Evidence map›Paper›PMID 20628382›Full record

ArticleBritish journal of cancer2010

Identification of thymidylate synthase as a potential therapeutic target for lung cancer.

K Takezawa, I Okamoto, S Tsukioka, J Uchida, M Kiniwa, M Fukuoka, K Nakagawa

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Thymidylate synthase protein expression by IHC and gene copy number by SISH correlate and show great variability in non-small cell lung cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2012
    Article
  15. Cell fate control gene therapy based on engineered variants of human deoxycytidine kinase.Molecular therapy : the journal of the American Society of Gene Therapy · 2012
    Article
  16. Article
  17. Article
4 · The record

Corrections and comments

  • Retraction · 2025-09-19Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · Unreliable Data · · See also: https://pubpeer.com/publications/7DDF4339DBB7C79F2A3BB7B53F008E; I Okamoto aka Isamu Okamoto (from cv); K Takezawa aka Ken Takezawa, S Tsukioka aka Sayaka Tsukioka, J Uchida aka Junji Uchida, M Kiniwa aka Mamoru Kiniwa, M Fukuoka aka Masahiro Fukuoka, and K Nakagawa aka Kazuhiko Nakagawa (from related article in same timme frame and coauthors;
  • Retracted
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

K TakezawaDepartment of Medical Oncology, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-Sayama, Osaka 589-8511, Japan.
I Okamoto
S Tsukioka
J Uchida
M Kiniwa
M Fukuoka
K Nakagawa
Kindai University · JPTaiho Pharmaceutical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThymidylate synthase (TS), a key enzyme in the de novo synthesis of thymidine, is an important chemotherapeutic target for malignant tumours including lung cancer. Although inhibition of TS has an antiproliferative effect in cancer cells, the precise mechanism of this effect has remained unclear.

methodsWe examined the effects of TS inhibition with an RNA interference-based approach. The effect of TS depletion on the growth of lung cancer cells was examined using colorimetric assay and flow cytometry.

resultsMeasurement of the enzymatic activity of TS in 30 human lung cancer cell lines revealed that such activity differs among tumour histotypes. Almost complete elimination of TS activity by RNA interference resulted in inhibition of cell proliferation in all tested cell lines, suggestive of a pivotal role for TS in cell proliferation independent of the original level of enzyme activity. The antiproliferative effect of TS depletion was accompanied by arrest of cells in S phase of the cell cycle and the induction of caspase-dependent apoptosis as well as by changes in the expression levels of cyclin E and c-Myc. Moreover, TS depletion induced downregulation of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP), and it seemed to activate the mitochondrial pathway of apoptosis.

conclusionOur data provide insight into the biological relevance of TS as well as a basis for clinical development of TS-targeted therapy for lung cancer.

Indexed as

AdenocarcinomaApoptosisCarcinoma, Large CellCarcinoma, Small CellCarcinoma, Squamous CellCaspase 3Cell CycleCell DivisionCell Line, TumorCyclin ECytosolGene DeletionGene Expression Regulation, NeoplasticHumansImmunoblottingLung NeoplasmsCaspase 3Cyclin EProto-Oncogene Proteins c-mycThymidylate Synthase

Identifiers

PMID20628382
PMCPMC2920030
OpenAlexW2025937740

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.