actually Holland-Frei Cancer Medicine, which is a well know reference book in oncology has an entire chapter on the role of corticosteroids in the treatment of neoplasms. Here an extract of the introduction:

Pharmacologic doses of steroid inhibited growth of various tumor systems. Tissue culture studies confirmed that lymphoid cells were the most sensitive to glucocorticoids, and responded to treatment with decreases in DNA, ribonucleic acid (RNA), and protein synthesis. Studies of proliferating human leukemic lymphoblasts supported the hypothesis that glucocorticoids have preferential lymphocytolytic effects. The mechanism of action was initially thought to be caused by impaired energy use via decreased glucose transport and/or phosphorylation; it was later discovered that glucocorticoids induce apoptosis, or programmed cell death, in certain lymphoid cell populations.

Here their conclusion, which gives a good summary:

Despite an incomplete understanding of the mechanism of action of glucocorticoids, it is clear they are of great clinical value in the treatment of lymphoid neoplasms. They are also sometimes used in therapeutic regimens for other endocrine-responsive cancers, are efficacious in the treatment of several frequently occurring side effects of malignancies, and are widely used for general palliative therapy.

So, yes, prednisolone has an antitumor effect. However, this effect is tumor type dependent and achieved with specific dosing (in humans 10 mg daily to 100 mg/m2/day (depending on indication)). Only a veterinary will be able to provide you with a more accurate and case specific response.

EDIT (after additional clarification was provided by OP)

I found one study which might help in providing some "time" reference points in rats. This study looked at rat mammary tumor cells and reported

After dexamethasone (a type of glucocorticoid) withdrawal, c-myc and cyclin D1 expression (both involved in cell cycle progression) transiently peak at 2 and 4 h

So this could possibly explain the event you have described although bear in mind these results apply for a particular tumor type and a particular dosage used.

Sources:

Prednison. Drug Information. Uptodate. http://www.uptodate.com/contents/prednisone-drug-information?source=search_result&search=prednisone&selectedTitle=1~150#F213063

McKay et al. Corticosteroids in the Treatment of Neoplasms in Holland-Frei Cancer Medicine. 6th edition http://www.ncbi.nlm.nih.gov/books/NBK13383/