Evidence map›Paper›PMID 40667288›Full record

ArticlebioRxiv : the preprint server for biology2025

CRISPR-Based Gene Dependency Screens reveal Mechanism of BRAF Inhibitor Resistance in Anaplastic Thyroid Cancer.

Shawn Noronha, Yue Liu, Gaga Geneti, Haojian Li, Xiaolin Wu, David Sun, Vaibhavi Gujar, Takashi Furusawa, Alexei Lobanov, Maggie Cam and 16 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors.

Shawn NoronhaSurgical Oncology Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Yue LiuInstitute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 7871.
Gaga GenetiLaboratory Animal Sciences Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Haojian LiDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Xiaolin WuNCI Genomics Technology Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research/Frederick, Maryland, USA.
David SunNCI Genomics Technology Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research/Frederick, Maryland, USA.
Vaibhavi GujarDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Takashi FurusawaDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Alexei LobanovCollaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. Advanced Biomedical Computational Sciences, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, 21701, USA.
Maggie CamCollaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. Advanced Biomedical Computational Sciences, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, 21701, USA.
Lipika R PalCancer Data Science Lab/Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD 20892, USA.
Nishanth NairCancer Data Science Lab/Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD 20892, USA.
Chi-Ping DayCancer Data Science Lab/Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD 20892, USA.
Eytan RuppinCancer Data Science Lab/Center for Cancer Research/National Cancer Institute/National Institutes of Health, Bethesda, MD 20892, USA.
Chandrayee GoshDepartment of Surgery and Stanford Cancer Institute, Stanford University, Stanford, CA, USA.
Jiangnan HuDepartment of Surgery and Stanford Cancer Institute, Stanford University, Stanford, CA, USA.
Suresh KumarDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Thorkell AndressonProtein Characterization Laboratory/Cancer Research Technology Program/Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA.
King ChanProtein Characterization Laboratory/Cancer Research Technology Program/Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA.
Maura O'NeillProtein Characterization Laboratory/Cancer Research Technology Program/Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA.
Raj ChariGenome Modification Core, Laboratory Animal Sciences Program, Frederick, Maryland, USA.
Yves PommierDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Jaydira Del RiveroDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Urbain WeyemiDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.
Electron KebebewDepartment of Surgery and Stanford Cancer Institute, Stanford University, Stanford, CA, USA.
Myriem BoufraqechSurgical Oncology Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic thyroid cancer (ATC) is the most aggressive form of thyroid cancer. Despite recent advances in treating BRAFV600E-driven ATC, therapy resistance remains a significant challenge, often resulting in disease progression and death. Leveraging a focused CRISPR/KO screen in parallel with a CRISPR/activation screen, both tailored on response to BRAFV600E inhibitor treatment, we identified TAZ (encoded by the WWTR1 gene) deficiency as synthetically lethal with BRAF inhibitor in ATC. TAZ is overexpressed in ATC compared to well-differentiated thyroid tumors. We demonstrate that TAZ-deficient ATC cells display heightened sensitivity to BRAF inhibitors both

Identifiers

PMID40667288
PMCPMC12262318

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Registered trials

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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.