BMC Cancer 2008, 8:84 http://www.biomedcentral.com/1471-2407/8/84 There is evidence that glucocorticoid may inhibit anti- body-dependent cellular cytotoxicity [97]. There are limitations to the meta-analyses presented in this study. Firstly, there may be unpublished randomized controlled trials that are not included. Secondly, survival was extrapolated from summary graphs and data, and the point estimates are not as accurate as those that could have been derived from the individual patient data. Thirdly, the number of trials and the number of patients in each trial tended to be small; this makes heterogeneity more likely. For each meta-analysis, a chi-square test was used to assess heterogeneity. However, a chi-square test has low power if there are few trials or sample sizes are small. There is evidence that glucocorticoids have an effect on the natural history of some nonhematologic malignan- cies. However, that is not the only source of glucocorti- coids that a cancer is exposed to. One's own body synthesizes endogenous glucocorticoids. This raises the question of what effect endogenous glucocorticoids have on nonhematologic malignancy. The possible effect of endogenous glucocorticoids on lung cancer is the subject of another review (manuscript in preparation). Breast cancer, prostate cancer and possibly lung cancer show sensitivity to glucocorticoids. There may be variabil- ity within cancers of each type in their sensitivity. This raises the issue of predictive factors, that might assist in assessing glucocorticoid sensitivity. Glucocorticoid recep- tor status or histologic subtype (in lung cancer) might be relevant. A genomic/proteomic approach to explore this possibility might be useful. Conclusion The effect of glucocorticoids in nonhematologic malig- nancy depend on the primary tumor site. Glucocorticoids have a beneficial effect in breast and prostate cancer as monotherapy. In combination with chemotherapy or other endocrine therapy in breast cancer; glucocorticoids increase response rate, but do not change survival. In GI cancer, they most likely have a neutral effect. High dose continuous glucocorticoids, in patients with nonhemato- logic malignancy, decrease survival. Such treatment should be avoided in patients with nonhematologic malignancy. Based on ASCO criteria, this is a grade B rec- ommendation based on level ll evidence. In lung cancer, glucocorticoids might have a deleterious effect by them- selves and when given with chemotherapy. It is recom- mended that glucocorticoid use in lung cancer patients be kept to the minimum required. This is a grade B recom- mendation based on level ll evidence. List of Abbreviations AV: adriamycin 60 mg/m2 IV day 1 and vincristine 1.2 mg/ m2 IV day 1 every 21 days, BCNU: carmustine, CI: confi- dence interval, CMF: cyclophosphamide 100 mg/m2 po daily days 1–14 and methotrexate 40 mg/m2 IV days 1 and 8 and 5-FU 600 mg/m2 IV days 1 and 8 every 28 days, CMFP: CMF and prednisone 40 mg/m2/day days 1–14, CR: complete response, ER: estrogen receptor, 5-FU: 5- fluorouracil, FUDR: fluorodeoxyuridine, IM: intramuscu- lar, IV: intravenous, m2: meters squared, MPA: medroxy- progesterone acetate, -ve: negative, ns: not significant, NR: not reported, NSC-17256: 6α-methylpreg-4-ene-3,11,20- trione, NSCLC: nonsmall cell lung cancer, PD: progressive disease, +ve: positive, PR: partial response, PgR: progester- one receptor, po: by mouth, SCLC: small cell lung cancer, SD: stable disease, SE: standard error, vs.: versus Competing interests The author(s) declare that they have no competing inter- ests. Additional material Additional file 1 Search strategies. Provides the search strategies for PubMed, EMBASE, the Cochrane Library (including ACP Journal Club) and CINAHL. Click here for file [http://www.biomedcentral.com/content/supplementary/1471- 2407-8-84-S1.doc] Acknowledgements I would like to thank Rob Hall for critically reviewing the manuscript. I would like to thank Kim Aslett, Christina Wallace and other librarians for their assistance. I would like to thank the libraries of the following institu- tions for their help: Sault Area Hospital, Windsor Regional Hospital, North- ern Ontario School of Medicine, Wayne State University, Michigan State University, University of Windsor, University of Michigan and the NCI. I would like to thank Larry Stitt for the statistical analysis. I would like to thank Olga Karkalas and other translators for their work. References 1. Rutz HP: Effects of corticosteroid use on treatment of solid tumours. Lancet 2002, 360(9349):1969-1970. 2. 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