Evidence map›Paper›PMID 32413516›Full record

ArticleGenomics, proteomics & bioinformatics2020

CRISPR Screens Identify Essential Cell Growth Mediators in BRAF Inhibitor-resistant Melanoma.

Ziyi Li, Binbin Wang, Shengqing Gu, Peng Jiang, Avinash Sahu, Chen-Hao Chen, Tong Han, Sailing Shi, Xiaoqing Wang, Nicole Traugh and 7 more

Open access · goldAbstract read
In one paragraph

Article in Genomics, proteomics & bioinformatics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  8. CDK4/6 and MAPK-Crosstalk as Opportunity for Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  9. Article
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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

17 authors at 3 institutions in 2 countries.

Ziyi LiClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Binbin WangClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; Department of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Shengqing GuDepartment of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Peng JiangDepartment of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Avinash SahuDepartment of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Chen-Hao ChenDepartment of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Tong HanClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Sailing ShiClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Xiaoqing WangDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Nicole TraughDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Hailing LiuClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Yin LiuDepartment of Clinical Laboratory, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Qiu WuClinical Translational Research Center, Shanghai Pulmonary Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Myles BrownDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Tengfei XiaoDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA. Electronic address: xtfmail@gmail.com.
Genevieve M BolandCenter for Cancer Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. Electronic address: GMBOLAND@partners.org.
X Shirley LiuDepartment of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02115, USA. Electronic address: xsliu@ds.dfci.harvard.edu.
Tongji University · CNDana-Farber Cancer Institute · USHarvard University · US

Funding

Identifying drug synergistic with cancer immunotherapyR00CA248953 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI SAHU, AVINASH DAS · 2023 to 2025
$716k
Identifying drug synergistic with cancer immunotherapyK99CA248953 · NCI · DANA-FARBER CANCER INST · PI SAHU, AVINASH DAS · 2020 to 2021
$240k
NCI NIH HHS K99 CA248953NCI NIH HHS R00 CA248953
6 · The paper itself

Abstract

BRAF is a serine/threonine kinase that harbors activating mutations in ∼7% of human malignancies and ∼60% of melanomas. Despite initial clinical responses to BRAF inhibitors, patients frequently develop drug resistance. To identify candidate therapeutic targets for BRAF inhibitor resistant melanoma, we conduct CRISPR screens in melanoma cells harboring an activating BRAF mutation that had also acquired resistance to BRAF inhibitors. To investigate the mechanisms and pathways enabling resistance to BRAF inhibitors in melanomas, we integrate expression, ATAC-seq, and CRISPR screen data. We identify the JUN family transcription factors and the ETS family transcription factor ETV5 as key regulators of CDK6, which together enable resistance to BRAF inhibitors in melanoma cells. Our findings reveal genes contributing to resistance to a selective BRAF inhibitor PLX4720, providing new insights into gene regulation in BRAF inhibitor resistant melanoma cells.

Indexed as

Drug Resistance, NeoplasmCell Line, TumorCell ProliferationClustered Regularly Interspaced Short Palindromic RepeatsHumansIndolesIntercellular Signaling Peptides and ProteinsMelanomaMutationProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSulfonamidesBRAF protein, humanIndolesIntercellular Signaling Peptides and ProteinsPLX 4720Protein Kinase InhibitorsProto-Oncogene Proteins B-rafSulfonamidesBRAF inhibitorCRISPR screenDrug resistanceGene regulationMelanoma

Identifiers

PMID32413516
PMCPMC7393575
OpenAlexW3025474283

What OpenQuestion holds

Textmetadata
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.