PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11747473

Sample size requirements for case-control study designs.

M D Edwardes
View original source ↗Export metadata ↓

Abstract

BACKGROUND: Published formulas for case-control designs provide sample sizes required to determine that a given disease-exposure odds ratio is significantly different from one, adjusting for a potential confounder and possible interaction. RESULTS: The formulas are extended from one control per case to F controls per case and adjusted for a potential multi-category confounder in unmatched or matched designs. Interactive FORTRAN programs are described which compute the formulas. The effect of potential disease-exposure-confounder interaction may be explored. CONCLUSIONS: Software is now available for computing adjusted sample sizes for case-control designs.

Explore related subjects

Case-Control StudiesModels, StatisticalResearch DesignSample SizeSoftwareJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M D Edwardes. 2001-11-19. Sample size requirements for case-control study designs.. https://doi.org/10.1186/1471-2288-1-11

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Does pizza protect against cancer?

We analyzed the potential role of pizza on cancer risk, using data from an integrated network of case-control studies conducted in Italy between 1991 and 2000. Cancer sites were: oral cavity and pharynx (598 cases), esophagus (304 cases), larynx (460 cases), colon (1,225 cases) and rectum (728 cases). Controls were 4,999 patients admitted for acute, non-neoplastic conditions to the same hospital network as cases. Odds ratios for regular pizza consumers were 0.66 (95% confidence interval, CI = 0.47-0.93) for oral and pharyngeal cancer, 0.41 (95% CI = 0.25-0.69) for oesophageal, 0.82 (95% CI = 0.56-1.19) for laryngeal, 0.74 (95% CI = 0.61-0.89) for colon and 0.93 (95% CI = 0.75-1.17) for rectal cancer. Pizza appears therefore to be a favorable indicator of risk for digestive tract neoplasms in this population.

Case-Control Studies↗
PubMed2003

Decreased gene expression of steroid 5 alpha-reductase 2 in human prostate cancer: implications for finasteride therapy of prostate carcinoma.

BACKGROUND: Steroid 5alpha-reductase 2 (SRD5A2) catalyzes the conversion of testosterone to the more potent androgen, DHT, in the prostate. The therapeutic influence of SRD5A2 inhibitor finasteride on prostate cancer is currently unknown. The direction and extent of changes in SRD5A2 expression in disease tissues is a relevant issue in this regard. METHODS: The expression differences of SRD5A2 in tissues representative of normal, benign, and malignant growth in the human prostate were examined in parallel by comparative analysis of relevant microarray gene expression data. Semiquantitative RT-PCR was used to further verify the gene expression differences of SRD5A2. RESULTS: Consistently decreased expression of SRD5A2 was observed in 25 prostate cancer samples when compared to 25 matched normal samples and nine BPH samples. Expression differences among these samples for six other genes were presented in parallel as indicators of the direction and extent of expression changes. These additional genes include SRD5A1, Hepsin (overexpressed in prostate cancer), AMACR (overexpressed in prostate cancer), Keratin 8 (epithelial marker), smooth muscle actin (stromal marker), Nell2 (overexpressed in BPH). Semiquantitative RT-PCR verified the expression differences for SRD5A2 in six normal, six BPH, and six prostate cancer samples. CONCLUSIONS: Results from this study, combined with those from previous studies, indicate an association of prostate cancer with reduced 5alpha-reductase enzymatic activity as a result of remarkably decreased expression of the SRD5A2 gene. The implications of this study for finasteride therapy of prostate cancer are discussed.

Case-Control Studies↗
PubMed2003

Role of MTHFR genetic polymorphisms in the susceptibility to childhood acute lymphoblastic leukemia.

The central role of methylenetetrahydrofolate reductase (MTHFR) in the folate metabolism renders MTHFR gene polymorphisms (C677T and A1298C) potential modulators of a variety of disorders whose development depends on folate/homocysteine imbalance. Here, we provide additional evidence on the protective role of these polymorphisms in acute lymphoblastic leukemia (ALL), the most common pediatric cancer. A case-control study was conducted in 270 ALL patients and 300 healthy controls of French-Canadian origin. The TT677/AA1298 and CC677/CC1298 individuals were associated with reduced risk of ALL (crude odds ratio [OR] = 0.4; 95% confidence interval [CI], 0.2-0.9; and OR = 0.3; 95% CI, 0.1-0.6; respectively). Further stratification in patients born before and after January 1996 (approximate time of Health Canada recommendation for folic acid supplement in pregnancy) revealed that the protective effect of MTHFR variants is accentuated and present only in children born before 1996. Similar results were obtained when a transmission disequilibrium test was performed on a subset of children (n = 95) in a family-based study. This finding suggests gene-environment interaction and its role in the susceptibility to childhood ALL, which is consistent with previous findings associating either folate deficiency or MTHFR polymorphisms with risk of leukemia.

Case-Control Studies↗