Related Experiment Video

Updated: Sep 20, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
00:07

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Pharmacological inactivation of MYC for the treatment of cancer

Dean W Felsher1, Nicole Bradon

  • 1Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California, USA. dfelsher@stanford.edu

Drug News & Perspectives
|September 16, 2003
PubMed

Insights

Overexpressing the MYC proto-oncogene drives cancer. Inactivating MYC shows promise for cancer treatment, with several novel drug strategies under development for effective neoplasia therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • The MYC proto-oncogene is frequently overexpressed in human cancers.
  • MYC overexpression is a key driver in the pathogenesis of many cancers.
  • Emerging evidence suggests MYC inactivation as a potential therapeutic strategy for cancer.

Purpose of the Study:

  • To review strategies for developing drugs targeting MYC inactivation.
  • To explore novel therapeutic approaches for MYC-driven cancers.
  • To discuss the potential of targeting MYC for cancer treatment.

Main Methods:

  • Literature review of experimental observations and drug development strategies.
  • Discussion of various approaches to target MYC inactivation.
  • Analysis of potential therapeutic applications.

Main Results:

  • MYC inactivation is a viable therapeutic target in oncology.
  • Several distinct strategies exist for developing MYC-targeting drugs.
  • These strategies aim to inhibit MYC's oncogenic functions.

Conclusions:

  • Targeting MYC inactivation offers a promising avenue for cancer therapy.
  • Further research into novel drug development is crucial.
  • MYC-targeted therapies hold potential for treating various neoplasias.

More Related Videos

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...
Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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...