Evidence map›Paper›PMID 25798073›Full record

ArticleCancer cell international2015

Combination of cyclophosphamide and double-stranded DNA demonstrates synergistic toxicity against established xenografts.

Ekaterina A Alyamkina, Valeriy P Nikolin, Nelly A Popova, Alexandra M Minkevich, Artem V Kozel, Evgenia V Dolgova, Yaroslav R Efremov, Sergey I Bayborodin, Oleg M Andrushkevich, Oleg S Taranov and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 23% 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, 19 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

20 authors at 5 institutions in 1 country.

Ekaterina A AlyamkinaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Valeriy P NikolinInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Nelly A PopovaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia ; Novosibirsk State University, Novosibirsk, 630090 Russia.
Alexandra M MinkevichInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Artem V KozelNovosibirsk State University, Novosibirsk, 630090 Russia.
Evgenia V DolgovaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Yaroslav R EfremovInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia ; Novosibirsk State University, Novosibirsk, 630090 Russia.
Sergey I BayborodinInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia ; Novosibirsk State University, Novosibirsk, 630090 Russia.
Oleg M AndrushkevichInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia ; Novosibirsk State University, Novosibirsk, 630090 Russia.
Oleg S TaranovThe State Research Center of Virology and Biotechnology VECTOR, Koltsovo, Novosibirsk region 630559 Russia.
Vladimir V OmigovThe State Research Center of Virology and Biotechnology VECTOR, Koltsovo, Novosibirsk region 630559 Russia.
Vladimir A RogachevInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Anastasia S ProskurinaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Evgeniy I VereschaginNovosibirsk State Medical Academy, Novosibirsk, 630091 Russia.
Elena V KiselevaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Maria V ZhukovaInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Alexandr 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.
Sergey S BogachevInstitute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva ave, 630090 Novosibirsk, Russia.
Mikhail A ShurdovLLC Panagen, Gorno-Altaisk, Russia.
Institute of Cytology and Genetics · RUState Research Center of Virology and Biotechnology VECTOR · RUGorno-Altaisk State University · RUNovosibirsk State Medical University · RUNovosibirsk State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExtracellular double-stranded DNA participates in various processes in an organism. Here we report the suppressive effects of fragmented human double-stranded DNA along or in combination with cyclophosphamide on solid and ascites grafts of mouse Krebs-2 tumor cells and DNA preparation on human breast adenocarcinoma cell line MCF-7.

methodsApoptosis and necrosis were assayed by electrophoretic analysis (DNA nucleosomal fragmentation) and by measurements of LDH levels in ascitic fluid, respectively. DNA internalization into MCF-7 was analyzed by flow cytometry and fluorescence microscopy.

resultsDirect cytotoxic activity of double-stranded DNA (along or in combination with cyclophosphamide) on a solid transplant was demonstrated. This resulted in delayed solid tumor proliferation and partial tumor lysis due to necrosis of the tumor and adjacent tissues. In the case of ascites form of tumor, extensive apoptosis and secondary necrosis were observed. Similarly, MCF-7 cells showed induction of massive apoptosis (up to 45%) as a result of treatments with double-stranded DNA preparation.

conclusionsDouble-stranded DNA (along or in combination with cyclophosphamide) induces massive apoptosis of Krebs-2 ascite cells and MCF-7 cell line (DNA only). In treated mice it reduces the integrity of gut wall cells and contributes to the development of systemic inflammatory reaction.

Indexed as

ApoptosisAscites Krebs-2CyclophosphamideDouble-stranded DNAMCF-7NecrosisSepsis

Identifiers

PMID25798073
PMCPMC4369063
OpenAlexW2157328586

What OpenQuestion holds

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Registered trials

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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.