Evidence map›Paper›PMID 33327495›Full record

ArticleCancers2020

HER3-Receptor-Mediated STAT3 Activation Plays a Central Role in Adaptive Resistance toward Vemurafenib in Melanoma.

Laura Hüser, Marianthi-Maria Kokkaleniou, Karol Granados, Jennifer Dworacek, Aniello Federico, Marlene Vierthaler, Daniel Novak, Ihor Arkhypov, Thomas Hielscher, Viktor Umansky and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. 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

12 authors at 1 institution in 1 country.

Laura HüserSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0001-7599-8192
Marianthi-Maria KokkaleniouSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0003-3863-2524
Karol GranadosSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Jennifer DworacekSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Aniello FedericoSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Marlene VierthalerSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Daniel NovakSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Ihor ArkhypovSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Thomas HielscherBiostatistics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Viktor UmanskySkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Peter AltevogtSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0002-5896-2152
Jochen UtikalSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
German Cancer Research Center · DE

Funding

Deutsche Forschungsgemeinschaft 259332240 / RTG 2099
6 · The paper itself

Abstract

Melanoma is an aggressive form of skin cancer that is often characterized by activating mutations in the Mitogen-Activated Protein (MAP) kinase pathway, causing hyperproliferation of the cancer cells. Thus, inhibitors targeting this pathway were developed. These inhibitors are initially very effective, but the occurrence of resistance eventually leads to a failure of the therapy and is the major obstacle for clinical success. Therefore, investigating the mechanisms causing resistance and discovering ways to overcome them is essential for the success of therapy. Here, we observed that treatment of melanoma cells with the B-Raf Proto-Oncogene, Serine/Threonine Kinase (BRAF) inhibitor vemurafenib caused an increased cell surface expression and activation of human epidermal growth factor receptor 3 (HER3) by shed ligands. HER3 promoted the activation of signal transducer and activator of transcription 3 (STAT3) resulting in upregulation of the STAT3 target gene SRY-Box Transcription Factor 2 (

Indexed as

adaptive resistanceBRAF inhibitorHER3melanomaSTAT3

Identifiers

PMID33327495
PMCPMC7764938
OpenAlexW3110836917

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.