Evidence map›Paper›PMID 30819925›Full record

ArticleBlood2019

HAP1 loss confers l-asparaginase resistance in ALL by downregulating the calpain-1-Bid-caspase-3/12 pathway.

Jung Kwon Lee, SungMyung Kang, Xidi Wang, Jesusa L Rosales, Xu Gao, Hee-Guk Byun, Yan Jin, Songbin Fu, Jinghua Wang, Ki-Young Lee

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. L-asparaginase induces IP3R-mediated ER CaCell death discovery · 2024
    Article
  5. Article
  6. Metabolism of asparagine in the physiological state and cancer.Cell communication and signaling : CCS · 2024
    Review
  7. PKA inhibition is a central step in D,L-methadone-induced ER CaFrontiers in cell and developmental biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Huntingtin Interacting Proteins and Pathological Implications.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Requirement for ER-mitochondria CaFrontiers in cell and developmental biology · 2023
    Article
  19. Review
  20. Biological functions and potential therapeutic applications of huntingtin-associated protein 1: progress and prospects.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 5 countries.

Jung Kwon LeeDepartment of Cell Biology & Anatomy, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada.ORCID 0000-0003-0940-2930
SungMyung KangDepartment of Cell Biology & Anatomy, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada.
Xidi WangDepartment of Cell Biology & Anatomy, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada.
Jesusa L RosalesDepartment of Cell Biology & Anatomy, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada.ORCID 0000-0002-2543-3801
Xu GaoBiochemistry & Molecular Biology.
Hee-Guk ByunDepartment of Marine Biotechnology, Gangneung-Wonju National University, Gangneung, South Korea; and.ORCID 0000-0001-8587-6834
Yan JinLaboratory of Medical Genetics, and.
Songbin FuLaboratory of Medical Genetics, and.
Jinghua WangDepartment of Hematology, Second Affiliated Hospital, Harbin Medical University, Harbin, China.
Ki-Young LeeDepartment of Cell Biology & Anatomy, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada.ORCID 0000-0002-5387-2692
University of Calgary · CAGangneung–Wonju National University · KRLaboratory of Molecular Genetics · PLHarbin Medical University · CN

Funding

CIHR MOP-123400
6 · The paper itself

Abstract

l-Asparaginase (l-ASNase) is a strategic component of treatment protocols for acute lymphoblastic leukemia (ALL). It causes asparagine deficit, resulting in protein synthesis inhibition and subsequent leukemic cell death and ALL remission. However, patients often relapse because of the development of resistance, but the underlying mechanism of ALL cell resistance to l-asparaginase remains unknown. Through unbiased genome-wide RNA interference screening, we identified huntingtin associated protein 1 (

Indexed as

AdultAntineoplastic AgentsAsparaginaseCalpainCaspasesDown-RegulationDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesHumansMaleNerve Tissue ProteinsPrecursor Cell Lymphoblastic Leukemia-LymphomaSignal TransductionTumor Cells, CulturedYoung AdultAntineoplastic AgentsAsparaginaseCalpainCAPN1 protein, humanCaspasesHAP1 protein, humanNerve Tissue Proteins

Identifiers

PMID30819925
PMCPMC6587669
OpenAlexW2920137816

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.