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In this research, we first show that single-image shape from shading (SFS) algorithms share an inherent limitation in the accuracy of reconstructed surfaces due to the property of the reflectance map. That is, surface orientations can be accurately recovered if they lie along the gradient direction of the reflectance map function, but cannot be easily recovered if lying along the tangential direction. Then, we consider two methods which incorporate stereo information with shading to improve the performance. One is to use multiple images taken under different lightening conditions known as photometric stereo, and the other is to incorporate the height information obtained from images taken from different viewing angles known as the geometric stereo. With photometric stereo, we compensate the weakness of each reflectance map by combining several reflectance maps in a proper way in the gradient space and hence improve the accuracy of the results. With geometric stereo, absolute heights at sparse feature points are obtained and used as constraints on the resulting surface so that the ambiguity can be resolved. Simulation results for several test images are given to show the performance of our new robust algorithms.© (1993) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

OBJECTIVES Common genetic SNPs in two genes, encoding catechol-O-methyltransferase (COMT) and methylenetetrahydrofolate reductase (MTHFR), which are interconnected with COMT gene regulation, have been reported to contribute to schizophrenia risk. In this study, we evaluated the association between functional polymorphisms in COMT and MTHFR and schizophrenia risk with a case-control study in a Korean population. METHODS We performed a case-control study by genotyping analysis using 360 cases and 348 controls in Korean subjects to determine the association between functional polymorphisms in COMT and MTHFR and schizophrenia risk. RESULTS Four functional SNPs in COMT (Val158Met and rs165599) and MTHFR (C677T and A1298C) were genotyped by primer extension assay. None of the genotype distributions for the four SNPs was significantly different between cases and controls. Stratified analysis did not show any significant gender difference for any polymorphism. In addition, we found no evidence of a gene-gene interaction in the analysis of combined genotypes. CONCLUSION Our results suggest no significant association between the selected functional polymorphisms of COMT or MTHFR in Korean schizophrenia subjects. However, further studies are required to confirm our findings in a larger number of subjects.

Genome-wide association studies of lung cancer reported in populations of European background have identified three regions on chromosomes 5p15.33, 6p21.33, and 15q25 that have achieved genome-wide significance with p-values of 10−7 or lower. These studies have been performed primarily in cigarette smokers, raising the possibility that the observed associations could be related to tobacco use, lung carcinogenesis, or both. Since most women in Asia do not smoke, we conducted a genome-wide association study of lung adenocarcinoma in never-smoking females (584 cases, 585 controls) among Han Chinese in Taiwan and found that the most significant association was for rs2736100 on chromosome 5p15.33 (p = 1.30×10−11). This finding was independently replicated in seven studies from East Asia totaling 1,164 lung adenocarcinomas and 1,736 controls (p = 5.38×10−11). A pooled analysis achieved genome-wide significance for rs2736100. This SNP marker localizes to the CLPTM1L-TERT locus on chromosome 5p15.33 (p = 2.60×10−20, allelic risk = 1.54, 95% Confidence Interval (CI) 1.41–1.68). Risks for heterozygote and homozygote carriers of the minor allele were 1.62 (95% CI; 1.40–1.87), and 2.35 (95% CI: 1.95–2.83), respectively. In summary, our results show that genetic variation in the CLPTM1L-TERT locus of chromosome 5p15.33 is directly associated with the risk of lung cancer, most notably adenocarcinoma., Author Summary Worldwide, approximately 15% of lung cancer cases occur among nonsmokers. Genome-wide association studies (GWAS) of lung cancer conducted in populations of European background have identified three regions on chromosomes 5, 6, and 15 that harbor genetic variants that confer risk for lung cancer. Prior studies were conducted primarily in cigarette smokers, raising the possibility that the associations could be related to tobacco use, lung carcinogenesis, or both. A GWAS of lung cancer among never-smokers is an optimal setting to discover effects that are independent of smoking. Since most women in Asia do not smoke, we conducted a GWAS of lung adenocarcinoma among never-smoking females (584 cases, 585 controls) in Taiwan, and observed a region on chromosome 5 significantly associated with risk for lung cancer in never-smoking women. The finding was independently replicated in seven studies from East Asia totaling 1,164 lung adenocarcinomas and 1,736 controls. To our knowledge, this study is the first reported GWAS of lung cancer in East Asian women, and together with the replication studies represents the largest genetic association study in this population. The findings provide insight into the genetic contribution of common variants to lung carcinogenesis.

Objective: In order to investigate possible genetic contribution to childhood leukemia in the immune system, we evaluated the associations between 786 SNPs in 68 genes/gene regions related to immune response and childhood leukemia risk. Methods: Incident childhood leukemia cases (n=136) and non-cancer controls (n=254) were recruited from three teaching hospitals in Seoul between 2003 and 2006. Candidate genes/gene regions were selected based on SNP databases (CGAP and SNP500 database), and genotype assay was performed using GoldenGate (Illumina) oligonucleotide pool assay (OPA). First, we selected SNPs with dose response effect (Ptrend Results: Among the 786 SNPs, 134 SNPs in 7 genes/gene regions were significantly associated with childhood leukemia risk (Ptrend Discussion: Our results suggest that genetic polymorphisms in immune regulatory may play a role in childhood leukemia development. Further large study is warranted confirm our findings. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 925.

Objective In a hospital-based case-control study in Korea, we evaluated the association between polymorphisms in genes involved in apoptosis and cell cycle control and brain tumor risk among children. Methods Incident brain tumor cases (n=70) and non-cancer controls (n=254) were recruited from three teaching hospitals in Seoul between May 2003 and August 2006. Information on the characteristics of children and their parents were collected by trained interviewers using structured questionnaire. Tagging single-nucleotide polymorphisms (SNPs) were selected using a pairwise linkage-disequilibrium (LD) based algorithm (n=304) were genotyped for 43 cases and 153 controls in this study. Odds ratios (ORs) and 95% confidence intervals (CIs) for SNP genotypes were estimated using unconditional logistic regression adjusted for age and birth weight. The false discovery rate (FDR) was estimated to evaluate the probability of false positive associations; we considered FDR Results Eleven tag SNPs in six genes, AICDA, LMO2, MYC, BCL2, BCL2A1, and CASP7 were significantly associated with childhood brain tumor (Ptrend ConclusionOur results suggest that genetic polymorphisms in AICDA may be associated with the risk of brain tumor in childhood. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2846.

Background: Leukemia is the most common malignancy in children. The etiology of childhood leukemia is mostly unknown, although some environmental factors such as ionizing radiation and parental alcohol and tobacco use may play a causative role in leukemia. Methods: To investigate the association between parental alcohol consumption and childhood leukemia in a hospital-based case-control study in Korea, histologically-confirmed incident childhood leukemia cases (n=365) aged 0-18 years old were recruited from three teaching hospitals located in Seoul, Korea, between May 2003 and August 2008. Non-cancer controls (n=558) aged 0-18 years old without medical history of childhood cancer were recruited from the Department of Pediatrics of the same hospitals. Controls were frequency-matched to cases by 5-year age intervals and sex (cases: controls=1:1). Leukemia risks were estimated as odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression analysis adjusted for age, sex, parent's education, and birth weight ( Results: Among general characteristics, higher birth weight and parental education were associated with childhood leukemia risk (P Conclusion: Our results suggest that maternal alcohol consumption is associated with AML among Korean children. However, larger studies need to be conducted to replicate our findings. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1825.

Background: Although the clinical relevance of molecular subtypes of breast cancer has been examined, little is known about risk factors for different tumor subtypes, especially the HER2-overexpressing and triple-negative subtypes. Previous epidemiologic findings imply these subtypes may also vary with respect to risk factor profiles; however, these results were based mainly on older or younger cases in western countries. Our objective was to determine the different risk factors by breast cancer subtypes in Korean. Methods: In this study, cases were diagnosed with breast cancer and underwent curative surgery at two teaching hospitals located in Seoul, Korea, between 2000 and 2007. Control subjects were selected from two sources: records of the hospital based case-control study and community based health examination in the same duration. Total 2,473 cases and matched controls were eligible to analysis further study. Information was collected using a standardized questionnaire and breast tumours were tested by immunohistochemistry. Odds ratios (OR) and 95% confidence intervals (CI) of risk of molecular subtypes of breast cancer were calculated using a multivariate polytomous regression model, adjusting age at diagnosis. Results: In our study, 1,590 (65.6%) tumors were considered luminal (ER+ and/or PR+), 327 (13.5%) HER-2 overexpressing (ER-, PR-, HER-2+), and 505 (20.9%) triple negative (ER-, PR-, and HER-2-). We observed statistically strong significant differences in means or frequencies by tumor subtypes for age at diagnosis, education level, menopausal status, a family history of breast cancer and tumor size (p=15 vs. 50 vs. < 40: OR=0.5, 95% CI 0.3-0.8, p-trend Conclusion: Our findings suggest that risk profiles may be different by molecular subtypes, especially body mass index in stratified analysis by menopausal status. However, underlying mechanisms need to be investigated in further study. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5704.

Background: DNA copy number variation (CNV) is a common phenomenon in human genome and some CNVs have been associated with susceptibility or resistance to disease. It has been suggested that gene copy number can be elevated in cancer cells. To evaluate potential role of CNV in breast cancer development, we conducted genome-wide association study of CNV in Seoul Breast Cancer Study. Methods: Cases were diagnosed with breast cancer and underwent curative surgery at two teaching hospitals located in Seoul, Korea, between 2001 and 2007 (n=2,386). Control subjects were selected from multi-center based cohort study in 2007 (n=2,386). The Affymetrix SNP assay 6.0 array, which includes 946,000 probes for the detection of copy number variation, was used. Nexus Copy Number version 4.1 was used for detecting CNVs (significance threshold=10−6; minimum number of probes per segment=4), and statistical analysis. After quality control step (i.e., robust variance sample QC), total 2,315 cases and 2,039 controls were compared for the difference of each CNV. In this study, we selected the CNVs that were different between cases and controls by at least 5% (P adjusted for multiple comparison Results: Between case and controls, thirteen CNV regions including chr115q11.2, chr3q26.1, chr6q16.3, chr17q31.1 were significantly different for copy number. We note that those regions include genes such as UGT2B17 (UDP glucuronosyltransferase 2 family, polypeptide B18), OR4C11 (olfactory receptor, family 4, subfamily C, member 11), LRRC37A2 (leucine rich repeat containing 37, member A2), ARL17P1 (ADP-ribosylation factor-like 17 pseudogene 1), LOC644974, and the others. We are planning validation study for the regions by quantitative PCR to verify the association with breast cancer risk found in this study. Conclusion: Our results suggest that common CNVs may be associated with breast cancer in Korean women. However, further variation study is essential to support our observation and underlying biological mechanisms for the associations needs to be elucidated. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4720.

AIM: To analyze the association between the p73 G4C14-to-A4T14 polymorphism (a.k.a., the GC/AT variation) and colorectal cancer risk and survival in the Korean population, and to evaluate the relationships between p73 polymorphism and the p73 protein expression or clinicopathological characteristics of colorectal cancer. METHODS: Three hundred and eighty-three histologically confirmed cases and 469 healthy controls, recruited at one teaching hospital in Pusan, Korea from 2001 and 2007, were genotyped for p73 G4C14-to-A4T14 by PCR with confronting two-pair primers (PCR-CTPP) and the expression profile of p73 in cancer tissues (n = 383) was analyzed by immunohistochemistry. RESULTS: Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression model adjusted for age and gender. Compared with the GC/GC genotypes, the GC/AT and AT/AT genotypes were significantly associated with colorectal cancer risk (GC/AT vs GC/GC: OR = 1.46, 95% CI: 1.10-1.94; AT/AT vs GC/GC: 1.72, 0.98-3.03; Ptrend = 0.01). When stratified by age and gender, the association was restricted to those less than 60 years of age (GC/AT or AT/AT vs GC/GC: 2.22, 1.39-3.55) and male (GC/AT or AT/AT vs GC/GC: 1.91, 1.31-2.77). The expression of p73 was associated with invasion depth (P = 0.003) and advanced Duke’s stage (P = 0.06) of colorectal cancer. The patients with the GC/GC genotype were associated with worse survival compared with those with the other genotypes (P = 0.02). However, no significant relationship was observed between the p73 G4C14-to-A4T14 polymorphism and p73 protein expression in cancer tissues. CONCLUSION: Our results suggest that the p73 GC/AT polymorphism is associated with an increased colorectal cancer risk and survival in the Korean population.

Biomarkers are characteristic biological properties that can be detected and measured in a variety of biological matrices in the human body, including the blood and tissue, to give an indication of whether there is a threat of disease, if a disease already exists, or how such a disease may develop in an individual case. Along the continuum from exposure to clinical disease and progression, exposure, internal dose, biologically effective dose, early biological effect, altered structure and/or function, clinical disease, and disease progression can potentially be observed and quantified using biomarkers. While the traditional discovery of biomarkers has been a slow process, the advent of molecular and genomic medicine has resulted in explosive growth in the discovery of new biomarkers. In this review, issues in evaluating biomarkers will be discussed and the biomarkers of environmental exposure, early biologic effect, and susceptibility identified and validated in epidemiological studies will be summarized. The spectrum of genomic approaches currently used to identify and apply biomarkers and strategies to validate genomic biomarkers will also be discussed.

A78 Background Increased risk of multiple myeloma has been observed among those who have a family history, suggesting a genetic component in multiple myeloma development. Also, a number of studies have shown that changes in immuoregulatory role of T cells may contribute to the development of multiple myeloma. Objective In light of the relationship between immune system dysregulation and multiple myeloma risk, we investigated whether genetic variation in 153 immune function genes are associated with multiple myeloma susceptibility in a population-based case-control study conducted among White Connecticut women. Methods Tagging single-nucleotide polymorphisms (SNPs; N=876) were selected using a pairwise linkage-disequilibrium based algorithm. Odds ratios (ORs) and 95% confidence intervals (CIs) for SNP genotypes were estimated using unconditional logistic regression. Tests of association for gene regions were conducted using the minP test. We applied the false discovery rate (FDR) method to the minP test results as a means of controlling for multiple comparisons. Haplotype analyses among subjects were performed using the haplo.stat statistical package in the R program. Haplotype frequencies were estimated from genotype data using the expectation-maximization algorithm while at the same time excluding those with frequencies less than 1%, and were evaluated by the global score test. Results Six out of 75 gene regions were significantly (P Conclusion Our findings suggest that genetic variation in CD4 may influence susceptibility to multiple myeloma. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A78.