Evidence map›Paper›PMID 14655749›Full record

ArticleBrain pathology (Zurich, Switzerland)2003

Frequent LOH at chromosome 12q22-23 and Apaf-1 inactivation in glioblastoma.

Takuya Watanabe, Yuichi Hirota, Yasuaki Arakawa, Hironori Fujisawa, Osamu Tachibana, Mitsuhiro Hasegawa, Junkoh Yamashita, Yutaka Hayashi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  7. MiR-21: an environmental driver of malignant melanoma?Journal of translational medicine · 2015
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  12. Evasion of apoptosis as a cellular stress response in cancer.International journal of cell biology · 2010
    Article
  13. miR-21: a small multi-faceted RNA.Journal of cellular and molecular medicine · 2009
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Pathology and molecular genetics of astrocytic gliomas.Journal of molecular medicine (Berlin, Germany) · 2004
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Takuya WatanabeDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Japan.
Yuichi Hirota
Yasuaki Arakawa
Hironori Fujisawa
Osamu Tachibana
Mitsuhiro Hasegawa
Junkoh Yamashita
Yutaka Hayashi
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GB) often has loss of heterozygosity on the chromosomes, 1p, 10p, 10q, 11p, 17p, 19q, 22q, and several others. In the case of chromosome 12q, however, it remains to be seen whether LOH occurs. Apaf-1, the apoptotic protease activating factor-1, located at chromosome 12q22-23, is a major effecter of the p53 mediated apoptosis pathway, and Apaf-1 inactivation due to chromosome 12q22-23 LOH and hypermethylation may be involved in some of the neoplasms in malignancy. However, little is known about the frequency of the 12q22-23 LOH or the state of Apaf-1 in GB. To elucidate their involvement in GB, we analyzed a series of 33 GBs for chromosome 12q22-23 LOH, Apaf-1 mRNA expression, and Apaf-1 protein expression, using microsatellite analysis, reverse transcription (RT)-PCR analysis, and immunohistochemical (IHC) analysis, respectively. We also evaluated if and how the 12q22-23 LOH correlated with the p53 gene mutation and EGFR gene amplification. Chromosome 12q22-23 LOH was detected in 14 (42%) of 33 cases. Among the examined cases with LOH at 12q22-23, a low expression of Apaf-1 mRNA was detected in 9 (69%) of 13 cases, and a low expression of Apaf-1 protein was detected in 12 (86%) of 14 cases. The 12q22-23 LOH was significantly correlated with low expression of mRNA and protein (p<0.05, p<0.001 respectively). The p53 gene mutation and EGFR gene amplification were found in 13 cases (39%) and 8 cases (24%), respectively, and these gene alterations were inversely correlated. However, 12q22-23 LOH had no correlations with the p53 gene mutation or EGFR gene amplification. Six of 9 GBs (67%) with neither p53 gene mutation nor EGFR gene amplification tested positive for 12q22-23 LOH. These GBs are likely to belong to another subset independent from the 2 common genetic subsets in GB (one with p53 gene mutation and without EGFR gene amplification, and the other with EGFR gene amplification and without p53 gene mutation). Twenty-three (70%) out of the 33 GBs with the 12q22-23 LOH also tested positive for Apaf-1 inactivation or p53 gene mutation. This high frequency of alterations in the apoptosis-associated factors prompts a speculation that abrogation of the Apaf-1 and p53 mediated apoptosis pathway may play an important role in the tumorigenesis of GB.

Indexed as

Chromosomes, Human, Pair 12Loss of HeterozygosityAdultAgedApoptotic Protease-Activating Factor 1Brain NeoplasmsGenes, erbB-1Genes, p53GlioblastomaHumansImmunohistochemistryMicrosatellite RepeatsMiddle AgedMutationProteinsReverse Transcriptase Polymerase Chain ReactionAPAF1 protein, humanApoptotic Protease-Activating Factor 1ProteinsRNA, Messenger

Identifiers

PMID14655749
PMCPMC8095738
OpenAlexW2023018711

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.