Evidence map›Paper›PMID 34249435›Full record

ArticleAmerican journal of cancer research2021

Glutamate-cysteine ligase catalytic subunit as a therapeutic target in acute myeloid leukemia and solid tumors.

Chiou-Hong Lin, John P Vu, Chen-Yen Yang, Mint Sirisawad, Chun-Te Chen, Hung Dao, Jing Liu, Xuan Ma, Chin Pan, Joseph Cefalu and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Targeting PAX8 sensitizes ovarian cancer cells to ferroptosis by inhibiting glutathione synthesis.Apoptosis : an international journal on programmed cell death · 2024
    Article
  4. Oxidative Stress and Age-Related Tumors.Antioxidants (Basel, Switzerland) · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
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

13 authors at 1 institution in 1 country.

Chiou-Hong LinAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
John P VuAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Chen-Yen YangAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Mint SirisawadAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Chun-Te ChenAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Hung DaoAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Jing LiuAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Xuan MaAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Chin PanAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Joseph CefaluAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Chris TseAbbVie Oncology Discovery North Chicago, IL 60064, USA.
Erica JacksonAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
Hsu-Ping KuoAbbVie Oncology Discovery Sunnyvale, CA 94085, USA.
AbbVie (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a highly heterogenous and aggressive disease with a poor prognosis, necessitating further improvements in treatment therapies. Recently, several targeted therapies have become available for specific AML populations. To identify potential new therapeutic targets for AML, we analyzed published genome wide CRISPR-based screens to generate a gene essentiality dataset across a panel of 14 human AML cell lines while eliminating common essential genes through integration analysis with core fitness genes among 324 human cancer cell lines and DepMap databases. The key glutathione metabolic enzyme, glutamate-cysteine ligase catalytic subunit (GCLC), met the selection threshold. Using CRISPR knockout, GCLC was confirmed to be essential for the cell growth, survival, clonogenicity, and leukemogenesis in AML cells but was comparatively dispensable for normal hematopoietic stem and progenitor cells (HSPCs), indicating that GCLC is a potential therapeutic target for AML. In addition, we evaluated the essentiality of GCLC in solid tumors and demonstrated that GCLC represents a synthetic lethal target for ARID1A-deficient ovarian and gastric cancers.

Indexed as

Acute myeloid leukemia (AML)CRISPRglutamate-cysteine ligase catalytic subunit (GCLC)glutathione metabolic enzymesynthetic lethality

Identifiers

PMID34249435
PMCPMC8263632
OpenAlexW3180772588

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.