Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Inhibition of Cdk Activity

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...

M-Cdk Drives Transition Into Mitosis

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...

Combination Therapies and Personalized Medicine

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

Targeted Cancer Therapies

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...

You might also read

Related Articles

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

Sort by

Same author

Stage-adapted treatment of HIV-associated Hodgkin lymphoma: Long-term results of a prospective, multicenter study.

HemaSphere·2024

Same author

Patients with Primary Central Nervous System Lymphoma Not Eligible for Clinical Trials: Prognostic Factors, Treatment and Outcome.

Cancers·2021

Same author

Incidence and risk factors for relapses in HIV-associated non-Hodgkin lymphoma as observed in the German HIV-related lymphoma cohort study.

Haematologica·2018

Same author

Loss-of-function but not dominant-negative intragenic <i>IKZF1</i> deletions are associated with an adverse prognosis in adult <i>BCR-ABL</i>-negative acute lymphoblastic leukemia.

Haematologica·2017

Same author

Early whole brain radiotherapy in primary CNS lymphoma: negative impact on quality of life in the randomized G-PCNSL-SG1 trial.

Journal of cancer research and clinical oncology·2017

Same author

HIV-Associated Lung Cancer.

Oncology research and treatment·2017

Search research articles

Related Experiment Video

Updated: Jul 14, 2026

Robotic Duodenal Sleeve Resection for Gastrointestinal Stromal Tumor with Rare Exon 8 KIT Mutation Following Neoadjuvant Imatinib

Robotic Duodenal Sleeve Resection for Gastrointestinal Stromal Tumor with Rare Exon 8 KIT Mutation Following Neoadjuvant Imatinib

Published on: April 3, 2026

C-kit, GIST, and imatinib.

Jan Siehl¹, Eckhard Thiel

¹Medizinische Klinik III (Hematology, Oncology and Transfusion Medicine), Charité Campus Benjamin Franklin, Berlin, Germany.

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer

|July 5, 2007

Summary

Gain-of-function mutations in c-kit drive gastrointestinal stromal tumors (GIST). Imatinib is a standard targeted therapy, but resistance necessitates exploring new treatments like sunitinib for improved outcomes.

Area of Science:

Oncology
Molecular Biology
Pharmacology

Background:

Gastrointestinal stromal tumors (GIST) are driven by activating mutations in the c-kit receptor tyrosine kinase.
Targeted therapies aim to inhibit the aberrant signaling pathways crucial for GIST development.

Observation:

Imatinib, a c-kit inhibitor, demonstrates significant objective response rates (>50%) and long-term tumor control in advanced GIST.
Resistance to imatinib typically emerges within 18-26 months, highlighting the need for alternative therapeutic strategies.

Findings:

Sunitinib, another tyrosine kinase inhibitor, shows promise, particularly in GIST patients with specific c-kit exon 9 mutations.
These mutations are often associated with a poorer response to imatinib, suggesting a role for sunitinib in this subset.

More Related Videos

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor

Published on: May 2, 2022

Related Experiment Videos

Last Updated: Jul 14, 2026

Robotic Duodenal Sleeve Resection for Gastrointestinal Stromal Tumor with Rare Exon 8 KIT Mutation Following Neoadjuvant Imatinib

Robotic Duodenal Sleeve Resection for Gastrointestinal Stromal Tumor with Rare Exon 8 KIT Mutation Following Neoadjuvant Imatinib

Published on: April 3, 2026

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor

Published on: May 2, 2022

Implications:

Precision medicine approaches, tailoring therapies based on specific c-kit mutations, may enhance clinical outcomes in GIST.
Further research into novel targeted therapies is essential to overcome imatinib resistance and improve patient prognosis.