Related Experiment Video

Updated: May 23, 2026

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
08:18

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

Published on: September 8, 2021

A potential role for nilotinib in KIT-mutated melanoma

An Tran1, Hussein A Tawbi

  • 1University of Pittsburgh, School of Medicine, Division of Hematology/Oncology, Department of Medicine, Pittsburgh, PA 15232, USA.

Expert Opinion on Investigational Drugs
|April 17, 2012
PubMed
Abstract

Insights

Nilotinib shows promise for treating metastatic melanoma with KIT mutations. Its established safety and efficacy in other cancers suggest it warrants further clinical investigation for this specific patient group.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • Metastatic melanoma treatment is evolving with immunotherapy and targeted therapies.
  • KIT mutations are oncogenic drivers in up to 3% of melanomas.
  • Understanding KIT mutations is crucial for developing new melanoma treatments.

Purpose of the Study:

  • To review the development of KIT-targeted agents for melanoma.
  • To present data on nilotinib's pharmacokinetics, pharmacodynamics, safety, and clinical activity.
  • To leverage experience from nilotinib use in CML and GIST to guide melanoma development.

Main Methods:

  • Review of current KIT-targeted agent development in melanoma.
  • Analysis of nilotinib's pharmacokinetic and pharmacodynamic profiles.
  • Evaluation of nilotinib's safety and clinical activity data.
  • Extrapolation of knowledge from nilotinib's use in CML and GIST.

Main Results:

  • Nilotinib is a potent second-generation tyrosine kinase inhibitor.
  • Nilotinib has demonstrated favorable safety and efficacy in CML and imatinib-resistant GISTs.
  • These characteristics suggest potential for nilotinib in treating KIT-mutated melanoma.

Conclusions:

  • Nilotinib is a promising agent for metastatic melanoma with KIT mutations.
  • Clinical investigation of nilotinib in this setting is warranted.
  • Leveraging prior experience can optimize nilotinib's development for melanoma.

More Related Videos

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...