Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Targeting PEAK1 sensitizes anaplastic thyroid carcinoma cells harboring BRAFV600E to Vemurafenib by Bim upregulation.

Histology and histopathology - 1 Sept 2024

Wang Qiuhan, Hao Fengyun, Ning Liang, Sun Chong

Abstract excerpt

Pseudopodium-enriched atypical kinase 1 (PEAK1) has been demonstrated to be upregulated in human malignancies and cells. Enhanced PEAK1 expression facilitates tumor cell survival and chemoresistance. However, the role of PEAK1 inhibition to anaplastic thyroid carcinoma cell (ATC) and vemurafenib resistance is still unknown. Here, we observed that targeting PEAK1 inhibited cell viability and colony formation, but...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bcl-2-Like Protein 11
Share to Cell Survival
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Proto-Oncogene Proteins B-raf

Share to Thyroid Carcinoma, Anaplastic

Share to Thyroid Neoplasms

Share to Up-Regulation

Share to Vemurafenib

Source

Identifiers

PMID: 38284248
DOI: 10.14670/HH-18-705

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeting PEAK1 sensitizes anaplastic thyroid carcinoma cells harboring BRAFV600E to Vemurafenib by Bim upregulation.PMID 38284248Read ↗

S100A4 Knockout Sensitizes Anaplastic Thyroid Carcinoma Cells Harboring BRAFV600E/Mt to Vemurafenib.Semantic proximity Read ↗

Dual targeting of PDPK1 and BRAF V600E is synthetically lethalSemantic proximity Read ↗

Role of the ETV5/p38 signaling axis in aggressive thyroid cancer cellsSemantic proximity Read ↗

The MEK1/2 Inhibitor AZD6244 Sensitizes BRAF-Mutant Thyroid Cancer to Vemurafenib.Semantic proximity Read ↗

Targeted therapy with vemurafenib in BRAF(V600E)-mutated anaplastic thyroid cancerSemantic proximity Read ↗

Dual Inhibition of BRAF-MAPK and STAT3 Signaling Pathways in Resveratrol-Suppressed Anaplastic Thyroid Cancer Cells with BRAF Mutations.Semantic proximity Read ↗

mTOR inhibitors sensitize thyroid cancer cells to cytotoxic effect of vemurafenib.Semantic proximity Read ↗

Role of Annexin 7 (ANXA7) as a tumor suppressor and a regulator of drug resistance in thyroid cancerSemantic proximity Read ↗

FOXM1 is a molecular determinant of the mitogenic and invasive phenotype of anaplastic thyroid carcinoma.Semantic proximity Read ↗

Sorafenib inhibits intracellular signaling pathways and induces cell cycle arrest and cell death in thyroid carcinoma cells irrespective of histological origin or BRAF mutational status.Semantic proximity Read ↗

Antitumor activity of extracellular signal-regulated kinases 1/2 inhibitor BVD-523 (ulixertinib) on thyroid cancer cells.Semantic proximity Read ↗

Synergistic Effect of Metformin and Vemurufenib (PLX4032) as a Molecular Targeted Therapy in Anaplastic Thyroid Cancer – An In Vitro StudySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.