Evidence map›Paper›PMID 34066147›Full record

ArticleCells2021

Transcriptional CDK Inhibitors CYC065 and THZ1 Induce Apoptosis in Glioma Stem Cells Derived from Recurrent GBM.

Viktorija Juric, Heiko Düssmann, Martine L M Lamfers, Jochen H M Prehn, Markus Rehm, Brona M Murphy

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  4. Non-histone lactylation: unveiling its functional significance.Frontiers in cell and developmental biology · 2025
    Review
  5. Review
  6. Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Viktorija JuricDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Dublin 2, Ireland.ORCID 0000-0003-2916-9080
Heiko DüssmannDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Dublin 2, Ireland.
Martine L M LamfersBrain Tumor Center, Department of Neurosurgery, Erasmus MC, 3015 CN Rotterdam, The Netherlands.ORCID 0000-0001-7745-9029
Jochen H M PrehnDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Dublin 2, Ireland.
Markus RehmInstitute of Cell Biology and Immunology, University of Stuttgart, 70569 Stuttgart, Germany.
Brona M MurphyDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, University of Medicine and Health Sciences, Dublin 2, Ireland.ORCID 0000-0002-6740-8858
Royal College of Surgeons in Ireland · IEErasmus MC Cancer Institute · NLUniversity of Stuttgart · DE

Funding

Horizon 2020 Framework Programme 766069Science Foundation Ireland (SFI) 16/RC/3948Science Foundation Ireland (SFI) 16/RI/3740
6 · The paper itself

Abstract

Glioma stem cells (GSCs) are tumour initiating cells which contribute to treatment resistance, temozolomide (TMZ) chemotherapy and radiotherapy, in glioblastoma (GBM), the most aggressive adult brain tumour. A major contributor to the uncontrolled tumour cell proliferation in GBM is the hyper activation of cyclin-dependent kinases (CDKs). Due to resistance to standard of care, GBMs relapse in almost all patients. Targeting GSCs using transcriptional CDK inhibitors, CYC065 and THZ1 is a potential novel treatment to prevent relapse of the tumour. TCGA-GBM data analysis has shown that the GSC markers, CD133 and CD44 were significantly upregulated in GBM patient tumours compared to non-tumour tissue. CD133 and CD44 stem cell markers were also expressed in gliomaspheres derived from recurrent GBM tumours. Light Sheet Florescence Microscopy (LSFM) further revealed heterogeneous expression of these GSC markers in gliomaspheres. Gliomaspheres from recurrent tumours were highly sensitive to transcriptional CDK inhibitors, CYC065 and THZ1 and underwent apoptosis while being resistant to TMZ. Apoptotic cell death in GSC subpopulations and non-stem tumour cells resulted in sphere disruption. Collectively, our study highlights the potential of these novel CKIs to induce cell death in GSCs from recurrent tumours, warranting further clinical investigation.

Indexed as

Drug Resistance, NeoplasmAC133 AntigenAdenosineAdultAntineoplastic AgentsApoptosisBrain NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationGliomaHumansHyaluronan ReceptorsMaleMiddle AgedNeoplasm Recurrence, LocalAC133 AntigenAdenosineAntineoplastic AgentsCD44 protein, humanCYC065Hyaluronan ReceptorsPROM1 protein, humanTemozolomideCD133CD44CDK inhibitorsCYC065cyclin-dependent kinasesglioma stem cellsrecurrent GBMTHZ1

Identifiers

PMID34066147
PMCPMC8151379
OpenAlexW3162721066

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.