Evidence map›Paper›PMID 26872383›Full record

ArticleOncotarget2016

A strategy to eradicate well-developed Krebs-2 ascites in mice.

Ekaterina A Potter, Evgenia V Dolgova, Anastasia S Proskurina, Alexandra M Minkevich, Yaroslav R Efremov, Oleg S Taranov, Vladimir V Omigov, Valeriy P Nikolin, Nelly A Popova, Sergey I Bayborodin and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 25 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

15 authors at 4 institutions in 1 country.

Ekaterina A PotterInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Evgenia V DolgovaInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Anastasia S ProskurinaInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Alexandra M MinkevichInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Yaroslav R EfremovInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Oleg S TaranovThe State Research Center of Virology and Biotechnology VECTOR, Novosibirsk 630559, Russia.
Vladimir V OmigovThe State Research Center of Virology and Biotechnology VECTOR, Novosibirsk 630559, Russia.
Valeriy P NikolinInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Nelly A PopovaInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Sergey I BayborodinInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Alexander A OstaninInstitute of Clinical Immunology, Siberian Branch of The Russian Academy of Medical Sciences, Novosibirsk 630099, Russia.
Elena R ChernykhInstitute of Clinical Immunology, Siberian Branch of The Russian Academy of Medical Sciences, Novosibirsk 630099, Russia.
Nikolay A KolchanovInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Mikhail A ShurdovLLC Panagen, Gorno-Altaisk 649000, Russia.
Sergey S BogachevInstitute of Cytology and Genetics, Siberian Branch of The Russian Academy of Sciences, Novosibirsk 630090, Russia.
Institute of Cytology and Genetics · RUNovosibirsk State University · RUState Research Center of Virology and Biotechnology VECTOR · RUGorno-Altaisk State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We describe the strategy, which allows curing experimental mice engrafted with Krebs-2 ascites. The strategy is based on the facts that i) Krebs-2 tumor-initiating stem cells (TISCs) are naturally capable of internalizing fragments of extracellular double-stranded DNA (dsDNA); ii) upon delivery into TISCs, these dsDNA fragments interfere with the on-going DNA repair process so that TISCs either die or lose their tumorigenic potential. The following 3-step regimen of therapeutic procedures leading to eradication of Krebs-2 ascites is considered. Firstly, three timed injections of cyclophosphamide (CP) exactly matching the interstrand cross-link (ICL) repair phases that lead to synchronization of ascites cells in late S/G2/M. Secondly, additional treatment of ascites 18 hours post each CP injection (at NER/HR transition timepoint) with a composite dsDNA-based preparation interfering with the NER and HR repair pathways, so that tumorigenic properties of ascites cells are compromised. Thirdly, final treatment of mice with a combination of CP and dsDNA injections as ascites cells undergo apoptotic destruction, and the surviving TAMRA+ TISCs arrested in late S/G2/M phases massively enter into G1/S, when they regain sensitivity to CP+dsDNA treatment. Thus, this regimen assures that no viable cells, particularly Krebs-2 TISCs, remain.

Indexed as

AnimalsAscitesCarcinoma, Krebs 2CyclophosphamideDisease Models, AnimalDNADrug Administration ScheduleFemaleHumansMaleMiceMice, Inbred C57BLNeoplastic Stem CellsTransfectionCyclophosphamideDNAascites Krebs-2cyclophosphamideextracellular dsDNArepairtumor-initiating stem cells

Identifiers

PMID26872383
PMCPMC4905495
OpenAlexW2288684139

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.