Evidence map›Paper›PMID 39175042›Full record

ArticleCell communication and signaling : CCS2024

Characterization of two melanoma cell lines resistant to BRAF/MEK inhibitors (vemurafenib and cobimetinib).

Magdalena Kot, Aleksandra Simiczyjew, Justyna Wądzyńska, Marcin Ziętek, Rafał Matkowski, Dorota Nowak

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. 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.

Magdalena Kot *Department of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, Joliot-Curie 14a, Wroclaw, 50-383, Poland.
Aleksandra Simiczyjew *Department of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, Joliot-Curie 14a, Wroclaw, 50-383, Poland. aleksandra.simiczyjew@uwr.edu.pl.
Justyna WądzyńskaDepartment of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, Joliot-Curie 14a, Wroclaw, 50-383, Poland.
Marcin ZiętekDepartment of Oncology, Division of Surgical Oncology, Wroclaw Medical University, Plac Hirszfelda 12, Wroclaw, 53-413, Poland.
Rafał MatkowskiDepartment of Oncology, Division of Surgical Oncology, Wroclaw Medical University, Plac Hirszfelda 12, Wroclaw, 53-413, Poland.
Dorota NowakDepartment of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, Joliot-Curie 14a, Wroclaw, 50-383, Poland.

Funding

National Science Center, Poland SONATA, 2020/39/D/NZ5/02330
6 · The paper itself

Abstract

backgroundBRAF (v-raf murine sarcoma viral oncogene homolog B1)/MEK (mitogen-activated protein kinase kinase) inhibitors are used for melanoma treatment. Unfortunately, patients treated with this combined therapy develop resistance to treatment quite quickly, but the mechanisms underlying this phenomenon are not yet fully understood. Here, we report and characterize two melanoma cell lines (WM9 and Hs294T) resistant to BRAF (vemurafenib) and MEK (cobimetinib) inhibitors.

methodsCell viability was assessed via the XTT test. The level of selected proteins as well as activation of signaling pathways were evaluated using Western blotting. The expression of the chosen genes was assessed by RT-PCR. The distribution of cell cycle phases was analyzed by flow cytometry, and confocal microscopy was used to take photos of spheroids. The composition of cytokines secreted by cells was determined using a human cytokine array.

resultsThe resistant cells had increased survival and activation of ERK kinase in the presence of BRAF/MEK inhibitors. The IC

conclusionsIn summary, this work describes BRAF/MEK-inhibitor-resistant melanoma cells, allowing for better understanding the underlying mechanisms of resistance. The results may thus contribute to the development of new, more effective therapeutic strategies.

Indexed as

AzetidinesDrug Resistance, NeoplasmMelanomaPiperidinesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafVemurafenibCell Line, TumorCell SurvivalHumansMitogen-Activated Protein Kinase KinasesAzetidinesBRAF protein, humancobimetinibMitogen-Activated Protein Kinase KinasesPiperidinesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafVemurafenibBRAFi/MEKiCobimetinibDrug resistanceMelanomaTargeted therapyVemurafenib

Identifiers

PMID39175042
PMCPMC11342534

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.