Evidence map›Paper›PMID 31462891›Full record

ArticleCancer cell international2019

Haploinsufficiency of

Haowen Xiao, Yingying Ding, Yang Gao, Li-Mengmeng Wang, Huafang Wang, Lijuan Ding, Xiaoqing Li, Xiaohong Yu, He Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  11. Frontiers in neurology · 2022
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  16. Association BetweenFrontiers in pharmacology · 2021
    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

9 authors at 3 institutions in 1 country.

Haowen Xiao *1Department of Hematology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No. 3 Qingchun East Rd., Hangzhou, 310016 Zhejiang People's Republic of China.
Yingying Ding *Department of Hematology, The People's Hospital of Zhongshan City, Zhongshan, Guangdong Province People's Republic of China.
Yang Gao *1Department of Hematology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No. 3 Qingchun East Rd., Hangzhou, 310016 Zhejiang People's Republic of China.
Li-Mengmeng Wang2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
Huafang Wang2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
Lijuan Ding2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
Xiaoqing Li2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
Xiaohong Yu2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
He Huang2Institute of Hematology, Zhejiang University, Hangzhou, Zhejiang People's Republic of China.
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CNZhongshan People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRelapse represents the leading cause of death in both child and adult patients with acute lymphoblastic leukemia (ALL). Development of chemo-resistance is ultimately responsible for treatment failure and relapse, therefore understanding the molecular basis underlying resistance is imperative for developing innovative treatment strategies. Glucocorticoids (GCs) such dexamethasone and prednisolone are the backbone of combination chemotherapy regimens for treating all lymphoid tumors. However, the biological mechanisms of primary GC resistance in ALL is not completely understood. We previously performed a longitudinal whole-exome sequencing analysis on diagnosis/relapse pairs from adult patients with ALL. Our data revealed that relapse-specific truncation mutations in the

methodsIn the current study, we used discovery-based strategies including RNA sequencing (RNA-seq) and CRISPR/Cas9, followed by confirmatory testing, in human ALL cell lines, bone marrow blast samples from ALL patients and xenograft models, to elucidate the mechanisms responsible for resistance.

resultsOur results revealed a positive correlation between endogenous expression of

conclusionsOur findings suggest that the status of

Indexed as

Acute lymphoblastic leukemiaBcl-2 blockageGlucocorticoid resistanceHaploinsufficiencyMitochondrial apoptosis axisNR3C1

Identifiers

PMID31462891
PMCPMC6708234
OpenAlexW2969726262

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.