BMC Cancer 2008, 8:84 http://www.biomedcentral.com/1471-2407/8/84 tion for case series [4]. No published quality criteria for meta-analyses were found, so one was devised. Information from the clinical trials, case series and the meta-analysis is presented in tables, with the results being synthesized in a narrative manner. Where RCTs were similar enough in patient characteris- tics, therapy and endpoints, meta-analyses were per- formed. Response definitions were those used by the authors of each RCT; only complete and partial responses were included as responses. Followup was assumed to be complete. Survival at selected time points was extrapo- lated from graphs. If survival graphs were not provided, exponential survival was assumed and the median sur- vival was used to generate survival data. Within trials, the response rates and survival in the two arms formed 2 by 2 tables for which odds ratios and their corresponding 95% confidence intervals and between trial comparisons were made using logistic regression. Homogeneity of the odds ratios across trials was evaluated using a Breslow-Day χ2 test. Odds ratio estimates and between-group compari- sons for the combined trials were made using the Mantel- Haenszel fixed effect model. A result had to have a p value of less than 0.05 to be considered statistically significant. Results Results of Literature Search The literature was searched for clinical studies of glucocor- ticoids. Studies were eligible if patients had nonhemato- logic malignancy, and if there were endpoints of tumor response or tumor control or survival. For RCTs and meta- analyses, trials comparing two glucocorticoid arms or a glucocorticoid arm to a nonglucocorticoid arm were eligi- ble. After excluding duplicate publications of the same trial, fifty four RCTs met the eligibility criteria ([5-54] and [55-61]); one meta-analysis met the eligibility criteria [62]. In nonhematologic malignancy other than breast or prostate cancer, four phase l/ll (nonrandomized) trials of glucocorticoid monotherapy were found [63-66]. In non- hematologic malignancy other than breast cancer or pros- tate cancer or thymoma, four case series of glucocorticoid monotherapy with tumor response data were identified [67-70]. One of the case series is a clinical trial; however, tumor response rate was not a preplanned endpoint, so it is presented as a case series [67]. Three clinical trials, with no available results, were identified [71-73]. Nine case reports of glucocorticoid monotherapy, other than breast cancer or prostate cancer or thymoma regressing in response to glucocorticoid monotherapy, were found [74- 83]. No article was excluded due to quality. Glucocorticoids are commonly given as premedication with chemotherapy to prevent nausea and vomiting. In the chemotherapy trials mentioned in this review, there are two trials where it is clear whether glucocorticoids were used as premedication in patients not on the gluco- corticoid arm [23,28]. In the other chemotherapy trials, there is no mention of whether such usage was permitted or not. Case Reports There are case reports of nonhematologic malignancy either regressing or having increased growth in response to glucocorticoids. It is reasonably well documented in the literature that thymoma can sometimes respond to glucocorticoids [84]. In melanoma, 2 doses of 100 mg of intravenous hydrocortisone 8 hours apart caused tumor lysis syndrome in a patient with melanoma [74]. There are case reports where glucocorticoids apparently stimulated the growth of melanoma [75,76]. There is a case report of liver metastasis of thymic carcinoid responding to pred- nisolone [77]. Metastatic renal cell carcinoma might have shown a complete response to glucocorticoids in two patients[78,79]. There are case reports where glucocorti- coids apparently stimulated the growth of breast cancers [80-83]. Case Series The four case series of glucocorticoid monotherapy are shown in Table 1[67-70]. They included patients with a variety of cancers, such as lung cancer, GI cancer, breast cancer and sarcoma. No tumor regression, objective improvement or relief of pain was noted. Glucocorticoid doses were not dissimilar taking into account relative glu- cocorticoid activities (Table 2). For any particular tumor type, the number of cases is small: the one exception is the 255 lung cancer patients in the case series of de Camp [69]. With regards to quality, two case series were from tertiary care centers; the two that were not originated from sec- ondary care institutions [67,69]. Three of the four case series had less than 50 patients [67,68,70]. None of the case series were multi-institutional. Three of the four case series did not describe eligibility criteria [68-70]. In one case series, patients were similar with regards to the state of cancer progression; in the other studies, not enough information was provided to assess similarity [67]. In one case series, followup was long enough to assess whether glucocorticoids could cause cancer to decrease in size; in the other studies, it was unclear if followup was sufficient to assess this [70]. In none of the case series was reduction in tumor size assessed using objective criteria. Phase l and Phase ll (Nonrandomized) Trials In phase l/ll (nonrandomized) trials, responses have been noted. Based on responses lasting at least 28 days, responses in the four trials were 0% [63], 6% [64], 6% [65] and 6% [66]. In the largest trial (407 patients), 13 of Page 3 of 19 (page number not for citation purposes)