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 Experiment Videos

Imatinib: paradigm or anomaly?

Brian J Druker1

  • 1Howard Hughes Medical Institute. drukerb@ohsu.edu

Cell Cycle (Georgetown, Tex.)
|July 16, 2004
PubMed
Summary
This summary is machine-generated.

Imatinib therapy for chronic myeloid leukemia (CML) shows targeted cancer treatment is effective. This success raises questions about applying this precision medicine approach to complex solid tumors.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Signaling Mutations Negate the Favorable Impact of NPM1 Mutations in Older Patients With Newly Diagnosed Acute Myeloid Leukemia Treated With VEN/HMA.

American journal of hematology·2026
Same author

Results of a phase 1 trial testing ruxolitinib plus venetoclax in patients with relapsed/refractory acute myeloid leukemia.

Blood neoplasia·2026
Same author

Clinical outcomes of older patients with NPM1-mutated or KMT2A-rearranged AML before menin inhibitors: a Beat AML report.

Blood advances·2026
Same author

DDX41-Mutated AML: A Case Report and Perspectives.

JCO precision oncology·2026
Same author

The aryl hydrocarbon receptor is associated with monocytic AML and innate immune resistance reversible with an AHR inhibitor.

Frontiers in immunology·2025
Same author

<i>IDH2</i> mutation is associated with favorable outcome among older adults with newly diagnosed acute myeloid leukemia treated with hypomethylating agent-based therapy.

Haematologica·2025
Same journal

ALDH18A1 fuels spermine biosynthesis to sustain ferroptosis resistance in cancer and ischemia-reperfusion injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.

Cell cycle (Georgetown, Tex.)·2026
Same journal

OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.

Cell cycle (Georgetown, Tex.)·2026
See all related articles

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Imatinib (Gleevec) represents a breakthrough in targeted cancer therapy, specifically for chronic myeloid leukemia (CML).
  • Its development validated the principle that understanding cancer's molecular drivers can yield more effective and less toxic treatments.
  • The success of imatinib in CML has spurred optimism for similar targeted approaches in other cancers.

Discussion:

  • This abstract discusses the potential applicability of the imatinib paradigm to solid tumors.
  • It addresses the skepticism surrounding targeted therapies for more complex cancers.
  • The discussion will explore whether this skepticism is justified based on current understanding.

Key Insights:

  • Targeted molecular therapy, exemplified by imatinib in CML, offers a promising model for cancer treatment.

Related Experiment Videos

  • Precision medicine hinges on a deep understanding of cancer-specific molecular pathogenesis.
  • The efficacy of imatinib highlights the potential for highly specific and less toxic cancer interventions.

    • Outlook:

    • Further research is needed to determine if the success of targeted agents like imatinib can be replicated in solid tumors.
    • Overcoming skepticism requires demonstrating the feasibility of targeting specific molecular events in complex solid tumor environments.
    • The future of cancer treatment may increasingly rely on personalized, molecularly targeted therapies.