Evidence map›Paper›PMID 39155782›Full record

ArticleJournal of Zhejiang University. Science. B2024

Genome-wide CRISPR screening identifies critical role of phosphatase and tensin homologous (

Liming Lin, Jingjing Tao, Ying Meng, Yichao Gan, Xin He, Shu Li, Jiawei Zhang, Feiqiong Gao, Dijia Xin, Luyao Wang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2024. 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

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

14 authors.

Liming LinDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Jingjing TaoZhejiang Provincial Key Laboratory of Pancreatic Disease, the First Affiliated Hospital and Institute of Translational Medicine, Cancer Center, Zhejiang University School of Medicine, Hangzhou 310029, China.
Ying MengZhejiang Provincial Key Laboratory of Pancreatic Disease, the First Affiliated Hospital and Institute of Translational Medicine, Cancer Center, Zhejiang University School of Medicine, Hangzhou 310029, China.
Yichao GanInstitute of Genetics, Zhejiang University, Hangzhou 310058, China.
Xin HeDivision of Hematopoietic Stem Cell & Leukemia Research, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Shu LiDepartment of Hematology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jiawei ZhangDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Feiqiong GaoDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Dijia XinDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Luyao WangDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Yili FanDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Boxiao ChenDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Zhimin LuZhejiang Provincial Key Laboratory of Pancreatic Disease, the First Affiliated Hospital and Institute of Translational Medicine, Cancer Center, Zhejiang University School of Medicine, Hangzhou 310029, China. zhiminlu@zju.edu.cn.
Yang XuDepartment of Hematology, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. zhiminlu@zju.edu.cn, yxu@zju.edu.cn.

Funding

the National Natural Science Foundation of China 81572920 and 82100171the Zhejiang Provincial Natural Science Foundation of China LY21H080005
6 · The paper itself

Abstract

Although significant progress has been made in the development of novel targeted drugs for the treatment of acute myeloid leukemia (AML) in recent years, chemotherapy still remains the mainstay of treatment and the overall survival is poor in most patients. Here, we demonstrated the antileukemia activity of a novel small molecular compound NL101, which is formed through the modification on bendamustine with a suberanilohydroxamic acid (SAHA) radical. NL101 suppresses the proliferation of myeloid malignancy cells and primary AML cells. It induces DNA damage and caspase 3-mediated apoptosis. A genome-wide clustered regularly interspaced short palindromic repeats (CRISPR) library screen revealed that phosphatase and tensin homologous (

Indexed as

ApoptosisClustered Regularly Interspaced Short Palindromic RepeatsLeukemia, Myeloid, AcutePTEN PhosphohydrolaseAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalCRISPR-Cas SystemsDrug Resistance, NeoplasmHumansProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsMTOR protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine KinasesAcute myeloid leukemia (AML)ChemotherapyGenome-wide clustered regularly interspaced short palindromic repeats (CRISPR) libraryPhosphatase and tensin homologous (PTEN)Rapamycin

Identifiers

PMID39155782
PMCPMC11337085

What OpenQuestion holds

Textmetadata
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.