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Munari FF, Dos Santos W, Evangelista AF, Carvalho AC, Pastrez PA, Bugatti D, Wohnrath DR, Scapulatempo-Neto C, Guimarães DP, Longatto-Filho A, Reis RM. Profile of esophageal squamous cell carcinoma mutations in Brazilian patients. Sci Rep 2021; 11:20596. [PMID: 34663841 PMCID: PMC8523676 DOI: 10.1038/s41598-021-00208-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2021] [Accepted: 10/08/2021] [Indexed: 12/24/2022] Open
Abstract
Esophageal cancer is an aggressive tumor that has a high rate of incidence and mortality worldwide. It is the 10th most frequent type in Brazil, being squamous cell carcinoma (ESCC) the predominant subtype. There is currently an incessant search to identify the frequently altered genes associated with esophageal squamous cell carcinoma biology that could be druggable. This study aimed to analyze the somatic mutation profile of a large panel of cancer-related genes in Brazilian ESCC. In a series of 46 ESCC diagnoses at Barretos Cancer Hospital, DNA isolated from paired fresh-frozen and blood tissue, a panel of 150 cancer-related genes was analyzed by next-generation sequencing. The genes with the highest frequency of mutations were TP53 (39/46, 84.8%), followed by NOTCH1 (7/46, 15.2%), NFE2L2 (5/46, 10.8%), RB1 (3/46, 6.5%), PTEN (3/46, 6.5%), CDKN2A (3/46, 6.5%), PTCH1 (2/46, 4.3%) and PIK3CA (2/46, 4.3%). There was no significant association between molecular and patients' clinicopathological features. Applying an evolutionary action score of p53 (EAp53), we observed that 14 (35.9%) TP53 mutations were classified as high-risk, yet no association with overall survival was observed. Concluding, this the largest mutation profile of Brazilian ESCC patients, which helps in the elucidation of the major cancer-related genes in this population.
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Affiliation(s)
- Fernanda Franco Munari
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil
| | - Wellington Dos Santos
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil
| | - Adriane Feijó Evangelista
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil
| | - Ana Carolina Carvalho
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil
| | - Paula Aguiar Pastrez
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil
| | - Diego Bugatti
- Department of Upper Digestive, Barretos Cancer Hospital, Barretos, Brazil
| | - Durval R Wohnrath
- Department of Upper Digestive, Barretos Cancer Hospital, Barretos, Brazil
| | - Cristovam Scapulatempo-Neto
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil.,Department of Pathology, Barretos Cancer Hospital, Barretos, Brazil
| | - Denise Peixoto Guimarães
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil.,Department of Endoscopy, Barretos Cancer Hospital, Barretos, Brazil
| | - Adhemar Longatto-Filho
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil.,Medical Laboratory of Medical Investigation (LIM) 14, Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil.,Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.,ICVS/3B's-PT Government Associate Laboratory, Braga, Guimarães, Portugal
| | - Rui Manuel Reis
- Molecular Oncology Research Center, Barretos Cancer Hospital, Antenor Duarte Villela, 1331, Barretos, São Paulo, 14784 400, Brazil. .,Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal. .,ICVS/3B's-PT Government Associate Laboratory, Braga, Guimarães, Portugal.
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Yi M, Wu X, Zhuang W, Xia L, Chen Y, Zhao R, Wan Q, Du L, Zhou Y. Tea Consumption and Health Outcomes: Umbrella Review of Meta-Analyses of Observational Studies in Humans. Mol Nutr Food Res 2019; 63:e1900389. [PMID: 31216091 DOI: 10.1002/mnfr.201900389] [Citation(s) in RCA: 64] [Impact Index Per Article: 10.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/29/2019] [Revised: 05/26/2019] [Indexed: 02/05/2023]
Abstract
SCOPE The aim of this article is to conduct an umbrella review to study the strength and validity of associations between tea consumption and diverse health outcomes. METHODS AND RESULTS Meta-analyses of observational studies examining associations between tea consumption and health outcomes in all human populations and settings are screened. The umbrella review identifies 96 meta-analyses with 40 unique health outcomes. Tea consumption shows greater benefits than harm to health in this review. Dose-response analyses of tea consumption indicates reduced risks of total mortality, cardiac death, coronary artery disease, stroke, and type 2 diabetes mellitus with increment of two to three cups per day. Beneficial associations are also found for several cancers, skeletal, cognitive, and maternal outcomes. Harmful associations are found for esophageal and gastric cancer when the temperature of intake is more than 55-60 °C. CONCLUSION Tea consumption, except for very hot tea, seems generally safe at usual levels of intake, with summary estimates indicating the largest reduction for diverse health outcomes at two to three cups per day. Generally, tea consumption seems more beneficial than harmful in this umbrella review. Randomized controlled trials are further needed to understand whether the observed associations are causal.
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Affiliation(s)
- Mengshi Yi
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Xiaoting Wu
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Wen Zhuang
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Lin Xia
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Yi Chen
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Rui Zhao
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Qianyi Wan
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Liang Du
- Chinese Evidence-Based Medicine/Cochrane Center, Chengdu, 610041, China
| | - Yong Zhou
- Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China
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Amorim CA, De Souza LP, Moreira JP, Luiz RR, De V. Carneiro AJ, De Souza HSP. Geographic distribution and time trends of esophageal cancer in Brazil from 2005 to 2015. Mol Clin Oncol 2019; 10:631-638. [PMID: 31086670 PMCID: PMC6488946 DOI: 10.3892/mco.2019.1842] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2018] [Accepted: 04/05/2019] [Indexed: 12/18/2022] Open
Abstract
The purpose of the present study was to investigate the geographical distribution and time trends of the incidence and lethality of esophageal cancer (EC) in Brazil. The present study conducted an ecological study of EC using records from January 2005 to December 2015 in the Health Informatics Department of the Brazilian Ministry of Health (DATASUS) registry. In addition to demographical data on the population, EC incidence and lethality rates were estimated from hospitalizations and in-hospital mortalities and were adjusted by total available hospital beds. The adjusted EC rates per 100,000 increased from 9.1 in 2005 to 12.1 in 2015. The prevalence among males increased from 69 to 78%, while the female rates remained stable over the same period. Although EC was the most common in South and Southeast Brazil, the rates increased proportionately more in the other regions of the country, especially among males. Geographical analysis revealed higher rates of EC in more urbanized areas, with a coast-to-inland gradient. While rates increased in people older than 50 years, they decreased among people below this age. However, the lethality rates remained stable and high during the study period, overlapping with hospital admission rates. The recent increasing trend in the EC incidence, with shifts from the south towards the north and from more urbanized towards rural areas, suggests that environmental factors are crucial in EC pathogenesis. The concentration of EC in South Brazil may reflect the presence of major environmental factors in association with a possible genetic predisposition. The unchanging high mortality associated with EC in the rapidly aging population suggests that EC will continue to impose a significant social and economic burden in the future.
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Affiliation(s)
- César Augusto Amorim
- Department of Internal Medicine, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
| | - Lucila Perrota De Souza
- Department of Internal Medicine, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
| | - Jessica P. Moreira
- Institute of Public Health Studies, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
| | - Ronir R. Luiz
- Institute of Public Health Studies, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
| | - Antonio José De V. Carneiro
- Department of Internal Medicine, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
| | - Heitor S. P. De Souza
- Department of Internal Medicine, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, Brazil
- D'Or Institute for Research and Education (IDOR), Rio de Janeiro 22281-100, Brazil
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Murphy G, McCormack V, Abedi-Ardekani B, Arnold M, Camargo MC, Dar NA, Dawsey SM, Etemadi A, Fitzgerald RC, Fleischer DE, Freedman ND, Goldstein AM, Gopal S, Hashemian M, Hu N, Hyland PL, Kaimila B, Kamangar F, Malekzadeh R, Mathew CG, Menya D, Mulima G, Mwachiro MM, Mwasamwaja A, Pritchett N, Qiao YL, Ribeiro-Pinto LF, Ricciardone M, Schüz J, Sitas F, Taylor PR, Van Loon K, Wang SM, Wei WQ, Wild CP, Wu C, Abnet CC, Chanock SJ, Brennan P. International cancer seminars: a focus on esophageal squamous cell carcinoma. Ann Oncol 2017; 28:2086-2093. [PMID: 28911061 PMCID: PMC5834011 DOI: 10.1093/annonc/mdx279] [Citation(s) in RCA: 142] [Impact Index Per Article: 17.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
The International Agency for Research on Cancer (IARC) and the US National Cancer Institute (NCI) have initiated a series of cancer-focused seminars [Scelo G, Hofmann JN, Banks RE et al. International cancer seminars: a focus on kidney cancer. Ann Oncol 2016; 27(8): 1382-1385]. In this, the second seminar, IARC and NCI convened a workshop in order to examine the state of the current science on esophageal squamous cell carcinoma etiology, genetics, early detection, treatment, and palliation, was reviewed to identify the most critical open research questions. The results of these discussions were summarized by formulating a series of 'difficult questions', which should inform and prioritize future research efforts.
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Affiliation(s)
- G. Murphy
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | | | | | - M. Arnold
- Cancer Surveillance, International Agency for Research on Cancer, Lyon, France
| | - M. C. Camargo
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - N. A. Dar
- Department of Biochemistry, University of Kashmir, Hazratbal, Srinagar, Jammu and Kashmir, India
| | - S. M. Dawsey
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - A. Etemadi
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - R. C. Fitzgerald
- MRC Cancer Unit, Hutchison-MRC Research Centre, University of Cambridge, Cambridge, UK
| | - D. E. Fleischer
- Department of Internal Medicine, Mayo Clinic, Scottsdale, Arizona, USA
| | - N. D. Freedman
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - A. M. Goldstein
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - S. Gopal
- University of North Carolina Project-Malawi, Lilongwe, Malawi
| | - M. Hashemian
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - N. Hu
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - P. L. Hyland
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - B. Kaimila
- University of North Carolina Project-Malawi, Lilongwe, Malawi
| | - F. Kamangar
- Department of Public Health Analysis, School of Community Health and Policy, Morgan State University, Baltimore, Maryland, USA
| | - R. Malekzadeh
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - C. G. Mathew
- Department of Medical and Molecular Genetics, Kings College London
- Sydney Brenner Institute for Molecular Bioscience, University of Witwatersrand, Johannesburg, South Africa
| | - D. Menya
- School of Public Health, Moi University, Eldoret, Kenya
| | - G. Mulima
- University of North Carolina Project-Malawi, Lilongwe, Malawi
| | | | - A. Mwasamwaja
- Kilimanjaro Christian Medical Centre, Moshi, Tanzania
| | - N. Pritchett
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - Y.-L. Qiao
- Department of Etiology and Carcinogenesis & Department of Cancer Epidemiology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
| | - L. F. Ribeiro-Pinto
- Molecular Carcinogenesis Program, Institute Nacional de Cancer, Sao Paulo, Brazil
| | - M. Ricciardone
- National Cancer Institute, Center for Global Health, National Institutes of Health, Bethesda, Maryland, USA
| | - J. Schüz
- Section of Environment and Radiation
| | - F. Sitas
- School of Public Health, University of Sydney, New South Wales, Australia
- School of Public Health & Community Medicine, University of New South Wales, Sydney, Australia
| | - P. R. Taylor
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - K. Van Loon
- Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California, USA
| | - S.-M. Wang
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
- Department of Etiology and Carcinogenesis & Department of Cancer Epidemiology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
| | - W.-Q. Wei
- Department of Etiology and Carcinogenesis & Department of Cancer Epidemiology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
| | - C. P. Wild
- Director's office, International Agency for Research on Cancer, Lyon, France
| | - C. Wu
- Department of Etiology and Carcinogenesis & Department of Cancer Epidemiology, Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
| | - C. C. Abnet
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
| | - S. J. Chanock
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda Maryland, USA
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5
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Lacerda CF, Cruvinel-Carloni A, de Oliveira ATT, Scapulatempo-Neto C, López RVM, Crema E, Adad SJ, Rodrigues MAM, Henry MACA, Guimarães DP, Reis RM. Mutational profile of TP53 in esophageal squamous cell carcinoma associated with chagasic megaesophagus. Dis Esophagus 2017; 30:1-9. [PMID: 28375484 DOI: 10.1093/dote/dow040] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/07/2016] [Accepted: 12/30/2016] [Indexed: 02/07/2023]
Abstract
Chaga's disease is an important communicable neglected disease that is gaining wider attention due to its increasing incidence worldwide. Achalasia due to chagasic megaesophagus (CM), a complication of this disease, is a known-yet, poorly understood-etiological factor for esophageal squamous cell carcinoma (ESCC) development. In this study, we aimed to perform the analysis of TP53 mutations in a series of Brazilian patients with ESCC that developed in the context CM (ESCC/CM), and to compare with the TP53 mutation profile of patients with benign CM and patients with nonchagasic ESCC. Additionally, we intended to correlate the TP53 mutation results with patient's clinical pathological features. By polymerase chain reaction (PCR) followed by direct sequencing of the hotspot regions of TP53 (exon 5 to 8), we found that TP53 mutations were present in 40.6% (13/32) of the ESCC/CM group, 45% (18/40) of the nonchagasic ESCC group, and in only 3% (1/33) of the benign CM group. Missense mutations were the most common in the three groups, yet, the type and mutated exon mutation varied significantly among the groups. Clinically, the groups exhibited distinct features, with both cancer groups (ESCC and ESCC/CM) been significantly associated higher consumption of alcohol and tobacco, older age, worse Karnofsky performance status, poor outcome than the patients with benign CM. No significant association was found between TP53 mutation profile and clinical-pathological features in any of the three groups. We describe first the time the analysis of TP53 mutations in ESCC that developed in the context of CM, and the observed high frequency of mutations, suggest that TP53 also plays an important role in the tumorigenic process of this unexplored etiological condition.
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Affiliation(s)
- C F Lacerda
- Department of Digestive Surgery, Barretos Cancer Hospital, Barretos, São Paulo, Brazil.,Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil
| | - A Cruvinel-Carloni
- Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil
| | | | - C Scapulatempo-Neto
- Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil.,Department of Pathology, Barretos Cancer Hospital, Barretos, São Paulo, Brazil
| | - R V M López
- Centre for Researcher Support, Barretos Cancer Hospital, Barretos, São Paulo, Brazil
| | - E Crema
- Department of Digestive Surgery and Pathology, Medical School, UFTM -Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil
| | - S J Adad
- Department of Digestive Surgery and Pathology, Medical School, UFTM -Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil
| | - M A M Rodrigues
- Department of Gastroenterology Surgery and Pathology, Medical School, UNESP - São Paulo State University, Botucatu, São Paulo, Brazil
| | - M A C A Henry
- Department of Gastroenterology Surgery and Pathology, Medical School, UNESP - São Paulo State University, Botucatu, São Paulo, Brazil
| | - D P Guimarães
- Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil.,Department of Endoscopy, Barretos Cancer Hospital, Barretos, São Paulo, Brazil
| | - R M Reis
- Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil.,Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.,ICVS/3B's - PT Government Associate Laboratory, Braga/Guimarães, Portugal
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6
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Sun P, Chen C, Zhang F, Yang H, Bi XW, An X, Wang FH, Jiang WQ. Combined heavy smoking and drinking predicts overall but not disease-free survival after curative resection of locoregional esophageal squamous cell carcinoma. Onco Targets Ther 2016; 9:4257-64. [PMID: 27471400 PMCID: PMC4948733 DOI: 10.2147/ott.s104182] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
INTRODUCTION The prognostic impact of smoking and drinking on esophageal squamous cell carcinoma (ESCC) was scarcely discussed. We investigated the prognostic value of smoking and drinking and their relationships with clinicopathological characteristics in a large cohort of patients with locoregional ESCC. PATIENTS AND METHODS We retrospectively analyzed 488 patients who underwent curative treatment at a single institution between January 2007 and December 2008. A chi-square test was used to evaluate the relationships between smoking and drinking and clinicopathological variables, the Kaplan-Meier method was used for 5-year overall survival (OS) and disease-free survival, and Cox proportional hazards models were applied for univariate and multivariate analyses of variables with respect to OS and disease-free survival. RESULTS Heavy smokers were more likely to have advanced Tumor-Node-Metastases (TNM) stage and higher neutrophil/lymphocyte ratio at diagnosis (P<0.05). Drinkers were more likely to have advanced TNM stage, to present with a larger tumor, and to undergo multidisciplinary treatment (P<0.05). For patients who used neither heavy tobacco nor alcohol, used either tobacco or alcohol, and used both, the 5-year OS rates and OS times were 57.4%, 46.4%, and 39.1% (P<0.05) and not reached, 55.2 months, and 41.2 months (P<0.05), respectively. On multivariate analysis, patients who both heavily smoked and drank had 1.392 times the risk of dying during follow-up compared with neither-users (95% CI =1.020-1.901, P=0.037). CONCLUSION We identified that combined heavy smoking and drinking might predict poor prognosis in ESCC patients.
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Affiliation(s)
- Peng Sun
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Cui Chen
- Department of Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong Province, People's Republic of China
| | - Fei Zhang
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Hang Yang
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Xi-Wen Bi
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Xin An
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Feng-Hua Wang
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
| | - Wen-Qi Jiang
- State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine; Department of Medical Oncology, Sun Yat-Sen University Cancer Center
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Chung CS, Lee YC, Wu MS. Prevention strategies for esophageal cancer: Perspectives of the East vs. West. Best Pract Res Clin Gastroenterol 2015; 29:869-83. [PMID: 26651249 DOI: 10.1016/j.bpg.2015.09.010] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/01/2015] [Accepted: 09/02/2015] [Indexed: 02/06/2023]
Abstract
Esophageal cancer is the eighth most common cancer worldwide. Esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) are the two major phenotypes in Western and Eastern countries, respectively. Because of different pathways in carcinogenesis, the risk factors and effective steps for prevention of esophageal cancer are different between EAC and ESCC. The carcinogenesis of EAC is initiated by the acid exposure of the esophageal mucosa from stomach while that of the ESCC are related to the chronic irritation of carcinogens mainly by the alcohol, cigarette, betel quid, and hot beverage. To eliminate the burden of esophageal cancer on the global health, the effective strategy should be composed of the primary, secondary, and tertiary prevention. In this article, we perform a systematic review of the preventive strategies for esophageal cancer with special emphasis on the differences from the perspectives of Western and Eastern countries.
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Affiliation(s)
- Chen-Shuan Chung
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan; College of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan
| | - Yi-Chia Lee
- Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan
| | - Ming-Shiang Wu
- Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
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8
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Chen Y, Tong Y, Yang C, Gan Y, Sun H, Bi H, Cao S, Yin X, Lu Z. Consumption of hot beverages and foods and the risk of esophageal cancer: a meta-analysis of observational studies. BMC Cancer 2015; 15:449. [PMID: 26031666 PMCID: PMC4457273 DOI: 10.1186/s12885-015-1185-1] [Citation(s) in RCA: 61] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2014] [Accepted: 03/12/2015] [Indexed: 12/30/2022] Open
Abstract
Background Previous studies have mostly focused on the effects of specific constituents of beverages and foods on the risk of esophageal cancer (EC). An increasing number of studies are now emerging examining the health consequences of the high temperature of beverages and foods. We conducted a meta-analysis to summarize the evidence and clarify the association between hot beverages and foods consumption and EC risk. Methods We searched the PubMed, Embase, and Web of Science databases for relevant studies, published before May 1, 2014, with the aim to estimate the association between hot beverage and food consumption and EC risk. A random-effect model was used to pool the results from the included studies. Publication bias was assessed by using the Begg test, the Egger test, and funnel plot. Results Thirty-nine studies satisfied the inclusion criteria, giving a total of 42,475 non-overlapping participants and 13,811 EC cases. Hot beverage and food consumption was significantly associated with EC risk, with an odds ratio (OR) of 1.82 (95% confidence interval [CI], 1.53–2.17). The risk was higher for esophageal squamous cell carcinoma, with a pooled OR of 1.60 (95% CI, 1.29–2.00), and was insignificant for esophageal adenocarcinoma (OR: 0.79; 95% CI: 0.53–1.16). Subgroup analyses suggests that the association between hot beverage and food consumption and EC risk were significant in Asian population (OR: 2.06; 95% CI: 1.62-2.61) and South American population (OR: 1.52; 95% CI: 1.25-1.85), but not significant in European population (OR: 0.95; 95% CI: 0.68-1.34). Conclusions Hot beverage and food consumption is associated with a significantly increased risk of EC, especially in Asian and South American populations, indicating the importance in changing people’s dietary habits to prevent EC.
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Affiliation(s)
- Yawen Chen
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Yeqing Tong
- Center for Disease Control and Prevention of Hubei Province, Wuhan, Hubei, China.
| | - Chen Yang
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Yong Gan
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Huilian Sun
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Huashan Bi
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Shiyi Cao
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Xiaoxv Yin
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
| | - Zuxun Lu
- School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
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Wu XC, Zheng YF, Tang M, Li XF, Zeng R, Zhang JR. Association Between Smoking and p53 Mutation in Oesophageal Squamous Cell Carcinoma: A Meta-analysis. Clin Oncol (R Coll Radiol) 2015; 27:337-44. [PMID: 25736278 DOI: 10.1016/j.clon.2015.02.007] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2014] [Revised: 01/09/2015] [Accepted: 02/12/2015] [Indexed: 01/10/2023]
Abstract
AIMS Several studies have evaluated the association between smoking and p53 mutation in oesophageal squamous cell carcinoma (ESCC), but the conclusions are inconsistent. The aim of the present study was to carry out a meta-analysis evaluating the relationship between smoking and p53 mutation in patients with ESCC. MATERIALS AND METHODS Eligible studies were identified through searches in PubMed and EMBASE. The odds ratio with 95% confidence interval was used to assess the association. In total, 20 studies were identified that met the selection criteria; these studies were analysed using STATA 12.0 software. RESULTS The 20 studies identified comprised 1524 ESCC patients, of whom 72.97% were smokers and 27.03% were non-smokers. The pooled odds ratio of p53 mutation in ESCC for any cigarette smoking versus no smoking was 1.28 (95% confidence interval=0.88-1.88). The estimated odds ratios were 1.06 (95% confidence interval=0.56-2.00, based on five studies, 129 light smokers and 70 non-smokers) for light smoking and 2.01 (95% confidence interval=1.12-3.60, based on five studies, 223 heavy smokers and 73 non-smokers) for heavy smoking. CONCLUSION The results of our meta-analysis indicate an overall positive relationship between heavy smoking and p53 mutation in ESCC. Heavy smokers with ESCC have a higher risk for p53 mutation than non-smokers. Large-scale clinical studies are still needed to draw a more precise conclusion.
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Affiliation(s)
- X C Wu
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
| | - Y F Zheng
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
| | - M Tang
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
| | - X F Li
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
| | - R Zeng
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
| | - J R Zhang
- Oncology Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China
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Adduri RSR, Katamoni R, Pandilla R, Madana SN, Paripati AK, Kotapalli V, Bashyam MD. TP53 Pro72 allele is enriched in oral tongue cancer and frequently mutated in esophageal cancer in India. PLoS One 2014; 9:e114002. [PMID: 25436609 PMCID: PMC4250174 DOI: 10.1371/journal.pone.0114002] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2014] [Accepted: 10/31/2014] [Indexed: 12/13/2022] Open
Abstract
Purpose The tumor suppressor p53 is known to be inactivated frequently in various cancers. In addition, germline polymorphisms in TP53 are known to affect protein function and influence risk of developing different types of cancers. In this study, we analyzed the association of TP53 Pro72Arg polymorphism with squamous cell carcinoma of oral tongue (SCCOT) and esophagus (ESCC) in India. Methods We assessed the distribution of TP53 Pro72Arg polymorphism in one hundred and fifteen and eighty two SCCOT and ESCC patients, respectively, with respect to one hundred and ten healthy controls from the same population. In addition, we analyzed association of the polymorphism with several clinico-pathological and molecular parameters. Results Pro72 allele was significantly enriched in SCCOT patients compared to the healthy control group but neither allele was enriched in ESCC. Interestingly, Pro72 allele was preferentially mutated in ESCC which was confirmed by analysis of samples heterozygous for Pro72Arg. Conclusions Our study revealed the association of Pro72 allele with SCCOT suggesting the effect of this polymorphism on SCCOT risk. Preferential mutation of Pro72 allele exclusively in ESCC indicates the need for further studies to understand the tissue specific effect of p53 polymorphism.
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Affiliation(s)
- Raju S. R. Adduri
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Rajender Katamoni
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Ramaswamy Pandilla
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Sandeep N. Madana
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Arun Kumar Paripati
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Viswakalyan Kotapalli
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
| | - Murali Dharan Bashyam
- Laboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad, India
- * E-mail:
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Zheng X, Xing S, Liu XM, Liu W, Liu D, Chi PD, Chen H, Dai SQ, Zhong Q, Zeng MS, Liu WL. Establishment of using serum YKL-40 and SCCA in combination for the diagnosis of patients with esophageal squamous cell carcinoma. BMC Cancer 2014; 14:490. [PMID: 25001061 PMCID: PMC4094903 DOI: 10.1186/1471-2407-14-490] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2014] [Accepted: 06/30/2014] [Indexed: 12/18/2022] Open
Abstract
Background Elevated serum YKL-40 levels have been observed in various cancers. We evaluated the diagnostic performance of serum YKL-40 alone or in combination with the CEA, CYFRA21-1 and SCCA tumor markers for patients with esophageal squamous cell carcinoma (ESCC). Methods YKL-40 was detected in ESCC cell lines and tissues by real-time RT-PCR, Western blotting and ELISA. YKL-40 protein expression was determined in 20 ESCC tumor tissues using immunohistochemistry. Serum YKL-40 was measured by ELISA in 126 healthy donors, 59 patients with benign esophageal diseases and 150 patients with ESCC. Serum CEA, CYFRA21-1 and SCCA were determined by electrochemiluminescence. Results YKL-40 mRNA and protein were observed in ESCC cancer cell lines, tissues and cell culture media, respectively. YKL-40 expression was observed in 17 of 20 ESCC samples (85%). Serum YKL-40 concentration was significantly elevated in patients with ESCC (Range: 6.95-502.10 ng/ml) compared with patients with benign diseases (Range: 1.21-429.30 ng/ml; P = 0.038) and healthy controls (Range: 2.56-132.26 ng/ml; P < 0.001). ROC curves demonstrated that serum YKL-40 has a sensitivity of 72.70%, a specificity of 84.13% and an AUC of 0.874 for the diagnosis of ESCC, which was superior to CEA (Sen: 8.00%; Spe: 96.80%, AUC = 0.652), CYFRA21-1 (Sen: 40.00%; Spe: 92.06%, AUC = 0.746) and SCCA (Sen: 32.67%; Spe: 94.44%, AUC = 0.789). The YKL-40 and SCCA combination was better for diagnosing ESCC (Sen: 82.00%, Spe: 79.37%, PPV: 82.55 and NPV: 78.74; AUC = 0.917) than the YKL-40 and CEA combination (Sen: 74.00%, Spe: 83.20%, PPV: 84.09 and NPV: 72.73; AUC = 0.877), the YKL-40 and CYFRA21-1 combination (Sen: 82.00%, Spe: 77.78%, PPV: 81.46% and NPV: 78.40%; AUC = 0.897) or the CEA, CYFRA21-1 and SCCA combination (Sen: 56.67%, Spe: 84.80%, PPV: 81.73 and NPV: 61.99; AUC = 0.831). Associations between serum YKL-40 levels and the clinic characteristics of ESCC were not significant, with the exception of age (p = 0.001). Conclusions ESCC tumor cells and tissues express YKL-40. Serum YKL-40 may be a potential biomarker for ESCC. Serum YKL-40 in combination with SCCA significantly increases the sensitivity of detecting ESCC.
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Affiliation(s)
| | | | | | | | | | | | | | | | | | - Mu-Sheng Zeng
- State Key Laboratory of Oncology in Southern China, Guangzhou, China.
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12
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Frequent expression of KIT in endometrial stromal sarcoma with YWHAE genetic rearrangement. Mod Pathol 2014; 27:751-7. [PMID: 24186140 DOI: 10.1038/modpathol.2013.199] [Citation(s) in RCA: 49] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2013] [Accepted: 09/08/2013] [Indexed: 12/15/2022]
Abstract
Endometrial stromal sarcomas with the YWHAE-NUTM2A/B genetic fusion characteristically contain high-grade round to epithelioid cell component that is strongly and diffusely cyclin D1-positive and it may or may not show an associated low-grade fibroblastic/myxoid cell component. They are clinically more aggressive than endometrial stromal sarcomas with the JAZF1-SUZ12 genetic fusion and frequently demonstrate extrauterine extension at initial clinical presentation. In this setting, the tumor may be misdiagnosed as gastrointestinal stromal tumor. This study examines the expression of KIT and ANO1 in 14 YWHAE-NUTM2A/B tumors by immunohistochemistry. Staining localization was determined as membranous and/or cytoplasmic, and the staining intensity was assessed (negative, weak, moderate and strong). Of the 14 tumors, 6 contained only a high-grade round cell component, 2 only a low-grade fibroblastic component and 6 had both components in the slides evaluated. The high-grade round cell component displayed moderate to strong membranous/cytoplasmic KIT staining in all tumors (12 of 12). The low-grade fibroblastic cell component showed only weak cytoplasmic KIT staining in 3 of 8 tumors. In contrast, ANO1 was negative in all 14 neoplasms, irrespective of the component evaluated. Sanger sequencing analysis (exons 9, 11, 13 and 17) and Ampliseq Cancer Panel mutation screen (Ion Torrent) demonstrated no KIT mutations in three KIT-positive YWHAE-NUTM2A/B tumors. This study shows that the high-grade round cell component of YWHAE-NUTM2A/B endometrial stromal sarcoma consistently expresses KIT but lacks KIT hotspot mutations. KIT expression may represent a potential diagnostic pitfall in the evaluation of YWHAE-NUTM2A/B endometrial stromal sarcoma presenting with pelvic/abdominal mass, particularly in situations where its uterine origin is not definitive, and thus a panel of antibodies that includes ANO1 and cyclin D1 is necessary.
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Esophageal Cancer, the Topmost Cancer at MTRH in the Rift Valley, Kenya, and Its Potential Risk Factors. ISRN ONCOLOGY 2013; 2013:503249. [PMID: 24490085 PMCID: PMC3893746 DOI: 10.1155/2013/503249] [Citation(s) in RCA: 50] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 09/08/2013] [Accepted: 10/08/2013] [Indexed: 12/15/2022]
Abstract
Esophageal cancer at Moi Teaching and Referral Hospital (MTRH) is the leading cancer in men with a poor prognosis. A case control study (n = 159) aimed at the histology type, gender, and risk indicators was carried out at MTRH. Mantel Haenszel chi-square and logistic regression were employed for analysis. Squamous-cell carcinoma was the common histological type occurring in the middle third portion of the oesophagus. The occurrence of the cancer in males was 1.4 times that of females. The mean age was 56.1 yrs. Low socioeconomic, smoking, snuff use, alcohol, tooth loss, cooking with charcoal and firewood, hot beverage, and use of mursik were independently associated with esophageal cancer (P < 0.05). Using logistic regression adjusted for various factors, alcohol consumption was associated with the increased risk of esophageal cancer. AHR was 0.45 and 95% CI: 0.205-0.985, P = 0.046. A societal component of low socioeconomic conditions, a lifestyle component with specific practices such as the consumption of mursik, chang'aa, busaa, snuff, smoking, hot tea, poor oral hygiene, and an environmental component with potential exposure to high levels of nitrosamines, passive smoking, and cooking with coal, could be involved. The increase in experts at MTRH capable of diagnosing could be responsible for the increase in reporting this neoplasm.
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The potential of molecular markers to improve interventions through the natural history of oesophageal squamous cell carcinoma. Biosci Rep 2013; 33:BSR20130063. [PMID: 23837802 PMCID: PMC3747595 DOI: 10.1042/bsr20130063] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
EC (oesophageal cancer) is one of the ten most frequent and fatal tumours worldwide and ESCC (oesophageal squamous cell carcinoma) accounts for about 80% of the cases. The first symptoms of ESCC arise late during the progression of the disease and, therefore, the diagnosis is usually done in advanced stages. This leads to an inefficient treatment and consequently to a poor prognosis. Thus, a comprehensive knowledge of ESCC biology is of major importance to identify risk factors, especially in high-incidence areas and biomarkers which could enable ESCC prevention and interventions throughout the natural history of the disease. In this review, we present the current knowledge regarding ESCC aetiology as well as the different genetic and epigenetic alterations already described in this tumour. We also discuss how these alterations could be used to anticipate ESCC diagnosis as well as how they can help improving treatment. A molecular natural history of the disease is proposed pointing out potential markers that may improve interventions at different points of ESCC development. Only when the different layers of complexity behind this tumour are elucidated, it will be possible to successfully perform prevention at different levels.
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15
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Abedi-Ardekani B, Kamangar F, Sotoudeh M, Villar S, Islami F, Aghcheli K, Nasrollahzadeh D, Taghavi N, Dawsey SM, Abnet CC, Hewitt SM, Fahimi S, Saidi F, Brennan P, Boffetta P, Malekzadeh R, Hainaut P. Extremely high Tp53 mutation load in esophageal squamous cell carcinoma in Golestan Province, Iran. PLoS One 2011; 6:e29488. [PMID: 22216294 PMCID: PMC3246475 DOI: 10.1371/journal.pone.0029488] [Citation(s) in RCA: 53] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2011] [Accepted: 11/29/2011] [Indexed: 01/29/2023] Open
Abstract
Background Golestan Province in northeastern Iran has one of the highest incidences of esophageal squamous cell carcinoma (ESCC) in the world with rates over 50 per 100,000 person-years in both sexes. We have analyzed TP53 mutation patterns in tumors from this high-risk geographic area in search of clues to the mutagenic processes involved in causing ESCC. Methodology/Principal Findings Biopsies of 119 confirmed ESCC tumor tissue from subjects enrolled in a case-control study conducted in Golestan Province were analyzed by direct sequencing of TP53 exons 2 through 11. Immunohistochemical staining for p53 was carried out using two monoclonal antibodies, DO7 and 1801. A total of 120 TP53 mutations were detected in 107/119 cases (89.9%), including 11 patients with double or triple mutations. The mutation pattern was heterogeneous with infrequent mutations at common TP53 “hotspots” but frequent transversions potentially attributable to environmental carcinogens forming bulky DNA adducts, including 40% at bases known as site of mutagenesis by polycyclic aromatic hydrocarbons (PAHs). Mutations showed different patterns according to the reported temperature of tea consumption, but no variation was observed in relation to ethnicity, tobacco or opium use, and alcoholic beverage consumption or urban versus rural residence. Conclusion/Significance ESCC tumors in people from Golestan Province show the highest rate of TP53 mutations ever reported in any cancer anywhere. The heterogeneous mutation pattern is highly suggestive of a causative role for multiple environmental carcinogens, including PAHs. The temperature and composition of tea may also influence mutagenesis.
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Affiliation(s)
- Behnoush Abedi-Ardekani
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
- International Agency for Research on Cancer, Lyon, France
- Social Security Organization, Tehran, Iran
| | - Farin Kamangar
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America
- Department of Public Health Analysis, School of Community Health and Policy, Morgan State University, Baltimore, Maryland, United States of America
| | - Masoud Sotoudeh
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | | | - Farhad Islami
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
- International Agency for Research on Cancer, Lyon, France
- Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York, United States of America
| | - Karim Aghcheli
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | - Dariush Nasrollahzadeh
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
- Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
| | - Noushin Taghavi
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | - Sanford M. Dawsey
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America
| | - Christian C. Abnet
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America
| | - Stephen M. Hewitt
- Tissue Array Research Program, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America
| | - Saman Fahimi
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
- Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
| | - Farrokh Saidi
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | - Paul Brennan
- International Agency for Research on Cancer, Lyon, France
| | - Paolo Boffetta
- Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York, United States of America
- International Prevention Research Institute, Lyon, France
| | - Reza Malekzadeh
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | - Pierre Hainaut
- International Agency for Research on Cancer, Lyon, France
- * E-mail:
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Thongsuksai P, Boonyaphiphat P, Puttawibul P, Sudhikaran W. Specific intronic p53 mutation in esophageal squamous cell carcinoma in Southern Thailand. World J Gastroenterol 2010; 16:5359-66. [PMID: 21072901 PMCID: PMC2980687 DOI: 10.3748/wjg.v16.i42.5359] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/12/2010] [Revised: 08/21/2010] [Accepted: 08/28/2010] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate p53 mutations in esophageal cancer in a high-risk population, and correlate them with smoking, alcohol consumption and betel chewing. METHODS One hundred and sixty-five tumor samples of esophageal squamous cell carcinoma (ESCC) obtained from a university hospital in Songkhla province, Southern Thailand were investigated for p53 mutations in exons 5-8, using polymerase chain reaction-single strand conformation polymorphism analysis, followed by direct sequencing. A polymerase chain reaction-restriction fragment length polymorphism (RFLP) assay was additionally used to confirm possible germline mutation in intron 6. A history of risk habits was obtained by interviews. The association between risk habits and mutation frequency was evaluated using the χ(2) test. RESULTS The studied specimens were from 139 male and 26 female patients with ESCC, treated at Songklanagarind Hospital. Most of the patients were smokers (86.7%) and alcohol consumers (72.73%), and 38.3% were betel chewers. Forty-three mutations of the p53 gene were detected in 25.5% (42/165) of tumor samples. Mutations were most commonly found in exon 5 (25.6%) and exon 8 (25.6%). Mutations in the hot-spot codon 248 were found in four cases (9.3% of all mutations). G:C→C:G (30.23%), G:C→A:T (27.90%) and G:C→T:A (16.28%) were the prevalent spectra of mutations. Unexpectedly, among 10 intronic mutations, eight cases harbored a similar mutation: G→C substitution in intron 6 (nucleotide 12759, GenBank NC_000017). These were additionally confirmed by the RFLP technique. Similar mutations were also detected in their matched blood samples using RFLP and direct sequencing, which suggested germline mutations. There was no significant correlation between risk habits and p53 mutation frequency. CONCLUSION A proportion of Thai ESCC patients harbored specific intronic p53 mutations, which might be germline mutations. Further studies are needed to explore this novel finding.
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Szymańska K, Levi J, Menezes A, Wünsch-Filho V, Eluf-Neto J, Koifman S, Matos E, Daudt A, Curado M, Villar S, Pawlita M, Waterboer T, Boffetta P, Hainaut P, Brennan P. TP53 and EGFR mutations in combination with lifestyle risk factors in tumours of the upper aerodigestive tract from South America. Carcinogenesis 2009; 31:1054-9. [DOI: 10.1093/carcin/bgp212] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
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TP53 mutation profile of esophageal squamous cell carcinomas of patients from Southeastern Brazil. Mutat Res 2009; 696:10-5. [PMID: 19944185 DOI: 10.1016/j.mrgentox.2009.11.005] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2009] [Revised: 11/10/2009] [Accepted: 11/13/2009] [Indexed: 11/24/2022]
Abstract
Esophageal cancer (EC) is among the 10 most common and fatal malignacies in the world, presenting a marked geographic variation in incidence rates between and within different countries. The TP53 tumor suppressor gene is highly mutated in esophageal tumors and its mutation pattern can offer clues to the etiopathology of the tumor. As Brazil presents one of the highest incidence areas in the West, a deeper knowledge of the molecular mechanisms related to EC development in the Brazilian population is needed. We analyzed the mutation profile of 110 esophageal squamous cell carcinomas (ESCC) of patients from Southeastern Brazil (Rio de Janeiro and São Paulo) and collected data regarding alcohol intake and tobacco smoking. We detected 41 mutations in tumor samples from 38 patients. There was no association between mutation frequency and tobacco smoking or alcohol drinking. The most frequently mutated codons were 179, 214, 220 and 248. Codons 179, 220 and 248 are hot-spots for ESCC, but codon 214 presents only 0.7% of the mutations registered in the IARC database. The mutation profile revealed a high percentage of mutations at A:T base pairs (34.1%) followed by deletions (17.1%). We concluded that the mutation profile detected in this study is different from that of patients from Southern Brazil but very similar to that previously seen in French patients, being characterized by a high frequency of mutations at A:T base pairs, which may be associated with acetaldehyde, the metabolic product of ethanol.
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Islami F, Boffetta P, Ren J, Pedoeim L, Khatib D, Kamangar F. High-temperature beverages and foods and esophageal cancer risk--a systematic review. Int J Cancer 2009; 125:491-524. [PMID: 19415743 PMCID: PMC2773211 DOI: 10.1002/ijc.24445] [Citation(s) in RCA: 192] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022]
Abstract
Coffee, tea and maté may cause esophageal cancer (EC) by causing thermal injury to the esophageal mucosa. If so, the risk of EC attributable to thermal injury could be large in populations in which these beverages are commonly consumed. In addition, these drinks may cause or prevent EC via their chemical constituents. Therefore, a large number of epidemiologic studies have investigated the association of an indicator of amount or temperature of use of these drinks or other hot foods and beverages with risk of EC. We conducted a systematic review of these studies and report the results for amount and temperature of use separately. By searching PubMed and the ISI, we found 59 eligible studies. For coffee and tea, there was little evidence for an association between amount of use and EC risk; however, the majority of studies showed an increased risk of EC associated with higher drinking temperature which was statistically significant in most of them. For maté drinking, the number of studies was limited, but they consistently showed that EC risk increased with both amount consumed and temperature, and these 2 were independent risk factors. For other hot foods and drinks, over half of the studies showed statistically significant increased risks of EC associated with higher temperature of intake. Overall, the available results strongly suggest that high-temperature beverage drinking increases the risk of EC. Future studies will require standardized strategies that allow for combining data and results should be reported by histological subtypes of EC.
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Affiliation(s)
- Farhad Islami
- Digestive Disease Research Center, Medical Sciences/ University of Tehran, Tehran, Iran
- Lifestyle, Environment and Cancer Group, International Agency for Research on Cancer, Lyon, France
- King’s College London, Thames Cancer Registry, London, UK
| | - Paolo Boffetta
- Lifestyle, Environment and Cancer Group, International Agency for Research on Cancer, Lyon, France
| | - JianSong Ren
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | - Leah Pedoeim
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | - Dara Khatib
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | - Farin Kamangar
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
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Silva JFD, Bidinotto LT, Furtado KS, Salvadori DMF, Rivelli DP, Barros SBDM, Rodrigues MAM, Barbisan LF. Maté attenuates DNA damage and carcinogenesis induced by diethylnitrosamine and thermal injury in rat esophagus. Food Chem Toxicol 2009; 47:1521-9. [DOI: 10.1016/j.fct.2009.03.040] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2008] [Revised: 03/18/2009] [Accepted: 03/28/2009] [Indexed: 11/26/2022]
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Islami F, Pourshams A, Nasrollahzadeh D, Kamangar F, Fahimi S, Shakeri R, Abedi-Ardekani B, Merat S, Vahedi H, Semnani S, Abnet CC, Brennan P, Møller H, Saidi F, Dawsey SM, Malekzadeh R, Boffetta P. Tea drinking habits and oesophageal cancer in a high risk area in northern Iran: population based case-control study. BMJ 2009; 338:b929. [PMID: 19325180 PMCID: PMC3269898 DOI: 10.1136/bmj.b929] [Citation(s) in RCA: 196] [Impact Index Per Article: 12.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
Abstract
OBJECTIVE To investigate the association between tea drinking habits in Golestan province, northern Iran, and risk of oesophageal squamous cell carcinoma. DESIGN Population based case-control study. In addition, patterns of tea drinking and temperature at which tea was drunk were measured among healthy participants in a cohort study. SETTING Golestan province, northern Iran, an area with a high incidence of oesophageal squamous cell carcinoma. PARTICIPANTS 300 histologically proved cases of oesophageal squamous cell carcinoma and 571 matched neighbourhood controls in the case-control study and 48 582 participants in the cohort study. MAIN OUTCOME MEASURE Odds ratio of oesophageal squamous cell carcinoma associated with drinking hot tea. RESULTS Nearly all (98%) of the cohort participants drank black tea regularly, with a mean volume consumed of over one litre a day. 39.0% of participants drank their tea at temperatures less than 60 degrees C, 38.9% at 60-64 degrees C, and 22.0% at 65 degrees C or higher. A moderate agreement was found between reported tea drinking temperature and actual temperature measurements (weighted kappa 0.49). The results of the case-control study showed that compared with drinking lukewarm or warm tea, drinking hot tea (odds ratio 2.07, 95% confidence interval 1.28 to 3.35) or very hot tea (8.16, 3.93 to 16.9) was associated with an increased risk of oesophageal cancer. Likewise, compared with drinking tea four or more minutes after being poured, drinking tea 2-3 minutes after pouring (2.49, 1.62 to 3.83) or less than two minutes after pouring (5.41, 2.63 to 11.1) was associated with a significantly increased risk. A strong agreement was found between responses to the questions on temperature at which tea was drunk and interval from tea being poured to being drunk (weighted kappa 0.68). CONCLUSION Drinking hot tea, a habit common in Golestan province, was strongly associated with a higher risk of oesophageal cancer.
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Affiliation(s)
- Farhad Islami
- Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, 14117 Tehran, Iran
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Hussain I, ul Rehman S, Afroze D, Zahoor L, Abdullah S, Hafiz A, Shah ZA, Iqbal S, Shaffi M, Das BC, Siddiqi MA. Mutational spectrum of conserved regions of TP53 and PTEN genes in Kangri cancer (of the skin) in the Kashmiri population. Mutat Res 2009; 676:5-10. [PMID: 19486858 DOI: 10.1016/j.mrgentox.2009.02.011] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2008] [Revised: 01/09/2009] [Accepted: 02/22/2009] [Indexed: 10/21/2022]
Abstract
Kangri cancer is a unique, thermally induced squamous cell carcinoma (SCC) of the skin that develops due to persistent use of a Kangri (a brazier) by the Kashmiri people to combat the cold temperature during winter. Unlike classical UV-induced SCC of the skin, Kangri cancer appears on the legs and abdomen. Its common features are erythematous patches, recurrence and metastasis. In the absence of any molecular etiology, we made a preliminary attempt to estimate the nature and frequency of mutations in the TP53 and PTEN genes in Kangri cancer patients from Kashmir. PCR-SSCP analysis followed by direct sequencing revealed that TP53 mutations account for 40% (12/30) of sporadic Kangri cancer patients and that PTEN mutations account for only 6.6% (2/30). There were 16 mutations in TP53 exons 5 and 7, found in 12 patients. They consisted of 11 substitutions (7 transitions, 3 transversions and 1 double-base) and 5 insertions. The 11 substitutions represent 8 distinct missense mutations, 3 of which were silent mutations. The mutations detected in the PTEN gene consisted of one insertion and one C>T transition. This high percentage of TP53 mutations (especially A>G) showed a statistically significant association with age and positive lymph node status. Our results indicate that TP53 is a predominant target of chronic hyperthermia in the development of Kangri cancer in the moderate risk Kashmiri population. The differences in the TP53 mutation spectrum of UV-induced SCC of the skin and Kangri cancer are probably due to the nature of the respective environmental carcinogens. The study also suggests that TP53 may function as a potential molecular marker and prognostic tool, at least in a subset of sporadic Kangri tumors.
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Affiliation(s)
- Ishraq Hussain
- Department of Immunology and Molecular Medicine, Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar 190011, Kashmir, India
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Egashira A, Morita M, Kakeji Y, Sadanaga N, Oki E, Honbo T, Ohta M, Maehara Y. p53 gene mutations in esophageal squamous cell carcinoma and their relevance to etiology and pathogenesis: results in Japan and comparisons with other countries. Cancer Sci 2007; 98:1152-6. [PMID: 17573896 PMCID: PMC11159086 DOI: 10.1111/j.1349-7006.2007.00524.x] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022] Open
Abstract
Esophageal squamous cell carcinoma is a form of cancer that has varying incidence rates among different countries, distinct geographic areas and different ethnic groups. According to previous reports, p53 gene mutations have been identified in 20-80% of these tumors, and these mutations have occurred at an early stage. These findings suggest that such mutations play an important role in esophageal carcinogenesis, and highlight the importance of mutagens, which cause sequence alterations in the p53 gene. In order to clarify the environmental factors and the molecular mechanisms that may be responsible for the occurrence and prevention of a specific mutation in the process of esophageal carcinogenesis, we analyzed p53 gene mutations in 95 samples of esophageal squamous cell carcinoma. We further reviewed published reports investigating the frequency of p53 gene mutations in esophageal cancer from high-risk areas to normal-risk areas and compared these findings to our results in Japan. The frequency of p53 gene mutations in Japanese esophageal cancer is 47.4% and there are three prominent features: (1) a predominance of transversions, in particular the G:C to T:A transversion; (2) a relatively low frequency of transitions; and (3) a relatively high percentage of frameshift mutations. These results indicate the possible importance of the benzo[a]pyrene metabolite and oxidative DNA damage in esophageal carcinogenesis and scarcely correlate with DNA replication errors or alkylation in comparison to other gastrointestinal cancers. In addition, we observed a peculiar sequence of frameshift mutations. Taken together, these data suggest that this tumor suppressor gene plays a critical role in the multistep carcinogenesis process for esophageal squamous cell cancer.
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Affiliation(s)
- Akinori Egashira
- Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
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Goan YG, Chang HC, Hsu HK, Chou YP, Cheng JT. Risk of p53 gene mutation in esophageal squamous cell carcinoma and habit of betel quid chewing in Taiwanese. Cancer Sci 2005; 96:758-65. [PMID: 16271069 PMCID: PMC11158869 DOI: 10.1111/j.1349-7006.2005.00115.x] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
Abstract
A recent report suggested that BQ (BQ) chewing significantly correlated with the occurrence of esophageal squamous cell carcinoma (ESCC) in Taiwanese. BQ chewing was shown to be associated with p53 mutation in oral cancers. However, the relationship between BQ chewing and p53 mutation in ESCC is unclear. Seventy-five primary ESCC patients were enrolled for mutational analysis of the p53 gene using polymerase chain amplification and direct sequencing of amplified product. Thirty-seven mutations of the p53 gene were detected in 45.5% (34/75) of tumor specimens. These mutations significantly clustered in exon 5 (21/37) of the p53 gene. The incidence of p53 mutations did not associate with clinicopathological characteristics or the habits of cigarette smoking or alcohol consumption. However, BQ chewers exhibited significantly higher incidence of p53 gene mutations than non-chewers (67.6% vs 32.4%, P = 0.007). After controlling the confounding factors of cigarette smoking and alcohol intake, BQ chewing still showed significant association with the incidence of p53 mutation in ESCCs (RR = 4.23; 95% CI, 1.317-13.60). The A:T to G:C transition (8/37, 21.6%) and G:C to T:A transversion (5/23, 13.5%) were the prevalent spectrum of p53 gene mutations. All A:T to G:C transitional mutations occurred in patients with the habits of BQ chewing and cigarette smoking. Noticeably, alcohol consumption could enhance this peculiar spectrum of p53 mutation in ESCC. Accordingly, p53 might be an important molecular target of BQ carcinogens in the development of ESCC in Taiwanese.
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Affiliation(s)
- Yih-Gang Goan
- Department of Surgery, Kaohsiung Veterans General Hospital, Taiwan, Republic of China
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Mir MM, Dar NA, Gochhait S, Zargar SA, Ahangar AG, Bamezai RNK. p53 mutation profile of squamous cell carcinomas of the esophagus in Kashmir (India): a high-incidence area. Int J Cancer 2005; 116:62-8. [PMID: 15761872 DOI: 10.1002/ijc.21002] [Citation(s) in RCA: 46] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Abstract
Esophageal squamous cell carcinoma (ESCC) has been reported to show geographical variation in its incidence, even within areas of ethnic homogeneity. Kashmir valley, in north of India, has been described as a high-risk area for ESCC. Here, we make a preliminary attempt to study mutations in exons 5-8 (the DNA binding domain) of the tumor suppressor gene, p53, in 55 ESCC patients from Kashmir. Polymerase chain reaction followed by direct sequencing analysis revealed the presence of mutations in 36.36% (20/55) tumors, assessed for the extent of allelic instability. The 20 mutations, found in 20 patients, comprised of 17 single-base substitutions (11 transitions + 6 transversions) and 3 deletions. The 17 single-base variations represented 12 missense mutations, 2 nonsense mutations and 3 variations located in intron 6, 1 of which resulted in a splicing variant. The patients when compared for the incidence of p53 mutation with various demographic features revealed females to be at increased risk (p = 0.016; OR = 4.13; 95% CI = 1.26-13.46). Comparison of mutation profile with other high-risk areas reflected both differences and similarities indicating coexposure to a unique set of risk factors. This might be due to the special dietary and cultural practices of Kashmir that needs validation, as does the gender-based difference in the incidence of p53 mutation observed in this study.
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Affiliation(s)
- Mohammad Muzaffar Mir
- Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir
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Abstract
AIM: To characterize the tumor suppressor gene p53 mutations in exon 4, esophageal cancer and adjacent non-cancerous tissues.
METHODS: We performed p53 (exons 4-8) gene mutation analysis on 24 surgically resected human esophageal cancer specimens by PCR, single-strand conformation polymorphism, and DNA sequencing.
RESULTS: p53 gene mutations were detected in 9 of 22 (40.9%) esophageal cancer specimens and 10 of 17 (58.8%) adjacent non-cancerous tissues. Eight of sixteen (50.0%) point mutations detected were G–A transitions and 9 of 18 (50.0%) p53 gene mutations occurred in exon 4 in esophageal cancer specimens. Only 1 of 11 mutations detected was G-A transition and 4 of 11 (36.4%) p53 gene mutations occurred in exon 4 in adjacent non-cancerous tissues.
CONCLUSION: Mutation of p53 gene in exon 4 may play an important role in development of esophageal cancer. The observation of p53 gene mutation in adjacent non-cancerous tissues suggests that p53 gene mutation may be an early event in esophageal carcinogenesis. Some clinical factors, including age, sex, pre-operation therapy and location of tumors, do not influence p53 gene mutation rates.
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Affiliation(s)
- Li-Ya Li
- Department of Oncology, China-Japan Friendship Hospital, Beijing 100029, China.
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de Moura Gallo CV, Azevedo E Silva Mendonça G, de Moraes E, Olivier M, Hainaut P. TP53 mutations as biomarkers for cancer epidemiology in Latin America: current knowledge and perspectives. Mutat Res 2005; 589:192-207. [PMID: 15878142 DOI: 10.1016/j.mrrev.2005.01.002] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2004] [Revised: 01/28/2005] [Accepted: 01/30/2005] [Indexed: 11/18/2022]
Abstract
Due to particular social and economical development, and to the impact of globalization of lifestyles, Latin America shows a superposition of cancers that are frequent in low resource countries (gastric, oesophageal squamous cell and cervical cancers) and high resource countries (cancers of breast, colon and rectum, lung and prostate). Latin America thus offers opportunities for investigating the impact on changing lifestyle patterns on the occurrence of cancer. At the molecular level, mutations in the tumor suppressor gene TP53 are common in many cancers and their distribution can be informative of the nature of the mutagenic mechanisms, thus giving clues to cancer etiology and molecular pathogenesis. However most of the data available are derived from studies in industrialized countries. In this review, we discuss current trends on cancer occurrence in Latin American countries, and we review the literature available on TP53 mutations and polymorphisms in patients from Latin America. Overall, a total of 285 mutations have been described in 1213 patients in 20 publications, representing 1.5% of the total number of mutations reported world-wide. Except for hematological cancers, TP53 mutation frequencies are similar to those reported in other regions of the world. The only tumor site presenting significant differences in mutation pattern as compared to other parts of the world is colon and rectum. However, this difference is based on a single study with 35 patients. Recently, a characteristic TP53 mutation at codon 337 (R337H) has been identified in the germline of children with adrenocortical carcinoma in Southern Brazil. Further and better focused analyses of TP53 mutation patterns in the context of epidemiological studies, should help to improve our understanding of cancer etiology in order to develop appropriate health policies and public health programs in Latin America.
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Affiliation(s)
- Claudia Vitória de Moura Gallo
- Departamento de Biologia Celular e Genética, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
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N/A. N/A. Shijie Huaren Xiaohua Zazhi 2004; 12:2478-2480. [DOI: 10.11569/wcjd.v12.i10.2478] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
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Goldenberg D, Golz A, Joachims HZ. The beverage maté: a risk factor for cancer of the head and neck. Head Neck 2003; 25:595-601. [PMID: 12808663 DOI: 10.1002/hed.10288] [Citation(s) in RCA: 50] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022] Open
Abstract
BACKGROUND Maté is a tealike beverage consumed habitually in South America and among South Americans throughout the world. It is brewed from the dried leaves and stemlets of the perennial tree Ilex paraguariensis (yerba maté), a species that belongs to the Aquifoliaceae family. Maté consumption has been associated with an increased rate of oral, oropharyngeal, esophageal, and laryngeal cancers. The purpose of this study is to review the literature and discuss the role of Maté consumption as a risk factor for head and neck cancers. MATERIALS AND METHODS We performed a thorough review of the relevant literature linking maté consumption with head and neck cancer and the proposed carcinogenicity of maté. Case control studies on maté-drinking populations and in vivo and in vitro studies on the carcinogenicity of maté were reviewed. The populations included in many of these studies also used alcohol and tobacco products, confounding the influence of maté as an independent risk factor. RESULTS Evidence in the literature suggests that maté consumption is carcinogenic and plays a role in the development of cancers of the oral cavity, pharynx, larynx, and esophagus. CONCLUSIONS The exact mechanism of carcinogenesis of maté is unknown. Both chemical and thermal carcinogenesis mechanisms have been suggested. Available information suggests that maté drinking is a risk factor for upper aerodigestive tract cancer.
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Affiliation(s)
- David Goldenberg
- Department of Otolaryngology-Head and Neck Surgery, Rambam Medical Center, Israel.
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Takata-Yahiro M, Fujii Y, Nodarse JF, Islam MR, Oda S, Zhang QM, Yonei S, Nakamura M. A Novel GT-Mismatch Binding Protein That Recognizes Strict DNA Sequences with High Affinity. TOHOKU J EXP MED 2003; 200:211-29. [PMID: 14580152 DOI: 10.1620/tjem.200.211] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022]
Abstract
Mismatched or damaged base pairs in DNA are mutagenic and both eukaryotes and prokaryotes have a series of repair systems that decrease a spontaneous mutation rate. All exocyclic amino groups of cytosine(C), adenine(A), and guanine(G) contribute to hydrogen bonds for base pairing. High temperature and oxidative stresses increase the deamination of these bases and methylated C. These deaminated sites would be initially recognized by components of DNA repair system. We discovered a novel G/thymine(T)-mismatch binding protein (nGTBP) that bound, with high affinity, to a minimal 14-mer DNA heteroduplex with a strict 5'-TRT GNB-3' sequence (R for purine, N for any bases, and B for "not A," namely for C, G, or T ). This italicized G position mismatched with T could be replaced by hypoxanthine, the deaminated A. The nGTBP, however, barely recognized DNA duplexes individually containing 8-oxo-G, thymine glycol, and 5-methylcytosine.
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Affiliation(s)
- Maki Takata-Yahiro
- Department of Host-Defense Biochemistry, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852-8523, Japan
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