Evidence map›Paper›PMID 29301323›Full record

ReviewBiomedicines2018

Programming of Cell Resistance to Genotoxic and Oxidative Stress.

Ilya O Velegzhaninov, Vitaly A Ievlev, Yana I Pylina, Dmitry M Shadrin, Olesya M Vakhrusheva

Abstract readReview
In one paragraph

Review in Biomedicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
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  5. 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

5 authors.

Ilya O VelegzhaninovInstitute of Biology of Komi Science Centre of Ural Branch of RAS, Syktyvkar 167982, Russia. vellio@yandex.ru.ORCID 0000-0002-4715-4053
Vitaly A IevlevBiology department of St. Olaf College, Northfield, MN 55057, USA. ievlev1@stolaf.edu.
Yana I PylinaInstitute of Biology of Komi Science Centre of Ural Branch of RAS, Syktyvkar 167982, Russia. yanapylina@yandex.ru.
Dmitry M ShadrinInstitute of Biology of Komi Science Centre of Ural Branch of RAS, Syktyvkar 167982, Russia. shdimas@yandex.ru.
Olesya M VakhrushevaPolytechnical Institute of Vyatka State University, Kirov 610000, Russia. nimf04ka@mail.ru.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different organisms, cell types, and even similar cell lines can dramatically differ in resistance to genotoxic stress. This testifies to the wide opportunities for genetic and epigenetic regulation of stress resistance. These opportunities could be used to increase the effectiveness of cancer therapy, develop new varieties of plants and animals, and search for new pharmacological targets to enhance human radioresistance, which can be used for manned deep space expeditions. Based on the comparison of transcriptomic studies in cancer cells, in this review, we propose that there is a high diversity of genetic mechanisms of development of genotoxic stress resistance. This review focused on possibilities and limitations of the regulation of the resistance of normal cells and whole organisms to genotoxic and oxidative stress by the overexpressing of stress-response genes. Moreover, the existing experimental data on the effect of such overexpression on the resistance of cells and organisms to various genotoxic agents has been analyzed and systematized. We suggest that the recent advances in the development of multiplex and highly customizable gene overexpression technology that utilizes the mutant Cas9 protein and the abundance of available data on gene functions and their signal networks open new opportunities for research in this field.

Indexed as

cell programmingchemical genotoxinsdiversity of mechanismsgene overexpressionmalignant transformationoxidative stressradiationstress resistance

Identifiers

PMID29301323
PMCPMC5874662

What OpenQuestion holds

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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.