Evidence map›Paper›PMID 25344912›Full record

ArticleOncotarget2014

Suppression of esophageal tumor growth and chemoresistance by directly targeting the PI3K/AKT pathway.

Bin Li, Jin Li, Wen Wen Xu, Xin Yuan Guan, Yan Ru Qin, Li Yi Zhang, Simon Law, Sai Wah Tsao, Annie L M Cheung

Registry-linked trialOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05660083 (Phase II Trial of Alpelisib With iNOS Inhibitor and Nab-paclitaxel in Patients With HER2 Negative Metastatic or Locally Advanced Metaplastic Breast Cancer), which is not on this map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.3field-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.

NCT05660083 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

Phase II Trial of Alpelisib With iNOS Inhibitor and Nab-paclitaxel in Patients With HER2 Negative Metastatic or Locally Advanced Metaplastic Breast Cancer (MpBC)

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2023 to 2028Enrolled36ConditionsHER2-negative Breast Cancer, Metastatic Breast Cancer, Metaplastic Breast Carcinoma, TNBC - Triple-Negative Breast CancerArmsL-NMMA
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  7. Factors that determine cell fate in mitotically arrested cancer cells.Frontiers in cell and developmental biology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Molecular mechanisms associated with chemoresistance in esophageal cancer.Cellular and molecular life sciences : CMLS · 2022
    Review
  13. In vitro anti-cancer effect of marmesin by suppression of PI3K/Akt pathway in esophagus cancer cells.Esophagus : official journal of the Japan Esophageal Society · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. 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

9 authors at 3 institutions in 3 countries.

Bin LiDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Centre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI), China.
Jin LiDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Present Address: Research Center for Molecular Medicine of The Austrian Academy of Sciences, Vienna, Austria.
Wen Wen XuDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI), China.
Xin Yuan GuanCentre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Department of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Yan Ru QinDepartment of Clinical Oncology, First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Li Yi ZhangDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Simon LawCentre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Department of Surgery, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Sai Wah TsaoDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Centre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Annie L M CheungDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Centre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI), China.
University of Hong Kong · HKAustrian Academy of Sciences · ATFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer is the sixth most common cause of cancer-related deaths worldwide. Novel therapeutic intervention is urgently needed for this deadly disease. The functional role of PI3K/AKT pathway in esophageal cancer is little known. In this study, our results from 49 pairs of human esophageal tumor and normal specimens demonstrated that AKT was constitutively active in the majority (75.5%) of esophageal tumors compared with corresponding normal tissues. Inhibition of the PI3K/AKT pathway with specific inhibitors, wortmannin and LY294002, significantly reduced Bcl-xL expression, induced caspase-3-dependent apoptosis, and repressed cell proliferation and tumor growth in vitro and in vivo without obvious toxic effects. Moreover, significantly higher expression level of p-AKT was observed in fluorouracil (5-FU)-resistant esophageal cancer cells. Inactivation of PI3K/AKT pathway markedly increased the sensitivity and even reversed acquired resistance of esophageal cancer cells to chemotherapeutic drugs in vitro. More importantly, the resistance of tumor xenografts derived from esophageal cancer cells with acquired 5-FU resistance to chemotherapeutic drugs was significantly abrogated by wortmannin treatment in animals. In summary, our data support PI3K/AKT as a valid therapeutic target and strongly suggest that PI3K/AKT inhibitors used in conjunction with conventional chemotherapy may be a potentially useful therapeutic strategy in treating esophageal cancer patients.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAndrostadienesAnimalsApoptosisCell Line, TumorCell ProliferationChromonesDrug Resistance, NeoplasmEnzyme InhibitorsEsophageal NeoplasmsFemaleFluorouracilHumansMiceMice, Nude2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAKT1 protein, humanAndrostadienesChromonesEnzyme InhibitorsFluorouracilMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktWortmannin

Identifiers

PMID25344912
PMCPMC4294385
OpenAlexW2117282329

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.