Linked Life Data

11100818

Source:http://linkedlifedata.com/resource/pubmed/id/11100818

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-3-8
pubmed:abstractText
Bcl-2 protein plays an important role in inhibiting apoptosis and protecting normal and neoplastic cells from toxicity. Bcl-2 overexpression in malignant tumors, on the other hand, may cause resistance against adjuvant treatment. Since there are subpopulations of patients with glioma that differ considerably in their treatment benefit, it is important to identify prognostic factors for outcome and to tailor adjuvant protocols in accordance with specific biological features of the respective tumor. The present study aimed at investigating the role of bcl-2 expression in higher-grade glioma (WHO grade III and IV). Bcl-2 expression was correlated with clinical and paraclinical parameters, and evaluated in univariate and multivariate statistical models. In addition, bcl-2-overexpressing human glioma cells in culture were used for modeling the in vivo findings and for investigating the importance of bcl-2 for tumor resistance against cytotoxic treatment. A group of 86 patients with higher-grade glioma were investigated. Anaplastic astrocytoma (AA; WHO G III, n = 29) showed bcl-2 expression in 48% of the cases, and immunohistochemical positivity was associated with a significantly shorter survival time (p = 0.0068). In glioblastoma patients (GBM; WHO G IV, n = 57), 51% of tumors were bcl-2 positive, but bcl-2 expression did not correlate significantly with survival (p = 0.39). In a Cox proportional hazards regression model, bcl-2 positivity was confirmed as a negative prognostic parameter in AA, but not in GBM. Bcl-2 overexpressing and control human glioma cell clones (T98MG line) were treated in culture with the cytotoxic drugs carmustine (BCNU), paclitaxel, vincristine, and doxorubicin. In addition, bcl-2-overexpressing and control cells were infected with a retrovirus carrying the herpes-simplex-virus thymidine kinase gene (HSV-tk), and then treated with ganciclovir (GCV). Bcl-2 overexpression significantly increased tumor cell resistance against all of the above cytotoxic drugs, and also against HSV-TK/GCV mediated gene therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0167-594X
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
207-16
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11100818-Astrocytoma, pubmed-meshheading:11100818-Brain Neoplasms, pubmed-meshheading:11100818-Glioblastoma, pubmed-meshheading:11100818-Glioma, pubmed-meshheading:11100818-Humans, pubmed-meshheading:11100818-Immunohistochemistry, pubmed-meshheading:11100818-Middle Aged, pubmed-meshheading:11100818-Neoplasm Proteins, pubmed-meshheading:11100818-Nuclear Proteins, pubmed-meshheading:11100818-Prognosis, pubmed-meshheading:11100818-Proportional Hazards Models, pubmed-meshheading:11100818-Proto-Oncogene Proteins, pubmed-meshheading:11100818-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:11100818-Proto-Oncogene Proteins c-mdm2, pubmed-meshheading:11100818-Receptor, Epidermal Growth Factor, pubmed-meshheading:11100818-Regression Analysis, pubmed-meshheading:11100818-Retrospective Studies, pubmed-meshheading:11100818-Survival Rate, pubmed-meshheading:11100818-Time Factors, pubmed-meshheading:11100818-Tumor Suppressor Protein p53
pubmed:year
2000
pubmed:articleTitle
Bcl-2 expression in higher-grade human glioma: a clinical and experimental study.
pubmed:affiliation
Department of Neurosurgery, Martin Luther University Halle Wittenberg, Halle (Saale), Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't