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

7.4K
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...
7.4K
Abnormal Proliferation02:23

Abnormal Proliferation

4.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.4K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

4.8K
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...
4.8K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.6K
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...
4.6K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.4K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.4K

You might also read

Related Articles

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

Sort by
Same author

BMX-001 acts as a selective chemoradioprotector in rectal cancer.

Redox biochemistry and chemistry·2026
Same author

Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury.

Acta neuropathologica communications·2026
Same author

Pembrolizumab Plus Quad-Shot Radiotherapy for Recurrent, Unresectable, or Metastatic Head and Neck Cancer: A Nonrandomized Clinical Trial.

JAMA otolaryngology-- head & neck surgery·2026
Same author

Effect of Dietary Linoleic Acid Intake on Eicosapentaenoic Acid Status and Lipoxygenase-Mediated Oxylipin Biosynthesis in Healthy Adults: A Randomized Controlled Trial.

Nutrients·2026
Same author

Lactylation landscape of mitochondrial proteins in myocardial infarction.

Redox biology·2026
Same author

Lactylation landscape of mitochondrial proteins in myocardial infarction.

bioRxiv : the preprint server for biology·2026
Same journal

Linperlisib enhances MUC1-Tn CAR T cell efficacy by inhibiting EGR1/DUSP2 axis to prevent CAR T cell exhaustion.

Leukemia·2026
Same journal

CD7 chimeric antigen receptor T cells in patients with relapsed or refractory CD7-positive acute myeloid leukemia.

Leukemia·2026
Same journal

Single-cell architecture of purinergic signaling in human cord blood hematopoietic stem and progenitor cells.

Leukemia·2026
Same journal

Feasibility and safety of rapid glofitamab ramp-up.

Leukemia·2026
Same journal

Single-cell DNA methylation analysis uncovers epigenetic pathways in the transformation of MDS to AML.

Leukemia·2026
Same journal

PD-L2 is associated with lineage-related transcriptional programs distinct from PD-L1 in primary mediastinal large B-cell lymphoma.

Leukemia·2026
See all related articles

Related Experiment Video

Updated: May 30, 2025

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
10:04

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis

Published on: May 1, 2015

13.0K

Targeting ABCD1-ACOX1-MET/IGF1R axis suppresses multiple myeloma.

Zhannan Han1, Zhibo Yan1, Zhehan Ma2

  • 1Department of Pathology, Duke University School of Medicine, Durham, NC, 27710, USA.

Leukemia
|January 30, 2025
PubMed
Summary
This summary is machine-generated.

Very long chain fatty acids (VLCFAs) influence multiple myeloma (MM) treatment effectiveness. Inhibiting VLCFA degradation enhances chemotherapy and targets key signaling pathways, offering new therapeutic strategies for this incurable cancer.

More Related Videos

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice
05:32

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice

Published on: January 7, 2019

6.8K
Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos
07:24

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

6.4K

Related Experiment Videos

Last Updated: May 30, 2025

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
10:04

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis

Published on: May 1, 2015

13.0K
Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice
05:32

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice

Published on: January 7, 2019

6.8K
Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos
07:24

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

6.4K

Area of Science:

  • Hematology
  • Cancer Biology
  • Metabolic Pathways

Background:

  • Multiple myeloma (MM) is an incurable blood cancer requiring new treatments.
  • Intracellular very long chain fatty acids (VLCFAs) are implicated in MM cell survival and drug resistance.

Purpose of the Study:

  • To investigate the role of VLCFA metabolism in modulating the efficacy of multiple myeloma chemotherapeutics.
  • To identify novel therapeutic targets by understanding the link between VLCFA levels and MM cell signaling.

Main Methods:

  • Assessing the impact of inhibiting VLCFA biosynthesis and degradation on MM cell death.
  • Evaluating the synergistic effects of an ACOX1 inhibitor with bortezomib in MM xenograft models.
  • Analyzing the effects of altered VLCFA levels on MET and IGF1R kinase activity and signaling.

Main Results:

  • Inhibition of VLCFA biosynthesis decreased bortezomib-induced cell death.
  • Suppression of VLCFA degradation via ACOX1 inhibition enhanced cytotoxicity of bortezomib, carfilzomib, and lenalidomide.
  • ACOX1 inhibition cooperated with bortezomib to suppress resistant MM xenograft growth, reduced MET and IGF1R activity, and altered kinase-cerebroside interactions.

Conclusions:

  • MM cells possess a metabolic vulnerability related to VLCFA levels.
  • Targeting the VLCFA metabolism axis, particularly ACOX1, represents a promising therapeutic strategy for multiple myeloma.
  • Modulating VLCFA levels can overcome resistance to existing MM therapies by affecting MET and IGF1R signaling.