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 Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.8K
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...
7.8K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

5.1K
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...
5.1K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.4K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.4K

You might also read

Related Articles

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

Sort by
Same author

Potent Anti-Glioblastoma Effects of Next-Generation MNK Inhibitors.

Cancers·2026
Same author

SLFN5 restrains type I interferon responses and promotes glioblastoma via its N-terminal Schlafen core domain.

Communications biology·2026
Same author

Multi-omics analysis reveals LARP1 as a key integrator of translation and metabolism in AML.

Oncogenesis·2026
Same author

Development of a Direct-to-Biology Platform to Discover Potent MNK Inhibitors.

Journal of medicinal chemistry·2026
Same author

PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.

Blood advances·2026
Same author

Schlafen 5 is an intracellular immune checkpoint and controls IFN responses in pancreatic ductal adenocarcinoma.

JCI insight·2026

Related Experiment Video

Updated: Sep 18, 2025

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.3K

Targeting SLFN11-regulated pathways restores chemotherapy sensitivity in AML.

Sara H Small1,2,3,4, Ricardo E Perez1, Elspeth M Beauchamp1,2,5

  • 1Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, IL.

Blood Neoplasia
|June 24, 2025
PubMed
Summary

Low expression of Schlafen 11 (SLFN11) predicts poor outcomes in acute myeloid leukemia (AML). Restoring SLFN11 function or inhibiting the ATR pathway may overcome chemoresistance in AML patients.

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.4K
Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.3K

Related Experiment Videos

Last Updated: Sep 18, 2025

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype
14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

3.3K
Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

8.4K
Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.3K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Chemoresistance is a major obstacle in treating acute myeloid leukemia (AML).
  • Understanding resistance mechanisms is crucial for developing effective AML therapies.

Purpose of the Study:

  • To investigate the role of Schlafen 11 (SLFN11) in AML chemoresistance.
  • To identify SLFN11 as a potential therapeutic target for AML.

Main Methods:

  • Correlating SLFN11 expression with patient survival and prognosis.
  • Assessing the impact of SLFN11 levels on AML cell apoptosis and chemotherapy sensitivity.
  • Investigating the role of the ATR/Chk1 pathway in SLFN11-mediated chemoresistance.
  • Evaluating the sensitivity of SLFN11 knockout AML cells to different therapeutic agents.

Main Results:

  • Low SLFN11 expression is linked to poor survival and prognosis in AML patients.
  • SLFN11 regulates chemotherapy sensitivity; its suppression leads to cytarabine resistance via ATR/Chk1 activation.
  • Inhibiting the ATR pathway restores cytarabine sensitivity in AML cells with low SLFN11.
  • SLFN11 knockout AML cells remain sensitive to hypomethylating agents and venetoclax.

Conclusions:

  • SLFN11 is a key regulator and predictor of chemotherapy sensitivity in AML.
  • Targeting pathways suppressed by SLFN11 may offer novel combination therapies to improve AML treatment outcomes.