An international case–control study of adult glioma and meningioma: the role of head trauma

University of Southern California, Department of Preventive Medicine, USC/Norris Comprehensive Cancer Center, Los Angeles 90033-0800, USA.
International Journal of Epidemiology (Impact Factor: 9.18). 09/1998; 27(4):579-86.
Source: PubMed


Increased brain tumour risk after head trauma suggested by case reports and clinical series has been previously studied epidemiologically with mixed results. An international multicentre case-control study investigated the role of head trauma from injury or sports participation in adult brain tumour risk.
In all, 1178 glioma and 330 meningioma cases were individually or frequency matched to 2236 controls. Only exposures that occurred at least 5 years before diagnosis and head injuries that received medical attention were considered.
Risk for ever having experienced a head injury was highest for male meningiomas (odds ratio [OR] = 1.5, 95% confidence interval [CI] : 0.9-2.6) but was lower for 'serious' injuries, i.e. those causing loss of consciousness, loss of memory or hospitalization (OR = 1.2, 95% CI: 0.6-2.3). Among male meningiomas, latency of 15 to 24 years significantly increased risk (OR = 5.4, 95% CI: 1.7-16.6), and risk was elevated among those who participated in sports most correlated with head injury (OR = 1.9, 95% CI: 0.7-5.3). Odds ratios were lower for male gliomas (OR = 1.2, 95% CI : 0.9-1.5 for any injury; OR = 1.1, 95% CI: 0.7-1.6 for serious injuries) and in females in general.
Evidence for elevated brain tumour risk after head trauma was strongest for meningiomas in men. Findings related to sports should be interpreted cautiously due to cultural variability in our data and our lack of complete data on physical exercise in general which appeared to be protective.

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Available from: Graham G Giles, Oct 12, 2015
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    • "There are also several case reports between previous trauma and subsequent development of meningioma (Sakai et al. 1981; Rodrigues et al. 2006; Francois et al. 2010; Kizilay et al. 2010), which is another of the primary brain tumor types observed by (Pearce et al. 2012). There is epidemiological evidence of this relationship as well, (Preston-Martin et al. 1998), including dose response relationships (Phillips et al. 2002). Past epidemiological evidence in large part shows an association between radiation exposure and brain tumors only after high doses characteristic of radiotherapy (UNSCEAR 2006; Mettler and Upton 2008). "
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    ABSTRACT: Several radiation-related professional societies have concluded that carcinogenic risks associated with doses below 50-100 mSv are either too small to be detected, or are nonexistent. This is especially important in the context of doses from medical imaging. Radiation exposure to the public from medical imaging procedures is rising around the world, primarily due to increased utilization of computed tomography. Professional societies and advisory bodies consistently recommend against multiplying small doses by large populations to predict excess radiation-induced cancers, in large part because of the potential for sensational claims of health impacts which do not adequately take the associated uncertainties into account. Nonetheless, numerous articles have predicted thousands of future cancers as a result of CT scanning, and this has generated considerable concern among patients and parents. In addition, some authors claim that we now have direct epidemiological evidence of carcinogenic risks from medical imaging. This paper critically examines such claims, and concludes that the evidence cited does not provide direct evidence of low-dose carcinogenicity. These claims themselves have adverse public health impacts by frightening the public away from medically justified exams. It is time for the medical and scientific communities to be more assertive in responding to sensational claims of health risks.
    Dose-Response 10/2014; 1(-1). DOI:10.2203/dose-response.14-030.Ulsh · 1.22 Impact Factor
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    • "In fact, evidence of a possible causal role of previous brain traumatic injury in the oncogenesis of intracranial gliomas is lacking in epidemiological studies [2, 13]. Some evidence has been found only for intracranial meningiomas [14]. This would mean that, concerning gliomas, there is not enough evidence for possible medico-legal implications between previous trauma and tumorigenesis [15]. "
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    ABSTRACT: For a long time, head injury has been considered as a possible causative factor for later development of brain tumors. However, the actual role of previous head trauma in the pathogenesis of intracranial tumors is still a matter of debate, also due to the possible medico-legal implications. Some authors have suggested several criteria for establishing a possible causal relationship between the aforementioned factors. We report a case of a left posterior paraventricular high-grade glioma which developed 20 years after a posttraumatic hematoma occurring in the same area. This case is reported in detail and the relevant literature is reviewed.
    Case Reports in Oncology 08/2013; 6(2):403-9. DOI:10.1159/000354340
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    • "Limited evidence suggests that gliomas are associated with traumatic brain injury, cigarette smoking, use of hair dyes, and exposure to certain chemicals and viruses. For instance, studies suggest associations between prior head injury and meningioma in men,9 between smoking unfiltered cigarettes and an increased risk of adult glioma,10,11 and a null or inverse association between glioma and alcohol consumption.12 An international case-control study showed an inverse association between allergic diseases and glioma, but not with meningioma.13 "
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    ABSTRACT: Primary brain tumors are among the top ten causes of cancer-related deaths in the US. Malignant gliomas account for approximately 70% of the 22,500 new cases of malignant primary brain tumors diagnosed in adults each year and are associated with high morbidity and mortality. Despite optimal treatment, the prognosis for patients with gliomas remains poor. The use of retinoids (vitamin A and its congeners) in the treatment of certain tumors was originally based on the assumption that these conditions were associated with an underlying deficiency of vitamin A and that supplementation with pharmacological doses would correct the deficiency. Yet the results of retinoid treatment have been only modestly beneficial and usually short-lived. Studies also indicate that vitamin A excess and supplementation have pro-oxidant effects and are associated with increased risks of mortality from cancer and other diseases. The therapeutic role of vitamin A in cancer thus remains uncertain and a new perspective on the facts is needed. The modest and temporary benefits of retinoid treatment could result from a process of feedback inhibition, whereby exogenous retinoid temporarily inhibits the endogenous synthesis of these compounds. In fact, repeated and/or excessive exposure of the tissues to endogenous retinoic acid may contribute to carcinogenesis. Gliomas, in particular, may result from an imbalance in retinoid receptor expression initiated by environmental factors that increase the endogenous production of retinoic acid in glia. At the receptor level, it is proposed that this imbalance is characterized by excessive expression of retinoic acid receptor-α (RARα) and reduced expression of retinoic acid receptor-β (RARβ). This suggests a potential new treatment strategy for gliomas, possibly even at a late stage of the disease, ie, to combine the use of a RARα antagonist and a RARβ agonist. According to this hypothesis, the RARα antagonist would be expected to inhibit RARα-induced gliomas, while the RARβ agonist would suppress tumor growth and possibly contribute to the regeneration of normal glia.
    Cancer Management and Research 08/2012; 4(1):233-41. DOI:10.2147/CMAR.S32449
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