Evidence map›Paper›PMID 26698156›Full record

ArticleMedical oncology (Northwood, London, England)2016

Increased lanosterol turnover: a metabolic burden for daunorubicin-resistant leukemia cells.

Claudia Stäubert, Rosanna Krakowsky, Hasanuzzaman Bhuiyan, Barbara Witek, Anna Lindahl, Oliver Broom, Anders Nordström

Open access · hybridAbstract read
In one paragraph

Article in Medical oncology (Northwood, London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Squalene Epoxidase: Its Regulations and Links with Cancers.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Cancers · 2019
    Article
  8. Review
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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

7 authors at 5 institutions in 2 countries.

Claudia StäubertDepartment of Molecular Biology, Umeå University, 90187, Umeå, Sweden.
Rosanna KrakowskyInstitute of Biochemistry, Faculty of Medicine, University of Leipzig, Leipzig, Germany.
Hasanuzzaman BhuiyanDoping Laboratory, Department of Clinical Pharmacology, Karolinska University Hospital, Stockholm, Sweden.
Barbara WitekDepartment of Molecular Biology, Umeå University, 90187, Umeå, Sweden.
Anna LindahlDepartment of Oncology-Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Oliver BroomDepartment of Molecular Biology, Umeå University, 90187, Umeå, Sweden.
Anders NordströmDepartment of Molecular Biology, Umeå University, 90187, Umeå, Sweden. anders.nordstrom@umu.se.ORCID http://orcid.org/0000-0003-3676-817X
Science for Life Laboratory · SEUmeå University · SEKarolinska University Hospital · SELeipzig University · DESwedish University of Agricultural Sciences · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cholesterol metabolism is essential for cancer cell proliferation. We found the expression of genes involved in the cholesterol biosynthesis pathway up-regulated in the daunorubicin-resistant leukemia cell line CEM/R2, which is a daughter cell line to the leukemia cell line CCRF-CEM (CEM). Cellular (2)H2O labelling, mass spectrometry, and isotopomer analysis revealed an increase in lanosterol synthesis which was not accompanied by an increase in cholesterol flux or pool size in CEM/R2 cells. Exogenous addition of lanosterol had a negative effect on CEM/R2 and a positive effect on sensitive CEM cell viability. Treatment of CEM and CEM/R2 cells with cholesterol biosynthesis inhibitors acting on the enzymes squalene epoxidase and lanosterol synthase, both also involved in the 24,25-epoxycholesterol shunt pathway, revealed a connection of this pathway to lanosterol turnover. Our data highlight that an increased lanosterol flux poses a metabolic weakness of resistant cells that potentially could be therapeutically exploited.

Indexed as

Antibiotics, AntineoplasticCell Line, TumorChromatography, LiquidDaunorubicinDrug Resistance, NeoplasmHumansLanosterolLeukemiaMass SpectrometryPolymerase Chain ReactionAntibiotics, AntineoplasticDaunorubicinLanosterolCancerCholesterol biosynthesisDrug resistanceLC–MSLeukemiaStable isotope labelling mass spectrometry

Identifiers

PMID26698156
PMCPMC4689760
OpenAlexW2265367197

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.