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

Modulating autophagy for therapeutic benefit.

Jennifer S Carew1, Steffan T Nawrocki, John L Cleveland

  • 1Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Autophagy
|May 15, 2007
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

Product-Intrinsic NF-κB-Driven Transcriptional Programs Connote Durability of CAR-T Response in Multiple Myeloma.

Blood·2026
Same author

p97 Inhibition Synergistically Enhances Hypomethylating Therapy through Targeting of PLK1 in Acute Myeloid Leukemia.

Cancer research communications·2026
Same author

Integrated Genomic and Epigenomic Analysis Reveals Epigenetic Plasticity in Disease Progression and Multidrug Resistance in Multiple Myeloma.

Cancer research·2026
Same author

Real-world prevalence and outcome of elevated right ventricular systolic pressure in myelofibrosis.

Cardio-oncology (London, England)·2026
Same author

Cardiovascular Adverse Events During Venetoclax-Based Treatment in Acute Myeloid Leukemia.

Journal of the American Heart Association·2026
Same author

Proteolysis targeting chimeras as senolytics: An emerging senotherapy for combating aging.

The Journal of pharmacology and experimental therapeutics·2025
Same journal

TRIM21 induces selective autophagy of viruses and bacteria.

Autophagy·2026
Same journal

OPTN (optineurin)-mediated selective substrate recognition in Golgi membrane-associated degradation.

Autophagy·2026
Same journal

Hypoxia-induced EPAS1/HIF2A-USP33-ATG101 axis drives oncogenic autophagy and peritoneal metastasis in gastric cancer.

Autophagy·2026
Same journal

Correction.

Autophagy·2026
Same journal

Targeting lysosomes with a novel chloroquine derivative induces irreversible lysosomal damage and disrupts autophagosome and lysosome assembly in cancer.

Autophagy·2026
Same journal

Targeting the SNAI1-LAMP3 axis to restore lysosomal function and alleviate autophagic flux impairment to delay retinal degeneration.

Autophagy·2026
See all related articles

Autophagy is a cell survival pathway exploited by cancer. Disrupting autophagy synergizes with SAHA to induce apoptosis in refractory chronic myelogenous leukemia (CML).

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Autophagy is a cellular survival mechanism crucial for biosynthesis and ATP regeneration under stress conditions like nutrient deprivation and hypoxia.
  • The tumor microenvironment often features hypoxia and nutrient scarcity, promoting autophagy in cancer cells.
  • Autophagy plays a significant role in cancer chemoresistance, particularly against therapies inducing apoptosis.

Purpose of the Study:

  • To investigate the role of autophagy in chemoresistance in Imatinib-refractory chronic myelogenous leukemia (CML).
  • To evaluate the potential of autophagy-disrupting agents to enhance the efficacy of therapeutic agents like SAHA in resistant CML models.

Main Methods:

  • Utilized a model of Imatinib-refractory CML.

Related Experiment Videos

  • Tested primary CML cells with Bcr-Abl mutations, including the T315I mutation conferring resistance to tyrosine kinase inhibitors.
  • Assessed the synergistic effect of autophagy inhibitors combined with SAHA on inducing apoptotic cell death.

    • Main Results:

    • Autophagy inhibition synergized with SAHA (a histone deacetylase inhibitor) in promoting apoptotic death of refractory CML cells.
    • This combination therapy proved effective against CML cells with mutations conferring resistance to standard treatments.
    • Demonstrated that agents disrupting autophagy can overcome chemoresistance in specific cancer contexts.

    Conclusions:

    • Disrupting the autophagy pathway is a promising strategy to enhance cancer therapy efficacy.
    • Combining autophagy inhibitors with agents like SAHA can overcome chemoresistance in refractory malignancies.
    • Supports the clinical application of autophagy-disrupting agents in treating chemorefractory cancers, especially CML with resistance mutations.