Evidence map›Paper›PMID 38939059›Full record

ReviewPrzeglad gastroenterologiczny2024

Resistance to death pathway induction as a potential targeted therapy in CRISPR/Cas-9 knock-out colorectal cancer cell lines.

Malgorzata Adamiec-Organisciok, Magdalena Wegrzyn, Lukasz Cienciala, Ngoni Magate, Magdalena Skonieczna, Joanna Nackiewicz

Abstract readReview
In one paragraph

Review in Przeglad gastroenterologiczny, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

6 authors.

Malgorzata Adamiec-OrganisciokDepartment of Systems Engineering and Biology, Silesian University of Technology, Faculty of Automatic Control, Electronics and Computer Science, Gliwice, Poland.
Magdalena WegrzynDepartment of Systems Engineering and Biology, Silesian University of Technology, Faculty of Automatic Control, Electronics and Computer Science, Gliwice, Poland.
Lukasz CiencialaDepartment of Systems Engineering and Biology, Silesian University of Technology, Faculty of Automatic Control, Electronics and Computer Science, Gliwice, Poland.
Ngoni MagateDepartment of Systems Engineering and Biology, Silesian University of Technology, Faculty of Automatic Control, Electronics and Computer Science, Gliwice, Poland.
Magdalena SkoniecznaDepartment of Systems Engineering and Biology, Silesian University of Technology, Faculty of Automatic Control, Electronics and Computer Science, Gliwice, Poland.
Joanna NackiewiczFaculty of Chemistry, University of Opole, Opole, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulated cell death is a fundamental biological process that plays a crucial role in maintaining tissue homeostasis and eliminating damaged or unnecessary cells. Ferroptosis is an iron-dependent process, characterized by the accumulation of oxidized and damaged lipids, which leads to programmed cell death. Among the ferroptotic pathway genes regulating this process, GPX4, TFRC, ACSL4, FSP1, SLC7A11, and PROM2 could be considered. There are many well-known ferroptotic pathway regulators, which are discussed in this compact review. Cells with tissues of different origin display sensitive or resistant phenotypes to such regulators. In some cases, unexpected changes during cell treatment occurred, suggesting the possibility of regulating the death pathway. We assumed that possible changing of ferro-sensitivity to ferro-resistance in cells, especially in colorectal cancer cell lines, is responded for induced chemoresistance. Using novel techniques, such as CRISPR/Cas-9 genome editing, an induced phenotype "switching" is possible.

Indexed as

antioxidant defence mechanismsCRISPR/Cas-9 genome editingferroptosisglutathione peroxidase GPX4regulated cell death

Identifiers

PMID38939059
PMCPMC11200076

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.