Evidence map›Paper›PMID 26119932›Full record

ArticleOncogene2016

Targeting melanoma with NT157 by blocking Stat3 and IGF1R signaling.

E Flashner-Abramson, S Klein, G Mullin, E Shoshan, R Song, A Shir, Y Langut, M Bar-Eli, H Reuveni, A Levitzki

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–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

22 citing papers in PubMed.

  1. Article
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  8. NT157 has antineoplastic effects and inhibits IRS1/2 and STAT3/5 in JAK2Signal transduction and targeted therapy · 2020
    Article
  9. Review
  10. My journey from tyrosine phosphorylation inhibitors to targeted immune therapy as strategies to combat cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Review
  12. Review
  13. Article
  14. Article
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

E Flashner-AbramsonDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
S KleinDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
G MullinDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
E ShoshanDepartment of Cancer Biology, Unit 173 UT, MD Anderson Cancer Center, Houston, TX, USA.
R SongDepartment of Cancer Biology, Unit 173 UT, MD Anderson Cancer Center, Houston, TX, USA.
A ShirDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Y LangutDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
M Bar-EliDepartment of Cancer Biology, Unit 173 UT, MD Anderson Cancer Center, Houston, TX, USA.
H ReuveniDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
A LevitzkiDepartment of Biological Chemistry, Unit of Cellular Signaling, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.

Funding

UT M.D. Anderson Cancer Center SPORE in MelanomaP50CA093459 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GRIMM, ELIZABETH A · 2004 to 2014
$23.7M
NCI NIH HHS P50 CA093459
6 · The paper itself

Abstract

It is well known that specific signal transduction inhibitors rarely suffice as anti-cancer agents. In most cases, tumors possess primary drug resistance due to their inherent heterogeneity, or acquire drug resistance due to genomic instability and acquisition of mutations. Here we expand our previous study of the novel compound, NT157, and show that it acts as a dual-targeting agent that invokes the blockage of two signal transduction pathways that are central to the development and maintenance of multiple human cancers. We show that NT157 targets not only IGF1R-IRS1/2, as previously reported, but also the Stat3 signaling pathway and demonstrates remarkable anti-cancer characteristics in A375 human melanoma cells and in a metastatic melanoma model in mice.

Indexed as

Antineoplastic AgentsCell Line, TumorDrug DiscoveryHumansMelanomaMolecular Targeted TherapyNeoplasm InvasivenessPyrogallolReceptor, IGF Type 1Receptors, SomatomedinSignal TransductionSTAT3 Transcription FactorSulfonamidesAntineoplastic AgentsIGF1R protein, humanNT157 compoundPyrogallolReceptor, IGF Type 1Receptors, SomatomedinSTAT3 Transcription FactorSulfonamides

Identifiers

PMID26119932

What OpenQuestion holds

Textmetadata
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.