Glioblastoma from a homogenous cohort of patients treated within clinical trial
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7696 | GEO | 2008/06/20
SECONDARY ACCESSION(S): PRJNA99459
REPOSITORIES: GEO
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Project description:Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent). Experiment Overall Design: 80 glioblastoma specimen and 4 non-tumoral brain samples
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Project description:Glioblastoma (GBM) is among the most aggressive cancers. Despite aggressive radiotherapy and treatment with the alkylating agent temozolomide (TMZ), patients ultimately succumb to the disease. Although much interest has focused on highly tumorigenic GBM stem cells (GSCs), adaption of a concept from microbial research proposes that a minor population of dormant âpersisterâ cells in cancer evade current therapies. To separate dormant and treatment-resistant tumor cells in human GBM tumorspheres, we have refined density gradient protocols previously used for separation of neurosphere-forming neural stem cells (NSCs). We find that a minor cell population in human GBM tumorsphere cultures and patient-derived tumor biopsies display increased cell density. These high-density GBM cells (HDGCs) display dormancy, variable expression of proposed GSC markers, and 10-100 fold higher levels of reprogramming gene expression compared to low-density GBM cells (LDGCs). Transcriptional profiling data confirmed the slow-cycling state of HDGCs. As a result, HDGCs show decreased tumorsphere formation capacity in vitro and reduced tumorigenicity in vivo. Using tumorspheres and xenografts, we demonstrated that HDGCs show increased treatment-resistance to ionizing radiation (IR) and temozolomide treatment compared to LDGCs. Similar to the NSC lineage, our data suggest that dormant HDGCs become increasingly sensitive to anti-proliferative therapies as they become activated and further differentiate. In conclusion, density gradients represents a marker-independent approach to separate dormant and treatment-resistant tumor cells in human GBMs and other solid cancers. 12 samples, no replicates, derived from 5 individual patients
2016-07-01 | E-GEOD-71116 | biostudies-arrayexpress
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Project description:Temozolomide resistance is a major obstacle in the therapy of glioblastoma. This is also due to the insufficient understanding of glioma heterogeneity in relation to temozolomide resistance. More in depth biological knowledge would benefit the development of different approaches to tackle the problem from its root. We explored the different outcomes derived from the long-term exposure to temozolomide and identified two different behavioral phenotypes associated to specific categories of pathways. In addition, we investigated the intra-tumoral heterogeneity of these phenotypes revealing the complexity of the temozolomide resistance phenomenon.
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2019-10-31 | GSE122920 | GEO
Project description:Objective: Insights about differences in tumor vasculature and how it reacts to VEGF inhibition is limited, but nevertheless of major relevance to anti-angiogenic therapy. In this study we therefore characterize the effect of bevacizumab combined with chemoradiotherapy (CRT), and explore molecular and genetic markers for response prediction to this combination treatment. Material and Methods: In an academic multicentric randomized phase II study, patients with advanced rectal cancer have been treated with bevacizumab (5mg/kg) in combination with capecitabine (1650mg/m2/day) and radiotherapy (45Gy; 1.8Gy/day) with (50mg/m2) or without oxaliplatin prior to surgery. Of 59 patients, tumor tissue and blood samples were collected before treatment and after the first loading dose of bevacizumab but before CRT (week 3). First, cDNA micro-arrays were performed on the biopsies to investigate differences in gene expression of tumors from patients with and without a pathological complete response (pCR) before start of treatment and to identify biological processes affected by bevacizumab delivery. The paraffin embedded tissue was stained for blood vessels (CD31/CD34) combined with α-SMA (pericytes) and CA-IX (hypoxia). To explore candidate blood-based biomarkers ELISAâs were performed for PDGF-AA, PDGF-BB, THBS-1, IL-8, CYR61 and Ang-2. The expression of all markers was correlated with the pathological response of the patients. Results: Differences in tumoral gene expression are observed between patients with and without a pCR, with the first response group presenting a more angiogenic phenotype before start of treatment and changes in angiogenic processes after bevacizumab delivery. One dose of bevacizumab leads to a decrease in the number of pericyte covered blood vessels, a decrease in circulating PDGF-AA, PDGF-BB and Thrombospondin-1. Patients showing a pCR having less pericyte covered blood vessels, more hypoxia, and less circulating PDGF-BB compared to patients who did not have a pCR after bevacizumab treatment with chemoradiation and bevacizumab. Conclusions: The translational data demonstrate that tumors with an angiogenic expression profile respond better to bevacizumab combined with CRT and points towards a possible role for PDGF, CA-IX and pericyte covered blood vessels for the early response prediction to this treatment. Our findings suggest a role for mural cell recruitment and vessel maturation for the susceptibility of the tumor vasculature to bevacizumab treatment. Further validation of our biological observations and hypothesis generating data in randomized trials is needed. This study involves samples of patients enrolled in the AXEbeam trail that were analysed by Primeview microarray (Affymetrix). Biopsies were taken at two different timepoints: before treatment (tumor and normal mucosa) and after the first loading dose of bevacizumab but before chemoradiation (only tumor, week 3). Patients were classified into two groups: with a complete pathological response at time of surgery (Responders=R) or non-responders (NR). For the responders, we collected 21 samples in total (7 tumor samples and 8 normal mucosa samples taken before treatment and 6 tumor samples collected at week 3). From the non-responders we had 26 samples in total (9 tumor and 10 mucosa samples before treatment and 7 tumor samples at week 3 after a single dose of bevacizumab). Microarrays were run in two batches (15xxx versus 16xxx CEL file samples; indicated in the description field). Three samples (NJ 04/003 T1, RVS 09/002 M and NJ 04/003 W3) were put twice on the array (15897+16789; 15893+16790; 15898+16791) to verify and exclude batch effects. Please note that, due to these three technical repeats the total number of microarray CEL files is 50 (21 Responders, 26 Non-responders and 3 repeats).
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Project description:Genome wide DNA methylation profiling of human blood samples. The Illumina Infinium EPIC DNA methylation Beadchip was used to obtain DNA methylation profiles Survival has increased in early stage breast cancer (BC), and the late effects of cancer treatment can persist for decades. The molecular mechanisms underlying acceleration of age-related diseases after chemotherapy and radiotherapy are poorly understood. We examined epigenetic changes in peripheral blood in early stage BC patients undergoing either adjuvant radiotherapy, or adjuvant chemotherapy and radiotherapy. DNA methylation experiments were performed on peripheral blood samples from women collected prior to and following completion of adjuvant therapy. Methylation profiles were used to estimate three measures of epigenetic age acceleration - intrinsic, extrinsic, and phenotypic - as well as estimated cell counts.
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Project description:Combined model of in vitro and in vivo resistance to alkylating agents (BCNU and Temozolomide) in glioblastoma multiforme. Three matched pairs of surgical specimens from initial (DI, ME, LX) and repeat (DIR, MER, LXR) tumor resection were used to establish cell lines. Patients received BCNU chemotherapy between the two operations, which rendered the sublines from repeat surgery more resistant to BCNU than those from initial surgery. Each the pre-chemotherapeutic set and the post-chemotherapeutic set of cell lines was selected in vitro for resistance to either BCNU or Temozolomide. 9 in vitro selected sublines were established. Of those 4 (2 selected for BCNU [ME-BCNU, DI-BCNU] and 2 selected for Temozolomide [ME-TMZ, LX-TMZ) were generated from the parental/sensitive pre-chemotherapeutic set and 5 (2 selected for BCNU [DIR-BCNU, MER-BCNU] and 3 selected for Temozolomide [DIR-TMZ, MER-TMZ, LXR-TMZ) from the in vivo resistant post-chemotherapeutic set. The model included a total of 15 sublines. Genome-wide high-resolution gene copy number profiling was performed on each subline using 42,000-feature cDNA microarrays. Utilizing the same microarray platform genome-wide gene expression profiles were generated. Biostatistical tools were employed to identify signatures of resistance to alkylating agents both at the genetic as well as at the transcriptomic levels. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Series_type = Logical Set Keywords: other
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