Descriptive epidemiology of cerebral gliomas in France

Fleury, Agnès; Ménegoz, F; Grosclaude, Pascale; Daurès, Jean‐Pierre; Henry‐Amar, M.; Raverdy, N.; Schaffer, Paul; Poisson, M; Delattre, Jean‐Yves

doi:10.1002/(sici)1097-0142(19970315)79:6<1195::aid-cncr19>3.0.co;2-v

Cited by 117 publications

(55 citation statements)

References 27 publications

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“…Because data in that population are calculated from the time of diagnosis, OS and PFS were calculated from the time of surgery and the time of study inclusion. PFS and OS were then stratified by age (Ͼ 75 years or Ͻ 75 years), KPS at study entry (postsurgery; Ͼ 60 or Ͻ 60), median tumor size (Ͼ 15.75 cm 2 or Ͻ 15.75 cm 2 ), and type of response (CR, PR, or SD). Survival curves were compared using the log-rank test at an ␣ level of 0.05.…”

Section: Methodsmentioning

confidence: 99%

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Phase II study of temozolomide without radiotherapy in newly diagnosed glioblastoma multiforme in an elderly populations

Chinot

Barrié

Frauger

et al. 2004

Cancer

135

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BACKGROUNDCurrently, the survival of patients age > 70 years with glioblastoma multiforme (GBM) ranges from 4 months to 6 months, although radiotherapy and/or chemotherapy may prolong survival in certain subgroups. Temozolomide is an oral chemotherapeutic agent with efficacy against malignant gliomas and a favorable safety profile. This open‐label, single‐center, Phase II study was designed to evaluate the efficacy and safety of temozolomide as first‐line chemotherapy and exclusive treatment in elderly patients with newly diagnosed GBM.METHODSChemotherapy‐naïve patients (age > 70 years) were treated with temozolomide at a dose of 150–200 mg/m2 per day for 5 consecutive days of a 28‐day cycle until they developed disease progression. No radiation therapy was administered. The primary endpoint was median overall survival (OS); secondary endpoints included progression‐free survival (PFS) and toxicity.RESULTSThirty‐two patients (median age, 75 years; median Karnofsky performance status, 70) experienced a median OS of 6.4 months and a median PFS of 5.0 months. Of 29 patients who were assessed for response, 9 patients (31%) achieved a partial response, 12 patients (41%) maintained stable disease, and 8 patients (28%) developed progressive disease. Adverse events primarily were mild, with NCI CTC Grade 3–4 thrombocytopenia and neutropenia reported to occur in 6% and 9% of patients, respectively. No neurotoxicity was observed. Treatment delays and dose reductions occurred in 13% and 14% of cycles, respectively.CONCLUSIONSTemozolomide represents a safe, easily administered, and effective therapeutic approach for elderly patients with newly diagnosed GBM. Cancer 2004. © 2004 American Cancer Society.

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Section: Methodsmentioning

confidence: 99%

“…[1][2][3] For example, some investigators have reported an increase of 5% per year in the portion of population age Ն 65 years. 2 Another study showed that, although it remained relatively stable in the younger segment of the population, the incidence of GBM increased by Ͼ 20% in patients ages 70 -74 years between 1980 and 1990.…”

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confidence: 99%

Phase II study of temozolomide without radiotherapy in newly diagnosed glioblastoma multiforme in an elderly populations

Chinot

Barrié

Frauger

et al. 2004

Cancer

135

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“…For example, the ageadjusted annual incidence rate of glioma in the United States is 7.6 in 100,000 in males and 5.4 in 100,000 in females (2), and the male-to-female excess has been stable over time and is evident internationally (7)(8)(9). Using New York State tumor registry data for the period from 1976 to 1995, McKinley et al (7) calculated crude, and age-and sex-specific incidence rates for three types of glial tumors: glioblastoma multiforme, astrocytoma not otherwise specified, and anaplastic astrocytoma.…”

Section: Descriptive Epidemiologymentioning

confidence: 99%

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Kabat

Etgen

Rohan

2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Gliomas are the most common type of primary malignant brain tumor and have a very poor prognosis. Little is known, however, about the etiology of these tumors. Evidence from a number of sources suggests that endogenous steroid hormones may play a role in the development of gliomas. First, the descriptive epidemiology of glioma suggests a relative protection of females compared with males, particularly during the premenopausal years. Second, some gliomas and glioblastomas express estrogen receptors (ER), especially ERβ, as well as aromatase, the enzyme responsible for the conversion of testosterone to estradiol, and possibly other steroid hormone receptors. Third, experimental studies indicate that glioblastomas transplanted into animals grow at a slower rate in females compared with males. Finally, experimental studies show that estradiol, 2-methoxyestradiol, and a number of selective estrogen receptor modulators inhibit proliferation of gliomas and induce cell death. These hormonal agonists and antagonists may act either through classical steroid hormone receptors or independently of such receptors. In view of these findings, further clinical, experimental, and epidemiologic studies are needed to elucidate the role of steroid hormone agonists and antagonists in the development and proliferation of glioma. If hormonal pathways are involved in gliomagenesis, this could eventually lead to the design of preventive strategies. Cancer Epidemiol Biomarkers Prev; 19(10); 2421-7. ©2010 AACR.Little is known about the etiology of brain neoplasms, which in general are highly fatal (1). Gliomas, which include astrocytomas, oligodendrogliomas, and ependymomas, are the most common type of primary malignant brain tumor, accounting for approximately 80% of cases (2). Gliomas originate from glial cells (astrocytes or oligodendrocytes). Gliobastoma multiforme, the highest grade of glioma, is the most common and most aggressive type of malignant glioma. Most cases of glioblastoma multiforme (∼90%), referred to as "primary glioblastoma multiforme," develop rapidly without detectable evidence of a less malignant precursor tumor, whereas about 10% of glioblastomas, referred to as "secondary glioblastoma multiforme," develop slowly from low-grade astrocytomas (3). The only established risk factors for gliomas are high-dose ionizing radiation and certain rare genetic conditions, which together account for only a small proportion of cases (1, 4, 5). However, evidence from a number of sources suggests a possible role of endogenous ovarian steroid hormones in the development of glioma. Given that this topic has received little attention in major reviews on brain tumor epidemiology to date (1, 4-6), we review here findings from descriptive and analytic epidemiology, clinical studies, and experimental animal and cell culture studies pertinent to the potential role of steroid hormones in the development of glioma. Descriptive EpidemiologyThe incidence rate of glioma in adulthood is 50% greater in men than in women (5, 7). For example...

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“…The annual incidence rates of primary brain tumours in the United Kingdom, France, Norway and Finland and mortalities per 100 000 population are similar to those in the United States (Muir et al, 1994;Fleury et al, 1997;Prados and Levin, 2000). The incidence of brain cancer may be increasing in older people (Muir et al, 1994).…”

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confidence: 65%

Effective treatment of experimental U-87MG human glioblastoma in nude mice with a targeted cytotoxic bombesin analogue, AN-215

et al. 2002

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Some brain tumours, such as glioblastomas express high levels of receptors for bombesin/gastrin releasing peptide. We investigated whether bombesin/gastrin releasing peptide receptors found in glioblastoma cell lines can be utilised for targeting of a cytotoxic bombesin analogue, AN-215 consisting of a potent derivative of doxorubicin, 2-pyrrolino-doxorubicin (AN-201) linked to a bombesin-like peptide carrier. This study reports the effect of AN-215 on the growth of U-87MG human glioblastomas xenografted into nude mice. High affinity binding of AN-215 to U-87MG tumours was characterised by an IC 50 value of 4.0+0.1 nM, as determined by radioreceptor assays. mRNA analyses revealed the presence of mRNA for BN receptor subtypes 1 and 2. Treatment with AN-215 significantly (P50.05) extended tumour doubling time from 4.54+0.2 days to 8.18+1.8 days and inhibited tumour growth as demonstrated by a 69.6% reduction in final tumour volume (P50.001) and a 64.6% decrease in tumour weight as compared to controls. Cytotoxic radical AN-201 at the same dose was ineffective. The antitumour effect of AN-215 could be blocked by pretreatment with an excess of a bombesin antagonist, indicating that the action of this cytotoxic analogue is receptor-mediated. Our results suggest that patients with inoperable brain tumours such as malignant gliomas may benefit from targeted chemotherapy based on cytotoxic bombesin analogue AN-215.

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Descriptive epidemiology of cerebral gliomas in France

Cited by 117 publications

References 27 publications

Phase II study of temozolomide without radiotherapy in newly diagnosed glioblastoma multiforme in an elderly populations

Phase II study of temozolomide without radiotherapy in newly diagnosed glioblastoma multiforme in an elderly populations

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Effective treatment of experimental U-87MG human glioblastoma in nude mice with a targeted cytotoxic bombesin analogue, AN-215

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