Evidence map›Paper›PMID 25582346›Full record

SynthesisScientific reports2015

The prognostic value of phosphorylated Akt in breast cancer: a systematic review.

Zu-Yao Yang, Meng-Yang Di, Jin-Qiu Yuan, Wei-Xi Shen, Da-Yong Zheng, Jin-Zhang Chen, Chen Mao, Jin-Ling Tang

Open access · goldAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. AKT-dependent nuclear localization of EPRS1 activates PARP1 in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Changes in Cells Associated with Insulin Resistance.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Article
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  19. The Role of mTOR Signaling as a Therapeutic Target in Cancer.International journal of molecular sciences · 2021
    Review
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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

8 authors at 3 institutions in 1 country.

Zu-Yao YangDivision of Epidemiology, JC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong.
Meng-Yang DiDivision of Epidemiology, JC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong.
Jin-Qiu YuanDivision of Epidemiology, JC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong.
Wei-Xi ShenCancer Institute, Shenzhen People's Hospital (2nd Clinical Medical College of Jinan University), Shenzhen, Guangdong Province, China.
Da-Yong ZhengDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China.
Jin-Zhang ChenDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China.
Chen Mao1] Division of Epidemiology, JC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong [2] Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute of The Chinese University of Hong Kong, Shenzhen, Guangdong Province, China.
Jin-Ling Tang1] Division of Epidemiology, JC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong [2] Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute of The Chinese University of Hong Kong, Shenzhen, Guangdong Province, China [3] The Hong Kong Branch of The Chinese Cochrane Centre, The Chinese University of Hong Kong, Hong Kong.
Chinese University of Hong Kong · CNSouthern Medical University · CNShenZhen People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prognostic value of phosphorylated Akt (pAkt) overexpression in breast cancer has been investigated by many studies with inconsistent results. This systematic review was conducted to evaluate the association of pAkt overexpression with breast cancer prognosis in terms of overall survival and disease-free survival. Three electronic databases (PubMed, EMBASE and Chinese Biomedical Literature Database) were comprehensively searched. Hazard ratios (HRs) with 95% confidence intervals (CIs) from different studies were combined using the random-effects model. In total, 33 studies with 9,836 patients were included for final analysis. The summary HR for overall survival and disease-free survival was 1.52 (95% CI: 1.29-1.78) and 1.28 (95% CI: 1.13-1.45), respectively, indicating higher risk of death and disease recurrence associated with pAkt overexpression. The results were robust in sensitivity analyses by omitting one study each time and by using the fixed-effects model instead. Subgroup and meta-regression analyses did not show that the prognostic effect of pAkt overexpression would change materially with such factors as population, status of hormone receptors, hormonal or trastuzumab treatment given, analyzing method (univariate versus multivariate) and methodological quality of the original studies. In conclusion, the available evidence suggests that pAkt overexpression is an adverse prognostic factor for breast cancer.

Indexed as

Breast NeoplasmsDisease-Free SurvivalFemaleHumansPhosphorylationProto-Oncogene Proteins c-aktPublication BiasRegression AnalysisProto-Oncogene Proteins c-akt

Identifiers

PMID25582346
PMCPMC4291578
OpenAlexW2050580690

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.