Incidence Of Malignant Brain Tumors Research Articles

293P Molecular biomarkers correlation in symptomatic tumor-related epilepsy: A preliminary study on 151 cases of brain tumors

The annual incidence of malignant brain tumors is 7.08 per 100,000 inhabitants in Italy and epilepsy is one of the most common presenting symptoms. Patients with brain tumor-related epilepsy (BTRE) suffer from two challenging pathologies simultaneously: glioma and epilepsy. The pathogenesis of BTRE is not fully described. The integration of molecular data and histology changed the diagnostic approach and prognostic characterization for patients with brain tumors. The aim of this study is to explore the associations between histo-molecular patterns and epilepsy features, in a group of patients suffering from brain tumors.

Epidemiology of central nervous system tumors

Brain tumors of the central nervous system have a very poor prognosis. They represent a significant mortality in the USA according to the CBTR US 2020 central brain tumor register in United state. These tumors differ according to histology, anatomical site, age, sex, race and ethnicity. The incidence of malignant brain tumors is higher in males and whites, and non-malignant tumors are most common in females and blacks. The 5-year relative survival went from 23 to 36 between 1975 and 2019, especially in young people, with less improvement in the elderly because of glioblastomas for which there is little progress; their 5-year survival increased by only 4-7%. Little is known about Brain tumors incriminating ionizing radiation, chemicals and genetics. Due to the aggressive nature of the malignant subtypes; continuous updates are needed to elucidate the causes of differences between gender, age and ethnicity.

Racial/ethnic and sex differences in young adult malignant brain tumor incidence by histologic type

BackgroundBrain tumors are among the top four cancers in young adults. We assessed important windows of tumor development and examined the interplay of race/ethnicity, age, and sex in young adult brain tumor incidence. MethodsUsing SEER 18 data (2000–2017), incidence rates were estimated by Poisson regression in individuals aged 20–39 years at diagnosis. Incidence rate ratios (IRR) and 95% confidence intervals (95% CI) were estimated by race/ethnicity, sex and age for 12 malignant histologies. ResultsWhite incidence for all histologies was higher (White vs. Black IRR: 2.09, 95% CI: 1.94, 2.24; White vs Asian Pacific Islander IRR: 1.88, 95% CI: 1.75, 2.03; White vs Hispanic IRR: 1.70, 95% CI: 1.62, 1.78; White vs American Indian IRR: 1.40, 95% CI: 1.14, 1.73). Minority groups had higher lymphoma incidence (White vs Black IRR: 0.32, 95% CI: 0.25, 0.40, White vs Hispanic HR: 0.55, 95% CI: 0.44, 0.68). Males had higher incidence than females for all histologies (IRR: 1.36, 95% CI: 1.31, 1.41). Male rates were highest for lymphoma (male-to-female [MF] IRR: 2.00, 95% CI: 1.65, 2.42) and glioblastoma (MF IRR: 1.61, 95% CI: 1.48, 1.75). The male excess in incidence was similar by race/ethnicity and increased with age (20–24-year-old IRR: 1.18, 95% CI: 1.07, 1.29; 35–39-year-old IRR: 1.44, 95% CI: 1.35, 1.54). ConclusionsA White race and male incidence excess was observed among brain tumors. ImpactThe male excess was similar by race/ethnicity and increased with age suggesting male sex may be an intrinsic risk factor for brain tumor development.

Brain and other central nervous system tumor statistics, 2021.

Brain and other central nervous system (CNS) tumors are among the most fatal cancers and account for substantial morbidity and mortality in the United States. Population-based data from the Central Brain Tumor Registry of the United States (a combined data set of the National Program of Cancer Registries [NPCR] and Surveillance, Epidemiology, and End Results [SEER] registries), NPCR, National Vital Statistics System and SEER program were analyzed to assess the contemporary burden of malignant and nonmalignant brain and other CNS tumors (hereafter brain) by histology, anatomic site, age, sex, and race/ethnicity. Malignant brain tumor incidence rates declined by 0.8% annually from 2008 to 2017 for all ages combined but increased 0.5% to 0.7% per year among children and adolescents. Malignant brain tumor incidence is highest in males and non-Hispanic White individuals, whereas the rates for nonmalignant tumors are highest in females and non-Hispanic Black individuals. Five-year relative survival for all malignant brain tumors combined increased between 1975 to 1977 and 2009 to 2015 from 23% to 36%, with larger gains among younger age groups. Less improvement among older age groups largely reflects a higher burden of glioblastoma, for which there have been few major advances in prevention, early detection, and treatment the past 4 decades. Specifically, 5-year glioblastoma survival only increased from 4% to 7% during the same time period. In addition, important survival disparities by race/ethnicity remain for childhood tumors, with the largest Black-White disparities for diffuse astrocytomas (75% vs 86% for patients diagnosed during 2009-2015) and embryonal tumors (59% vs 67%). Increased resources for the collection and reporting of timely consistent data are critical for advancing research to elucidate the causes of sex, age, and racial/ethnic differences in brain tumor occurrence, especially for rarer subtypes and among understudied populations.

The incidence of malignant brain tumors is increased in patients with obstructive sleep apnea: A national health insurance survey.

The association between obstructive sleep apnea (OSA) and malignant brain tumors has yet to be fully investigated. Therefore, the purpose of this study was to elucidate the effect of OSA on brain tumor incidence based on the Korea National Health Insurance Service (KNHIS) dataset. The KNHIS data between 2007 and 2014 were analyzed, and the primary endpoint was newly diagnosed malignant brain tumor. A total of 198,574 subjects aged ≥ 20 years with newly diagnosed OSA were enrolled in the study, and 992,870 individuals were selected as a control group based on propensity score matching (PSM) by gender and age. The average follow-up duration was 4.8 ± 2.3 years. The hazard ratios (HRs) for brain tumor for patients with OSA were 1.78 (95% confidence interval [CI]: 1.42–2.21) in Model 1 (not adjusted with any covariate) and 1.67 (95% CI: 1.34–2.09) in Model 2 (adjusted for income level, diabetes, hypertension, dyslipidemia, and COPD). In subgroup analysis by gender, the odds ratios (OR) of OSA were 1.82 (95% CI: 1.41–2.33) in men and 1.26 (95% CI: 0.74–2.03) in women. The ORs were 1.97 (95% CI: 1.15–3.24) in the older (age ≥ 65 years) group, 1.66 (95% CI: 1.25–2.17) in the middle-aged (40 ≤ age < 65 years) group, and 1.41 (0.78–2.44) in the young (20 ≤ age < 40 years) group. In conclusion, OSA may increase the incidence of brain tumors.

Global incidence of brain and spinal tumors by geographic region and income level based on cancer registry data

While obtaining accurate estimates of tumor incidence volume is a difficult technical problem because it requires collating and analyzing data from dozens of world-wide sources curated under different conditions, our study aims to determine the global incidence of brain and spinal tumors. We analyzed 207 tumor registries on five continents, and calculated age-standardized rates to compare tumor incidence between geographic regions and income levels. Based on data available in current cancer registries, the apparent global incidence of malignant brain tumors was 4.25 cases per 100,000 person-years (95% CI [4.21–4.29]), and varied by region from 6.76 [6.71–6.80] in Europe to 2.81 [2.64–2.99] in Africa. Incidence also varied by World Bank income group, ranging from 6.29 [6.26–6.32] cases per 100,000 in high income countries (HICs), to 4.81 [4.77–4.86] in low and middle-income countries (LMICs). Malignant spinal tumors were much less frequent globally (0.098 [0.093–0.104]) and varied similarly by region and income group. The incidence of brain and spinal tumors varies by region and income group, although case ascertainment bias driven by limited resources in low income regions likely plays a role in variance. The burden of neurosurgical disease in LMICs is large, and similar in scale to HICs.

Simulation of the incidence of malignant brain tumors in birth cohorts that started using mobile phones when they first became popular in Japan.

Over 20 years have passed since the initial spread of mobile phones in Japan. Epidemiological studies of mobile phone use are currently being conducted around the world, but scientific evidence is inconclusive. The present study aimed to simulate the incidence of malignant brain tumors in cohorts that began using mobile phones when they first became popular in Japan. Mobile phone ownership data were collected through an Internet-based questionnaire survey of subjects born between 1960 and 1989. The proportion of mobile phone ownership between 1990 and 2012 was calculated by birth cohort (1960s, 1970s, and 1980s). Subsequently, using the ownership proportion, the incidence of malignant brain tumors was calculated under simulated risk conditions. When the relative risk was set to 1.4 for 1,640 h or more of cumulative mobile phone use and the mean daily call duration was 15 min, the incidence of malignant brain tumors in 2020 was 5.48 per 100,000 population for the 1960s birth cohort, 3.16 for the 1970s birth cohort, and 2.29 for the 1980s birth cohort. Under the modeled scenarios, an increase in the incidence of malignant brain tumors was shown to be observed around 2020. © 2019 Bioelectromagnetics Society.

Trends in the incidence of primary malignant brain tumors in Taiwan and correlation with comorbidities: A population-based study

ObjectivePrimary malignant brain tumors are relatively uncommon, and their incidence and survival rates have seldom been reported. Patients and methodsWe identified all patients with malignant brain tumors in Taiwan between 1997 and 2012 using the National Health Insurance database. We estimated the stratified incidence of malignant brain tumors by age and sex. We estimated the median 1-, 2-, and 5-year survival, taking comorbidities into account. Trends for incidence and survival were analyzed using Joinpoint regression. The incidence in different geographic areas was also evaluated. ResultsA total of 7746 men and 5846 women were identified. The incidence of malignant brain tumor was 3.34 (95% CI, 3.09–3.59) per 100,000 person-years in 1997 and 3.82 (95% CI, 3.56–4.08) per 100,000 person-years in 2012. The average annual percentage change (APC) of the standardized incidence over this period was 0.1 (95% CI, −1.9 to 2.2), suggesting a relatively stable incidence. However, the incidence significantly decreased between 1999 and 2012, with an APC of −1.8 [95% CI, −2.5 to −1.0]. One- and 5-year survival was 53.8% (50.0%–57.5%) and 27.5% (24.1%–30.9%) in 1997 and 67.6% (64.3%–70.7%) and 32.8% (29.6%–35.9%) in 2012. The average APC was 1.1 (95% CI, 0.7–1.5) for 1-year survival and 0.2 (95% CI, −1.0–1.4) for 5-year survival. The trend of improvement in the survival rate was seen for short-term but not long-term survival, especially in the group with more comorbidities. ConclusionsA slightly decreased trend in incidence of primary malignant brain tumors was observed in Taiwanese general population since 1999. Over the past 15 years, the short-term survival of malignant brain tumors has improved, especially in adults.

Global incidence of malignant brain and other central nervous system tumors by histology, 2003-2007.

Previous reports have shown that overall incidence of malignant brain and other central nervous system (CNS) tumors varied significantly by country. The aim of this study was to estimate histology-specific incidence rates by global region and assess incidence variation by histology and age. Using data from the Central Brain Tumor Registry of the United States (CBTRUS) and the International Agency for Research on Cancer's (IARC) Cancer Incidence in Five Continents X (including over 300 cancer registries), we calculated the age-adjusted incidence rates (AAIR) per 100000 person-years and 95% CIs for brain and other CNS tumors overall and by age groups and histology. There were significant differences in incidence by region. Overall incidence of malignant brain tumors per 100000 person-years in the US was 5.74 (95% CI = 5.71-5.78). Incidence was lowest in Southeast Asia (AAIR = 2.55, 95% CI = 2.44-2.66), India (AAIR = 2.85, 95% CI = 2.78-2.93), and East Asia (AAIR = 3.07, 95% CI = 3.02-3.12). Incidence was highest in Northern Europe (AAIR = 6.59, 95% CI = 6.52-6.66) and Canada (AAIR = 6.53, 95% CI = 6.41-6.66). Astrocytic tumors showed the broadest variation in incidence regionally across the globe. Brain and other CNS tumors are a significant source of cancer-related morbidity and mortality worldwide. Regional differences in incidence may provide clues toward genetic or environmental causes as well as a foundation for broadening knowledge of their epidemiology. Gaining a comprehensive understanding of the epidemiology of malignant brain tumors globally is critical to researchers, public health officials, disease interest groups, and clinicians and contributes to collaborative efforts in future research.

Measles may be a Risk Factor for Malignant Brain Tumors.

BackgroundA possible risk factor for brain tumor might be measles, since late neurologic sequelae are part of measles pathology. Subacute sclerosing panencephalitis, a devastating neurologic illness, is prone to develop years after measles infection.MethodsBecause measles damage to the brain might increase the risk of brain tumor, we examined the relationship of measles incidence in 1960 and brain tumor incidence in 50 US States and the District of Columbia, 2004-2007. Data on number of cases of measles by state in 1960 are from the Morbidity and Mortality Weekly Report. In 1960 measles was a childhood illness. We calculated measles incidence by obtaining the population of each state from the 1960 US Census and then age adjusting our results to the cumulative percent of the state population under age 21, since this would have been the measles-infected group. Data on the percentage white population by state are from the US Census (www.census.gov). Age-adjusted incidence (to the 2000 US standard population) of brain tumors is from the Central Brain Tumor Registry of the United States 2011 report.ResultsThere was a significant correlation between 1960 measles incidence and incidence of malignant brain tumors in persons 20 and older in 2004-2007 (r=0.321, p=0.026). Because glioblastoma is more frequent in whites and males, multivariate linear regression was performed with tumor incidence as the dependent variable, measles incidence, percent white population, and sex ratio by state as independent variables. Measles incidence was significantly correlated with malignant brain tumor incidence (β=0.361, p<0.001) and independent of the effect of race (β=0.734, p<0.001) and sex ratio m/f (β=-0.478, p<0.001). There was no correlation of measles incidence with brain tumor incidence in persons younger than 20.ConclusionInflammation is a critical component of tumor development. The inflammation of measles-induced subacute sclerosing panencephalitis, even subclinical cases, could well promote tumor formation, since many tumors arise from sites of infection, chronic irritation and inflammation.

EDL-360: A Potential Novel Antiglioma Agent

Glioma is a brain tumor that arises from glial cells or glial progenitor cells, and represents 80% of malignant brain tumor incidence in the United States. Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor malignancy with fewer than 8% of patients with GBM surviving for more than 3 years. Over the past 10 years, despite improvement in diagnosis and therapies for cancer, the survival rate for high-grade glioma patients remains dismal. The main focus of our research is to identify potent novel antiglioma small molecules. We previously showed that EDL-360, a tetrahydroisoquinoline (THIQ) analog, as being highly cytotoxic to human glioma cell cultures. Here we show that EDL-360 significantly induced apoptosis in human glioma cell lines (U87 and LN18). However, in normal astrocytic cells, EDL-360 induced a modest G0/G1 cell cycle arrest but did not induce apoptosis. In an attempt to enhance EDL-360 induced cell death, we tested simultaneous treatment with EDL-360 and embelin (an inhibitor of the anti-apoptotic protein, XIAP). We found that, glioma cells had significant lower viability when EDL-360 and embelin were used in combination when compared to EDL-360 alone. We also used combination treatment of EDL-360 with decylubiquinone (dUb), a caspase-9 inhibitor, and found that the combination treatment induced a significant cell death when compared to treatment with EDL-360 alone. This is the first report that suggests that dUb has anticancer activity, and perhaps acts as a XIAP inhibitor. Finally, our in vivo data showed that EDL-360 treatment induced a partial regression in glioma tumorigenesis and induced cell death in the treated tumors as shown by H&E staining. Taken together these data suggests that EDL-360 has a potential therapeutic application for treating glioma, especially when combined with XIAP inhibitors.

Cell phones and glioma risk: a review of the evidence

Recently cell phones have become the target of much controversy because they are increasingly being viewed as potential carcinogenic agents with a causal role in brain tumor development. The overall incidence of malignant brain tumors in the United States from 1992 to 2007 declined slightly from 6.8 to 6.2 per 100,000, while the incidence in children has risen slightly over the past three decades [1, 2]. According to the Central Brain Tumor Registry (CBTRUS) [3] in 1995 the incidence of both benign and malignant brain tumors was 13.4 per 100,000 and in 2004 it was 18.2 per 100,000. The cause of the clear increase in benign tumor incidence is unknown, but there is concern that cell phones can trigger biological effects and that several decades of cell phone use in an individual may significantly increase the risk of a malignant brain tumor. The potential public health problem is sizeable as the most common malignant brain tumors are highly lethal and cell phone use in the U.S. alone has escalated dramatically, with approximately 70 million new cell phone subscriptions between 2006 and 2010, and 250 million subscriptions overall in 2007 [4, 5]. The concern relating to cell phone use and brain cancer is underscored by the fact that teens and children are beginning to use cell phones at younger ages [6]. Moreover, greater than 4 of 5 children/teens 12 years and older sleep with a cell phone next to them, often under the pillow [7]. Children and young adults are more susceptible to the harmful effects of carcinogenic agents such as radiation [8]. Therefore, a shift in incidence of brain tumors in younger age groups may emerge as their exposure to cell phones reaches long-term status and attains the 10-year or greater mark. A recent study revealed that children exposed to 1,800 MHz cell phone electromagnetic fields (EMF) can experience significantly higher exposures to cortical regions, hippocampus, hypothalamus and the eye than adults, and that this difference can be greater than one order of magnitude [6]. The most feared brain tumors in adults and children are the gliomas, which include the astrocytomas and oligodendrogliomas. These tumors are graded on a progressive scale of malignancy, and astrocytomas that have progressed to the Grade IV World Health Organization (WHO) classification level are also known as glioblastomas [9]. Glioblastomas are common brain tumors and most frequently arise de novo as primary cancers. The gliomas as a whole comprise approximately 33% of all brain tumors and 79% of malignant brain tumors [3]. Cure is not typical and the therapy of even low grade gliomas can be challenging. The glioblastomas are highly lethal and despite aggressive treatment efforts patients are dead at a median of 14 months after diagnosis [10]. Five year survival is dismal, less than 10%. This review will focus specifically on glioma risk from cell phone use, and will begin with a brief overview of the state of the relevant cell phone—brain tumor risk literature. The two significant, comprehensive databases concerning cell phone use and brain cancer risk are the often cited Hardell (Sweden) and the multicenter European Interphone studies [11, 12]. These two groups each include multiple studies, and they comprise the major focus of the current review. Glioma risk data derived from Hardell and Interphone, as well as from some smaller studies, is partitioned Courtney Corle and Milan Makale are co-first authors.

Induction of Cell Death through Alteration of Oxidants and Antioxidants in Lung Epithelial Cells Exposed to High Energy Protons

Radiation affects several cellular and molecular processes, including double strand breakage and modifications of sugar moieties and bases. In outer space, protons are the primary radiation source that poses a range of potential health risks to astronauts. On the other hand, the use of proton irradiation for tumor radiation therapy is increasing, as it largely spares healthy tissues while killing tumor tissues. Although radiation-related research has been conducted extensively, the molecular toxicology and cellular mechanisms affected by proton irradiation remain poorly understood. Therefore, in this study, we irradiated rat lung epithelial cells with different doses of protons and investigated their effects on cell proliferation and death. Our data show an inhibition of cell proliferation in proton-irradiated cells with a significant dose-dependent activation and repression of reactive oxygen species and antioxidants glutathione and superoxide dismutase, respectively, compared with control cells. In addition, the activities of apoptosis-related genes such as caspase-3 and -8 were induced in a dose-dependent manner with corresponding increased levels of DNA fragmentation in proton-irradiated cells compared with control cells. Together, our results show that proton irradiation alters oxidant and antioxidant levels in cells to activate the apoptotic pathway for cell death.

Glioblastoma and dementia may share a common cause

The cause of most glioblastomas is unknown. One cause might lie in the surrounding brain tissue. The interactions between glioblastoma cells and their micro- and macro-environment could create a context that promotes or suppresses tumor growth and protects or exposes the malignant cells to immune attack. Alzheimer's disease has been identified as a protein misfolding disorder (proteopathy), caused by accumulation of abnormally folded A-beta and tau proteins in the brain. These or other changed proteins or as yet unrecognized biochemical brain changes of dementia might promote glioblastoma development. Published data indicate that there is an association between Alzheimer's disease prevalence and malignant brain tumor incidence in 19 US states. Hypothetically, Alzheimer's and glioblastoma may share an as yet unknown peripheral tissue pathway that can promote the progression of both diseases. If this pathway can be identified, new treatments for both conditions may follow.

Primary malignant brain tumor incidence and Medicaid enrollment

To the Editor: I read with interest the article by Sherwood et al.1 discussing malignant brain tumor incidence and Medicaid enrollment at any time during a patient’s illness with a brain tumor (model 1A), and for a month prior to diagnosis for the years analyzed (model 1B). The incidence and relative risk was smaller in model 1B. Many patients with malignant and benign brain tumors (oligodendroglioma, astrocytoma, and neoplasm not otherwise specified) developed …

Long-Term Mortality and Cancer Risk in Irradiated Rhesus Monkeys

Continuous, 24-year observations on a group of 358 rhesus monkeys reveal that life shortening from exposure to protons in the energy range encountered in the Van Allen belts and solar proton events is influenced primarily by the dose rather than by the energy of radiation. Life shortening in groups exposed to similar surface doses of 138- to 2300-MeV and 32- to 55-MeV protons are not significantly different, but the low-energy protons are associated with more deaths in the early years, while the high-energy protons contribute more to mortality in later years. In males, the most significant cause of life shortening is nonleukemia cancers. In females, radiation increased the risk of endometriosis (an abnormal proliferation of the lining of the uterus) which resulted in significant mortality in the years before early detection and treatment methods were employed. Animals exposed to 55-MeV protons had a high incidence of malignant brain tumors with latent periods ranging from 13 months to 20 years. The first fatal cancer among nonirradiated controls occurred 18 years after the study began. Analysis of the dose-response data supports the 1989 guidelines of the NCRP for maximum permissible radiation exposures in astronauts (NCRP, Guidance on Radiation Received in Space Activities, Report No. 98, National Council on Radiation Protection and Measurements, Bethesda, MD, 1989).