Evidence map›Paper›PMID 19491896›Full record

ArticleBritish journal of cancer2009

The oncogenic mutation in the pleckstrin homology domain of AKT1 in endometrial carcinomas.

K Shoji, K Oda, S Nakagawa, S Hosokawa, G Nagae, Y Uehara, K Sone, Y Miyamoto, H Hiraike, O Hiraike-Wada and 6 more

Abstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. The structural heterogeneity of AKT autoinhibition.Protein science : a publication of the Protein Society · 2026
    Article
  6. Ipatasertib in Patients with Tumors with AKT Mutations: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Subprotocol Z1K.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  7. Article
  8. Article
  9. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
  10. Article
  11. Review
  12. Could cannabinoids provide a new hope for ovarian cancer patients?Pharmacology research & perspectives · 2023
    Review
  13. Article
  14. Genomic landscape of endometrial carcinomas of no specific molecular profile.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Novel polymer-based system for intrauterine delivery of everolimus for anti-cancer applications.Journal of controlled release : official journal of the Controlled Release Society · 2021
    Article
  19. Article
  20. Targeting Akt in cancer for precision therapy.Journal of hematology & oncology · 2021
    Review

18 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

K ShojiDepartment of Obstetrics and Gynecology, The University of Tokyo, Tokyo, Japan.
K Oda
S Nakagawa
S Hosokawa
G Nagae
Y Uehara
K Sone
Y Miyamoto
H Hiraike
O Hiraike-Wada
T Nei
K Kawana
H Kuramoto
H Aburatani
T Yano
Y Taketani

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe phosphatidylinositol 3'-kinase (PI3K)-AKT pathway is activated in many human cancers and plays a key role in cell proliferation and survival. A mutation (E17K) in the pleckstrin homology domain of the AKT1 results in constitutive AKT1 activation by means of localisation to the plasma membrane. The AKT1 (E17K) mutation has been reported in some tumour types (breast, colorectal, ovarian and lung cancers), and it is of interest which tumour types other than those possess the E17K mutation.

methodsWe analysed the presence of the AKT1 (E17K) mutation in 89 endometrial cancer tissue specimens and in 12 endometrial cancer cell lines by PCR and direct sequencing.

resultsWe detected two AKT1 (E17K) mutations in the tissue samples (2 out of 89) and no mutations in the cell lines. These two AKT1 mutant tumours do not possess any mutations in PIK3CA, PTEN and K-Ras.

interpretationOur results and earlier reports suggest that AKT1 mutations might be mutually exclusive with other PI3K-AKT-activating alterations, although PIK3CA mutations frequently coexist with other alterations (such as HER2, K-Ras and PTEN) in several types of tumours.

Indexed as

Mutation, MissenseBlood ProteinsCell Line, TumorDNA MethylationEndometrial NeoplasmsFemaleHumansPhosphatidylinositol 3-KinasesPhosphoproteinsPolymorphism, Single NucleotideProtein Structure, TertiaryProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseAKT1 protein, humanBlood ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsplatelet protein P47Proto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID19491896
PMCPMC2713716

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.