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1.
Int Wound J ; 21(1): e14628, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-38272817

RESUMO

High-grade gliomas (HGGs) may be amenable to the neurosurgical technique known as laser interstitial thermal therapy (LITT), which delivers thermal energy to interstitial brain injuries and wounds with pinpoint accuracy. The purpose of this extensive meta-analysis was to evaluate the effects of LITT on wound complications among patients who have brain tumours. Diverse conclusions emerge from a systematic review of pertinent studies, necessitating a comprehensive examination. The meta-analysis, performed utilizing the meta library provided by the R package meta, reveals an initial significant overall effect (RR: -2.1262, 95% CI [-2.7466, -1.5059], p < 0.0001) accompanied by considerable heterogeneity among studies (I2 = 61.13%). Following analyses that specifically examined the incidence of wounds, a complex correlation was found (RR: 0.0471, 95% CI [0.0264, 0.0842], p < 0.0001), indicating that LITT has a discernible but insignificant effect on the occurrence of wounds. Although the meta-analysis emphasizes a notable decrease in wound complications subsequent to LITT treatment, additional research is warranted due to constraints in standardized reporting, data accessibility, and small sample sizes. The results of this study underscore the need for exhaustive protocols to analyse wound complications in patients with brain tumours undergoing LITT.


Assuntos
Neoplasias Encefálicas , Hipertermia Induzida , Terapia a Laser , Humanos , Neoplasias Encefálicas/etiologia , Neoplasias Encefálicas/cirurgia , Hipertermia Induzida/efeitos adversos , Hipertermia Induzida/métodos , Terapia a Laser/efeitos adversos , Terapia a Laser/métodos , Lasers , Cicatrização
2.
Neuro Oncol ; 25(7): 1368-1376, 2023 07 06.
Artigo em Inglês | MEDLINE | ID: mdl-36638155

RESUMO

BACKGROUND: Computed tomography (CT) scans make substantial contributions to low-dose ionizing radiation exposures, raising concerns about excess cancers caused by diagnostic radiation. METHODS: Deidentified medicare records for all Australians aged 0-19 years between 1985-2005 were linked to national death and cancer registrations to 2012. The National Cancer Institute CT program was used to estimate radiation doses to the brain from CT exposures in 1985-2005, Poisson regression was used to model the dependence of brain cancer incidence on brain radiation dose, which lagged by 2 years to minimize reverse causation bias. RESULTS: Of 10 524 842 young Australians, 611 544 were CT-exposed before the age of 20 years, with a mean cumulative brain dose of 44 milligrays (mGy) at an average follow-up of 13.5 years after the 2-year lag period. 4472 were diagnosed with brain cancer, of whom only 237 had been CT-exposed. Brain cancer incidence increased with radiation dose to the brain, with an excess relative risk of 0.8 (95% CI 0.57-1.06) per 100 mGy. Approximately 6391 (95% CI 5255, 8155) persons would need to be exposed to cause 1 extra brain cancer. CONCLUSIONS: For brain tumors that follow CT exposures in childhood by more than 2 years, we estimate that 40% (95% CI 29%-50%) are attributable to CT Radiation and not due to reverse causation. However, because of relatively low rates of CT exposure in Australia, only 3.7% (95% CI 2.3%-5.4%) of all brain cancers are attributable to CT scans. The population-attributable fraction will be greater in countries with higher rates of pediatric scanning.


Assuntos
Neoplasias Encefálicas , Neoplasias Induzidas por Radiação , Criança , Humanos , Idoso , Incidência , Neoplasias Induzidas por Radiação/epidemiologia , Neoplasias Induzidas por Radiação/etiologia , Doses de Radiação , Austrália/epidemiologia , Programas Nacionais de Saúde , Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Tomografia Computadorizada por Raios X/efeitos adversos , Tomografia Computadorizada por Raios X/métodos
3.
Int J Cancer ; 146(9): 2442-2449, 2020 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-31304976

RESUMO

Tea and coffee have antioxidant and neuroprotective effects. Observational studies suggest that tea and coffee intake may reduce cancer risk, but data on glioma risk are inconclusive. We evaluated the association between tea, coffee and caffeine intake and glioma risk in the female Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII) and the male Health Professionals Follow-Up Study (HPFS). Cumulative intake was derived from validated quadrennial food frequency questionnaires. Glioma cases were confirmed by medical record review. Multivariable-adjusted hazard ratios of glioma by beverage intake category were estimated using Cox proportional hazards models. We documented 554 incident cases of glioma (256 in NHS, 87 in NHSII and 211 in HPFS). Compared to <1 cup/week, higher tea consumption was borderline inversely associated with glioma risk in pooled cohorts (hazard ratio [HR] = 0.73, 95% confidence interval [CI]: 0.49-1.10 for >2 cups/day, p-trend = 0.05), but not in women (HR = 0.74, 95% CI: 0.47-1.18 for >2 cups/day, p-trend = 0.11) or men (HR = 0.70, 95% CI: 0.30-1.60 for >2 cups/day, p-trend = 0.30) separately. Overall, we observed no significant associations between caffeinated, decaffeinated or total coffee intake and glioma risk. There were no material differences in the results with baseline values, 8-year lagged responses, or when limited to glioblastoma (n = 362). In three large prospective cohort studies, tea intake was borderline inversely associated with glioma risk. No significant associations were observed for coffee intake and glioma risk. These results merit further exploration in prospective studies.


Assuntos
Neoplasias Encefálicas/epidemiologia , Café/efeitos adversos , Glioma/epidemiologia , Chá/efeitos adversos , Adulto , Idoso , Neoplasias Encefálicas/etiologia , Neoplasias Encefálicas/prevenção & controle , Estudos de Casos e Controles , Feminino , Seguimentos , Glioma/etiologia , Glioma/prevenção & controle , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Prospectivos , Fatores de Risco , Inquéritos e Questionários , Estados Unidos/epidemiologia
4.
BMC Cancer ; 19(1): 1092, 2019 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-31718568

RESUMO

BACKGROUND: The evasion of apoptosis is a hallmark of cancer. Understanding this process holistically and overcoming apoptosis resistance is a goal of many research teams in order to develop better treatment options for cancer patients. Efforts are also ongoing to personalize the treatment of patients. Strategies to confirm the therapeutic efficacy of current treatments or indeed to identify potential novel additional options would be extremely beneficial to both clinicians and patients. In the past few years, system medicine approaches have been developed that model the biochemical pathways of apoptosis. These systems tools incorporate and analyse the complex biological networks involved. For their successful integration into clinical practice, it is mandatory to integrate systems approaches with routine clinical and histopathological practice to deliver personalized care for patients. RESULTS: We review here the development of system medicine approaches that model apoptosis for the treatment of cancer with a specific emphasis on the aggressive brain cancer, glioblastoma. CONCLUSIONS: We discuss the current understanding in the field and present new approaches that highlight the potential of system medicine approaches to influence how glioblastoma is diagnosed and treated in the future.


Assuntos
Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/terapia , Glioblastoma/diagnóstico , Glioblastoma/terapia , Biologia de Sistemas/métodos , Apoptose/genética , Biomarcadores Tumorais , Neoplasias Encefálicas/etiologia , Neoplasias Encefálicas/mortalidade , Gerenciamento Clínico , Suscetibilidade a Doenças , Glioblastoma/etiologia , Glioblastoma/mortalidade , Humanos , Modelos Biológicos , Avaliação de Resultados em Cuidados de Saúde , Medicina de Precisão/métodos , Prognóstico
5.
Bioelectromagnetics ; 39(1): 53-59, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29171064

RESUMO

This study aimed to clarify the distribution of the ear side of mobile phone use in the general population of Japan and clarify what factors are associated with the ear side of mobile phone use. Children at elementary and junior high schools (n = 2,518) and adults aged ≥20 years (n = 1,529) completed an Internet-based survey. Data were subjected to a logistic regression analysis. In children, due to the tendency to use the dominant hand, we analyzed the factors associated with the use of right ear in right-handed people. Statistically significant differences were observed only in talk time per call (odds ratio (OR) = 2.17; 95% confidence interval (CI): 1.22-3.99). In adults, due to the tendency to use the left ear, we analyzed factors associated with the use of left ear in right-handed people. Significant differences were observed in those aged 30-39 years (OR = 2.55; 95% CI: 1.79-3.68), those aged 40-49 years (OR = 3.08; 95% CI: 2.15-4.43), those aged >50 years (OR = 1.85; 95% CI: 1.20-2.85), and in those with a percentage of total talk time when using mobile phones at work of 51-100% (OR = 1.75; 95% CI: 1.21-2.55). We believe that future epidemiological studies on mobile phone use can be improved by considering the trends in mobile phone use identified in this study. Bioelectromagnetics. 39:53-59, 2018. © 2017 Wiley Periodicals, Inc.


Assuntos
Uso do Telefone Celular/estatística & dados numéricos , Orelha , Adolescente , Adulto , Encéfalo/efeitos da radiação , Neoplasias Encefálicas/etiologia , Uso do Telefone Celular/efeitos adversos , Criança , Feminino , Humanos , Japão , Masculino , Pessoa de Meia-Idade , Risco , Inquéritos e Questionários , Adulto Jovem
6.
Neurotoxicology ; 61: 214-232, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-27212451

RESUMO

The overall aim of this systematic review was to identify risk factors for onset and natural progression, which were shown to increase, decrease, or have a null association with risk of primary brain tumour. For onset, the project was separated into two phases. The first phase consisted of a systematic search of existing systematic reviews and meta-analyses. Moderate to high methodological quality reviews were incorporated and summarized with relevant observational studies published since 2010, identified from a systematic search performed in phase 2. For natural progression, only the first phase was conducted. Standard systematic review methodology was utilized. Based on this review, various genetic variants, pesticide exposures, occupational farming/hairdressing, cured meat consumption and personal hair dye use appear to be associated with increased risk of onset amongst adults. The specific EGF polymorphsm 61-A allele within Caucasian populations and having a history of allergy was associated with a decreased risk. For progression, M1B-1 antigen was shown to increase the risk. High birth weight, pesticide exposure (childhood exposure, and parental occupational exposure) and maternal consumption of cured meat during pregnancy may also increase the risk of onset of childhood brain tumours. Conversely, maternal intake of pre-natal supplements (folic acid) appeared to decrease risk. Children with neurofibromatosis 2 were considered to have worse overall and relapse free survival compared to neurofibromatosis 1, as were those children who had grade III tumours compared to lesser grades.


Assuntos
Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Progressão da Doença , Idade de Início , Neoplasias Encefálicas/genética , Fator de Crescimento Epidérmico/genética , Humanos , Antígeno Ki-67/genética , Mutação/genética , Neurofibromatose 1/genética , Neurofibromatose 2/genética , Praguicidas/toxicidade , Fatores de Risco , Proteína Supressora de Tumor Von Hippel-Lindau/genética
7.
Int J Cancer ; 139(12): 2714-2721, 2016 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-27560973

RESUMO

Few prospective studies have investigated the etiology of brain tumor, especially among Asian populations. Both coffee and green tea are popular beverages, but their relation with brain tumor risk, particularly with glioma, has been inconsistent in epidemiological studies. In this study, we evaluated the association between coffee and greed tea intake and brain tumor risk in a Japanese population. We evaluated a cohort of 106,324 subjects (50,438 men and 55,886 women) in the Japan Public Health Center-Based Prospective Study (JPHC Study). Subjects were followed from 1990 for Cohort I and 1993 for Cohort II until December 31, 2012. One hundred and fifty-seven (70 men and 87 women) newly diagnosed cases of brain tumor were identified during the study period. Hazard ratio (HR) and 95% confidence intervals (95%CIs) for the association between coffee or green tea consumption and brain tumor risk were assessed using a Cox proportional hazards regression model. We found a significant inverse association between coffee consumption and brain tumor risk in both total subjects (≥3 cups/day; HR = 0.47, 95%CI = 0.22-0.98) and in women (≥3 cups/day; HR = 0.24, 95%CI = 0.06-0.99), although the number of cases in the highest category was small. Furthermore, glioma risk tended to decrease with higher coffee consumption (≥3 cups/day; HR = 0.54, 95%CI = 0.16-1.80). No association was seen between green tea and brain tumor risk. In conclusion, our study suggested that coffee consumption might reduce the risk of brain tumor, including that of glioma, in the Japanese population.


Assuntos
Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Café , Comportamento de Ingestão de Líquido , Chá , Adulto , Estudos de Coortes , Feminino , Seguimentos , Humanos , Incidência , Japão/epidemiologia , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Vigilância da População , Modelos de Riscos Proporcionais , Risco , Inquéritos e Questionários
8.
Cancer Epidemiol ; 42: 53-9, 2016 06.
Artigo em Inglês | MEDLINE | ID: mdl-27018750

RESUMO

BACKGROUND: Individuals with Neurofibromatosis Type 1 (NF1) are strongly predisposed to developing pediatric brain tumors (PBTs), especially optic pathway gliomas (OPGs). Although developmental factors have been implicated in the origins of PBTs in both human and animal studies, associations between early-life factors and PBTs have not been evaluated in individuals with NF1. Our objective was to evaluate associations between peri-gestational characteristics and PBTs in this population. METHODS: We conducted a cross-sectional study, ascertaining questionnaire and medical record data for 606 individuals<18years old who enrolled in the NF1 Patient Registry Initiative (NPRI) from 6/9/2011-6/29/2015. One hundred eighty-four individuals had reported PBT diagnoses, including 65 who were identified with OPG diagnoses. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between PBT and OPG diagnoses and peri-gestational characteristics (prematurity, birth weight, parental age, plurality, family history of NF1, assisted reproductive technology, maternal vitamin supplementation, and parental smoking). RESULTS: We observed no significant associations between any of the assessed characteristics and PBTs overall or OPGs with the exception of birth weight. After controlling for potential confounding variables, we observed a significant positive association between birth weight quartile and OPGs with a HR of 3.32 (95% CI 1.39-7.94) for the fourth (≥3915.5g) compared to the first (≤3020g) quartile (p for trend=0.001). CONCLUSIONS: Consistent with results for PBTs in the general population, these results suggest that higher birth weights increase OPG risk in individuals with NF1.


Assuntos
Peso ao Nascer/genética , Neoplasias Encefálicas/etiologia , Neurofibromatose 1/complicações , Glioma do Nervo Óptico/etiologia , Adolescente , Criança , Pré-Escolar , Estudos Transversais , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Fatores de Risco
9.
Cancer Epidemiol ; 40: 52-9, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26625087

RESUMO

Little is known about the aetiology of childhood brain tumours. We investigated anthropometric factors (birth weight, length, maternal age), birth characteristics (e.g. vacuum extraction, preterm delivery, birth order) and exposures during pregnancy (e.g. maternal: smoking, working, dietary supplement intake) in relation to risk of brain tumour diagnosis among 7-19 year olds. The multinational case-control study in Denmark, Sweden, Norway and Switzerland (CEFALO) included interviews with 352 (participation rate=83.2%) eligible cases and 646 (71.1%) population-based controls. Interview data were complemented with data from birth registries and validated by assessing agreement (Cohen's Kappa). We used conditional logistic regression models matched on age, sex and geographical region (adjusted for maternal age and parental education) to explore associations between birth factors and childhood brain tumour risk. Agreement between interview and birth registry data ranged from moderate (Kappa=0.54; worked during pregnancy) to almost perfect (Kappa=0.98; birth weight). Neither anthropogenic factors nor birth characteristics were associated with childhood brain tumour risk. Maternal vitamin intake during pregnancy was indicative of a protective effect (OR 0.75, 95%-CI: 0.56-1.01). No association was seen for maternal smoking during pregnancy or working during pregnancy. We found little evidence that the considered birth factors were related to brain tumour risk among children and adolescents.


Assuntos
Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adolescente , Ordem de Nascimento , Peso ao Nascer , Estudos de Casos e Controles , Criança , Dinamarca , Feminino , Humanos , Recém-Nascido , Modelos Logísticos , Masculino , Idade Materna , Noruega , Gravidez , Nascimento Prematuro/epidemiologia , Fumar , Suécia , Suíça , Adulto Jovem
10.
Int J Oncol ; 46(5): 1865-71, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25738972

RESUMO

Quickly changing technologies and intensive uses of radiofrequency electromagnetic field (RF-EMF)­emitting phones pose a challenge to public health. Mobile phone users and uses and exposures to other wireless transmitting devices (WTDs) have increased in the past few years. We consider that CERENAT, a French national study, provides an important addition to the literature evaluating the use of mobile phones and risk of brain tumors. The CERENAT finding of increased risk of glioma is consistent with studies that evaluated use of mobile phones for a decade or longer and corroborate those that have shown a risk of meningioma from mobile phone use. In CERENAT, exposure to RF­EMF from digitally enhanced cordless telephones (DECTs), used by over half the population of France during the period of this study, was not evaluated. If exposures to DECT phones could have been taken into account, the risks of glioma from mobile phone use in CERENAT are likely to be higher than published. We conclude that radiofrequency fields should be classified as a Group 2A ̔probable̓ human carcinogen under the criteria used by the International Agency for Research on Cancer (Lyon, France). Additional data should be gathered on exposures to mobile and cordless phones, other WTDs, mobile phone base stations and Wi­Fi routers to evaluate their impact on public health. We advise that the as low as reasonable achievable (ALARA) principle be adopted for uses of this technology, while a major cross­disciplinary effort is generated to train researchers in bioelectromagnetics and provide monitoring of potential health impacts of RF­EMF.


Assuntos
Neoplasias Encefálicas/etiologia , Carcinógenos/classificação , Telefone Celular , Campos Eletromagnéticos/efeitos adversos , Glioma/etiologia , Neoplasias Encefálicas/epidemiologia , França/epidemiologia , Glioma/epidemiologia , Humanos , Fatores de Risco
11.
Cancer Causes Control ; 26(6): 871-9, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-25791129

RESUMO

PURPOSE: The etiology of childhood brain tumors (CBT) is poorly understood, but dietary factors could be involved. In this case-control study of CBT, the possible associations of childhood intake of dietary and supplemental folate, vitamin B6, and vitamin B12 with the risk of CBT were investigated, along with various food groups. METHODS: Cases diagnosed between 2005 and 2010 were identified from 10 pediatric oncology centers in Australia and controls by nationwide random-digit dialling. For study children of ages 3-14 years, diet in the year before diagnosis (or recruitment) was assessed using food frequency questionnaires. Folate intake was adjusted for bioavailability, and dietary micronutrient intake was energy-adjusted. Micronutrients and food groups were analyzed using logistic regression adjusting for relevant confounders. Principal components analysis was conducted to assess food group intake patterns for analysis. RESULTS: Food and micronutrient data were available for 216 cases and 523 controls. Folate intake was associated with a reduced risk of CBT overall (odds ratio for highest tertile vs. lowest: 0.63, 95% confidence interval 0.41, 0.97) and particularly low-grade gliomas (odds ratio for highest tertile vs. lowest: 0.52, 95% confidence interval 0.29, 0.92). Vitamin B6 and B12 intake was not associated with CBT risk, nor was processed meat. CONCLUSIONS: High folate intake during childhood may reduce the risk of CBT. This potentially important finding needs to be corroborated in other studies. If replicated, these results could have important implications for public health recommendations regarding diet during childhood.


Assuntos
Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Dieta , Ácido Fólico/administração & dosagem , Vitamina B 12/administração & dosagem , Vitamina B 6/administração & dosagem , Adolescente , Austrália , Estudos de Casos e Controles , Criança , Pré-Escolar , Inquéritos sobre Dietas , Suplementos Nutricionais , Ingestão de Alimentos , Feminino , Humanos , Masculino , Micronutrientes , Risco
12.
J Stem Cells ; 10(4): 287-94, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-27144830

RESUMO

The mobile phones (MP) are low power radio devices which work on electromagnetic fields (EMFs), in the frequency range of 900-1800 MHz. Exposure to MPEMFs may affect brain physiology and lead to various health hazards including brain tumors. Earlier studies with positron emission tomography (PET) have found alterations in cerebral blood flow (CBF) after acute exposure to MPEMFs. It is widely accepted that DNA double-strand breaks (DSBs) and their misrepair in stem cells are critical events in the multistage origination of various leukemia and tumors, including brain tumors such as gliomas. Both significant misbalance in DSB repair and severe stress response have been triggered by MPEMFs and EMFs from cell towers. It has been shown that stem cells are most sensitive to microwave exposure and react to more frequencies than do differentiated cells. This may be important for cancer risk assessment and indicates that stem cells are the most relevant cellular model for validating safe mobile communication signals. Recently developed technology for recording the human bio-electromagnetic (BEM) field using Electron photonic Imaging (EPI) or Gas Discharge Visualisation (GDV) technique provides useful information about the human BEM. Studies have recorded acute effects of Mobile Phone Electromagnetic Fields (MPEMFs) using EPI and found quantifiable effects on human BEM field. Present manuscript reviews evidences of altered brain physiology and stem cell functioning due to mobile phone/cell tower radiations, its association with increased cancer risk and explores early diagnostic value of EPI imaging in detecting EMF induced changes on human BEM.


Assuntos
Neoplasias Encefálicas/etiologia , Telefone Celular , Campos Eletromagnéticos/efeitos adversos , Células-Tronco/efeitos da radiação , Encéfalo/irrigação sanguínea , Encéfalo/patologia , Encéfalo/efeitos da radiação , Neoplasias Encefálicas/patologia , Quebras de DNA de Cadeia Dupla/efeitos da radiação , Hemodinâmica/efeitos da radiação , Humanos , Fatores de Risco , Células-Tronco/patologia
13.
Cancer Causes Control ; 24(2): 267-76, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23247638

RESUMO

BACKGROUND: Coffee contains many compounds, including antioxidants, which could prevent cancerogenesis, and coffee has been related with lower incidence of cancer at several sites. Tea is also rich in antioxidants, mainly polyphenols. To provide a quantitative overall estimate on the relation between coffee and tea consumption and glioma, we combined all published data, using a meta-analytic approach. METHODS: In September 2012, a bibliography search was carried out in both PubMed and Embase to identify observational studies providing quantitative estimates on the issue. Pooled estimates of the relative risks (RR) and the corresponding 95 % confidence intervals (CI) were calculated using random-effects models. RESULTS: Six studies (four cohort and two case-control studies) were available for meta-analysis, for a total of about 2100 cases. The summary RRs and 95 % CIs of glioma for drinkers versus non/occasional drinkers were 0.96 (95 % CI: 0.81-1.13) for coffee and 0.86 (95 % CI: 0.78-0.94) for tea, with no heterogeneity between studies. When we compared the highest versus the lowest categories of consumption, the RRs were 1.01 (95 % CI: 0.83-1.22) for coffee, 0.88 (95 % CI: 0.69-1.12) for tea, and 0.75 (95 % CI: 0.54-1.05) for coffee plus tea. CONCLUSIONS: This meta-analysis, although based on few studies, suggests a lack of association between coffee intake and glioma risk, and a tendency, if any, to a lower risk for tea and coffee plus tea drinkers.


Assuntos
Neoplasias Encefálicas/epidemiologia , Café , Glioma/epidemiologia , Chá , Adulto , Neoplasias Encefálicas/etiologia , Neoplasias Encefálicas/prevenção & controle , Glioma/etiologia , Glioma/prevenção & controle , Humanos , Fatores de Risco
14.
Cancer Causes Control ; 23(5): 757-68, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22457000

RESUMO

PURPOSE: We utilized the large, prospective NIH-AARP Diet and Health Study to further explore the hypothesis, suggested by two recent prospective cohort studies, that increased intake of coffee, tea, soda, and/or caffeine is associated with reduced adult glioma risk. METHODS: At baseline in 1995-1996, dietary intake, including coffee, tea, and soda, was assessed with a food frequency questionnaire. We used Cox proportional hazards models to calculate adjusted hazard ratios (HR) and 95 % confidence intervals (CI) for glioma risk in relation to beverage intake. RESULTS: During follow-up of 545,771 participants through 2006, 904 participants were diagnosed with glioma. We found no trends of decreasing glioma risk with increasing intake of specific beverages or total caffeine. HR patterns for consumption of the caffeinated versus decaffeinated form of each beverage were inconsistent with a specific caffeine effect. HR patterns of reduced glioma risk for most categories of beverage intake greater than "none" prompted a post hoc analysis that revealed borderline-significant inverse associations for any versus no intake of tea (HR = 0.84; 95 % CI, 0.69-1.03), total coffee plus tea (HR = 0.70; 95 % CI, 0.48-1.03), and soda (HR = 0.82; 95 % CI, 0.67-1.01). CONCLUSIONS: The borderline-significant inverse associations could be explained by a threshold effect in which any beverage intake above a low level confers a beneficial effect, most likely due to beverage constituents other than caffeine. They could also be explained by non-drinkers of these beverages sharing unknown extraneous characteristics associated with increased glioma risk, or by chance.


Assuntos
Neoplasias Encefálicas/epidemiologia , Cafeína/efeitos adversos , Bebidas Gaseificadas/efeitos adversos , Café/efeitos adversos , Glioma/epidemiologia , Chá/efeitos adversos , Idoso , Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/etiologia , Estudos de Coortes , Feminino , Glioma/diagnóstico , Glioma/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , National Institutes of Health (U.S.) , Estudos Prospectivos , Fatores de Risco , Inquéritos e Questionários , Estados Unidos/epidemiologia
15.
Curr Drug Metab ; 12(6): 587-93, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-21434862

RESUMO

The incidence of brain tumor and other types of cancer are markedly increased during the last few decades. There are many etiological and environmental factors involved in the initiation of different types of cancers including brain tumors. Mutations in tumor suppressor gene p53 and its expression are associated with shorter survival and higher mortality rate of patients with brain tumors. Another factor, N-nitrosamines have received much attention as a potential risk factor for brain tumor. These compounds are potent carcinogens and occur widely in the environment, and also can be formed endogenously in the stomach from the interaction of ingested nitrate or nitrite with secondary amines. Free radicals are another etiological factor of brain tumor and are removed by cellular antioxidants in the human body. Brain tissue is vulnerable to the damaging effects of free radicals as a result of low antioxidant levels. Interestingly, there is an inverse correlation between the total antioxidant levels and oxidative DNA damage in transitional meningioma compared with normal brain tissues. Also, an inverse relationship between antioxidant levels and grades of malignancy has been found after histopathological examination of brain tumors. Moreover, high intake of vitamin E is correlated with greater survival for all patients diagnosed as Grade III malignant glioma. Dietary supplementation with antioxidants [e.g. vitamins C & E] was found to reduce the incidence of brain tumors in children whose mothers took these vitamins throughout pregnancy. On the other hand, decreases in antioxidant levels were correlated with the severity of malignancy of brain tumors, and also with accumulation of considerable amounts of oxidative stress products including free radicals which damage this tissue. The mechanisms of protection of these antioxidants against brain tumors might be due to inhibition of the nitrosation process, decreasing of tumor necrotic factor, scavenging of free radicals, inhibition of telomerase activity which facilitates telomere attrition. It is concluded that administration of antioxidants could reduce the incidence of brain tumors and probably other types of cancer.


Assuntos
Antioxidantes/farmacologia , Neoplasias Encefálicas/prevenção & controle , Suplementos Nutricionais , Animais , Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Dieta , Feminino , Humanos , Incidência , Gravidez , Fatores de Risco
16.
Bioelectromagnetics ; 32(2): 164-7, 2011 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21225893

RESUMO

The Interphone Study on brain cancer rests upon a case-control design with recall of past exposures recorded with substantial inaccuracy and low participation rates. This commentary questions the wisdom in choosing this design and argues that funding could and should have been used better by setting up a large-scale cohort study that could address other potential endpoints besides cancer. Bioelectromagnetics 32:164-167, 2011. © 2010 Wiley-Liss, Inc.


Assuntos
Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Telefone Celular , Projetos de Pesquisa Epidemiológica , Neoplasias Induzidas por Radiação/epidemiologia , Poluentes Atmosféricos/efeitos adversos , Telefone Celular/estatística & dados numéricos , Humanos , Neoplasias Induzidas por Radiação/etiologia
17.
Adv Tech Stand Neurosurg ; 34: 3-35, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19368079

RESUMO

Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses. Glioblastoma patients have a median survival expectancy of only 14 months on the current standard treatment of surgical resection to the extent feasible, followed by adjuvant radiotherapy plus temozolomide, given concomitantly with and after radiotherapy. Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management. Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy. Resistance to apoptosis results from changes at the genomic, transcriptional and post-transcriptional level of proteins, protein kinases and their transcriptional factor effectors. The PTEN/ PI3K/Akt/mTOR/NF-kappaB and the Ras/Raf/MEK/ERK signaling cascades play critical roles in the regulation of gene expression and prevention of apoptosis. Components of these pathways are mutated or aberrantly expressed in human cancer, notably glioblastomas. Monoclonal antibodies and low molecular-weight kinase inhibitors of these pathways are the most common classes of agents in targeted cancer treatment. However, most clinical trials of these agents as monotherapies have failed to demonstrate survival benefit. Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe. Temozolomide brings significant therapeutic benefits in glioblastoma treatment. Part of temozolomide cytotoxic activity is exerted through pro-autophagic processes and also through the induction of late apoptosis. Autophagy, type II programmed cell death, represents an alternative mechanism to overcome, at least partly, the dramatic resistance of many cancers to pro-apoptotic-related therapies. Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs. Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells. The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.


Assuntos
Astrocitoma/patologia , Astrocitoma/terapia , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/terapia , Antineoplásicos/uso terapêutico , Astrocitoma/etiologia , Autofagia , Terapia Biológica , Neoplasias Encefálicas/etiologia , Terapia Combinada , Humanos , Imunidade Inata , Procedimentos Neurocirúrgicos
18.
Cancer Invest ; 27(2): 184-92, 2009 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-19235591

RESUMO

In this study we examined by QRT-PCR the mRNA expression of TGF-beta 1, IGF-1, EGF, FGF-2 and YY1 in human brain tumors. Our findings introduce YY1, for the first time, as a novel gene implicated in brain gliomatogenesis and meningioma establishment. We present a positive correlation between the autocrine expression of YY1 and TGF-beta 1, IGF-1 and FGF-2, known to be involved in the progression of gliomas and meningiomas. We suggest that mRNA profiling of the above genes in the early stages of disease development could be useful for prognostic purposes, and these genes can be considered as potential targets for therapeutic approaches against brain tumors.


Assuntos
Neoplasias Encefálicas/metabolismo , Fator 2 de Crescimento de Fibroblastos/genética , Glioma/metabolismo , Fator de Crescimento Insulin-Like I/genética , Meningioma/metabolismo , RNA Mensageiro/análise , Fator de Crescimento Transformador beta1/genética , Fator de Transcrição YY1/genética , Adulto , Idoso , Neoplasias Encefálicas/etiologia , Feminino , Glioma/etiologia , Humanos , Masculino , Meningioma/etiologia , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase Via Transcriptase Reversa
19.
J Occup Environ Med ; 49(7): 791-802, 2007 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-17622853

RESUMO

Work-related exposures potentially associated with a cluster of brain tumors at a petroleum exploration and extraction research facility were evaluated in a nested case-control study. Fifteen cases were identified in the original cohort and 150 matched controls were selected. Odds ratios (ORs) for occupational exposure to petroleum, radiation, solvents, magnetic fields, and work activities were near or below 1.0. ORs near 1.5 were observed for: working with computers (OR = 1.47; 95% confidence interval [CI] = 0.30-9.35); work-related travel (OR = 1.48; 95% CI = 0.25-5.95), and travel immunizations (OR = 1.62; 95% CI = 0.23-9.45). Higher ORs were observed for work in administrative and marketing buildings and for achieving a master's or higher degree (OR = 2.0, 95% CI = 0.4-10.7). While some ORs above 1.5 were noted, no work-related chemical and physical exposures were significantly associated with the occurrence of brain tumors among employees at this facility.


Assuntos
Neoplasias Encefálicas/epidemiologia , Doenças Profissionais/epidemiologia , Exposição Ocupacional , Petróleo , Pesquisadores , Idoso , Neoplasias Encefálicas/etiologia , Neoplasias Encefálicas/mortalidade , California/epidemiologia , Estudos de Casos e Controles , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Medição de Risco
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