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Search Results: 1 - 10 of 341 matches for " Parviz Ghadirian "
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Weight History, Smoking, Physical Activity and Breast Cancer Risk among French-Canadian Women Non-Carriers of More Frequent BRCA1/2 Mutations
Vishnee Bissonauth,Bryna Shatenstein,Eve Fafard,Christine Maugard,André Robidoux,Steven Narod,Parviz Ghadirian
Journal of Cancer Epidemiology , 2009, DOI: 10.1155/2009/748367
Abstract: Several lifestyle factors play a significant role in determining an individual's risk of breast cancer. Many of them could be modified to protect against the malignancy. A nested case-control study was conducted to examine the association between selected lifestyle factors and non-BRCA-related breast cancer risk among French-Canadian women. Some 280 women with breast cancer and who were nongene carriers of mutated BRCA gene were recruited as cases. Another 280 women, without any cancer and nongene carriers of mutated BRCA gene served as controls. A tested lifestyle questionnaire was interviewer administered to incident cases to obtain information on weight history, smoking, physical activity, and other lifestyle risk factors. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated in logistic regression models. Comparing cases to controls, breast cancer risk was higher among subjects who reached their maximum body mass index (BMI) at an older age (>50 years) (OR=2.83; 95% CI: 2.34–2.91). A positive association was noted between breast cancer risk and weight gain of >34 lbs compared to weight gain of ≤15 lbs, since the age of 20 (OR=1.68; 95% CI: 1.10–2.58). Weight gain of >24 lbs compared to weight gain of ≤9 lbs, since the age of 30 also resulted in the same relationship (OR=1.96; 95% CI: 1.46–3.06). Similarly, since the age of 40, weight gain of >12 lbs compared to weight gain of ≤1 lb was associated with increased breast cancer risk (OR=1.91; 95% CI: 1.53–2.66). Women who smoked >9 pack-years of cigarettes had a 59% higher breast cancer risk (=.05). Subjects who engaged in >24.8 metabolic-equivalent- (MET-) hours per week compared to ≤10.7 MET-hours per week of moderate physical activity had a 52% (=.01) decreased risk and total physical activity between 16.2 and 33.2 MET-hours per week compared to ≤16.2 MET-hours per week, resulted in a 43% (=.05) lower risk of breast cancer. In conclusion, weight history did affect breast cancer risk. Moreover, smoking appeared to raise the risk, whereas moderate physical activity had a protective effect.
RAD51C germline mutations in breast and ovarian cancer patients
Mohammad R Akbari, Patricia Tonin, William D Foulkes, Parviz Ghadirian, Marc Tischkowitz, Steven A Narod
Breast Cancer Research , 2010, DOI: 10.1186/bcr2619
Abstract: In order to confirm these findings, we sequenced the nine coding exons of RAD51C in the germline DNA of 454 patients with familial breast/ovarian cancer. The mean age at diagnosis of the breast cancers was 44.7 years (range 21 to 65) and the mean age of diagnosis of the ovarian cancers was 47.9 years (range 23 to 60 years). All patients were previously found to be negative for BRCA1 and BRCA2 mutations. Each proband had at least two affected first- or second-degree relatives. Eighty-five percent of the families contained at least one case of ovarian cancer. One-hundred patients were Jewish, 152 were French-Canadian and 202 were of various other ethnic origins. All subjects provided written informed consent to participate in the study. The study protocol was approved by the ethics committee of the Women's College Research Institute, protocol number 2007-0036-B.We found no deleterious RAD51C mutation among the 454 patients. We found a novel c.146-8A > G splicing variant in three of 100 Jewish breast cancer patients, but this variant was also present in 12 of 190 Jewish controls. In addition, we found one polymorphic missense variant (p.126Ala > Thr or rs61758784) in three patients and one (p.287Thr > Ala or rs28363317) in four patients. Based on the prevalence of mutations in the initial report [2], we expected to identify approximately five families with a deleterious germline RAD51C mutation. It is of interest that the mutations in the German families were all different, and therefore the discrepant results cannot be explained by the presence of RAD51C founder alleles in Germany. Perhaps RAD51C mutations are not as common as the initial report suggests.The authors declare that they have no competing interests.
Haplotype analysis of TP53 polymorphisms, Arg72Pro and Ins16, in BRCA1 and BRCA2 mutation carriers of French Canadian descent
Luca Cavallone, Suzanna L Arcand, Christine Maugard, Parviz Ghadirian, Anne-Marie Mes-Masson, Diane Provencher, Patricia N Tonin
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-96
Abstract: The frequencies of the TP53 alleles, genotypes and haplotypes of 157 index breast cancer cases comprised of 42 BRCA1 mutation carriers, 57 BRCA2 mutation carriers, and 58 BRCA mutation-negative cases, where each case was drawn from independently ascertained families were compared. The effect of TP53 variants on the age of diagnosis was also investigated for these groups. The TP53 polymorphisms were also investigated in 112 women of French Canadian descent with no personal history of cancer.The BRCA mutation-positive groups had the highest frequency of homozygous carriers of the 72Pro allele compared with mutation-negative group. The TP53 polymorphisms exhibited linkage disequilibrium (p < 0.001), where the 72Arg and Ins16minus alleles occurred in strong disequilibrium. The highest frequency of carriers of Ins16minus-72Arg haplotype occurred in the BRCA mutation-negative groups. The BRCA1 mutation carriers homozygous for the 72Pro allele had the youngest ages of diagnosis of breast cancer. However none of these observations were statistically significant. In contrast, the BRCA2 mutation carriers homozygous for the 72Pro allele had a significantly older age of diagnosis of breast cancer (p = 0.018). Moreover, in this group, the mean age of diagnosis of breast cancer in carriers of the Ins16minus-72Arg haplotype was significantly younger than that of the individuals who did not this carry this haplotype (p = 0.009).We observed no significant association of breast cancer risk with TP53 genetic variants based on BRCA1/2 mutation carrier status. Although the small sample size did not permit analysis of all possible haplotypes, we observed that BRCA2 mutation carriers harboring the Ins16minus-72Arg haplotype had a significantly younger mean age of diagnosis of breast cancer. These observations suggest that investigations in a larger French Canadian sample are warranted to further elucidate the effects of TP53 variants on age of diagnosis of breast cancer among BRCA1 and BR
Human Infection with Uncinaria in North of Iran
E Ghadirian
Iranian Journal of Parasitology , 2007,
Abstract: NO ABSTRACT
Identification of a novel CHEK2 variant and assessment of its contribution to the risk of breast cancer in French Canadian women
David J Novak, Long Chen, Parviz Ghadirian, Nancy Hamel, Phil Zhang, Vanessa Rossiny, Guy Cardinal, André Robidoux, Patricia N Tonin, Francois Rousseau, Steven A Narod, William D Foulkes
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-239
Abstract: The 14 coding exons of CHEK2 were fully sequenced for variant alleles in a panel of 25 affected French Canadian women and 25 healthy controls. Two variants were identified of which one novel variant was further screened for in an additional panel of 667 breast cancer patients and 6548 healthy controls. Additional genotyping was conducted using allele specific PCR and a restriction digest assay. Significance of amino acid substitutions were deduced by employing comparative analysis techniques.Two variants were identified: the previously reported silent substitution 252A>G (E84E) and the novel missense variant, 1217G>A (R406H). No significant difference in allele distribution between French Canadian women with breast cancer and healthy controls was observed (3/692, 0.43% vs. 22/6573, 0.33%, respectively, P = 0.73).The novel CHEK2 missense variant identified in this study, R406H, is unlikely to contribute to breast cancer risk in French Canadian women.Breast cancer is the most common form of malignancy amongst females in the western world. Specifically, one in ten of all new diagnosed cancer cases are of the female breast [1]. Typically, less than five percent of these cases are inherited in a mendelian fashion, specifically from the segregation of highly penetrant alleles, such as mutations in BRCA1 and BRCA2 [2]. The existence of a large number of breast cancer families who lack linkage to either BRCA1 or BRCA2 [3] suggested that other breast cancer susceptibility genes remained undiscovered. One such candidate gene, CHEK2, encodes a multifunctional kinase enzyme involved in the induction of cell cycle arrest, DNA repair and apoptosis [4-6]. Several large-scale studies have characterized known variants of the CHEK2 gene [7-9], conclusively proving that CHEK2 is a breast cancer susceptibility gene.One CHEK2 mutation present in the general population, 1100delC, occurs independently of BRCA1/2 mutations [7,8]. The 1100delC variant results in a premature stop codon withi
Haplotype analysis suggest common founders in carriers of the recurrent BRCA2 mutation, 3398delAAAAG, in French Canadian hereditary breast and/ovarian cancer families
Kathleen K Oros, Guy Leblanc, Suzanna L Arcand, Zhen Shen, Chantal Perret, Anne-Marie Mes-Masson, William D Foulkes, Parviz Ghadirian, Diane Provencher, Patricia N Tonin
BMC Medical Genetics , 2006, DOI: 10.1186/1471-2350-7-23
Abstract: The frequency was estimated by assaying the mutation in series of French Canadian breast cancer cases diagnosed before age 41 (n = 60) or 80 (n = 127) years of age, and ovarian cancer cases (n = 80) unselected for family history of cancer by mutation analysis. Haplotype analysis was performed to determine if mutation carriers shared a common ancestry. Members from 11 families were analyzed using six polymorphic microsatellite markers (cen-D13S260-D13S1699-D13S1698-D13S1697-D13S1701-D13S171-tel) spanning approximately a 3.6 cM interval at the chromosomal region 13q13.1, which contains BRCA2. Allele frequencies were estimated by genotyping 47 unaffected female individuals derived from the same population. Haplotype reconstruction of unaffected individuals was performed using the program PHASE.The recurrent BRCA2 mutation occurred in 1 of 60 (1.7%) women diagnosed with breast cancer before 41 years of age and one of 80 (1.3%) women with ovarian cancer. No mutation carriers were identified in the series of breast cancer cases diagnosed before age 80. Mutation carriers harboured one of two haplotypes, 7-3-9-3 – [3/4]-7, that varied with marker D13S1701 and which occurred at a frequency of 0.001. The genetic analysis of D13S1695, a polymorphic marker located approximately 0.3 cM distal to D13S171, did not favour a genetic recombination event to account for the differences in D13S1701 alleles within the haplotype. Although mutation carriers harbour genotypes that are frequent in the French Canadian population, neither mutation-associated haplotype was plausible in reconstructed haplotypes of 47 individuals of French Canadian descent.These results suggest that mutation carriers share a related ancestry; further supporting the concept that recurrent BRCA1 and BRCA2 mutations in the French Canadian population could be attributed to common founders. This finding provides further support for targeted screening of recurrent mutations in this population before large-scale mutatio
Changes in body weight and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers
Joanne Kotsopoulos, Olufunmilayo I Olopade, Parviz Ghadirian, Jan Lubinski, Henry T Lynch, Claudine Isaacs, Barbara Weber, Charmaine Kim-Sing, Peter Ainsworth, William D Foulkes, Andrea Eisen, Ping Sun, Steven A Narod
Breast Cancer Research , 2005, DOI: 10.1186/bcr1293
Abstract: A matched case–control study was conducted in 1,073 pairs of women carrying a deleterious mutation in either BRCA1 (n = 797 pairs) or BRCA2 (n = 276 pairs). Women diagnosed with breast cancer were matched to control subjects by year of birth, mutation, country of residence, and history of ovarian cancer. Information about weight was derived from a questionnaire routinely administered to women who were carriers of a mutation in either gene. Conditional logistic regression was used to estimate the association between weight gain or loss and the risk of breast cancer, stratified by age at diagnosis or menopausal status.A loss of at least 10 pounds in the period from age 18 to 30 years was associated with a decreased risk of breast cancer between age 30 and 49 (odds ratio (OR) = 0.47; 95% confidence interval (CI) 0.28–0.79); weight gain during the same interval did not influence the overall risk. Among the subgroup of BRCA1 mutation carriers who had at least two children, weight gain of more than 10 pounds between age 18 and 30 was associated with an increased risk of breast cancer diagnosed between age 30 and 40 (OR = 1.44, 95% CI 1.01–2.04). Change in body weight later in life (at age 30 to 40) did not influence the risk of either premenopausal or postmenopausal breast cancer.The results from this study suggest that weight loss in early adult life (age 18 to 30) protects against early-onset BRCA-associated breast cancers. Weight gain should also be avoided, particularly among BRCA1 mutation carriers who elect to have at least two pregnancies.The inheritance of a deleterious mutation in either of the two breast cancer susceptibility genes, BRCA1 or BRCA2, has been associated with a lifetime risk of breast cancer of 45% to 87% [1,2]. Reports of increasing penetrance among women born in recent cohorts in comparison with those born in earlier years has prompted the search for factors that may influence the risk of cancer in genetically susceptible women [2-5]. To date, bo
Identification of a novel truncating PALB2 mutation and analysis of its contribution to early-onset breast cancer in French-Canadian women
William D Foulkes, Parviz Ghadirian, Mohammed Akbari, Nancy Hamel, Sylvie Giroux, Nelly Sabbaghian, Andrew Darnel, Robert Royer, Aletta Poll, Eve Fafard, André Robidoux, Ginette Martin, Tarek A Bismar, Marc Tischkowitz, Francois Rousseau, Steven A Narod
Breast Cancer Research , 2007, DOI: 10.1186/bcr1828
Abstract: We screened all coding exons of PALB2 in a sample of 50 French-Canadian women diagnosed with either early-onset breast cancer or familial breast cancer at a single Montreal hospital. The genetic variants identified in this sample were then studied in 356 additional women with breast cancer diagnosed before age 50 and in 6,448 newborn controls.We identified a single protein-truncating mutation in PALB2 (c.2323 C>T, resulting in Q775X) in 1 of the 50 high-risk women. This variant was present in 2 of 356 breast cancer cases and in none of 6,440 newborn French-Canadian controls (P = 0.003). We also identified two novel new non-synonymous single nucleotide polymorphisms in exon 4 of PALB2 (c.5038 A>G [I76V] and c.5156 G>T [G115V]). G115V was found in 1 of 356 cases and in 15 of 6,442 controls (P = 0.6). The I76V variant was not identified in either the extended case series or the controls.We have identified a novel truncating mutation in PALB2. The mutation was found in approximately 0.5% of unselected French-Canadian women with early-onset breast cancer and appears to have a single origin. Although mutations are infrequent, PALB2 can be added to the list of breast cancer susceptibility genes for which founder mutations have been identified in the French-Canadian population.Approximately 3% to 5% of breast cancer is estimated to be due to a dominantly inherited gene, and two breast cancer genes, BRCA1 and BRCA2, account for approximately 85% of families with four or more cases of breast and ovarian cancer [1]. Soon after these genes were discovered, it became apparent that specific founder mutations in these genes were present in different ethnic groups [2,3], including individuals of French-Canadian descent [4]. Five founder mutations account for 75% to 85% of all BRCA1/2 mutations in the French-Canadian population of Quebec [5,6]. However, for approximately one half of strongly hereditary breast cancer families, no BRCA1/2 mutation has been identified and other genes a
Effect of Prior Bilateral Oophorectomy on the Presentation of Breast Cancer in BRCA1 and BRCA2 Mutation Carriers
Kelly A Metcalfe, William D Foulkes, Henry T Lynch, Parviz Ghadirian, Nadine Tung, Ivo A Olivotto, Ellen Warner, Olufunmilayo Olopade, Andrea Eisen, Barbara Weber, Jane McLennan, Ping Sun, Steven A Narod
Hereditary Cancer in Clinical Practice , 2005, DOI: 10.1186/1897-4287-3-2-53
Abstract: Women with a BRCA1 or BRCA2 mutation with the diagnosis of invasive breast cancer were identified from ten cancer genetics clinics. The medical history, medical treatment records and pathology reports for the breast cancers were reviewed. Information was abstracted from medical charts, including history (and date) of oophorectomy, date of breast cancer diagnosis, stage of disease, and pathologic characteristics of the breast cancer. Women with prior bilateral oophorectomy were matched by age, year of diagnosis, and mutation with one or more women who had two intact ovaries at the time of breast cancer diagnosis. Characteristics of the breast tumours were compared between the two groups.Women with prior bilateral oophorectomy presented with smaller tumours on average compared to women without prior oophorectomy (mean size 1.50 cm vs. 1.95 cm; p = 0.01). Additionally, although not statistically significant, women with intact ovaries were more likely to have high-grade tumour (70% vs. 54%: p = 0.10) and to have positive lymph nodes (34% vs. 18%; p = 0.11) compared to women with prior bilateral oophorectomy.Bilateral oophorectomy prior to breast cancer appears to favourably influence the biological presentation of breast cancer in BRCA1 and BRCA2 mutation carriers.Women with a BRCA1 or BRCA2 mutation have up to an 87% lifetime risk of developing invasive breast cancer [1]. The surgical removal of the ovaries in women with a BRCA1 or BRCA2 mutation has been shown to reduce the risk of developing breast cancer [2]. Nevertheless, some women who have had bilateral oophorectomy go on to develop breast cancer. Previous research has suggested that there may be an association between menopausal status and prognostic features of breast cancer [3], but this association has not been studied in women with a BRCA1 or BRCA2 mutation.Women with a BRCA1 or BRCA2 mutation are encouraged to consider the option of prophylactic oophorectomy to prevent both breast and ovarian cancers. The r
Price and Income Elasticities of Gasoline Demand in Iran: Using Static, ECM, and Dynamic Models in Short, Intermediate, and Long Run  [PDF]
Vahid Mohamad Taghvaee, Parviz Hajiani
Modern Economy (ME) , 2014, DOI: 10.4236/me.2014.59087
Abstract:

Price and income elasticities of gasoline demand show whether the price policy, pursued by the Iranian government, can decrease the high gasoline consumption sufficiently or not. Since the two oil price shocks in 1970 and 1973, interest in the study of oil products demand has increased considerably, especially on gasoline. High gasoline consumption is a serious crisis in Iran, posing economically, politically, and environmentally threats. In this study, the elasticities are estimated over three intervals, short run, intermediate run, and long run in Iran during 1976-2010, by putting the estimates of Error Correction Model (ECM), static model, and dynamic model in an increasing order, respectively. The short run, intermediate run, and long run price elasticities are -0.1538, -0.1618, and -0.3612 and the corresponding income elasticities are 0.2273 - 0.3581, 0.4636, and 0.7284, respectively. Not only do these elasticities imply that the gasoline demand is price and income inelastic but also the adjustment velocity, estimated by ECM, is a low point at -0.1942. Based on the estimations, the gasoline demand responds to the changes of price and income slightly and slowly. Therefore, policy makers should develop more strategies to reduce gasoline consumption, for example, substitute goods, public transportation systems, and environmental standards settings.

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