Evidence map›Paper›PMID 27458138›Full record

ArticleMolecular cancer therapeutics2016

Hypoxia-Driven Mechanism of Vemurafenib Resistance in Melanoma.

Yong Qin, Jason Roszik, Chandrani Chattopadhyay, Yuuri Hashimoto, Chengwen Liu, Zachary A Cooper, Jennifer A Wargo, Patrick Hwu, Suhendan Ekmekcioglu, Elizabeth A Grimm

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Three-DimensionalInternational journal of biological sciences · 2024
    Review
  6. Article
  7. Hypoxia in Skin Cancer: Molecular Basis and Clinical Implications.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. HO-1 Limits the Efficacy of Vemurafenib/PLX4032 in BRAFAntioxidants (Basel, Switzerland) · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Hypoxia-dependent drivers of melanoma progression.Journal of experimental & clinical cancer research : CR · 2021
    Review
  15. Article
  16. Review
  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

10 authors at 1 institution in 1 country.

Yong QinDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jason RoszikDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Chandrani ChattopadhyayDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Yuuri HashimotoDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Chengwen LiuDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Zachary A CooperDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jennifer A WargoDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Patrick HwuDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Suhendan EkmekciogluDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Elizabeth A GrimmDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. egrimm@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
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
Exploring synergy of combined BRAF-targeted therapy & immunotherapy for melanomaK08CA160692 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WARGO, JENNIFER A. · 2012 to 2016
$713k
NCI NIH HHS K08 CA160692NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA093459
6 · The paper itself

Abstract

Melanoma is molecularly and structurally heterogeneous, with some tumor cells existing under hypoxic conditions. Our cell growth assays showed that under controlled hypoxic conditions, BRAF(V600E) melanoma cells rapidly became resistant to vemurafenib. By employing both a three-dimensional (3D) spheroid model and a two-dimensional (2D) hypoxic culture system to model hypoxia in vivo, we identified upregulation of HGF/MET signaling as a major mechanism associated with vemurafenib resistance as compared with 2D standard tissue culture in ambient air. We further confirmed that the upregulation of HGF/MET signaling was evident in drug-resistant melanoma patient tissues and mouse xenografts. Pharmacologic inhibition of the c-Met/Akt pathway restored the sensitivity of melanoma spheroids or 2D hypoxic cultures to vemurafenib. Mol Cancer Ther; 15(10); 2442-54. ©2016 AACR.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalFemaleHepatocyte Growth FactorHumansHypoxiaIndolesMelanomaMiceMutationPhosphorylationAntineoplastic AgentsHepatocyte Growth FactorIndolesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metSulfonamidesTumor Suppressor Protein p53Vemurafenib

Identifiers

PMID27458138
PMCPMC5079683
OpenAlexW2489443540

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.