The role of glioma stem cells in chemotherapy resistance and glioblastoma multiforme recurrence

Auffinger, Brenda; Spencer, Drew A.; Pytel, Peter; Ahmed, Atique U.; Lesniak, Maciej S.

doi:10.1586/14737175.2015.1051968

Cited by 235 publications

(202 citation statements)

References 107 publications

(145 reference statements)

Supporting

Mentioning

184

Contrasting

Order By: Relevance

“…Human BTSC are a slowlydividing, small population within a heterogeneous glioblastoma which can recapitulate a whole tumor and differentiate into other specific GBM subpopulations [51]. Human BTSC tend to preferentially reside within the hypoxic core of tumor mass [52].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of carbonic anhydrase IX in glioblastoma multiforme

Amiri

Moquin

et al. 2016

European Journal of Pharmaceutics and Biopharmaceutics

View full text Add to dashboard Cite

a b s t r a c tCarbonic anhydrase IX (CA IX) is a transmembrane enzyme upregulated in several types of tumors including glioblastoma multiforme (GBM). GBM is among the most aggressive tumors among gliomas. Temozolomide (TMZ) therapy combined with surgical or radiation approaches is the standard treatment but not effective in long term. In this study we tested the treatment with acetazolamide (ATZ), an inhibitor of CA IX, alone or combined with TMZ. The experiments were performed in 2D and 3D cultures (spheroids) using glioblastoma U251N and human brain tumor stem cells (BTSCs). Several proteins implicated in tumor cell death were also investigated. The key results from these studies suggest the following: (1) Cell death of human glioblastoma spheroids and BTSC is significantly increased with combined treatment after 7 days, and (2) the effectiveness of ATZ is significantly enhanced against BTSC and U251N when incorporated into nano-carriers. Collectively, these results point toward the usefulness of nano-delivery of CA IX inhibitors and their combination with chemotherapeutics for glioblastoma treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibition of carbonic anhydrase IX in glioblastoma multiforme

Amiri

Moquin

et al. 2016

European Journal of Pharmaceutics and Biopharmaceutics

View full text Add to dashboard Cite

show abstract

“…10,[13][14][15] On the other hand, GBM also appears to have a cellular hierarchy, whereby there exists a subpopulation of GBM cells that are enriched with the capacity for tumor initiation and propagation, and these cells drive tumor growth and treatment resistance. [16][17][18][19] A large number of studies have suggested that WNT signaling is aberrantly activated in GBM and that it promotes GBM growth and invasion via the maintenance of stem cell properties. [20][21][22][23] Here, we will review recent studies from the literature that have described the functions of WNT/β-catenin signaling in development and cancer, with particular emphasis on [24][25][26][27][28][29] genetic and epigenetic alterations that lead to aberrant WNT pathway activation in GBM.…”

mentioning

confidence: 99%

WNT signaling in glioblastoma and therapeutic opportunities

Lee

Ahn

et al. 2016

Laboratory Investigation

224

182

View full text Add to dashboard Cite

WNTs and their downstream effectors regulate proliferation, death, and migration and cell fate decision. Deregulation of WNT signaling is associated with various cancers including GBM, which is the most malignant primary brain cancer. In this review, we will summarize the experimental evidence supporting oncogenic roles of WNT signaling in GBM and discuss current progress in the targeting of WNT signaling as an anti-cancer approach. In particular, we will focus on (1) genetic and epigenetic alterations that lead to aberrant WNT pathway activation in GBM, (2) WNT-mediated control of GBM stem cell maintenance and invasion, and (3) cross-talk between WNT and other signaling pathways in GBM. We will then review the discovery of agents that can inhibit WNT signaling in preclinical models and the current status of human clinical trials.

show abstract

“…Glioblastoma multiforme typically features a high capacity to infi ltrate normal surrounding tissue which is, together with the high radioresistance, the main reason for the poor prognosis for GBM [ 42 ]. Due to the infi ltration a total removal of those TICs is nearly impossible, as physicians can resect the visible tumour but not the cells migrated in adjacent tissues developing metastasis.…”

Section: Glioblastoma Multiforme Treatmentmentioning

confidence: 99%