scholarly journals Differential Distribution of erbB Receptors in Human Glioblastoma Multiforme: Expression of erbB3 in CD133-Positive Putative Cancer Stem Cells

2010 ◽  
Vol 69 (6) ◽  
pp. 606-622 ◽  
Author(s):  
Véronique Duhem-Tonnelle ◽  
Ivan Bièche ◽  
Sophie Vacher ◽  
Anne Loyens ◽  
Claude-Alain Maurage ◽  
...  
2016 ◽  
Vol 8 (1) ◽  
pp. 100-114 ◽  
Author(s):  
Simona Daniele ◽  
Simona Sestito ◽  
Deborah Pietrobono ◽  
Chiara Giacomelli ◽  
Grazia Chiellini ◽  
...  

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 106 ◽  
Author(s):  
Novi Silvia Hardiany ◽  
Purnamawati Huang ◽  
Syarifah Dewi ◽  
Reni Paramita ◽  
Septelia Inawati Wanandi

Background: Glioblastoma multiforme (GBM) is the most aggressive form of malignant glioma and is also known as grade IV astrocytoma. This might be due to the presence of cancer stem cells with high pluripotency and ability of self-renewal. Recently, it has been reported that tumor stroma cells, including mesencyhmal stem cells (MSCs), secrete factors that affect cancer cell growth. Until now, the role of MSC secretomes in cancer stem cell pluripotency remains unclear. The aim of this study was to analyze the effect of MSC secretomes in conditioned medium (CM) on the expression of pluripotency markers of GBM cells. Methods: Umbilical cord-derived MSCs (UCSCs) were grown on serum-free alphaMEM for 24 hours to prepare the UCSC-CM. Human GBM T98G cells were treated with UCSC-CM for 24 hours. Following this treatment, expression of pluripotency markers SOX2, OCT4 and NANOG genes was analyzed using quantitative RT-PCR. Results: SOX2 and OCT mRNA expression was 4.7-fold (p=0.02) and 1.3-fold (p=0.03) higher in CM-treated cells compared to the control. However, there was no change in NANOG mRNA expression. This might be due to there being others factors regulating NANOG mRNA expression. Conclusions: UCSC-CM could affect the expression of SOX2 and OCT4 in human glioblastoma multiforme T98G cells. Further research is needed to elucidate the mechanism by which pluripotency markers are expressed when induced by the UCSC secretome.


1971 ◽  
Vol 18 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Eiichi Tani ◽  
Toshio Ametani

2021 ◽  
Vol 22 (13) ◽  
pp. 6781
Author(s):  
Anna Kirstein ◽  
Daniela Schilling ◽  
Stephanie E. Combs ◽  
Thomas E. Schmid

Background: Treatment resistance of glioblastoma multiforme to chemo- and radiotherapy remains a challenge yet to overcome. In particular, the O6-methylguanine-DNA-methyltransferase (MGMT) promoter unmethylated patients have only little benefit from chemotherapy treatment using temozolomide since MGMT counteracts its therapeutic efficacy. Therefore, new treatment options in radiotherapy need to be developed to inhibit MGMT and increase radiotherapy response. Methods: Lomeguatrib, a highly specific MGMT inhibitor, was used to inactivate MGMT protein in vitro. Radiosensitivity of established human glioblastoma multiforme cell lines in combination with lomeguatrib was investigated using the clonogenic survival assay. Inhibition of MGMT was analyzed using Western Blot. Cell cycle distribution and apoptosis were investigated to determine the effects of lomeguatrib alone as well as in combination with ionizing radiation. Results: Lomeguatrib significantly decreased MGMT protein and reduced radiation-induced G2/M arrest. A radiosensitizing effect of lomeguatrib was observed when administered at 1 µM and increased radioresistance at 20 µM. Conclusion: Low concentrations of lomeguatrib elicit radiosensitization, while high concentrations mediate a radioprotective effect.


2015 ◽  
Vol 35 (5) ◽  
pp. 1333-1340 ◽  
Author(s):  
LAIZANG WANG ◽  
ZHI WANG ◽  
JIANHUA LI ◽  
WEIGUANG ZHANG ◽  
FUBIN REN ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Kristen Abernathy ◽  
Jeremy Burke

Despite improvements in cancer therapy and treatments, tumor recurrence is a common event in cancer patients. One explanation of recurrence is that cancer therapy focuses on treatment of tumor cells and does not eradicate cancer stem cells (CSCs). CSCs are postulated to behave similar to normal stem cells in that their role is to maintain homeostasis. That is, when the population of tumor cells is reduced or depleted by treatment, CSCs will repopulate the tumor, causing recurrence. In this paper, we study the application of the CSC Hypothesis to the treatment of glioblastoma multiforme by immunotherapy. We extend the work of Kogan et al. (2008) to incorporate the dynamics of CSCs, prove the existence of a recurrence state, and provide an analysis of possible cancerous states and their dependence on treatment levels.


1995 ◽  
Vol 83 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Se Hyuck Park ◽  
Tatsuhiro Maeda ◽  
Gayatry Mohapatra ◽  
Frederic M. Waldman ◽  
Richard L. Davis ◽  
...  

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