umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Synergistic killing of Glioblastoma Stem-like cells by Bortezomib and HDAC Inhibitors
Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Show others and affiliations
2012 (English)In: Anticancer Research, ISSN 0250-7005, E-ISSN 1791-7530, Vol. 32, no 7 ; Special Issue, 2407-2413 p.Article in journal (Refereed) Published
Abstract [en]

Background: The malignant brain tumour glioblastoma is a devastating disease that remains a therapeutic challenge. Materials and Methods: Effects of combinations of the US Food and Drug Administation (FDA) approved proteasome inhibitor bortezomib and the histone deacetylase (HDAC) inhibitors vorinostat, valproic acid and sodium phenylbutyrate were studied on primary glioblastoma stem cell lines and conventional glioblastoma cell lines. Cell survival, proliferation and death were analyzed by fluorometric microculture cytotoxicity assay (FMCA), propidium iodide labeling and flow cytometry, and cell cloning through limiting dilution and live-cell bright-field microscopy. Results: Bortezomib and the HDAC inhibitors showed synergistic cell killing at clinically relevant drug concentrations, while the conventional cell lines cultured in serum-containing medium were relatively resistant to the same treatments. Conclusion: These findings of synergistic glioblastoma stem cell killing by bortezomib and three different FDA-approved HDAC inhibitors confirm and expand previous observations on co-operative effects between these classes of drugs.

Place, publisher, year, edition, pages
International Institute of Anticancer Research, 2012. Vol. 32, no 7 ; Special Issue, 2407-2413 p.
Keyword [en]
Glioblastoma, stem cells, proteasome inhibitor, HDAC inhibitor, TB101, R11 stem cells, U251 MG, GL15 cells
National Category
Cancer and Oncology
Identifiers
URN: urn:nbn:se:umu:diva-57605ISI: 000306254300003OAI: oai:DiVA.org:umu-57605DiVA: diva2:543575
Available from: 2012-08-08 Created: 2012-08-08 Last updated: 2017-12-07Bibliographically approved

Open Access in DiVA

No full text

Search in DiVA

By author/editor
Asklund, ThomasKvarnbrink, SamuelHolmlund, CamillaWibom, CarlBergenheim, TommyHenriksson, RogerHedman, Håkan
By organisation
OncologyClinical Neuroscience
In the same journal
Anticancer Research
Cancer and Oncology

Search outside of DiVA

GoogleGoogle Scholar

urn-nbn

Altmetric score

urn-nbn
Total: 213 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf