PMID- 15685439
OWN - NLM
STAT- MEDLINE
DCOM- 20050617
LR  - 20221109
IS  - 0001-6322 (Print)
IS  - 0001-6322 (Linking)
VI  - 109
IP  - 1
DP  - 2005 Jan
TI  - Epidemiology and etiology of gliomas.
PG  - 93-108
AB  - Gliomas of astrocytic, oligodendroglial and ependymal origin account for more 
      than 70% of all brain tumors. The most frequent (65%) and most malignant 
      histological type is the glioblastoma. Since the introduction of computerized 
      tomography and magnetic resonance imaging, the incidence rates of brain tumors 
      have been rather stable, with a tendency of higher rates in highly developed, 
      industrialized countries. Some reports indicate that Caucasians have higher 
      incidence than black or Asian populations, but to some extent, this may reflect 
      socio-economic differences and under-ascertainment in some regions, rather than a 
      significant difference in genetic susceptibility. With the exception of pilocytic 
      astrocytomas, the prognosis of glioma patients is still poor. Less than 3% of 
      glioblastoma patients are still alive at 5 years after diagnosis, higher age 
      being the most significant predictor of poor outcome. Brain tumors are a 
      component of several inherited tumor syndromes, but the prevalence of these 
      syndromes is very low. Several occupations, environmental carcinogens, and diet 
      (N-nitroso compounds) have been reported to be associated with an elevated glioma 
      risk, but the only environmental factor unequivocally associated with an 
      increased risk of brain tumors, including gliomas, is therapeutic X-irradiation. 
      In particular, children treated with X-irradiation for acute lymphoblastic 
      leukemia show a significantly elevated risk of developing gliomas and primitive 
      neuroectodermal tumor (PNET), often within 10 years after therapy. TP53 mutations 
      are frequent in low-grade gliomas and secondary glioblastomas derived therefrom. 
      Approximately 60% of mutations are located in the hot spot codons 248 and 273, 
      and the majority of these are G:C-->A:T transitions at CpG sites. TP53 mutations 
      are significantly more frequent in low-grade astrocytomas with promoter 
      methylation of the O(6)-methylguanine-DNA methyltransferase repair gene, 
      suggesting that, in addition to deamination of 5-methylcytosine, exogenous or 
      endogenous alkylation in the O(6) position of guanine may contribute to the 
      formation of these mutations.
FAU - Ohgaki, Hiroko
AU  - Ohgaki H
AD  - International Agency for Research on Cancer, Lyon, France. ohgaki@iarc.fr
FAU - Kleihues, Paul
AU  - Kleihues P
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20050201
PL  - Germany
TA  - Acta Neuropathol
JT  - Acta neuropathologica
JID - 0412041
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - Age Factors
MH  - Central Nervous System Viral Diseases/complications
MH  - Craniocerebral Trauma/complications
MH  - Educational Status
MH  - Electromagnetic Fields/adverse effects
MH  - Glioma/*epidemiology/*etiology/genetics/mortality
MH  - Humans
MH  - Hypersensitivity/complications
MH  - Incidence
MH  - Models, Biological
MH  - Mortality
MH  - Mutation/genetics
MH  - Occupational Exposure
MH  - Radiation, Ionizing
MH  - *Risk Factors
MH  - Sex Factors
MH  - Smoking/adverse effects
MH  - Tumor Suppressor Protein p53/genetics
RF  - 153
EDAT- 2005/02/03 09:00
MHDA- 2005/06/18 09:00
CRDT- 2005/02/03 09:00
PHST- 2004/10/27 00:00 [received]
PHST- 2004/11/01 00:00 [accepted]
PHST- 2005/02/03 09:00 [pubmed]
PHST- 2005/06/18 09:00 [medline]
PHST- 2005/02/03 09:00 [entrez]
AID - 10.1007/s00401-005-0991-y [doi]
PST - ppublish
SO  - Acta Neuropathol. 2005 Jan;109(1):93-108. doi: 10.1007/s00401-005-0991-y. Epub 
      2005 Feb 1.