Evidence map›Paper›PMID 30082471›Full record

ArticleMolecular cancer therapeutics2018

Hexosamine Biosynthetic Pathway Inhibition Leads to AML Cell Differentiation and Cell Death.

Abhishek Asthana, Parameswaran Ramakrishnan, Yorleny Vicioso, Keman Zhang, Reshmi Parameswaran

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  8. CanPharmaceuticals (Basel, Switzerland) · 2024
    Review
  9. Article
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  11. Article
  12. Metabolic targeting of malignant tumors: a need for systemic approach.Journal of cancer research and clinical oncology · 2023
    Review
  13. Review
  14. Article
  15. Biomolecules · 2022
    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

5 authors at 1 institution in 1 country.

Abhishek AsthanaDivision of Hematology/Oncology, Department of Medicine, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio.
Parameswaran RamakrishnanDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio.
Yorleny ViciosoDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio.
Keman ZhangDivision of Hematology/Oncology, Department of Medicine, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio.
Reshmi ParameswaranDivision of Hematology/Oncology, Department of Medicine, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio. rxp278@case.edu.
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
NRSA Training CoreTL1TR002549 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 2018 to 2022
$2.9M
Transcriptional regulation by O-GlcNAcylation in T lymphocytesR01AI116730 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI RAMAKRISHNAN, PARAMESWARAN · 2016 to 2020
$2.0M
Targeting B cell activating factor receptor (BAFF-R) as a novel therapeutic strategy for drug resistant Acute Lymphoblastic Leukemia (ALL)R21CA201775 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI PARAMESWARAN, RESHMI · 2016 to 2017
$379k
NCATS NIH HHS TL1 TR002549NCI NIH HHS P30 CA043703NCI NIH HHS R21 CA201775NIAID NIH HHS R01 AI116730NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

Treatment for acute myeloid leukemia (AML) has remained unchanged for past 40 years. Targeting cell metabolism is a promising avenue for future cancer therapy. We found that enzymes involved in metabolic hexosamine biosynthetic pathway (HBP) are increased in patients with AML. Inhibiting GFAT (the rate-limiting enzyme of HBP) induced differentiation and apoptosis in AML cells, sparing normal cells. UDP-GlcNAc, the end product of HBP, is the substrate for O-GlcNAcylation, a posttranslational modification. O-GlcNAc transferase (OGT) is the enzyme which transfers GlcNAc from UDP-GlcNAc to target proteins. Inhibition of O-GlcNAcylation, using OGT inhibitors as well as genetic knockdown of OGT, also led to cell differentiation and apoptosis of AML cells. Finally, HBP inhibition

Indexed as

AnimalsAntineoplastic AgentsApoptosisBiosynthetic PathwaysCell DeathCell DifferentiationCell Line, TumorDisease Models, AnimalHexosaminesHumansLeukemia, Myeloid, AcuteMicePhosphorylationXenograft Model Antitumor AssaysAntineoplastic AgentsHexosamines

Identifiers

PMID30082471
PMCPMC6168390
OpenAlexW2886117058

What OpenQuestion holds

Textmetadata
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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.