Evidence map›Paper›PMID 25944801›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2015

Inhibition of Survivin with YM155 Induces Durable Tumor Response in Anaplastic Thyroid Cancer.

Amit Mehta, Lisa Zhang, Myriem Boufraqech, Yi Liu-Chittenden, Yaqin Zhang, Dhaval Patel, Sean Davis, Avi Rosenberg, Kris Ylaya, Rachel Aufforth and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Combined Inhibition ofInternational journal of molecular sciences · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. A Combinatorial Strategy for TargetingClinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. CAR T Therapy Targeting ICAM-1 Eliminates Advanced Human Thyroid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  16. Dual Inhibition of HDAC and Tyrosine Kinase Signaling Pathways with CUDC-907 Inhibits Thyroid Cancer Growth and Metastases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  17. Article
  18. Article
  19. Review
  20. 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

13 authors at 1 institution in 1 country.

Amit MehtaEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. Geisel School of Medicine at Dartmouth, Hanover, New Hampshire.
Lisa ZhangEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Myriem BoufraqechEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Yi Liu-ChittendenEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Yaqin ZhangNational Center for Advancing Translational Sciences, NIH, Bethesda, Maryland.
Dhaval PatelEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Sean DavisCancer Genetics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Avi RosenbergLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Kris YlayaLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Rachel AufforthEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Zhuyin LiNational Center for Advancing Translational Sciences, NIH, Bethesda, Maryland.
Min ShenNational Center for Advancing Translational Sciences, NIH, Bethesda, Maryland.
Electron KebebewEndocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. kebebewe@mail.nih.gov.
Dartmouth College · US

Funding

Therapeutic targets and novel anticancer agents for endocrine cancersZIABC011286 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NILUBOL, NARIS · 2010 to 2025
$16.6M
Genomic and genetic studies of endocrine cancersZIABC011275 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KEBEBEW, ELECTRON · 2010 to 2018
$8.2M
Howard Hughes Medical InstituteIntramural NIH HHS ZIA BC011275Intramural NIH HHS ZIA BC011286
6 · The paper itself

Abstract

purposeAnaplastic thyroid cancer (ATC) is a rare but lethal malignancy without any effective therapy. The aim of this study is to use a high-throughput drug library screening to identify a novel therapeutic agent that targets dysregulated genes/pathways in ATC. EXPERIMENTALDESIGN: We performed quantitative high-throughput screening (qHTS) in ATC cell lines using a compound library of 3,282 drugs. Dysregulated genes in ATC were analyzed using genome-wide expression analysis and immunohistochemistry in human ATC tissue samples and ATC cell lines. In vitro and in vivo studies were performed for determining drug activity, effectiveness of targeting, and the mechanism of action.

resultsqHTS identified 100 active compounds in three ATC cell lines. One of the most active agents was the first-in-class survivin inhibitor YM155. Genome-wide expression analysis and immunohistochemistry showed overexpression of survivin in human ATC tissue samples, and survivin was highly expressed in all ATC cell lines tested. YM155 significantly inhibited ATC cellular proliferation. Mechanistically, YM155 inhibited survivin expression in ATC cells. Furthermore, YM155 treatment reduced claspin expression, which was associated with S-phase arrest in ATC cells. In vivo, YM155 significantly inhibited growth and metastases and prolonged survival.

conclusionsOur data show that YM155 is a promising anticancer agent for ATC and that its target, survivin, is overexpressed in ATC. Our findings support the use of YM155 in clinical trials as a therapeutic option in advanced and metastatic ATC.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell CycleCell Line, TumorCell ProliferationCell SurvivalGene Expression ProfilingGene Expression Regulation, NeoplasticGenome-Wide Association StudyHeLa CellsHumansImidazolesImmunohistochemistryInhibitor of Apoptosis ProteinsInhibitory Concentration 50MiceAdaptor Proteins, Signal TransducingBIRC5 protein, humanCLSPN protein, humanImidazolesInhibitor of Apoptosis ProteinsNaphthoquinonesRNA, Small InterferingsepantroniumSurvivin

Identifiers

PMID25944801
PMCPMC4573822
OpenAlexW1844771852

What OpenQuestion holds

Textmetadata
LicenceTDM
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.