Evidence map›Paper›PMID 35225010›Full record

ArticleCancer control : journal of the Moffitt Cancer Center

Glucose Influences the Response of

Anna M Bielecka-Wajdman, Tomasz Ludyga, Daria Smyk, Wojciech Smyk, Magdalena Mularska, Patrycja Świderek, Wojciech Majewski, Christina Susanne Mullins, Michael Linnebacher, Ewa Obuchowicz

Open access · goldAbstract read
In one paragraph

Article in Cancer control : journal of the Moffitt Cancer Center. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Anna M Bielecka-WajdmanDepartment of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.ORCID https://orcid.org/0000-0002-5133-5164
Tomasz LudygaDepartment of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Daria SmykStudent Research Circle at the Department of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Wojciech SmykStudent Research Circle at the Department of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Magdalena MularskaStudent Research Circle at the Department of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Patrycja ŚwiderekStudent Research Circle at the Department of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Wojciech MajewskiDepartment of Radiotherapy, 49598Maria Sklodowska-Curie Institute Oncology Center, Branch in Gliwice, Gliwice, Poland.
Christina Susanne MullinsDepartment of Thoracic Surgery, 39071Rostock University Medical Center, Rostock, Germany.
Michael LinnebacherDepartment of General Surgery, Molecular Oncology and Immunotherapy, 39071Rostock University Medical Center, Rostock, Germany.
Ewa ObuchowiczDepartment of Pharmacology, School of Medicine in Katowice, 49613Medical University of Silesia, Katowice, Poland.
Medical University of Silesia · PLUniversity of Rostock · DEThe Maria Sklodowska-Curie National Research Institute of Oncology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCurrent research indicates that weakness of glucose metabolism plays an important role in silencing of invasiveness and growth of hypoxic tumors such as GBM. Moreover, there are indications that DXM, frequently used in treatment, may support GBM energy metabolism and provoke its recurrence.

methodsWe carried out in vitro experiments on the commercial T98G cell line and two primary GBM lines (HROG02, HROG17) treated with TMZ and/or DXM in physiological oxygen conditions for GBM (2.5% oxygen) and for comparison, in standard laboratory conditions (20% oxygen). The influence of different glucose levels on selected malignancy features of GBM cells-cellular viability and division, dynamic of cell culture changes, colony formation and concentration of InsR have been elevated.

resultsUnder 2.5% oxygen and high glucose concentration, an attenuated cytotoxic effect of TMZ and intensification of malignancy features in all glioblastoma cell lines exposed to DXM was seen. Furthermore, preliminary retrospective analysis to assess the correlation between serum glucose levels and Ki-67 expression in surgical specimens derived from patients with GBM (IV) treated with radio-chemotherapy and prophylactic DXM therapy was performed.

conclusionThe data suggest a link between the in vitro study results and clinical data. High glucose can influence on GBM progression through the promotion of the following parameters: cell viability, dispersal, InsR expression and cell proliferation (Ki-67). However, this problem needs more studies and explain the mechanism of action studied drugs.

Indexed as

Brain NeoplasmsGlioblastomaCell Line, TumorDexamethasoneDrug Resistance, NeoplasmGlucoseHumansRetrospective StudiesTemozolomideDexamethasoneGlucoseTemozolomideadjuvant treatment in brain cancerbrain tumorchemotherapy in brain cancerglioblastomaglucose in cancer

Identifiers

PMID35225010
PMCPMC8891890
OpenAlexW4214551260

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.