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

Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

4.0K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
4.0K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
4.5K
Master Transcription Regulators02:23

Master Transcription Regulators

6.9K
Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
6.9K
Epigenetic Regulation01:37

Epigenetic Regulation

3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.8K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

4.7K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.7K

You might also read

Related Articles

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

Sort by
Same author

Intrinsic promoter responsiveness dictates sensitivity to transcriptional activation by enhancers.

bioRxiv : the preprint server for biology·2026
Same author

Publisher Correction: Tumor transcriptional state predicts survival in immune-checkpoint-blockade-treated glioblastoma.

Nature cancer·2026
Same author

Tumor transcriptional state predicts survival in immune-checkpoint-blockade-treated glioblastoma.

Nature cancer·2026
Same author

Pharmacological targeting of IRF4 as a therapeutic strategy for multiple myeloma.

Nature chemical biology·2026
Same author

New Insights into the Role of Clonotypic B Cells in Plasma-cell Neoplasia.

Blood cancer discovery·2026
Same author

A Perturb-seq screen guided by species divergence uncovers pathways for collateral artery formation.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Jun 12, 2025

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

27.8K

Selective Enhancer Gain-of-Function Deregulates MYC Expression in Multiple Myeloma.

Mahshid Rahmat1,2, Kendell Clement2,3, Jean-Baptiste Alberge1,2,4

  • 1Dana-Farber Cancer Institute, Boston, Massachusetts.

Cancer Research
|September 23, 2024
PubMed
Summary
This summary is machine-generated.

Researchers discovered a new epigenetic mechanism driving MYC gene overexpression in multiple myeloma. This involves increased accessibility of a specific enhancer, leading to higher MYC expression and disease progression, offering potential new therapeutic targets.

More Related Videos

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
09:16

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

7.5K
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

9.9K

Related Experiment Videos

Last Updated: Jun 12, 2025

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

27.8K
Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
09:16

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

7.5K
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

9.9K

Area of Science:

  • Hematology
  • Molecular Biology
  • Epigenetics

Background:

  • MYC deregulation is common in multiple myeloma, correlating with poor prognosis.
  • Known drivers (translocations, amplifications) explain only ~40% of MYC overexpression cases.

Purpose of the Study:

  • To investigate epigenetic mechanisms of MYC regulation in multiple myeloma.
  • To identify novel drivers of MYC overexpression beyond genetic aberrations.

Main Methods:

  • CRISPR interference (CRISPRi) was employed to assess enhancer activity.
  • Analysis of transcription factor binding (cMAF, IRF4, SPIB) and enhancer accessibility.
  • Investigation of focal amplification events at the enhancer region.

Main Results:

  • An epigenetic mechanism involving increased plasma cell enhancer accessibility was identified, leading to MYC overexpression.
  • This enhancer activity was independent of enhancer hijacking but driven by transcription factors cMAF, IRF4, and SPIB.
  • Focal amplification of this enhancer occurred in ~3.4% of multiple myeloma patients.

Conclusions:

  • A novel epigenetic pathway for MYC deregulation in multiple myeloma has been elucidated.
  • Noncoding regulatory elements and transcription factor networks are critical drivers of multiple myeloma.
  • This enhancer may serve as a predictive biomarker and therapeutic target for improving patient outcomes.