DNA repair gene polymorphisms in the nucleotide excision repair pathway and lung cancer risk: A meta-analysis

Objective: A number of studies have reported the association of "XPA", "XPC", "XPD/ERCC2" gene polymorphisms with lung cancer risk. However, the results were conflict. To clarify the impact of polymorphisms of "XPA", "XPC", "XPD/ERCC2", on lung cancer risk, a meta-analysis was performed in this study. Methods: The electronic databases PubMed and Embase were retrieved for studies included in this meta-analysis by "XPA", "XPC", "XPD/ERCC2", "lung", "cancer/neoplasm/tumor/carcinoma", "polymorphism" (An upper date limit of October, 31, 2009). A meta-analysis was performed to evaluate the relationship among XPA, XPC and XPD polymorphism and lung cancer risks. Results: A total of 31 publications retrieved from Pubmed and Embase included in this study. XPC A939C CC genotype increased lung cancer risk in total population (recessive genetic model: OR=1.23, 95% CI:1.05-1.44; homozygote comparison: OR=1.21,95%CI:1.02-1.43and CC vs. CA contrast: OR=1.25,95%CI:1.06-1.48), except in Asians. XPD A751C, 751C allele and CC genotype also increased lung cancer risk in total population and in Caucasians (recessive genetic model: Total population: OR=1.20, 95%CI:1.07-1.35). No significant correlation was found between XPD A751C and lung cancer risk in Asians and African Americans. XPD G312A AA genotype increased lung cancer risk in total population, in Asians and Caucasians(recessive genetic model: Total population: OR=1.20, 95%CI: 1.06-1.36). No significant association was found between XPA G23A, XPC C499T, XPD C156A and lung cancer risk. Conclusion: Our results suggest that the polymorphisms in XPC and XPD involve in lung cancer risks. XPA polymorphisms is less related to lung cancer risk.     

53. Studies for Effects on Fertility and Early Embryonic Development to Implantation of Qingling-Sibutramine hydrochloride in Mice

To better understand the safety property to reproductive and development in human of Qingling-Sibutramine hydrochloride (Ql-Sibutramine), a study of toxic effects/disturbances resulting from treatment from before mating (males/females) through mating and implantation of Ql-Sibutramine in mice were conduc-ted. Ql-Sibutramine was administrated in drink water. A premating treatment interval of 8 weeks for male and 2 weeks for female were done in mice. Treatment was continued throughout mating to termination of males and through implantation for female. The dosages were 32 mg*kg-1*d-1 (1/5 LD50), 2.83 mg*kg-1*d-1, 0.25 mg*kg-1*d-1, and a control group. Assessment of maturation of gametes, mating behavior, fertility, preimplantation stages of the embryo, implantation and toxicity to the parent mice were done. The boby weight lose was observed in the group of 32 mg*kg-1*d-1 in male mice. No other toxic effects in the parent mice and offspring were observed.     

Epidemiology and trend analysis on malignant mesothelioma in China

Objective:Population-based cancer registration data were used to analyze the epidemiology and trend of malignant mesothelioma in China,and the result would provide basic data for its prevention and control.Methods:Malignant mesothelioma data in 2013 were retrieved from the database of National Cancer Registry.Malignant mesothelioma incidence and mortality were estimated using age-specific rate by urban/rural and gender according to the national population in 2013.Malignant mesothelioma data from 22 cancer registries were used for trend analysis during 2000-2013.Results:It is estimated that there were 2,041 new malignant mesothelioma cases and 1,659 malignant mesothelioma deaths occurred in 2013.The crude incidence rate in China were 1.50/106 (males 1.67/106,females 1.32/106),age-standardized incidence rates by Chinese standard population (ASIRC) and by world standard population (ASIRW) were 1.03/106 and 1.02/106,respectively.The crude mortality rate in China was 1.22/106(males 1.67/106,females 1.32/106),age-standardized mortality rates by Chinese standard population (ASMRC) and by world standard population (ASMRW) were 0.83/106 and 0.81/106,respectively.There was an increasing trend of incidence rate for malignant mesothelioma in registration areas of China during 2000-2013 with annual percentage change (APC) of 2.5％ [95％ confidence interval (95％ CI):0.6％-4.5％].After age standardization,no significant differences were observed.No matter for crude mortahty rates or age-standardized mortality rates,no significant differences were observed during 2000-2013.Conclusions:Malignant mesothelioma is the major occupational and environmental neoplasm associated with asbestos exposure.The increasing incidence trend suggests that more attention should be paid on this disease.     

Evolution of viral RNA in a Chinese patient to interferon/ribavirin therapy for hepatitis C

Objective:The combination of interferon(IFN)and ribavirin(RBV)is the standard therapy for hepatitis C virus(HCV)infection.HCV genotype 2a has proved more amenable to the therapy,but its efficacy is yet limited.This study aimed to investigate the mechanism of the poor response in a case of HCV genotype 2a infection.methods:We analyzed dynamic change of HCV RNA from a patient,infected with HCV genotype 2a,showing a poor virological response to IFN/RBV as judged 12 weeks after initiation of the therapy by HCV clone sequencing.Then we constructed subgenomic Japanese fulminant hepatitis-1(JFH1)replicon and different chimeric replicons with humanized Gaussia luciferase gene.The chimeric replicons were derived from subgenomic JFH1 replicon,in which the NS5A region was replaced by the patient’s sequence from the pre/posttreatment,and the chimeric replicons’ susceptibility to IFN were evaluated by relative Gausia Luciferase activity.Results:The pretreatment HCV sequences appeared almost uniform,and the quasispecies variation was further more simplified after 12 weeks of therapy.Besides,the quasispecies variation seemed to be more diversified in the NS5A,relatively,a region crucial for IFN response,and each of chimeric replicons exhibited distinct response to IFN.Conclusions:During the course of the chronic infection,HCV population seems to be adapted to the patient’s immunological system,and further to be selected by combination of IFN/RBV therapy,indicating quasispecies may completely eliminated by addition of other drugs with targets different from those of IFN.In addition,each different response of chimeric replicon to IFN is most likely related to amino acid changes in or near the IFN-sensitivity determining region(ISDR) of NS5A during chronic infection and IFN/RBV therapy.     

The Preliminary Study on Relationship between HPV－associated Cervical Cancer and p53 Codon 72 Polymorphism in Sichuan Province

Objective: To study the relationship between HPV-associated cervical cancer and p53 codon 72 polymorphism in Sichuan Province. Methods: Three groups of women were studied: 30 women for normal control; 30 women with ovarian cancer; 50 women with cervical cancer. DNA from peripheral blood samples and from pathologic tissue sections was examined by PCR with allele-specific primers. Results:The proportions of individuals homozygons for the arginine allele, homozygous for the proline allele and heterozygous for the two alleles were 33.3%, 6.7% and 60% respectively among normal women; 40%, 6.7% and 53.3% in women with ovarian cancer respectively; 80%, 6% and 14% in women with cervical cancer respectively. X2 analysis showed significant differences in the proportions. Conclusion: In this population,individuals homozygons for the arginine variant of codon 72 of the p53 gene were at increased risk of cervical cancer.     

An Inhibitory Effect of MAD1 on Bladder Tumor Cellular Proliferation in Vivo

OBJECTIVE To observe the inhibitory effect on bladder tumor prolivera-tion after transfection with the expression plasmid pcDNA3.1( )/Mad1. METHODS Bladder tumors were induced in SD rats by intravesical instillation of MNU . The tumor-bearing rats were randomly divided into 3 groups: group A, transfected with pcDNA3.1 ( )/Mad1, group B, trans-fected with an empty vector and group C, transfected with saline. Rat body weight (RBW), bladder absolute weight (BAW) and bladder relative weight (BRW) were measured and expression levels of Mad1 and TERT were assayed. Flow cytometer analysis was used to observe the effect of Mad1 on the bladder tumors. RESULTS Comparions of RBW among the 3 groups showed there were no differences (P>0.05). But the BAW and BRW for group A were significantly decreased (P<0.01, P<0.05, respectively) comparded to groups B and C. In group A, the Mad1 mRNA expression level was markedly improved, while the TERT mRNA expression level was decreased. Flow cy-tometry showed an increase in G0/G1-phase cells and a decrease of S-phase cells after transfection with Mad1. CONCLUSION Over expression of Mad1 can inhibit the cellular proliferation of bladder tumors.     

58. Susceptibility to lung cancer is associated with genetic polymorphisms of CYP1A1、GSTM1

Objective: To investigate the association of lung cancer susceptibility with genetic Polymorphism of CYP1A1 and GSTM1. Methods: The study was conducted on 65 lung cancer cases and 60 no-cancer controls. The genetic polymorphism both CYP1A1 and GSTM1 were performed in cancer tissues of all patients and peripheral blood leukocytes of no-cancer controls. First by RFLP-PCR, then after incubating with restriction enzyme Ncol and Hinfl. Results: ①There were no significant differences in the frequency distribution of CYP1A1 polymorphisms between lung cancer patients and controls, but the frequency of CYP1A1(Val/Val) was significant higher than that controls (P<0.05). ②If OR for CYP1A1 (Ile/Ile) genotype was 1.0, the OR of CYP1A1 (Ile/VaL)、CYP1A1 (Val/Val) was 1.68 (95%CI, 0.79～3.59) and 3.2 (95%CI, 1.06～10.26), respectively. ③The significant difference were observed that GSTM1(-) became markedly expressed (63.1%, 41/65) in elung cancer patients than in the corresponding controls (45%, 27/60) (P<0.05), OR was 2.09 (95%CI, 1.02～4.26); ④When analysis combined CYP1A1 and GSTM1 genotype, we found that individual who take along CYP1A1 (Ile/Ile)/GSTM1 (-) or CYP1A1 (Ile/Val+Val/Val)/GSTM1 (+) genotype had higher odds ratio than CYP1A1 (Ile/Ile)/GSTM1 (+) genotype, the OR was 3.82 (95%CI, 1.27～11.45) and 3.5 (95%CI 1.18～10.41), respectively, but the CYP1A1 (Val/Val) / GSTM1 (-) genotype was the hightest odds ratio, the OR was 10.5 (95%CI, 1.70～64.73). ⑤We observed that the individual who carry CYP1A1(Val/Val) genotype can increased risk of squamous cell carcinoma of lung (P<0.05), OR was 2.75 (95%CI, 1.24～6.17), there was no significant associated of pathologic with GSTM1 genotype. ⑥Stratified analysis suggested an interaction between cigarettes smoking and CYP1A1 (Ile/Val+Val/Val)、GSTM1 (-) genotype. Conclusion: ①The individuals who carried genotype of CYP1A1 (Val/Val) and GSTM1 (-) were susceptible to lung cancer. ②the individuals who carried CYP1A1 (Ile/Ile) /GSTM1 (-) or CYP1A1 (Ile/Val+Val/Val) /GSTM1 (+) genotype with higher risk of developing lung cancer than that CYP1A1 (Ile/Ile)/GSTM1 (+) genotype. ③There were interaction between smoking and CYP1A1 (Ile/Val+Val/Val)、GSTM1 (-)     

A FIVE-YEAR PROSPECTIVE STUDY ON THE RELATIONSHIP BETWEEN GARLIC AND GASTRIC CANCER

A prospective study on the relationship between garlic and gastric cancer of 4552 subjects was made from Oct., 1980 through 1985. The volunteers, aged 50-59, were healthy males and came from different incidence areas of gastric cancer where they lived for long periods. The result of this study showed that the death rates of gastric cancer in < 2500 g and > 2500 g groups of annual garlic intake were 10.40/ 10000 and 0, respectively. The relative risk of gastric cancer was significantly much higher in the former than in the latter, and showed a dose-response relationship. Protective effect of garlic for the population equal annual garlic intake was roughly the same in different districts. It was further confirmed that garlic played important role in preventing gastric cancer and had no regional differences.     

DNA methylation patterns in alcoholics and family controls

AIM: To assess whether DNA methylation patterns in chronic alcoholics are different from non-alcoholic sibling controls. METHODS: We examined the methylation patterns in DNA samples from 25 chronic alcoholics and 22 matched siblings as controls (one per family). DNA was extracted from peripheral blood and analyzed for differences in the methylation patterns after bisulfite-conversion. We used the Illumina GoldenGate Methylation Cancer Panel I (Illumina, San Diego, CA), which probes the methylation profile at 1505 CpG sites from 807 cancer related genes. We excluded the 84 X-chro- mosome CpG sites and 134 autosomal CpG sites that failed to show a within sample reliability score of at least 95% for all samples, leaving 1287 autosomal CpG sites (associated with 743 autosomal genes) with reliable signals for all samples. A methylation score was calculated as the average methylation for the 1287 CpG sites examined. Differences were assessed by a two-sample t-test. We also examined the average sib pair differences in methylation scores at each of the 1287 sites. All analyses were performed using SPSS, version 9.0, P < 0.05 was considered significant. RESULTS: Methylation levels at the 1287 CpG sites averaged 28.2% for both alcoholics and controls. The mean difference in methylation scores between alcoholic and non-alcoholic sibs by CpG site was < 1% with small inter-individual variances; and only 5 CpG sites had an average sib difference > 5%. Subgroup analysis showed that methylation scores were significantly lower for the alcoholic-dependent subjects who smoked compared to their non-smoking unaffected siblings. Specifically, among smokers who are alcoholic, global methylation indices were significantly lower than in nonalcoholic sib controls, whereas among non-smoking alcoholics, the global indices were significantly higher (P = 0.008). CONCLUSION: Although we observed no effect of alcoholism alone on DNA methylation, there is a decrease in alcoholics who smoke, suggesting a mechanism for alcohol-tobacco synergy for carcinogenesis.     

Association between genetic variations in tumor necrosis factor receptor genes and survival of patients with T-cell lymphoma

The prognosis of T-cell lymphoma (TCL) has been shown to be associated with the clinical characteristics of patients. However, there is little knowledge of whether genetic variations also affect the prognosis of TCL. This study investigated the associations between single nucleotide polymorphisms(SNPs) in tumor necrosis factor receptor superfamily(TNFRSF) genes and the survival of patients with TCL. A total of 38 tag SNPs in 18 TNFRSF genes were genotyped using Sequenom platform in 150 patients with TCL. Kaplan-Meier survival estimates were plotted and significance was assessed using log-rank tests. Cox proportional hazard models were used to analyze each of these 38 SNPs with adjustment for covariates that might influence patient survival, including sex and international prognostic Index score. Hazard ratios (HRs) and their 95% confidence intervals(CIs) were calculated. Among the 38 SNPs tested, 3 were significantly associated with the survival of patients with TCL. These SNPs were located at LTβR (rs3759333CT) and TNFRSF17(rs2017662CT and rs2071336CT). The 5-year survival rates were significantly different among patients carrying different genotypes and the HRs for death between the different genotypes ranged from 0.45 to 2.46. These findings suggest that the SNPs in TNFRSF genes might be important determinants for the survival of TCL patients.     

The Immuno-fluorescence Quantity Analysis of α-Tubulin and γ-Tubulin Protein in Precancerous Lesion and Carcinoma of the Breast and Its Significance

OBJECTIVE To investigate the changes and values of the expression of α-tubulin and γ-tubulin in atypical ductal hyperplasia （ADH）, ductal carcinoma in situ （DCIS） and invasive ductal carcinoma （IDC） of the breast. The relationship between centrosome abnormalities and breast tumor development was further discussed. METHODS There were three groups including ADH, DCIS and IDC with 30 cases in each group. They were analyzed by immuno-fiuorescence quantity analysis. The expression levels of α-tubulin and γ-tubulin protein in these tissues were detected by flow cytometry immuno-fiuorescence analysis and compared with the results from normal tissues. Immunohistochemistry was also performed in this research. RESULTS The results showed significant differences of the average of the positive （FITC labeled） cells （P=0.000） among the four groups. The level of the IDC group was the highest, while normal breast tissue showed the lowest level. The results suggested that the expression levels of α-tubulin and γ-tubulin both increased as the grade of cellular proliferation and differentiation increased. The expressions showed significant differences among all the groups, except between the ADH and DCIS. There were no significant differences between α-tubulin and γ-tubulin expression in each group （P〈0.05）, as there was agreement in the immuno-fluorescence and immunohistochemical analysis for protein expression. CONCLUSION There is abnormal expression of centrosome tubulin as an early event in the development of breast tumor. Furthermore these aberrations may play a key role during oncogenesis and promote cellular transformation to malignancy. The immuno-fiuorescence quantitive analysis and immunohistochemistry can complement each other.     

Trial of the correlation between cytochrome oxidase CYP3A4 with the susceptibility of paclitaxel-based regimen for advanced gastric cancer

Objective： The aim of the study was to investigate the relationship between susceptibility of paclitaxel-based regimen and gene polymorphisms of cytochrome oxidase CYP3A4 for advanced gastric cancer. Methods： Peripheral venous blood sample of 53 advanced gastric cancer patients were enrolled to test the mutation of CYP3A4 gene by denaturing high performance liquid chromatography（DHPLC） and DNA sequencing. The relation between the efficacy of paclitaxel-based regimen and CYP3A4 gene polymorphisms was further analyzed. Results： DHPLC indicated that among the 53 patients, 21 cases showed biomodal type（mutation） and 32 cases were of unimodal type（wild-type）. Sequencing results showed that the deletion mutation was found at the 27 th basic group of C in exon 10 of CYP3A4 gene. The response rate（RR） and disease control rate（DCR） of wild-type group were 40.6% and 84.4%, while in mutation group they were 33.3% and 85.7%, respectively, with no significances between the two groups（P 0.05）. Of all 53 cases, the median progression-free survival（PFS） was 6.5 months（95% CI： 3.576–9.424 months）, and the median overall survival（OS） was 11.0 months（95% CI： 6.955–15.045 months）. The median PFS and OS in wild-type group had no differences compared with those in mutation group（7.0 months vs. 7.0 months, P 0.05; 10.0 months vs. 14.0 months, P 0.05）. Between wild-type and mutation groups, the median PFS of patients applied with oxaliplatin containing regimen and the median OS in patients applied with/without oxaliplatin had no significant differences（P 0.05）, while the median PFS in patients received non-oxaliplatin regime had statistical differences（P = 0.024）. The median PFS and OS in patients receiving 3-drug or 2-drug regimes had no correlation with CYP3A4 gene polymorphisms. The adverse effects in the two groups were mild, mainly in grades 1–2. The common adverse effects were anorexia, nausea/vomiting and leucopenia. Conclusion： Deletion mutation was located in     

Mitochondrial DNA mutations---candidate biomarkers for breast cancer diagnosis in Bangladesh

Breast cancer is a major health problem that affects more than 24% of women in Bangladesh. Furthermore, among low-income countries including Bangladesh, individuals have a high risk for developing breast cancer. This study aimed to identify candidate mitochondrial DNA (mtDNA) biomarkers for breast cancer diagnosis in Bangladeshi women to be used as a preventive approach. We screened the blood samples from 24 breast cancer patients and 20 healthy controls to detect polymorphisms in the D-loop and the ND3-and ND4-coding regions of mtDNA by direct sequencing. Among 14 distinct mutations, 10 polymorphisms were found in the D-loop, 3 were found in the ND3-coding region, and 1 was found in the ND4-coding region. The frequency of two novel polymorphisms in the D-loop, one at position 16290 (Tins) and the other at position 16293 (A-del), was higher in breast cancer patients than in control subjects (position 16290: odds ratio = 6.011, 95% confidence interval = 1.2482 to 28.8411, P = 0.002; position 16293: odds ratio = 5.6028, 95% confidence interval = 1.4357 to 21.8925, P = 0.010). We also observed one novel mutation in the ND3-coding region at position 10316 (A > G) in 69% of breast cancer patients but not in control subjects. The study suggests that two novel polymorphisms in the D-loop may be candidate biomarkers for breast cancer     

CYP1A1基因多态性与p16基因甲基化对中国人肺癌发病的影响

Objective:To investigate the relationship between the genetic polymorphism of CYP1A1 and the genetic susceptibility to lung cancer as well as to study the effects of the methylation in p16 gene on the risk of lung cancer in a Chinese population.Methods:A case control study was conducted among 47 cases of lung cancer and 94 controls.The genetic polymorphism of CYP1A1 was tested with method of PCR-RFLP,and a methylation-specific PCR(MSP)was performed to detect p16 methylation.Results:It showed that there was no significant difference in frequencies of the genotypes of CYP1A1 between the two groups(P>0.05).Synergistic effects were not found between smoking and CYP1A1.Methylated p16 gene was found in 44.7%(21/47)of lung cancer tissues and in 17.0%(8/47)of normal lung tissues with significant difference(P< 0.05).Conclusion:The genetic polymorphism of CYP1A1 does not increase the risk of lung cancer in a Chinese population. The methylation in p16 gene may be the most common mechanism to inactivate p16 gene in lung cancer,and is not significantly associated with genotype of CYP1A1.     

Comparison of Cancer Incidence between China and the USA

Objective The incidence of cancer varies around the globe,especially between less-developed and developed regions.The aim of this study is to explore differences in cancer incidence between China and the USA. Methods Data were obtained from the GLOBOCAN 2008 database.Estimated numbers of new cancer cases in the USA were obtained from the American Cancer Society,while the numbers of cases in China,including those in urban and rural areas,were obtained from 36 cancer registries(2003-2005).Cancer incidence for major sites between China and the USA were analyzed. Results In China,lung cancer was the predominant type of cancer detected in males;in females,breast cancer was the main type of cancer.Gastrointestinal cancers,such as those of the liver,stomach,and esophagus,were more commonly seen in China than in the USA.A significant difference in the incidence of melanoma of the skin was observed between China and the USA.During comparison of differences in the age-standardized rates by world population(ASRWs) of major cancer sites between the two countries,4 sites in males(i.e.,nasopharynx,esophagus,stomach,and liver) and 6 sites in females(i.e.,nasopharynx,esophagus,stomach,liver, gallbladder,and cervix uteri) showed higher cancer incidence rates in China than in the USA. Conclusions Significant differences in cancer incidence sites were found between the two countries.Cancer may be prevented through public education and awareness.Programs to promote cancer prevention in China,especially those of the lung,breast,and gastrointestinal region,must also be implemented.     

Debate about TGFBR1 and the susceptibility to colorectal cancer

Recent years have witnessed enormous progress in our understanding of the genetic predisposition to colorectal cancer (CRC). Estimates suggest that all or most genetic susceptibility mechanisms proposed so far, ranging from high-penetrance genes to low-risk alleles, account for about 60% of the population-attributable fraction of CRC predisposition. In this context, there is increasing interest in the gene encoding the transforming growth factor β receptor 1 (TGFBR1 ); first when over a decade ago a common polymorphism in exon 1 (rs11466445, TGFBR1 *6A/9A) was suggested to be a risk allele for CRC, then when linkage studies identified the chromosomal region where the gene is located as susceptibility locus for familial CRC, and more recently when the allele-specific expression (ASE) of the gene was proposed as a risk factor for CRC. Published data on the association of TGFBR1 with CRC, regarding polymorphisms and ASE and including sporadic and familial forms of the disease, are often contradictory. This review gives a general overview of the most relevant studies in order to clarify the role of TGFBR1 in the field of CRC genetic susceptibility.     

Helicobacter pylori associated Asian enigma: Does diet deserve distinction?

Helicobacter pylori(H. pylori) is one of the most widespread infections in humans worldwide that chronically infects up to 50% of the world’s population. The infection is involved in the pathogenesis of chronic active gastritis, peptic ulcer, mucosa-associated lymphoid tissue lymphoma and gastric cancer, therefore, it has been classified as class Ⅰ definite carcinogen by the World Health Organization. Despite the established etiological role of H. pylori, its actual distribution and association with related diseases is controversial and there is a large intercountry variation especially among Asian countries. H. pylori infection is more frequent in developing countries like India, Pakistan, and Bangladesh as compared to developed Asian countries like Japan, China and South Korea. However, the frequency of gastric cancer is comparatively lower in India, Pakistan, and Bangladesh with that of Japan, China and South Korea. Such phenomenon of clinical diversity, defined as enigma, is judged by genetic variability of the infecting H. pylori strains, differences in the host genetic background in various ethnic groups, and environmental factors such as dietary habits. Most of the studies have so far focused on the bacterial factor while environmental issues, including dietary components, were not given due attention as one of the factors related with H. pylori associated gastric carcinogenesis. The dietary factor has been suggested to play an important role in H. pylori related carcinogenesis, and in this respect several studies have corroborated the intake of various dietary components as modulatory factors for gastric cancer risk. In this review, such studies, from in vitro experiments to clinical trials, are being focused in detail with respect to enigma associated with H. pylori. It may be conceivably concluded from the available evidence that dietary factor can be a game changer in the scenario of Asian enigma, particularly in high risk population infected with virulent H. pylori strains, however further affirmation studies are desperately needed to achieve conclusive outcomes.     

The effects of CYPIA1 gene polymorphism and p16 gene methylation on the risk of lung cancer in a Chinese population

Objective： To investigate the relationship between the genetic polymorphism of CYP1A1 and the genetic susceptibility to lung cancer as well as to study the effects of the methyiation in p16 gene on the risk of lung cancer in a Chinese population. Methods： A case control study was conducted among 47 cases of lung cancer and 94 controls. The genetic polymorphism of CYP1A1 was tested with method of PCR-RFLP, and a methylation-specific PCR （MSP） was performed to detect p16 methylation. Results： It showed that there was no significant difference in frequencies of the genotypes of CYP1A1 between the two groups （P 〉 0.05）. Synergistic effects were not found between smoking and CYP1AI. Methylated p16 gene was found in 44.7% （21/47） of lung cancer tissues and in 17.0% （8/47） of normal lung tissues with significant difference （P 〈 0.05）. Conclusion： The genetic polymorphism of CYP1A1 does not increase the risk of lung cancer in a Chinese population. The methylation in p16 gene may be the most common mechanism to inactivate p16 gene in lung cancer, and is not significantly associated with genotype of CYP1A1,     

Incidence and mortality of colorectal cancer in China, 2011

Objective: Colorectal cancer is the third most common type of cancer and the fourth leading cause of cancer-related death in the world. This article provides the most up-to-date overview of colorectal cancer burden in China.Methods: Totally 234 cancer registries submitted data of 2011 to the National Central Cancer Registry(NCCR). Qualified data from 177 registries was pooled and analyzed. The crude incidence and mortality rates of colorectal cancer were calculated by age, gender and geographic area. The numbers of new cases and deaths were estimated using the 5-year age-specific cancer incidence/mortality rates and the corresponding populations. China census in 2000 and Segi’s world population were applied for age standardized rates.Results: The estimate of new cases diagnosed with colorectal cancer of China in 2011 was 310,244(178,404 for males and 131,840 for females, 195,117 in urban areas and 115,128 in rural areas), accounting for 9.20% of overall new cancer cases. The crude incidence of colorectal cancer ranked fourth in all cancer sites with rate of 23.03/100,000(25.83/100,000 for males and 20.08/100,000 for female, 28.25/100,000 in urban areas and 17.54/100,000 in rural areas). The age-standardized rates by China population and by World population were 16.79/100,000 and 16.52/100,000, respectively. The estimated number of colorectal cancer deaths of China in 2011 was 149,722(86,427 for males and 63,295 for females, 91,682 in urban areas and 58,040 in rural areas), accounting for 7.09% of overall cancer deaths. The crude mortality rate for colorectal cancer ranked fifth leading cause of cancer-related death in all cancer sites with rate of 11.11/100,000(12.51/100,000 for males and 9.64/100,000 for female, 13.27/100,000 in urban areas and 8.84/100,000 in rural areas). The age-standardized rates by China population and by World population for mortality were 7.77/100,000 and 7.66/100,000, respectively. For both of incidence and mortality, the rates of colorectal cancer were much higher in males than in females, and in rural areas than in urban areas. The rate of colorectal cancer increased greatly with age, especially after 40 or 45 years old.Conclusions: Colorectal cancer is a relative common cancer in China, especially for males in urban areas. Targeted prevention and early detection programs should be carried out.