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1.  Cancer Prevention Health Services Research: An Emerging Field 
In October 2009, The University of Texas MD Anderson Cancer Center hosted a symposium, “Future Directions in Cancer Prevention and Control: Workforce Implications for Training, Practice, and Policy.” This article summarizes discussions and an Internet and literature review by the symposium's Health Services Infrastructure Working Group. We agree on the need for the recognition of Cancer Prevention Health Services Research (CP-HSR) as a unified research field. With advances in cancer screening and increased emphasis on preventive services under healthcare reform, there is a growing need for investigators with both cancer prevention and HSR expertise to consider the comparative effectiveness of cancer screening methods, the cost-effectiveness of early detection technologies, and the accessibility of preventive care for individuals at risk of cancer. Defining CP-HSR as a field will provide investigators with credibility and will serve to draw more researchers to the field. Increasing funding to train individuals in CP-HSR will be important to help meet the anticipated demand for investigators with this specialized multidisciplinary expertise.
doi:10.1007/s13187-012-0330-7
PMCID: PMC3880141  PMID: 22311693
Cancer prevention; Health service research; Cancer screening; Cost-effectiveness; Comparative effectiveness; Workforce
2.  Trends in Breast Cancer Incidence Rates by Age and Stage at Diagnosis in Gharbiah, Egypt, over 10 Years (1999–2008) 
Journal of Cancer Epidemiology  2013;2013:916394.
Background. This study was undertaken to evaluate trends in breast cancer incidence in Egypt from 1999 to 2008 and to make projections for breast cancer occurrence for the years 2009–2015. Patients and Methods. We utilized joinpoint regression and average annual percent change (AAPC) measures with 95% confidence intervals (CI) to describe the trends in breast cancer incidence rates from the Gharbiah Cancer Registry by age and stage at diagnosis and to estimate expected breast cancer caseloads for 2009–2015. Results. From 1999 to 2008, the AAPC in breast cancer incidence rates in Gharbiah significantly increased among women 50 years and older and among localized tumors (AAPC %, 95% CI, 3.1% to 8.0%). Our results predict a significant increase in breast cancer caseloads from 2009 to 2015 among women aged 30–39 (AAPC %, 95% CI, 0.9% to 1.1%) and among women aged 40–49 years (AAPC %, 95% CI, 1.0% to 2.6%). Conclusion. These results have important implications for allocating limited resources, managing treatment needs, and exploring the consequences of prior interventions and/or changing risk factors in Egypt and other developing countries at the same stages of demographic and health transitions.
doi:10.1155/2013/916394
PMCID: PMC3824336  PMID: 24282410
3.  Characterizing inflammatory breast cancer among Arab Americans in the California, Detroit and New Jersey Surveillance, Epidemiology and End Results (SEER) registries (1988–2008) 
SpringerPlus  2013;2:3.
Introduction
Inflammatory breast cancer (IBC) is characterized by an apparent geographical distribution in incidence, being more common in North Africa than other parts of the world. Despite the rapid growth of immigrants to the United States from Arab nations, little is known about disease patterns among Arab Americans because a racial category is rarely considered for this group. The aim of this study was to advance our understanding of the burden of IBC in Arab ethnic populations by describing the proportion of IBC among different racial groups, including Arab Americans from the Detroit, New Jersey and California Surveillance, Epidemiology and End Results (SEER) registries.
Methods
We utilized a validated Arab surname algorithm to identify women of Arab descent from the SEER registries. Differences in the proportion of IBC out of all breast cancer and IBC characteristics by race and menopausal status were evaluated using chi-square tests for categorical variables, t-tests and ANOVA tests for continuous variables, and log-rank tests for survival data. We modeled the association between race and IBC among all women with breast cancer using hierarchical logistic regression models, adjusting for individual and census tract-level variables.
Results
Statistically significant differences in the proportion of IBC out of all breast cancers by race were evident. In a hierarchical model, adjusting for age, estrogen and progesterone receptor, human epidermal growth receptor 2, registry and census-tract level education, Arab-Americans (OR=1.5, 95% CI=1.2,1.9), Hispanics (OR=1.2, 95% CI=1.1,1.3), Non-Hispanic Blacks (OR=1.3, 95% CI=1.2, 1.4), and American Indians/Alaskans (OR=1.9, 95% CI=1.1, 3.4) had increased odds of IBC, while Asians (OR=0.6, 95% CI=0.6, 0.7) had decreased odds of IBC as compared to Non-Hispanic Whites.
Conclusions
IBC may be more common among certain minority groups, including Arab American women. Understanding the descriptive epidemiology of IBC by race may generate hypotheses about risk factors for this aggressive disease. Future research should focus on etiologic factors that may explain these differences.
doi:10.1186/2193-1801-2-3
PMCID: PMC3568481  PMID: 23420611
Inflammatory breast cancer; Arab; Race; Hierarchical logistic regression
4.  Sociodemographic Characteristics, Health Beliefs, and the Accuracy of Cancer Knowledge 
Journal of Cancer Education  2009;24(1):58-64.
Background
Recent studies have found that knowledge about cancer prevention and treatment differs across ethnic and socioeconomic status (SES) backgrounds, which could directly impact our decisions to engage in protective health behaviors. In this study, we examined sociodemographic-based differences in cancer knowledge and health beliefs and examined differences in the accuracy of the cancer knowledge based on health beliefs.
Methods
Cross-sectional surveys were conducted between July 1995 and March 2004 on adult, healthy, cancer-free control participants (N = 2074; 50% male) enrolled into a molecular epidemiological case-control study. Most were non-Hispanic white, 14% were African American, and 8% were Hispanic. Participants were personally interviewed on 6 items assessing health beliefs and 10 items assessing cancer knowledge.
Results
Unadjusted differences in cancer knowledge were observed by gender, age, ethnicity, household income, educational attainment, and smoking status. After adjusting for the other sociodemographic characteristics, women had more accurate knowledge than men, the accuracy of knowledge increased with higher educational attainment and annual household income, and never smokers had more accurate knowledge than ever smokers (P < .01 for all). Moreover, accurate cancer knowledge was associated with protective health beliefs; eg, the belief that changing health habits was worthwhile was associated with more accurate knowledge.
Conclusions
Results emphasize the need to develop health education programs that enhance cancer knowledge among individuals of low SES and foster protective health beliefs.
doi:10.1080/08858190802664834
PMCID: PMC3381329  PMID: 19259867
5.  Association between a Functional Polymorphism (-1195T>C) in the IGFBP5 Promoter and Head and Neck Cancer Risk 
Head & neck  2010;33(5):650-660.
Background
No studies have evaluated roles of insulin-like growth factor binding protein 5 (IGFBP-5) polymorphisms in risk of squamous cell carcinoma of the head and neck (SCCHN).
Methods
A hospital-based study of 1082 SCCHN patients and 1120 cancer-free controls was performed to investigate associations between two functional polymorphisms -1195T>C and -709G>C in the IGFBP5 promoter region and SCCHN risk.
Results
We demonstrated that the transcription factor AP-1 differentially bound to T or C variants at -1195 in the promoter to regulate the IGFBP5 promoter activity and that the C variant genotypes were associated with deferential risk of late-stage SCCHN, compared with the TT genotype, particularly for HPV-unrelated sites (adjusted OR, 2.21; 95% CI, 1.19-4.11 for CC vs. TT).
Conclusion
The IGFBP5 -1195T>C polymorphism is functional and may potentially be a biomarker for susceptibility to late-stage SCCHN.
doi:10.1002/hed.21514
PMCID: PMC3023825  PMID: 20949447
IGFBP5; head neck cancer; TNM stage; polymorphism; association
6.  Genetic variations of the PI3K–AKT–mTOR pathway and clinical outcome in muscle invasive and metastatic bladder cancer patients 
Carcinogenesis  2010;31(8):1387-1391.
The phosphoinositide-3 kinase (PI3K)–AKT– mammalian target of rapamycin (mTOR) pathway is an important cellular pathway controlling cell growth, tumorigenesis, cell invasion and drug response. We hypothesized that genetic variations in the PI3K–AKT–mTOR pathway may affect the survival in muscle invasive and metastatic bladder cancer (MiM-BC) patients. We conducted a follow-up study of 319 MiM-BC patients to systematically evaluate 289 single-nucleotide polymorphisms (SNPs) of 20 genes in the PI3K–AKT–mTOR pathway as predicators of survival. In multivariate Cox regression, AKT2 rs3730050, PIK3R1 rs10515074 and RAPTOR rs9906827 were significantly associated with survival. In combined analysis, we found a cumulative effect of these three SNPs on survival. With the increasing number of unfavorable genotypes, there was a significant trend of higher risk of death in multivariate Cox regression (P for trend <0.001) and shorter median survival time in Kaplan–Meier estimates (P log rank <0.001). This is the first study to evaluate the role of germ line genetic variations in the PI3K–AKT–mTOR pathway genes as predictors of MiM-BC clinical outcomes. These findings warrant further replication in independent populations and may provide information on disease management and development of target therapies.
doi:10.1093/carcin/bgq110
PMCID: PMC2915631  PMID: 20530239
7.  Genetic variations in PI3K-AKT-mTOR pathway and bladder cancer risk 
Carcinogenesis  2009;30(12):2047-2052.
Genetic variations in phosphoinositide-3 kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway may affect critical cellular functions and increase an individual's cancer risk. We systematically evaluate 231 single-nucleotide polymorphisms (SNPs) in 19 genes in the PI3K-AKT-mTOR signaling pathway as predictors of bladder cancer risk. In individual SNP analysis, four SNPs in regulatory associated protein of mTOR (RAPTOR) remained significant after correcting for multiple testing: rs11653499 [odds ratio (OR): 1.79, 95% confidence interval (CI): 1.24–2.60, P = 0.002], rs7211818 (OR: 2.13, 95% CI: 1.35–3.36, P = 0.001), rs7212142 (OR: 1.57, 95% CI: 1.19–2.07, P = 0.002) and rs9674559 (OR: 2.05, 95% CI: 1.31–3.21, P = 0.002), among which rs7211818 and rs9674559 are within the same haplotype block. In haplotype analysis, compared with the most common haplotypes, haplotype containing the rs7212142 wild-type allele showed a protective effect of bladder cancer (OR: 0.83, 95% CI: 0.70–0.97). In contrast, the haplotype containing the rs7211818 variant allele showed a 1.32-fold elevated bladder cancer risk (95% CI: 1.09–1.60). In combined analysis of three independent significant RAPTOR SNPs (rs11653499, rs7211818 and rs7212142), a significant trend was observed for increased risk with an increase in the number of unfavorable genotypes (P for trend <0.001). Compared with the subjects without any of the unfavorable genotypes, those carrying all three unfavorable genotypes showed a 2.22-fold (95% CI: 1.33–3.71) increased bladder cancer risk. This is the first study to evaluate the role of germ line genetic variations in PI3K-AKT-mTOR pathway as cancer susceptibility factors that will help us identify high-risk individuals for bladder cancer.
doi:10.1093/carcin/bgp258
PMCID: PMC2792319  PMID: 19875696
8.  Genotypes and haplotypes of ERCC1 and ERCC2/XPD genes predict levels of benzo[a]pyrene diol epoxide-induced DNA adducts in cultured primary lymphocytes from healthy individuals: a genotype–phenotype correlation analysis 
Carcinogenesis  2008;29(8):1560-1566.
Benzo[a]pyrene diol epoxide (BPDE)-induced DNA adducts are a risk factor for tobacco-related cancers. Excision repair cross-complementing complementation group 1 (ERCC1) and excision repair cross-complementing complementation group 2/xeroderma pigmentosum D (ERCC2/XPD) participate in the nucleotide excision repair (NER) pathway that removes BPDE–DNA adducts; however, few studies have provided population-based evidence for this association. Therefore, we assayed for levels of in vitro BPDE-induced DNA adducts and genotypes of single-nucleotide polymorphisms (SNPs) of the NER genes ERCC1 (rs3212986 and rs11615) and ERCC2/XPD (rs13181, rs1799793 and rs238406) in 707 healthy non-Hispanic whites. The linear trend test of increased adduct values in never to former to current smokers was statistically significant (Ptrend = 0.0107). The median DNA adduct levels for the ERCC2 rs1799793 GG, GA and AA genotypes were 23, 29 and 30, respectively (Ptrend = 0.057), but this trend was not observed for other SNPs. After adjustment for covariates, adduct values larger than the median value were significantly associated with the genotypes ERCC1 rs3212986TT [odds ratio (OR) = 1.89, 95% confidence interval (CI) = 1.03–3.48] and ERCC2/XPD rs238406AA (OR = 0.64, 95% CI = 0.41–0.99) and rs238406CA (OR = 0.63, 95% CI = 0.45–0.89) compared with their corresponding wild-type homozygous genotypes. The results of haplotype analysis further suggested that haplotypes CAC and CGA of ERCC2/XPD, TC of ERCC1 and CACTC of ERCC2/XPD and ERCC1 were significantly associated with high levels of DNA adducts compared with their most common haplotypes. Our findings suggest that the genotypes and haplotypes of ERCC1 and ERCC2/XPD may have an effect on in vitro BPDE-induced DNA adduct levels.
doi:10.1093/carcin/bgn089
PMCID: PMC2516484  PMID: 18635523

Results 1-8 (8)