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

STI571 as a targeted therapy for CML.

Michael E O'Dwyer1, Michael J Mauro, Brian J Druker

  • 1Leukemia Center, Oregon Health & Science University Cancer Institute, Portland, Oregon, USA.

Cancer Investigation
|August 7, 2003
PubMed
Summary
This summary is machine-generated.

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

Targeting intrinsic apoptosis rewires human NK cell persistence: NOXA as a dominant survival switch.

Molecular therapy. Oncology·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

STI571 (imatinib mesylate) is a targeted therapy that effectively treats chronic myelogenous leukemia (CML) by inhibiting the Bcr-Abl tyrosine kinase. This drug offers expanded treatment options for CML patients across all disease phases.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Chronic myelogenous leukemia (CML) is a stem cell disorder characterized by the Bcr-Abl fusion gene.
  • The Bcr-Abl tyrosine kinase is constitutively active and essential for CML pathogenesis.
  • CML progresses through distinct phases, with malignant clones losing differentiation capacity.

Purpose of the Study:

  • To evaluate the efficacy of STI571 (imatinib mesylate) as a targeted therapy for CML.
  • To assess the impact of STI571 across different phases of chronic myelogenous leukemia.
  • To establish STI571 as a paradigm for gene product targeted therapy.

Main Methods:

  • Preclinical studies involving STI571, a specific Bcr-Abl tyrosine kinase inhibitor.
  • In vitro and in vivo assessment of STI571's effect on Bcr-Abl-expressing cells.

Related Experiment Videos

  • Clinical evaluation of STI571 in patients with all phases of CML.

    • Main Results:

    • STI571 specifically inhibited the proliferation of Bcr-Abl-expressing cells.
    • Remarkable therapeutic results were observed with STI571 in all phases of CML.
    • Durable responses to STI571 were most frequent in earlier stage CML patients.

    Conclusions:

    • STI571 is a highly effective targeted therapy for chronic myelogenous leukemia.
    • The drug demonstrates significant efficacy across all CML disease phases.
    • STI571 represents a breakthrough in targeted cancer therapy, expanding treatment options for CML patients.