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  • 1
    Keywords: CANCER ; DIAGNOSIS ; LUNG-CANCER ; HISTORY ; RISK ; GENE ; GENES ; METABOLISM ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; DELETION ; MUTANT ; GLUTATHIONE ; AGE ; smoking ; cancer risk ; CARRIERS ; case-control studies ; TOBACCO ; CANCER-RESEARCH ; M1 ; glutathione-S-transferase ; GLUTATHIONE S-TRANSFERASE ; case-control study ; ENVIRONMENTAL CARCINOGENS ; GSTM1 ; GSTT1 ; METAANALYSIS ; CLASS-MU ; GSTT1 POLYMORPHISMS
    Abstract: The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile--〉Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86-1.12) with the GSTM1 null, 1.11 (0.87-1.41) with the GSTT1 null, 1.01 (0.79-1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62-1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk
    Type of Publication: Journal article published
    PubMed ID: 15342448
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  • 2
    Keywords: CANCER ; EXPRESSION ; Germany ; FOLLOW-UP ; DISEASE ; RISK ; ACTIVATION ; ASSOCIATION ; LYMPHOMA ; AGE ; CIGARETTE-SMOKING ; smoking ; DOSE-RESPONSE ; case-control studies ; TOBACCO ; ALCOHOL ; SMOKERS ; EUROPE ; INTERVIEW ; Hodgkin's lymphoma ; DRINKING ; ONCOLOGY ; case-control study ; RE ; alcohol drinking ; case control studies ; INTERVAL ; NEVER SMOKERS ; odds ratio ; HEMATOLYMPHOPOIETIC MALIGNANCIES ; STERNBERG CELLS
    Abstract: We analysed the effects of tobacco and alcohol in the aetiology of Hodgkin's lymphoma (HL), based on 340 cases and 2465 controls enrolled in Spain, France, Italy, Germany, Ireland and Czech Republic, between 1998 and 2004. Current smokers showed a significantly increased odds ratio (OR) of HL of 1.39 (95% confidence interval (CI) = 1.04-1.87). Analyses were also conducted separately for subjects younger than 35 years (179 cases) and for older subjects (161 cases). For subjects below age 35, no association was observed between tobacco and HL, whereas for older subjects, ever-smokers experienced a doubled risk of HL as compared to never smokers and the OR of HL for current smoking was 2.35 (95% CI = 1.52-3.61), with suggestion of a dose response relationship. A protective effect of alcohol was observed in both age groups. The OR for ever-regular drinking was 0.58 (95% CI = 0.38-0.89) for younger subjects and 0.50 (95% CI = 0.34-0.74) for older subjects. There was no evidence of interaction between tobacco and alcohol. Our results are consistent with previous studies, suggesting a protective effect of alcohol on HL. An effect of tobacco was suggested for HL occurring in middle and late age, although this finding might have occurred by chance
    Type of Publication: Journal article published
    PubMed ID: 16819547
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  • 3
    Keywords: CANCER ; SURVIVAL ; Germany ; neoplasms ; DIAGNOSIS ; COHORT ; DISEASE ; DISEASES ; MORTALITY ; POPULATION ; RISK ; RISKS ; PATIENT ; RISK-FACTORS ; BREAST ; LYMPHOMA ; NUMBER ; CLINICAL-TRIALS ; risk factors ; case-control studies ; INHIBITORS ; case-control study ; case control studies ; INTERVAL ; DRUGS ; RISK-FACTOR ; PRAVASTATIN ; PROTEIN GERANYLGERANYLATION
    Abstract: Background: Statins, drugs used to treat dyslipidemia, may have anticancer properties. We have evaluated lymphoma risk associated with regular statin use in an international case-control study. Methods: This case-control study included 2,362 cases of incident B- and T-cell lymphoma from Czech Republic, France, Germany, Ireland, Italy, and Spain and 2,206 hospital or population controls. Information on drug use, diagnosis at admission (for hospital controls), and putative risk factors for lymphoma was collected with personal interviews. Hospital controls admitted for diseases possibly entailing use of statins were excluded from the analysis. Results: The odds ratio for regular statin use was 0.61 (95% confidence interval, 0.45-0.84); all major lymphoma subtypes showed similarly decreased risks. Decreased risks were observed in all centers. Duration of statin use was not associated with a greater reduction in the risk of lymphoma. Use of other lipid lowering drugs, such as fibrates, did not significantly modify the risk of lymphoma (odds ratio, 0.75; 95% confidence interval, 0.44-1.27). Conclusion: Statin use was associated with an important reduction in lymphoma risk, adding to the growing evidence of anticancer properties of this group of drugs. These results are reassuring for the increasing number of patients taking statins on a regular basis
    Type of Publication: Journal article published
    PubMed ID: 16702371
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  • 4
    Keywords: CANCER ; Germany ; human ; neoplasms ; RISK ; TIME ; ASSOCIATION ; LYMPHOMA ; MALIGNANCIES ; WOMEN ; MEN ; leukemia ; cancer risk ; CARCINOGENS ; hair dyes ; case-control studies ; NON-HODGKINS-LYMPHOMA ; MALIGNANCY ; PRODUCTS ; HUMAN CANCER ; INCREASE ; INTERVAL ; odds ratio ; population-based ; CANCER-RISK ; lymphatic system
    Abstract: Hair dyes have been evaluated as possibly being mutagenic and carcinogenic in animals. Studies of the association between human cancer risk and use of hair dyes have yielded inconsistent results. The authors evaluated the risk of lymphoid malignancies associated with personal use of hair dyes. The analysis included 2,302 incident cases of lymphoid neoplasms and 2,417 hospital- or population-based controls from the Czech Republic, France, Germany, Ireland, Italy, and Spain (1998-2003). Use of hair dyes was reported by 74% of women and 7% of men. Lymphoma risk among dye users was significantly increased by 19% in comparison with never use (odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.00, 1.41) and by 26% among persons who used hair dyes 12 or more times per year (OR = 1.26, 95% CI: 1.00, 1.60; p for linear trend = 0.414). Lymphoma risk was significantly higher among persons who had started coloring their hair before 1980 (OR = 1.37, 95% CI: 1.09, 1.72) and persons who had used hair dyes only before 1980 (OR = 1.62, 95% CI: 1.10, 2.40). Personal use of hair dyes is associated with a moderate increase in lymphoma risk, particularly among women and persons who used dyes before 1980. Specific compounds associated with this risk remain to be elucidated
    Type of Publication: Journal article published
    PubMed ID: 16731576
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  • 5
    Keywords: CANCER ; radiotherapy ; carcinoma ; human ; neoplasms ; DIAGNOSIS ; RISK ; PATIENT ; kidney ; RISK-FACTORS ; CARCINOGENESIS ; colon ; ASSOCIATION ; BREAST ; LYMPHOMA ; AGE ; OVARIAN-CANCER ; risk factors ; CERVICAL-CANCER ; RATES ; cancer risk ; REGISTRATION ; CANCER-PATIENTS ; adenocarcinoma ; TOBACCO ; pancreatic cancer ; LONG-TERM SURVIVORS ; YOUNG ; REGISTRY ; REPRODUCTIVE FACTORS ; ASSOCIATIONS ; ENDOMETRIAL ; PANCREATIC-CANCER ; cancer registries ; TESTICULAR CANCER ; LYMPHOMAS ; cancer registry ; pooled analysis ; RISK-FACTOR ; CANCERS ; REGISTRIES ; CANCER-DIAGNOSIS ; pancreatic neoplasms ; MALIGNANT NEOPLASMS ; neoplasms,second primary
    Abstract: Studies of pancreatic cancer in the setting of second primary malignant neoplasms can provide etiologic clues. An international multicenter study was carried out using data from 13 cancer registries with a registration period up to year 2000. Cancer patients were followed up from the initial cancer diagnosis, and the occurrence of second primary malignant neoplasms was compared with expected values derived from local rates, adjusting for age, sex, and period of diagnosis. Results from individual registries were pooled by use of a fixed-effects model. People were at higher risk of developing pancreatic cancer within 10 years of a diagnosis of cancers of the pharynx, stomach, gallbladder, larynx, lung, cervix, corpus uteri, bladder, and eye and 10 years or later following a diagnosis of cancers of the stomach, colon, gallbladder, breast, cervix, placenta, corpus uteri, ovary, testis, bladder, kidney, and eye, as well as Hodgkin's and non-Hodgkin's lymphomas. Pancreatic cancer was connected with smoking-related cancers, confirming the etiologic role of tobacco. The associations with uterine and ovarian cancers suggest that reproductive factors might be implicated in pancreatic carcinogenesis. The elevated pancreatic cancer risk in young patients observed among several types of cancer implies a role of genetic factors. Radiotherapy is also suggested as a risk factor
    Type of Publication: Journal article published
    PubMed ID: 16421239
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  • 6
    Keywords: CANCER ; carcinoma ; neoplasms ; DIAGNOSIS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; incidence ; POPULATION ; RISK ; RISKS ; SITE ; PATIENT ; prognosis ; RISK-FACTORS ; treatment ; LINKAGE ; DESIGN ; NUMBER ; AGE ; risk factors ; CANCER-PATIENTS ; CANCER PATIENTS ; TRENDS ; REGISTRY ; cancer registries ; PRIMARY TUMORS ; SWITZERLAND ; INTERVAL ; PRIMARY NEOPLASMS ; second primary cancers ; cancer registry ; pooled analysis ; RISK-FACTOR ; CANCERS ; REGISTRIES ; population-based ; PRIMARY MALIGNANCIES ; second primary cancer
    Abstract: Context: Increasing incidence and improved prognosis of thyroid cancer have led to concern about the development of second primary cancers, especially after radioiodine treatment. Thyroid cancer can also arise as a second primary neoplasm after other cancers. Objective: The objective of the study was to assess the risk of second primary cancer after thyroid cancer and vice versa. Design: This was a multinational record linkage study. Setting: The study was conducted at 13 population-based cancer registries in Europe, Canada, Australia, and Singapore. Patients or Other Participants: A cohort of 39,002 people (356,035 person-yr of follow-up) with primary thyroid cancer were followed up for SPN for up to 25 yr, and 1,990 cases of thyroid cancer were diagnosed after another primary cancer. Main Outcome Measures: To assess any possible excess of second primary neoplasms after thyroid cancer, the observed numbers of neoplasms were compared with expected numbers derived from age-, the cancer registries, yielding standardized incidence ratios (SIRs). The SIR of second primary thyroid cancer after various types of cancer was also calculated. Results: During the observation period, there were 2821 second primary cancers (all sites combined) after initial diagnosis of thyroid cancer, SIR of 1.31 ( 95% confidence interval 1.26 - 1.36) with significantly elevated risks for many specific cancers. Significantly elevated risks of second primary thyroid cancer were also seen after many types of cancer. Conclusion: Pooled data from 13 cancer registries show a 30% increased risk of second primary cancer after thyroid cancer and increased risks of thyroid cancer after various primary cancers. Although bias (detection, surveillance, misclassification) and chance may contribute to some of these observations, it seems likely that shared risk factors and treatment effects are implicated in many. When following up patients who have been treated for primary thyroid cancer, clinicians should maintain a high index of suspicion for second primary cancers
    Type of Publication: Journal article published
    PubMed ID: 16478820
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  • 7
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; CELL LUNG-CANCER ; Germany ; POPULATION ; RISK ; GENE ; GENES ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; HEALTH ; PROMOTER ; case-control studies ; squamous cell carcinoma ; GASTRIC-CANCER ; EUROPE ; inflammation ; molecular epidemiology ; CYTOKINE ; CELL CARCINOMA ; ONCOLOGY ; case-control study ; RE ; INTERLEUKIN-1 ; PROMOTER POLYMORPHISM ; CYCLOOXYGENASE-2 ; case control studies ; methods ; INTERLEUKIN-8 ; oral cancer ; CANCERS ; ESOPHAGEAL CANCER ; SQUAMOUS-CELL ; INTERLEUKIN-8 PROMOTER ; larynx cancer ; pharynx cancer ; upper aerodigestive tract cancers
    Abstract: Objectives The purpose of this study was to investigate the role of polymorphisms of genes involved in inflammation in the risk of cancers of the upper aerodigestive tract (UADT). Methods We have evaluated the role of polymorphisms in key genes related to inflammation, namely IL1B (rs1143627), COX2/PTGS2 (rs5275), and IL8 (rs4073) in a large case-control study comprising 811 UADT cancer cases and 1,083 controls. Results An association was observed for squamous cell carcinoma of the pharynx for a polymorphism in the promoter of the IL1B gene, with an OR of 2.39 (95% CI = 1.19-4.81) for the homozygotes for the minor allele A promoter polymorphism of IL8 was associated with decreased risk of laryngeal cancer, with an OR of 0.70 (95% CI = 0.50-0.98) for carriers of the minor allele. Conclusions To our knowledge, this is the first report on the role of these polymorphisms with respect to UADT carcinogenesis. Our results suggest that inflammation-related polymorphisms play a role, albeit minor, in the risk of developing cancers of the upper aerodigestive tract
    Type of Publication: Journal article published
    PubMed ID: 17356794
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  • 8
    Keywords: CANCER ; CELL ; human ; LUNG ; MODEL ; PATHWAY ; PATHWAYS ; lung cancer ; LUNG-CANCER ; SUPPORT ; SYSTEM ; SYSTEMS ; RISK ; RISKS ; SITE ; ENZYMES ; GENE ; GENES ; GENOME ; PATIENT ; DNA ; MARKER ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CYCLE ; SEQUENCE ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; HEALTH ; DNA-REPAIR ; REPAIR ; COMPONENT ; MARKERS ; DAMAGE ; HUMAN GENOME ; REGION ; REGIONS ; DNA-DAMAGE ; CANCER-PATIENTS ; CANCER PATIENTS ; CYCLE CONTROL ; MULTICENTER ; DNA repair ; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE ; ONCOLOGY ; RE ; VARIANT ; CHECKPOINT ; biomarker ; INTERVAL ; ENZYME ; analysis ; DNA damage ; HAPLOTYPE ; USA ; odds ratio ; cancer research ; cell cycle checkpoints ; modeling ; cell cycle control ; block ; nonsmokers ; INTEGRITY
    Abstract: The DNA repair systems maintain the integrity of the human genome and cell cycle checkpoints are a critical component of the cellular response to DNA damage. We hypothesized that genetic variants in DNA repair and cell cycle control pathways will influence the predisposition to lung cancer, and studied 27 variants in 17 DNA repair enzymes and 10 variants in eight cell cycle control genes in 1,604 lung cancer patients and 2,053 controls. To improve the estimation of risks for specific variants, we applied a Bayesian approach in which we allowed the prior knowledge regarding the evolutionary biology and physicochemical properties of the variant to be incorporated into the hierarchical model. Based on the estimation from the hierarchical modeling, MGMT 143V or 178R, and CHEK2 157I had an odds ratio of lung cancer equal to 1.45 [95% confidence interval (95% CI), 1.05-2.00], 1.18 (95% CI, 1.01-1.40), and 1.58 (95% CI, 1.14-2.17). The association of CHEK2 1571 seems to be overestimated in the conventional analysis. Nevertheless, this association seems to be robust in the hierarchical modeling. None of the pathways seem to have a prominent effect. In general, our study supports the notion that sequence variation may explain at least some of the variation of inherited susceptibility. In particular, further investigation of OGG1, MGMT, and CHEK2 focusing on the genetic regions where the present markers are located or the haplotype blocks tightly linked with these markers might be warranted
    Type of Publication: Journal article published
    PubMed ID: 18086781
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  • 9
    Keywords: CANCER ; IONIZING-RADIATION ; LUNG-CANCER ; EXPOSURE ; HISTORY ; POPULATION ; RISK ; GENE ; GENES ; radiation ; DNA ; FAMILY ; INDEX ; BIOMARKERS ; ASSOCIATION ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; FREQUENCIES ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; family history ; WOMEN ; DNA-REPAIR ; REPAIR ; smoking ; COLORECTAL-CANCER ; BLADDER-CANCER ; cancer risk ; INSTABILITY ; PARAMETERS ; TRANSFORMATION ; genetic polymorphism ; case-control studies ; TOBACCO ; ALCOHOL ; BODY ; FLUORESCENCE ; DNA repair ; SKIN-CANCER ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; MASSES ; BODIES ; case control study ; case-control study ; RE ; FAMILIES ; CAPACITY ; ALLELE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; XPD ; individual susceptibility ; biomarker ; case control studies ; INTERVAL ; analysis ; PREMENOPAUSAL WOMEN ; FAMILY-HISTORY ; PREMENOPAUSAL ; odds ratio ; CANCER-RISK ; TOXICOLOGY ; microbiology ; CHINESE POPULATION ; - ; BODY-MASS ; BODY-MASS-INDEX ; biotechnology ; XRCC3 ; REPAIR GENE XRCC3
    Abstract: The X- ray repair cross- complementing group 3 gene ( XRCC3) belongs to a family of genes responsible for repairing DNA double- strand breaks caused by normal metabolic processes and exposure to ionizing radiation. Polymorphisms in DNA repair genes may alter an individual's capacity to repair damaged DNA and may lead to genetic instability and contribute to malignant transformation. We examined the role of a polymorphism in the XRCC3 gene ( rs861529; codon 241: threonine to methionine change) in determining breast cancer risk in Thai women. The study population consisted of 507 breast cancer cases and 425 healthy women. The polymorphism was analysed by fluorescence- based melting curve analysis. The XRCC3 241Met allele was found to be uncommon in the Thai population ( frequency 0.07 among cases and 0.05 among controls). Odds ratios ( OR) adjusted for age, body mass index, age at menarche, family history of breast cancer, menopausal status, reproduction parameters, use of contraceptives, tobacco smoking, involuntary tobacco smoking, alcohol drinking, and education were calculated for the entire population as well as for pre- and postmenopausal women. There was a significant association between 241Met carrier status and breast cancer risk ( OR 1.58, 95% confidence interval ( CI) 1.02 - 2.44). Among postmenopausal women, a slightly higher OR ( 1.82, 95% CI 0.95 - 3.51) was found than among premenopausal women ( OR 1.48, 95% CI 0.82 - 2.69). Our findings suggest that the XRCC3 Thr241Met polymorphism is likely to play a modifying role in the individual susceptibility to breast cancer among Thai women as already shown for women of European ancestry
    Type of Publication: Journal article published
    PubMed ID: 17701750
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  • 10
    Keywords: CANCER ; carcinoma ; CELL ; LUNG ; PROSTATE ; COHORT ; EXPOSURE ; incidence ; liver ; RISK ; PATIENT ; kidney ; primary ; SKIN ; BREAST ; BREAST-CANCER ; LYMPHOMA ; DIFFERENCE ; DECREASE ; NUMBER ; AGE ; COUNTRIES ; PROSTATE-CANCER ; RATES ; skin cancer ; MELANOMA ; SWEDEN ; COLON-CANCER ; STOMACH ; SIR ; UNITED-STATES ; AUSTRALIA ; second cancer ; SKIN-CANCER ; basal cell carcinoma ; NON-HODGKINS-LYMPHOMA ; CELL CARCINOMA ; ONCOLOGY ; REGISTRY ; pancreas ; cancer registries ; non-Hodgkin lymphoma ; methods ; cancer registry ; CANCER INCIDENCE ; female ; CANCERS ; REGISTRIES ; E ; colorectal ; BASAL-CELL CARCINOMA ; second primary cancer ; SUN EXPOSURE ; vitamin D ; VITAMIN-D ; ULTRAVIOLET-RADIATION ; SUBSEQUENT RISK ; D METABOLITES
    Abstract: Background: Skin cancers are known to be associated with sun exposure, whereas sunlight through the production of vitamin D may protect against some cancers. The aim of this study was to assess whether patients with skin cancer have an altered risk of developing other cancers. Methods: The study cohort consisted of 416,134 cases of skin cancer and 3,776,501 cases of non-skin cancer as a first cancer extracted from 13 cancer registries. 10,886 melanoma and 35,620 non-melanoma skin cancer cases had second cancers. The observed numbers (0) of 46 types of second primary cancer after skin melanoma, basal cell carcinoma or non-basal cell carcinoma, and of skin cancers following non-skin cancers were compared to the expected numbers (E) derived from the age, sex and calendar period specific cancer incidence rates in each of the cancer registries (O/E = SIR, standardised incidence ratios). Rates from cancer registries classified to sunny countries (Australia, Singapore and Spain) and less sunny countries (Canada, Denmark, Finland, Iceland, Norway, Scotland, Slovenia and Sweden) were compared to each other. Results: SIR of all second solid primary cancers (except skin and lip) after skin melanoma were significantly lower for the sunny countries (SIR(S) = 1.03; 95% CI 0.99-1.08) than in the less sunny countries (SIR(L) = 1.14; 95%CI 1.11-1.17). The difference was more obvious after non-melanoma skin cancers: after basal cell carcinoma SIR(S)/SIR(L) = 0.65 (9S%CI = 0.58-0.72); after non-basal cell carcinoma SIR(S)/SIR(L) = 0.58 (95%CI = 0.50-0.67). In sunny countries, the risk of second primary cancer after non-melanoma skin cancers was lower for most of the cancers except for lip, mouth and non-Hodgkin lymphoma. Conclusions: Vitamin D production in the skin seems to decrease the risk of several solid cancers (especially stomach, colorectal, liver and gallbladder, pancreas, lung, female breast, prostate, bladder and kidney cancers). The apparently protective effect of sun exposure against second primary cancer is more pronounced after non-melanoma skin cancers than melanoma, which is consistent with earlier reports that non-melanoma skin cancers reflect cumulative sun exposure, whereas melanoma is more related to sunburn. (c) 2007 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17540555
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