Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.6K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.6K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.9K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.9K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.8K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.8K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

5.9K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.9K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.9K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.9K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

79.5K
Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
79.5K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Where Does Liquid Biopsy Add Value in Thyroid Cancer? Biological Rationale, Technological Innovation, and Clinical Utility.

Biomedicines·2026
Same author

Identification and Characterization of ERK2 Dimerization Inhibitors by Integrated In Silico and In Vitro Screening.

International journal of molecular sciences·2025
Same author

Targeted radioiodine therapy of ovarian cancer via the sodium/iodide symporter (NIS).

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025
Same author

BRAF V600E in thyroid cancer: navigating prognostic uncertainty and therapeutic opportunity.

European thyroid journal·2025
Same author

DNA Methylation Dynamics and Prognostic Implications in Metastatic Differentiated Thyroid Cancer.

Thyroid : official journal of the American Thyroid Association·2025
Same author

RBM10 loss promotes metastases by aberrant splicing of cytoskeletal and extracellular matrix mRNAs.

The Journal of experimental medicine·2025

Related Experiment Video

Updated: Aug 30, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

1.7K

Inhibiting ERK dimerization ameliorates BRAF-driven anaplastic thyroid cancer.

Miguel A Zaballos1,2, Adrián Acuña-Ruiz3,4, Marta Morante5,6

  • 1Instituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid (CSIC-UAM), 28029, Madrid, Spain. mazaballos@iib.uam.es.

Cellular and Molecular Life Sciences : CMLS
|September 3, 2022
PubMed
Summary
This summary is machine-generated.

DEL-22379, an ERK dimerization inhibitor, shows significant anti-tumor effects in BRAF-mutant anaplastic thyroid carcinoma (ATC) models. This study reveals differential responses in BRAF- vs. RAS-mutant ATC, suggesting personalized treatment strategies.

Keywords:
BRAFDEL-22379ERK dimerizationRASThyroid cancer

More Related Videos

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

21.2K
Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

6.1K

Related Experiment Videos

Last Updated: Aug 30, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
05:39

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

1.7K
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

21.2K
Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

6.1K

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • RAS-to-ERK signaling is critical in advanced thyroid carcinoma.
  • ERK dimerization inhibition offers a therapeutic strategy for carcinomas.
  • DEL-22379 is a specific ERK dimerization inhibitor investigated for thyroid cancer.

Purpose of the Study:

  • To analyze DEL-22379's effects on RAS-to-ERK signaling.
  • To evaluate DEL-22379's impact on tumor processes in vitro and in vivo.
  • To determine differential responses in BRAF- vs. RAS-mutant anaplastic thyroid carcinoma (ATC).

Main Methods:

  • Utilized four human ATC cell lines with BRAF or RAS mutations.
  • Assessed ERK dynamics and tumor characteristics.
  • Performed RNA-sequencing for transcriptional landscape analysis and in vivo efficacy testing in an orthotopic mouse model.

Main Results:

  • DEL-22379 impaired ERK activation in BRAF-mutant cells but not RAS-mutant cells.
  • Cell viability and metastasis were reduced, primarily in BRAF-mutant cells.
  • In vivo, tumor growth and dissemination were significantly reduced in BRAF-mutant and mildly in RAS-mutant models.

Conclusions:

  • BRAF- and RAS-mutant thyroid cells exhibit distinct responses to DEL-22379.
  • DEL-22379 shows significant anti-tumor activity against BRAF-mutant ATC with low toxicity.
  • Driver mutation type is crucial for thyroid cancer progression and treatment considerations.