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Abstract A38: Genome-wide CRISPR-Cas9 screens reveal modulators of temozolomide sensitivity in glioblastoma

2017· article· en· W2768045733 on OpenAlexaff
Graham MacLeod, Nishani Rajakulendran, Traver Hart, Helen Yu, Peter B. Dirks, Stéphane Angers

Bibliographic record

VenueMolecular Cancer Therapeutics · 2017
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCRISPR and Genetic Engineering
Canadian institutionsHospital for Sick ChildrenUniversity of Toronto
Fundersnot available
KeywordsTemozolomideMSH6CRISPRCancer researchBiologySynthetic lethalityGeneDNA repairMedicineGlioblastomaGeneticsDNA mismatch repair

Abstract

fetched live from OpenAlex

Abstract Glioblastoma (GBM) is a prevalent and highly lethal form of primary brain tumour. Presently, median survival time for GBM patients is only 15 months and thus improved treatment methods are in great need. Treatment of GBM consists of surgery, radiotherapy and the chemotherapeutic agent temozolomide (TMZ). Unfortunately, many GBMs are refractory to TMZ and most others ultimately develop resistance leading to localized disease recurrence and brain tumor invasion. With the aim of identifying new therapeutic targets for GBM we performed genome-wide CRISPR-Cas9 screens to identify genes that modulate TMZ sensitivity in GBM. The TKO library of single-guide RNAs (gRNAs) targeting over 89,000 exons in 17,232 human genes was used to screen a panel of 5 patient-derived human GBM stem cell (GSC) lines. GSCs treated with DMSO were grown in parallel with GSCs treated with either a lethal, or sub-lethal dose of TMZ. Next-generation sequencing was used to identify gRNAs that were increased/decreased in abundance in TMZ treated pools of cells. Positive selection screening revealed that loss of key components of the mismatch repair pathway–MLH1, MSH2, MSH6 and PMS2 confers resistance to lethal doses of TMZ, as has previously been observed in GBM patients. Negative selection screening using sub-lethal doses of TMZ showed that loss of a conserved set of 15 genes that conferred TMZ hypersensitivity in four MGMT-negative GSC lines while the lone MGMT-positive GSC line in our set had a completely different set of hypersensitivity genes. Functional annotation revealed enrichment for genes involved in multiple DNA repair pathways, most prominently Fanconi Anemia and interstrand cross-link repair. Further studies validated that deletion of either member of the MCM8/9 helicase complex sensitizes GBM cells to TMZ and characterized the previously undescribed gene ZC3H7A which was revealed to be a cytoplasmic, stress-granule associated protein. In addition, our results revealed that in drug resistant MGMT expressing GSCs, TMZ resistance can be restored via the PARP inhibitor ABT-888. In conclusion, our results have identified a core set of genes that can be targeted to increase sensitivity to the chemotherapeutic agent TMZ responsive GBMs and elucidated opportunities for restoring TMZ sensitivity in resistant GBMs. These genes, many of which are targetable enzymes represent promising therapeutic targets for increasing efficacy of chemotherapy and decreasing lethality in GBM. Citation Format: Graham MacLeod, Nishani Rajakulendran, Traver Hart, Helen Yu, Peter B. Dirks, Stephane Angers. Genome-wide CRISPR-Cas9 screens reveal modulators of temozolomide sensitivity in glioblastoma [abstract]. In: Proceedings of the AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; Jan 4-7, 2017; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2017;16(10 Suppl):Abstract nr A38.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.205
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.015
GPT teacher head0.310
Teacher spread0.295 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2017
Admission routes1
Has abstractyes

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