Volume 5
Archive

1: Br J Neurosurg. 2006 Oct;20(5):275-80.

 
OMICS and brain tumour biomarkers.

Petrik V, Loosemore A, Howe FA, Bell BA, Papadopoulos MC.

Centre for Clinical Neuroscience, Division of Cardiac and Vascular Sciences, St George's University of London, UK.

Currently, brain tumours are diagnosed by surgical biopsy and light microscopic examination of tissue, with immunohistochemistry in difficult cases. We review research in the field of brain tumour diagnosis and discuss several new approaches. In future, tumour type, optimal treatment, and prognosis could be obtained by studying the gene (genomics), protein (proteomics) or metabolite (metabolomics) content of tumour cells. These techniques generate complex data, analysed using techniques such as pattern recognition software to identify biomarker signatures of different tumours. Compared with individual biomarkers, biomarker signatures appear to increase diagnostic accuracy and may produce an improved brain tumour classification system.

PMID: 17129872 [PubMed - in process]

 

2: J Clin Oncol. 2006 Dec 1;24(34):5427-33.

 
Detrimental effects of tumor progression on cognitive function of patients with high-grade glioma.

Brown PD, Jensen AW, Felten SJ, Ballman KV, Schaefer PL, Jaeckle KA, Cerhan JH, Buckner JC.

Mayo Clinic, Rochester, MN 55905, USA. brown.paul@mayo.edu

PURPOSE: There is growing recognition that the primary cause of cognitive deficits in adult patients with primary brain tumors is the tumor itself and more significantly, tumor progression. To assess the cognitive performance of high-grade glioma patients, prospectively collected cognitive performance data were analyzed. PATIENTS AND METHODS: We studied 1,244 high-grade brain tumor patients entered onto eight consecutive North Central Cancer Treatment Group treatment trials that used radiation and nitrosourea-based chemotherapy. Imaging studies and Folstein Mini-Mental State Examination (MMSE) scores recorded at baseline, 6, 12, 18, and 24 months were analyzed to assess tumor status and cognitive function over time. RESULTS: The proportion of patients without tumor progression who experienced clinically significant cognitive deterioration compared with baseline was stable at 6, 12, 18, and 24 months (18%, 16%, 14%, and 13%, respectively). In patients without radiographic evidence of progression, clinically significant deterioration in MMSE scores was a strong predictor of a more rapid time to tumor progression and death. At evaluations preceding interval radiographic evidence of progression, there was significant deterioration in MMSE scores for patients who were to experience progression, whereas the scores remained stable for the patients who did not have tumor progression. CONCLUSION: The proportion of high-grade glioma patients with cognitive deterioration over time is stable, most consistent with the constant pressure of tumor progression over time. Although other factors may contribute to cognitive decline, the predominant cause of cognitive decline seems to be subclinical tumor progression that precedes radiographic changes.

Publication Types:

• Research Support, N.I.H., Extramural
• Research Support, Non-U.S. Gov't

PMID: 17135644 [PubMed - in process]

 

3: J Clin Oncol. 2006 Dec 1;24(34):5419-26.

 
Significance of necrosis in grading of oligodendroglial neoplasms: a clinicopathologic and genetic study of newly diagnosed high-grade gliomas.

Miller CR, Dunham CP, Scheithauer BW, Perry A.

Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA.

PURPOSE: High-grade gliomas (HGGs; WHO grades 3-4) are highly diverse, with survival times ranging from months to years. WHO 2000 grading criteria for high-grade oligodendroglial neoplasms [anaplastic oligoastrocytoma (AOA) and anaplastic oligodendroglioma (AO)] remain subjective, and the existence of grade 4 variants is controversial. PATIENTS AND METHODS: Overall survival (OS) of 1,093 adult patients with a cerebral HGG newly diagnosed between 1990 and 2005 was analyzed by univariate and multivariate models for significance of the following factors: patient age, surgery type, year of diagnosis, endothelial proliferation, necrosis, oligodendroglial histology, treatment center, and chromosome 1p, 19q, 7p (EGFR), and 10q (PTEN) abnormalities by fluorescence in situ hybridization (FISH). RESULTS: Necrosis was a statistically significant predictor of poor OS on univariate and multivariate analyses in AOA but not in AO. Median OS for patients with necrotic AOA (22.8 months) was significantly worse than for patients with non-necrotic AOA (86.9 months; P < .0001) but was better than conventional glioblastomas (9.8 months; P < .0001). In addition to patient age, the following were significant independent prognostic factors (P .001): grade and surgery type for the entire HGG cohort; modified grade for AOA (3 v 4); and modified grade, 1p/19q codeletion status, and oligodendroglial histology for the 586 HGGs analyzed by FISH. CONCLUSION: Stratification of AOA, but not of pure AO, into grades 3 and 4 on the basis of necrosis is prognostically justified and is more powerful than the current approach. Both routine histology and genetic testing provide independent, prognostically useful information.

Publication Types:

• Research Support, N.I.H., Extramural

PMID: 17135643 [PubMed - in process]

 

4: Neurology. 2006 Nov 28;67(10):1863-6.

 
Tumor suppressor in lung cancer-1 (TSLC1) functions as a glioma tumor suppressor.

Houshmandi SS, Surace EI, Zhang HB, Fuller GN, Gutmann DH.

Department of Neurology, Washington University School of Medicine, Box 8111; 660 S. Euclid Avenue, St. Louis, MO 63110, USA.

Tumor suppressor in lung cancer-1 (TSLC1) loss is common in many human cancers, including meningioma. In this study, we demonstrate that TSLC1 protein and RNA expression is lost in 60% to 65% of high-grade gliomas, and that TSLC1 reintroduction into glioma cells results in growth suppression. Moreover, Tslc1 loss in mice results in increased astrocyte proliferation in vivo and in vitro. These data indicate that TSLC1 functions as a glioma tumor suppressor.

Publication Types:

• Research Support, N.I.H., Extramural
• Research Support, Non-U.S. Gov't
• Research Support, U.S. Gov't, Non-P.H.S.

PMID: 17130425 [PubMed - in process]

 

5: Oncogene. 2006 Nov 30;25(56):7440.

 
Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptosis pathway in glioma cells.

Sawada M, Nakashima S, Banno Y, Yamakura H, Takenaka K, Shinoda J, Nishimura Y, Sakai N, Nozawa Y.

PMID: 17136113 [PubMed - in process]

 

6: Pediatr Hematol Oncol. 2007 Jan-Feb;24(1):79-84.

Progress in the treatment of childhood brain tumors: no room for complacency.

Finlay JL, Erdreich-Epstein A, Packer RJ.

Department of Hematology/Oncology, Children's Hospital, Los Angeles, California 90027, USA. neuronc514@aol.com

PMID: 17130118 [PubMed - in process]