Evidence map›Paper›PMID 10027302›Full record

ArticleBritish journal of cancer1999

Inflammatory cell-mediated tumour progression and minisatellite mutation correlate with the decrease of antioxidative enzymes in murine fibrosarcoma cells.

F Okada, K Nakai, T Kobayashi, T Shibata, S Tagami, Y Kawakami, T Kitazawa, R Kominami, S Yoshimura, K Suzuki and 8 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-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

12 citing papers in PubMed, 27 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

18 authors at 7 institutions in 1 country.

F OkadaLaboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Sapporo, Japan.
K Nakai
T Kobayashi
T Shibata
S Tagami
Y Kawakami
T Kitazawa
R Kominami
S Yoshimura
K Suzuki
N Taniguchi
O Inanami
M Kuwabara
H Kishida
D Nakae
Y Konishi
T Moriuchi
M Hosokawa
Hokkaido University · JPNara Medical University · JPNiigata University · JPOsaka University · JPSapporo University · JPHealth Sciences University of Hokkaido · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We isolated six clones of weakly tumorigenic fibrosarcoma (QR) from the tumorigenic clone BMT-11 cl-9. The QR clones were unable to grow in normal C57BL/6 mice when injected s.c. (1x10(5) cells). However, they formed aggressive tumours upon co-implantation with a 'foreign body', i.e. a gelatin sponge, and the rate of tumour take ranged from 8% to 58% among QR clones. The enhanced tumorigenicity was due to host cell-mediated reaction to the gelatin sponge (inflammation). Immunoblot analysis and enzyme activity assay revealed a significant inverse correlation between the frequencies of tumour formation by QR clones and the levels of manganese superoxide dismutase (Mn-SOD, P<0.005) and glutathione peroxidase (GPchi, P<0.01) in the respective tumour clones. Electron spin resonance (ESR) revealed that superoxide-scavenging ability of cell lysates of the QR clone with high level of Mn-SOD was significantly higher than that with low level of the antioxidative enzyme in the presence of potassium cyanide, an inhibitor for copper-zinc superoxide dismutase (CuZn-SOD) (P<0.001). Minisatellite mutation (MSM) induced by the inflammatory cells in tumour cells were investigated by DNA fingerprint analysis after QR clones had been co-cultured with gelatin-sponge-reactive cells. The MSM rate was significantly higher in the subclones with low levels of Mn-SOD and GPchi (P<0.05) than in the subclones with high levels of both enzymes. The MSM of the subclones with low levels of both enzymes was inhibited in the presence of mannitol, a hydroxyl radical scavenger. The content of 8-hydroxydeoxyguanosine (8-OHdG) by which the cellular DNA damage caused by active oxygen species can be assessed was significantly low in the tumours arising from the QR clone with high levels of Mn-SOD and GPchi even if the clone had been co-implanted with gelatin sponge, compared with the arising tumour from the QR clone with low levels of those antioxidative enzymes (P<0.001). In contrast, CuZn-SOD and catalase levels in the six QR clones did not have any correlation with tumour progression parameters. These results suggest that tumour progression is accelerated by inflammation-induced active oxygen species particularly accompanied with declined levels of intracellular antioxidative enzymes in tumour cells.

Indexed as

AnimalsAntioxidantsDisease ProgressionDNA, NeoplasmFemaleFibrosarcomaForeign BodiesGlutathione PeroxidaseInflammationMiceMice, Inbred C57BLMinisatellite RepeatsReactive Oxygen SpeciesSuperoxide DismutaseTumor Cells, CulturedAntioxidantsDNA, NeoplasmGlutathione PeroxidaseReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID10027302
PMCPMC2362451
OpenAlexW2012706488

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY
measurements read2
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.