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  • Mousavi, Seyed Mohsen, et al. (författare)
  • Risk of Kaposi Sarcoma Among Immigrants to Sweden
  • 2014
  • Ingår i: Acta Dermato-Venereologica. - Medical Journals Limited. - 1651-2057. ; 94:4, s. 476-477
  • Tidskriftsartikel (refereegranskat)abstract
    • Kaposi sarcoma (KS) is a locally aggressive endothelial tumour that is classified into 4 clinico-epidemiological forms: classic KS affecting lower limbs in elderly Mediterranean or East European men; endemic KS occurring in extremities among Equatorial African middle-aged men and children; iatrogenic KS involving lower limbs in immunosuppressive patients; and AIDS-associated (epidemic) KS observed among homo- and bisexual HIV-1-infected young men (1, 2). The world-wide epidemiology of KS has changed by spreading of HIV infection (1). For example, KS represented 7% of all cancers in Sub-Saharan African men in the 1960s, whereas in the 1980s the rate increased to 50%. Furthermore, the age distribution of KS has changed from elderly (in classic form) to the late thirties (in epidemic form). KS is a rare tumour in Nordic countries; the incidence is 0.1-0.2/100,000 according to the Cancer Incidence in Five Continents (CI5) report (3). According to this source, the rate in many Asian countries is <0.5/100,000, whereas African American men have a rate of 6.2/100,000. The highest rate is in men from Zimbabwe (52.2/100,000) (3). Human herpesvirus 8 (HHV-8) is the recognised cause of all forms of KS (2). There is discrepancy between the prevalence of HHV-8 and KS incidence in some populations suggesting underreporting of KS or the existance of some unknown protective factors for KS (1). Migrant studies provide data on international differences in cancer rates (4). Furthermore, studies on immigrants may provide supplementary and confirmatory data on the incidence of cancer in countries without local cancer registries. A few available studies on immigrants have focused only on classic KS (5, 6). In the present study, we report mean age at diagnosis and KS rates by site in first-generation immigrants to Sweden.
  • Mousavi, Seyed Mohsen, et al. (författare)
  • Risk of lung cancer by histology among immigrants to Sweden
  • 2012
  • Ingår i: Lung Cancer. - Elsevier. - 1872-8332. ; 76:2, s. 159-164
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We wanted to define lung cancer incidence rates by histological subtype among immigrants in Sweden to explore the effect of new environments on the incidence of lung cancer by histological subtype in different ethnic populations. Methods: The nationwide Swedish Family-Cancer Database w used to calculate age-standardized incidence rates (ASR) (per 100,000) and standardized incidence ratios (SIRs). The patient series covered 19,255 male and 14,601 female Swedes, and 3236 male and 1751 female immigrants. Results: By time since immigration, Former Yugoslavian (ASR = 46.4) and Asian Arab (38.8) men, and Danish (23.3), Norwegian (19.5) and Finnish (14.5) women had the highest rates for lung cancer, while the lowest rate was seen among Asian Arab women (5.8). The highest adenocarcinoma rates were seen among South European men (11.5), and Danish (7.4) and Norwegian (6.9) women, while squamous cell (SCC) and small cell carcinomas rates were the highest among former Yugoslavian (16.0) and Baltic (8.8) men, respectively. Former Yugoslavian men (2.6) had the highest rate for large cell carcinoma. Compared to Swedes, former Yugoslavian men had the highest significant risk for SCC (SIR = 3.62), small cell (3.14) and large cell (4.21) carcinomas, whereas the highest adenocarcinoma risk was seen among Asian Arabs (2.35). Danish women had the highest risks for SCC (1.91) and small cell carcinoma (2.56). Conclusion: The ethnic-specific lung cancer rates by histology followed the rates in the countries of origin. Our findings may suggest that preservation of smoking habits in the host country is linked to the ethnic diversity of lung cancer incidence by histology. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
  • Mousavi, Seyed Mohsen, et al. (författare)
  • Risk of transitional-cell carcinoma of the bladder in first- and second-generation immigrants to Sweden
  • 2010
  • Ingår i: European Journal of Cancer Prevention. - Lippincott Williams & Wilkins. - 1473-5709. ; 19:4, s. 275-279
  • Tidskriftsartikel (refereegranskat)abstract
    • Environmental risk factors, particularly tobacco smoking, are important for transitional-cell carcinoma of the bladder. Studies in migrants may provide valuable insight into the environmental and genetic etiology of cancer. The nationwide Swedish Family-Cancer Database was used to calculate standardized incidence ratios (SIRs) for transitional-cell carcinoma among the immigrants compared with native Swedes. SIRs for lung cancer were also calculated as a proxy for smoking prevalence. Significantly decreased risks of bladder cancer were observed for male (SIR=0.89) and female (0.71) Finns and male East Asian (0.39) first-generation immigrants. Male immigrants from many countries showed increased risks, ranging from 1.18 to 2.29. Only female immigrants from Denmark (1.40) and Norway (1.27) had increased risks. The risks for bladder and lung cancers correlated, except for Finnish and Iranian men. The sons of immigrants born in high-risk countries had an increased SIR (1.51) whereas the daughters of immigrants born in low-risk countries had a decreased risk (0.32). The risk in the second-generation immigrants born in Sweden was equal to that of natives. In conclusion, the observed bladder cancer risks in the first-generation immigrants, the changes in risks in the second-generation immigrants, and the covariation of the risk patterns of bladder and lung cancers suggested a main contribution by tobacco smoking. The exceptional patterns among the Finns and Iranians may point to the existence of modifying factors. The changes in incidence in second-generation immigrants, yet based on small case numbers, lend little support to the involvement of genetic factors. European Journal of Cancer Prevention 19:275-279 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
  • Mousavi, Seyed Mohsen, et al. (författare)
  • Risks of papillary and follicular thyroid cancer among immigrants to Sweden
  • 2011
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 129:9, s. 2248-2255
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies have indicated that ionizing radiation, particularly during childhood, is the main established risk factor for thyroid cancer. History of benign nodules/adenoma, goiter, iodine deficiency or high-iodine intake might be other associated factors. We wanted to define the histology-specific thyroid cancer risk in the first-generation immigrants to Sweden. We used the 2010 update of the nation-wide Swedish Family-Cancer Database (>12 million individuals; 1.8 million immigrants; histology code in force since 1958) to calculate standardized incidence ratios (SIRs) for histology-specific thyroid cancer among immigrants compared to the native Swedes. The patient series covered 2,604 male and 6,406 female Swedes, and 247 and 863 immigrants. The median age at immigration was 29 years, and the median age at thyroid cancer diagnosis was 46 years. Increased risks for female papillary carcinoma were observed for Finns (SIR = 1.63), former Yugoslavians (2.36), Russians (2.34), other East Europeans (2.14), Turks (3.16), Iranians (2.68), Iraqis (2.77), East and Southeast Asians (2.92), other Asians (1.69) and South Americans (2.23). Male Iranians (2.85), East and Southeast Asians (3.57) and other Asians (2.26) had an increased risk for papillary carcinoma. Only male East and Southeast Asians (2.93) had an increased risk for follicular carcinoma. The data might suggest that immigrant populations in Sweden from areas of low or high-iodine intake are at risk of papillary carcinoma, implicating iodine imbalance as a contributing factor to our findings. The increased risk of thyroid cancer among Asian immigrants may confirm the role of childhood-ionizing radiation on thyroid cancer risk.
  • Naccarati, A., et al. (författare)
  • Mutations and polymorphisms in TP53 gene-an overview on the role in colorectal cancer
  • 2012
  • Ingår i: Mutagenesis. - Oxford University Press. - 0267-8357. ; 27:2, s. 211-218
  • Tidskriftsartikel (refereegranskat)abstract
    • A functionally normal TP53 is essential to protect organisms from developing cancer. Somatic mutations in the gene represent one of the highest recurring perturbations in human tumours, including colorectal cancer (CRC). However, the variegated phenotype of wide spectrum of somatic mutations in TP53 and the complexity of the disease prevent a straight interpretation of the mutational analysis in tumours. In addition to the presence of somatic mutations, polymorphic features of the gene may also contribute to alteration of the normal TP53 functioning and variants, mainly in the form of single nucleotide polymorphisms, can be expected to impact susceptibility to sporadic CRC. In the present study, we reviewed the potential role of alterations in the TP53 gene, both somatic mutations and inherited sequence variations, in predisposition to CRC and in the prognosis and response to therapy. The available data from association studies have mostly shown contradictory outcomes. The majority of the studies were based on limited sample sizes and focussed on a limited number of polymorphisms, with main being the rs1042522 (Arg72Pro). Thus far, there is no possible generalisation of the role of TP53 as also a predictor of therapeutic response and prognosis. The effects of TP53, and its abnormalities, on the response of tumours to cytotoxic drugs, radiation and chemoradiation are complex. However, from studies it is emerging that the inherited genetics of TP53 pathway components could be utilised to further define patient populations in their abilities to induce p53 activity in response to either DNA damaging or p53-targeted therapies.
  • Nagore, Eduardo, et al. (författare)
  • TERT promoter mutations in melanoma survival.
  • 2016
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 139:1, s. 75-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Despite advances in targeted therapies, the treatment of advanced melanoma remains an exercise in disease management, hence a need for biomarkers for identification of at risk primary melanoma patients. In this study we aimed to assess the prognostic value of TERT promoter mutations in primary melanomas. DNA from 300 patients with stage I/II melanoma was sequenced for TERT promoter and BRAF/NRAS mutations. Cumulative curves were drawn for patients with and without mutations with progression free and melanoma specific survival as outcomes. Cox proportional hazard regression models were used to determine the effect of the mutations on survivals. Individually, presence of TERT promoter and BRAF/NRAS mutations associated with poor disease free and melanoma specific survival with modification of the effect by the rs2853669 polymorphism within the TERT promoter. Hazard ratio (HR) for simultaneous occurrence of TERT promoter and BRAF/NRAS mutations for disease free survival was 2.25 (95%CI 1.2-4.4) and for melanoma specific survival 5.8 (95%CI 1.8-18.1). The effect of the mutations on melanoma-specific survival in non-carriers of variant allele of the polymorphism was significant (HR 4.4, 95%CI 1.3-14.9) but could not be calculated for the carriers due to low number of events. The variant allele per se showed association with increased survival (HR 0.4, 95%CI 0.1-0.9). The data in this study provides preliminary evidence that TERT promoter mutations in combination with BRAF/NRAS mutations can be used to identify patients at risk of aggressive disease and the possibility of refinement of the classification with inclusion of the rs2853669 polymorphism within TERT promoter. This article is protected by copyright. All rights reserved.
  • Narod, S A, et al. (författare)
  • The risk of contralateral breast cancer in daughters of women with and without breast cancer.
  • 2015
  • Ingår i: Clinical Genetics. - Wiley-Blackwell. - 0009-9163.
  • Tidskriftsartikel (refereegranskat)abstract
    • We aimed to estimate the 15-year and lifetime risks of contralateral breast cancer in breast cancer patients according to the age of diagnosis of the first cancer and the history of breast cancer in the mother. The risks of contralateral breast cancer were estimated for all 78,775 breast cancer patients in the Swedish Family-Cancer Database (age at diagnosis of first breast cancer <70 years). The risk of experiencing a contralateral breast cancer within 15 years of diagnosis was 8.4% [95% confidence interval (CI): 8.1-8.7%] for women with an unaffected mother, was 12% (95%CI: 11-13%) for a woman with a mother with unilateral breast cancer and was 13% (95%CI: 9.5-17%) for women with a mother with bilateral breast cancer. In early-onset diagnosed women (<50 years) with an unaffected mother, the risk of contralateral breast cancer until age 80 was 23% (95%CI: 20-26%) and for late-onset (50-69 years) diagnosed women it was 17% (95%CI: 14-21%). In a woman with a mother with an early-onset unilateral breast cancer, risk of contralateral breast cancer by age 80 was 35% (95%CI: 25-46%). Women with a mother with early-onset bilateral breast cancer had 31% (95%CI: 12-67%) lifetime risk of contralateral breast cancer. The risk of contralateral breast cancer is higher for daughters of breast cancer patients than for daughters of women without breast cancer. Maternal cancer history and age at onset of first breast cancer in women should be taken into account when counseling breast cancer patients about their risk of contralateral breast cancer.
  • Niazi, Yasmeen, et al. (författare)
  • Distinct pathways associated with chromosomal aberration frequency in a cohort exposed to genotoxic compounds compared to general population
  • ????
  • Ingår i: Mutagenesis. - Oxford University Press. - 0267-8357. ; 34:4, s. 323-330
  • Tidskriftsartikel (refereegranskat)abstract
    • Non-specific structural chromosomal aberrations (CAs) observed in peripheral blood lymphocytes of healthy individuals can be either chromosome-type aberrations (CSAs) or chromatid-type aberrations (CTAs) depending on the stage of cell division they are induced in and mechanism of formation. It is important to study the genetic basis of chromosomal instability as it is a marker of genotoxic exposure and a predictor of cancer risk. For that purpose, we conducted two genome-wide association studies (GWASs) on healthy individuals in the presence and absence of apparent genotoxic exposure from the Czech Republic and Slovakia. The pre-GWAS cytogenetic analysis reported the frequencies of CSA, CTA and total CA (CAtot). We performed both linear and binary logistic regression analysis with an arbitrary cut-off point of 2% for CAtot and 1% for CSA and CTA. Using the statistical threshold of 1.0 × 10-5, we identified five loci with in silico predicted functionality in the reference group and four loci in the exposed group, with no overlap between the associated regions. A meta-analysis on the two GWASs identified further four loci with moderate associations in each of the studies. From the reference group mainly loci within genes related to DNA damage response/repair were identified. Other loci identified from both the reference and exposed groups were found to be involved in the segregation of chromosomes and chromatin modification. Some of the discovered regions in each group were implicated in tumourigenesis and autism.
  • Niazi, Yasmeen, et al. (författare)
  • Genetic variation associated with chromosomal aberration frequency : A genome-wide association study
  • 2018
  • Ingår i: Environmental and Molecular Mutagenesis. - John Wiley and Sons Inc.. - 0893-6692.
  • Tidskriftsartikel (refereegranskat)abstract
    • Chromosomal aberrations (CAs) in human peripheral blood lymphocytes (PBL) measured with the conventional cytogenetic assay have been used for human biomonitoring of genotoxic exposure for decades. CA frequency in peripheral blood is a marker of cancer susceptibility. Previous studies have shown associations between genetic variants in metabolic pathway, DNA repair and major mitotic checkpoint genes and CAs. We conducted a genome-wide association study on 576 individuals from the Czech Republic and Slovakia followed by a replication in two different sample sets of 482 (replication 1) and 1288 (replication 2) samples. To have a broad look at the genetic susceptibility associated with CA frequency, the sample sets composed of individuals either differentially exposed to smoking, occupational/environmental hazards, or they were untreated cancer patients. Phenotypes were divided into chromosome- and chromatid-type aberrations (CSAs and CTAs, respectively) and total chromosomal aberrations (CAtot). The arbitrary cutoff point between individuals with high and low CA frequency was 2% for CAtot and 1% for CSA and CTA. The data were analyzed using age, sex, occupation/cancer and smoking history as covariates. Altogether 11 loci reached the P-value of 10−5 in the GWAS. Replication 1 supported the association of rs1383997 (8q13.3) and rs2824215 (21q21.1) in CAtot and rs983889 (5p15.1) in CTA analysis. These loci were found to be associated with genes involved in mitosis, response to environmental and chemical factors and genes involved in syndromes linked to chromosomal abnormalities. Identification of new genetic variants for the frequency of CAs offers prediction tools for cancer risk in future. 2018 Wiley Periodicals, Inc.
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