Evidence map›Paper›PMID 25714025›Full record

ArticleOncotarget2015

The over-expression of survivin enhances the chemotherapeutic efficacy of YM155 in human hepatocellular carcinoma.

Hongping Xia, Jianxiang Chen, Ming Shi, Amudha Deivasigamani, London Lucien P J Ooi, Kam M Hui

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Prognostic stratification based on mFrontiers in immunology · 2022
    Article
  4. Article
  5. Review
  6. Assessment of Current Gene Therapy Practices in Hepatocellular Carcinoma.Gastrointestinal disorders (Basel, Switzerland) · 2020
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
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

6 authors at 2 institutions in 2 countries.

Hongping XiaLaboratory of Cancer Genomics, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore.
Jianxiang ChenLaboratory of Cancer Genomics, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore.
Ming ShiDepartment of Hepatobiliary Oncology, Cancer Center, Sun Yat-sen University, Guangzhou, P.R. China.
Amudha DeivasigamaniLaboratory of Cancer Genomics, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore.
London Lucien P J OoiDepartment of Surgical Oncology, National Cancer Centre, Singapore.
Kam M HuiLaboratory of Cancer Genomics, Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore.
National Cancer Centre Singapore · SGSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. The inability of chemotherapeutic drugs to selectively target HCC tumor cells because of their predominant resistant phenotype to most conventional anticancer agents bestows a major obstacle for the clinical management of HCC. In this report, we have examined and demonstrated the remarkable heterogeneity of expression of survivin and its phosphorylated active form (p-survivin) in HCC patients' tissues and cell lines. Furthermore, the expression of survivin and p-survivin in HCC cell lines was found to be associated with response to the small-molecule survivin suppressant YM155. Therefore, in the HCC cell lines that express elevated level of survivin and p-survivin, YM155 efficiently inhibited their proliferation, induced cell cycle arrest and apoptosis resulting in DNA damage through the dysregulation of cell-cycle checkpoint-related regulatory genes. Importantly, YM155 yielded significantly better therapeutic effect than sorafenib when tested in an orthotopic mouse model using patient-derived HCC xenografts with elevated survivin and p-survivin expression. Our results clearly demonstrated that the level of survivin and p-survivin expression could serve as molecular predictive biomarkers to select potential YM155-responsive patients, in a move towards delivering precision medicine for HCC patients.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, HepatocellularCell Line, TumorDNA DamageHumansImidazolesInhibitor of Apoptosis ProteinsLiver NeoplasmsMiceMice, NudeNaphthoquinonesRepressor ProteinsSurvivinXenograft Model Antitumor AssaysAntineoplastic AgentsBirc5 protein, mouseImidazolesInhibitor of Apoptosis ProteinsNaphthoquinonesRepressor ProteinssepantroniumSurvivincancer heterogeneityDNA damagehepatocellular carcinomasurvivinYM155

Identifiers

PMID25714025
PMCPMC4467416
OpenAlexW1527782622

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.