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Related Concept Videos

The Ras Gene02:38

The Ras Gene

6.6K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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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...
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Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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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...
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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...
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Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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...
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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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Related Experiment Video

Updated: Oct 26, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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ASN007 is a selective ERK1/2 inhibitor with preferential activity against RAS-and RAF-mutant tumors.

Ana Portelinha1, Scott Thompson2, Roger A Smith2

  • 1Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Cell Reports. Medicine
|August 2, 2021
PubMed
Summary

ASN007, a new ERK1/2 inhibitor, shows strong anticancer activity in preclinical models with RAS/RAF mutations. Combining it with PI3K inhibitors enhances its effectiveness in treating resistant cancers.

Keywords:
ASN007ERKKRASPI3KRAF/RAS-driven cancersbiomarkercombinational therapykinase inhibitorlymphomasolid tumors

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • The RAS/RAF/MEK/ERK signaling pathway is frequently activated in various cancers.
  • Targeting extracellular signal-regulated kinases ERK1 and ERK2 (ERK1/2) is a key therapeutic strategy.
  • Development of novel inhibitors is crucial for overcoming resistance mechanisms.

Purpose of the Study:

  • To characterize ASN007, an orally bioavailable and selective ERK1/2 inhibitor.
  • To evaluate the efficacy of ASN007 in preclinical cancer models.
  • To explore the combination therapy of ASN007 with PI3K inhibitors.

Main Methods:

  • Preclinical studies using cancer cell lines and tumor models.
  • Assessment of antiproliferative activity of ASN007.
  • Evaluation of combination therapy with PI3K inhibitor copanlisib in vitro and in vivo.

Main Results:

  • ASN007 demonstrated significant antiproliferative activity against tumors with BRAF and RAS mutations.
  • ASN007 showed efficacy in a BRAFV600E melanoma model resistant to BRAF and MEK inhibitors.
  • Combination of ASN007 with copanlisib enhanced antitumor activity through dual pathway inhibition.

Conclusions:

  • ASN007 is a promising therapeutic agent for RAS/RAF-driven cancers.
  • Dual inhibition of RAS/MAPK and PI3K pathways offers a rational combination strategy.
  • Further clinical evaluation of ASN007, particularly in combination therapy, is warranted.