Evidence map›Paper›PMID 15195139›Full record

ArticleOncogene2004

Characterization of loss-of-inactive X in Klinefelter syndrome and female-derived cancer cells.

Takahiro Kawakami, Cheng Zhang, Takanobu Taniguchi, Chul Jang Kim, Yusaku Okada, Hiroyuki Sugihara, Takanori Hattori, Anthony E Reeve, Osamu Ogawa, Keisei Okamoto

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

56 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Xq24/HemaSphere · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. The Molecular and Nuclear Dynamics of X-Chromosome Inactivation.Cold Spring Harbor perspectives in biology · 2022
    Review
  11. Review
  12. Frontiers in cell and developmental biology · 2021
    Article
  13. Biological Function of Long Non-coding RNA (LncRNA) Xist.Frontiers in cell and developmental biology · 2021
    Review
  14. Review
  15. Review
  16. Abnormal X chromosome inactivation and tumor development.Cellular and molecular life sciences : CMLS · 2020
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

10 authors at 4 institutions in 2 countries.

Takahiro KawakamiDepartment of Urology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Cheng Zhang
Takanobu Taniguchi
Chul Jang Kim
Yusaku Okada
Hiroyuki Sugihara
Takanori Hattori
Anthony E Reeve
Osamu Ogawa
Keisei Okamoto
Shiga University of Medical Science · JPAsahikawa Medical College Hospital · JPKyoto University · JPUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased risk of several types of cancer in Klinefelter syndrome (47XXY) suggests that the extra X chromosome may be involved in the tumorigenesis associated with this syndrome. Here, we show that cancer cells (PSK-1) derived from a patient with Klinefelter syndrome (47XXY) showing loss of an inactive X chromosome subsequently gained active X chromosomes. We found that this abnormal X chromosome composition in PSK-1 is caused by a loss of an inactive X chromosome followed by multiplication of identical active X chromosomes, not by reactivation of an inactive X chromosome. Furthermore, we extended the characterization of loss-of-inactive X in a series of 22 female-derived cancer cell lines (eight breast cancer cell lines, seven ovarian cancer cell lines, and seven cervical cancer cell lines). The data demonstrate that loss-of-inactive X in the female-derived cancer cells is mainly achieved by loss of an inactive X chromosomes followed by multiplication of an identical active X chromosomes. However, distinctive pathways, including reactivation of an inactive X chromosome, are also involved in the mechanisms for loss-of-inactive X and gain-of-active X in female-derived cancer cells. The biological significance of the loss-of-inactive X and gain-of-active X in the oncogenesis of Klinefelter syndrome and female-derived cancer cells are discussed.

Indexed as

Chromosomes, Human, XBreast NeoplasmsCell Line, TumorDNA MethylationDosage Compensation, GeneticFemaleGenes, p53HumansKlinefelter SyndromeMaleNeoplasmsOvarian NeoplasmsPolymorphism, GeneticRNA, Long NoncodingRNA, UntranslatedUterine Cervical NeoplasmsRNA, Long NoncodingRNA, UntranslatedXIST non-coding RNA

Identifiers

PMID15195139
OpenAlexW1967949850

What OpenQuestion holds

Textmetadata
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.