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Thesis (M.S.)--Northern Michigan University, 2008. / Bibliography: leaves 40-47.

Thesis (doctoral)--Lund University, 1992. / Added t.p. with thesis statement inserted.

Thesis (M. Phil.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 120-145).

Thesis (doctoral)--Lund University, 1992. / Added t.p. with thesis statement inserted.

Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas. Programa de Pós-Graduação em Neurociências. / Made available in DSpace on 2012-10-20T01:09:47Z (GMT). No. of bitstreams: 0 / Neste estudo foi avaliado o efeito da derrota social sobre a progressão tumoral de células de glioma C6 inoculadas no cérebro de ratos. Os animais foram divididos em 4 grupos: inoculados com salina (grupo S, controle), inoculados com glioma C6 (grupo I), inoculados com glioma e depois submetidos a dupla derrota social (grupo I/D) e derrotados e depois inoculados com glioma (grupo D/I). Após 15 dias da inoculação, os animais foram avaliados quanto à progressão tumoral, sobrevivência, atividade motora (teste de campo aberto) e parâmetros imunológicos (níveis séricos de IgG contra glioma C6 e contagem sanguínea de linfócitos, granulócitos e monócitos). A progressão tumoral nos grupos inoculado e depois derrotado (I/D) e derrotado e depois inoculado (D/I) aumentou 69% e 41%, respectivamente, em relação ao grupo inoculado (I); o grupo I/D apresentou uma progressão tumoral 19% maior do que o grupo D/I. A atividade motora dos animais dos grupos I/D e D/I foi reduzida em 52% e 26%, respectivamente. Os animais I/D e D/I sofreram uma redução da sobrevivência de 34% e de 16%, respectivamente, quando comparados ao grupo I. Os níveis séricos de IgG contra glioma C6 foram aumentados nos animais inoculados com glioma (grupos I, I/D e D/I); entretanto no grupo I/D este aumento foi menor. No grupo I/D também mostrou uma redução no número de linfócitos e de granulócitos. Em conclusão, os resultados indicaram que a derrota social em ratos aumentou a progressão tumoral de glioma e reduziu a sobrevivência e alguns parâmetros da resposta imune dos animais observadas no modelo experimental proposto.

Source: Dissertation Abstracts International, Volume: 70-03, Section: B, page: 1570. Advisers: Michael E. Scheurer; Jan M. Risser. Includes bibliographical references.

Thesis (M.Sc.)--University of Alberta, 2010. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Science, Department of Computing Science. Title from pdf file main screen (viewed on June 13, 2010). Includes bibliographical references.

Chromosome banding analysis of human glial tumors was performed using G- and Q-banding techniques in an attempt to establish recurring sites of chromosome change. Results revealed a nonrandom karyotypic profile including aneuploidy and considerable variation in chromosome number (range 40 → 200). All tumors examined displayed numerical abnormalities, with the most common numeric change being a gain of chromosome 7. Chromosomes most frequently involved in structural abnormalities included #1, #3, #7, and #11. Double minutes, reported to be frequently associated with human glial tumors, were observed in only one of ten tumors examined. These results (taken in conjunction with previously published reports) suggest that the single most frequently altered chromosome in human glial tumors is chromosome 7. An attempt was then made to correlate the observed chromosome 7 changes with activation of the cellular proto-oncogene c-erb-B, whose product is the epidermal growth factor receptor (EGFR). Six human glial tumors were analyzed for ¹²⁵I-EGF binding, EGFR gene copy number, EGFR gene rearrangement, mRNA expression, and karyotypic profile. Saturation analysis at 4°C revealed significant numbers of EGFR's in all 6 tumors. Southern blotting analysis utilizing cDNA probes for the EGFR failed to demonstrate significant amplification or structural rearrangement of the EFGR gene. Analysis of EGFR mRNA revealed significant levels in 3 of the tumors studied as compared to the A341 cell line. Karyotypic analysis revealed that all six cell lines displayed extra copies of both whole and structurally altered chromosome 7. These results may suggest that EGFR overexpression is associated with alterations of chromosome 7 (the locus for the EGFR gene). In contrast to previous reports, EGFR mRNA levels did not directly parallel EGF receptor numbers. These results suggest that overexpression of the EGFR may be related to an alternative mechanism, other than gene amplification and elevated mRNA levels, such as the regulation of receptor biosynthesis and degradation. In summary, findings indicate that alterations of chromosome 7 are the most prevalent chromosomal change in human glial tumors, and that these alterations may lead to overexpression of the proto-oncogene c-erb-B.

The overall survival for patients with glioblastoma multiforme (GBM) has not improved in two decades. A better understanding of the molecular basis for gliomagenesis would aid therapeutic advances. Recombinational based alternative lengthening of telomeres (ALT) is a telomere maintenance mechanism (TMM) distinct from telomerase, which serves as a prognostic factor in GBM. In this thesis, I have compared components of the p53 axis, namely p53, p21[WAF-1] and the paired box-containing transcription factors (PAX) PAX2, 5, and 8, with TMM in gliomas. Analysis of TP53 status in relation to TMM in 110 gliomas revealed that activation of ALT during tumorigenesis possibly requires loss of normal TP53 function (P < 0.0001). Overexpression of p21[WAF-1] was also found to correlate with telomerase-positive gliomas (P = 0.0002). Moreover, high p21[WAF-1] expression is a poor prognostic factor in patients under 56 years (P = 0.015). Telomere length (TL) was also found as a prognostic factor, such that short TL (< 5 kb) is a poor prognostic factor in the group without defined TMM ("None")(P = 0.0160). Pax2,5 and 8 belong to Group II of the PAX family. They are expressed at the midbrain-hindbrain boundary (MHB) and in the neural tube of the vertebrate embryo, whereas their expression levels are low in the adult brain. To explore their roles in glioma pathology, I analyzed mRNA levels in 54 gliomas and 16 established glioma cell lines. Increased levels of PAX8 mRNA were detected in 74.1% of gliomas and 62.5% of established glioma cell lines by real time PCR. Sixty-six percent of glioma specimens expressed high levels of active PAX2, 5, and 8 by immunohistochemistry. There were more males than females having high PAX2 expression (P = 0.0408). Suppression of PAX8 by small interfering RNA induced glioma cell death, independent of TP53 status. These findings identify PAX8 as a survival factor for GBM, and PAX2, 5, and 8 expression as contributing to the aggressive behavior of gliomas. The mRNA level of PAX8 showed a positive correlation with telomerase activity in glioma biopsies (r� = 0.75, P < 0.001). The relationship was explored and I found that PAX2 and PAX8 are able to activate the reporter constructs of both the catalytic subunit (hTERT) and the RNA component (hTR) of telomerase. PAX8 had a stronger effect than PAX2 on the activation of the hTERT and hTR promoters. By electrophoretic mobility shift assay, Western blotting and telomerase activity assay, I showed that PAX8 bound directly to hTERT and hTR promoters, and upregulated hTERT protein and telomerase activity. Moreover, gliomas carrying wild type TP53 had higher levels of PAX8 expression compared to those with mutant TP53 (P = 0.0075) suggesting that PAX8 is significant only in some GBMs during gliomagenesis. These results show that the oncofetal proteins, PAX2 and PAX8, may have roles in telomerase regulation. Taken together, molecular markers examined in this thesis suggest gliomas with different TMMs are derived from different pathways.