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

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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
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...
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...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...

You might also read

Related Articles

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

Sort by
Same author

A novel serum metabolite classifier for identifying Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) integrating metabolomics and machine learning.

BMC gastroenterology·2026
Same author

Metagenomic next-generation sequencing for comprehensive pathogen detection in intraocular infection.

European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology·2026
Same author

A newly developed chiral Ru-phe probe for highly sensitive enantioselective detection of tryptophan.

Mikrochimica acta·2026
Same author

Panx1 deficiency exacerbates GAN diet-induced obesity by destabilizing β-catenin via GSK3β.

iScience·2026
Same author

CD27 expression is a clinically accessible biomarker for predicting immunotherapy response in melanoma.

NPJ precision oncology·2026
Same author

Mode-division multiplexing enabled 2D optical phased array with large scale and wide field of view.

Optics letters·2026

Related Experiment Video

Updated: Jun 10, 2026

Reconstruct Human Retinoblastoma In Vitro
06:52

Reconstruct Human Retinoblastoma In Vitro

Published on: October 11, 2022

Targeting Rb mutant cancers by inactivating TSC2.

Jennifer S Searle1, Binghui Li, Wei Du

  • 1Ben May Department for Cancer Research, Chicago, IL 60637, USA.

Oncotarget
|August 14, 2010
PubMed
Summary

Inactivating TSC2 in retinoblastoma (Rb) mutant cancers causes cell death by increasing cellular stress. This suggests targeting TSC2 and inducing stress may be a new cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Retinoblastoma (Rb) is a crucial tumor suppressor gene.
  • Inactivation of Rb is common in various cancers.
  • Therapeutic strategies targeting the loss of Rb function are not well-established.

Purpose of the Study:

  • To investigate novel therapeutic approaches for Rb-mutant cancers.
  • To explore the consequences of TSC2 inactivation in Rb-deficient cancer cells.

Main Methods:

  • Utilizing cancer cell lines with inactivated Rb.
  • Inducing TSC2 inactivation.
  • Assessing cellular stress markers (metabolic, ER, oxidative).
  • Evaluating synergistic cell death.
Keywords:
ROSRbSOD2TORTSC2synthetic lethal

Related Experiment Videos

Last Updated: Jun 10, 2026

Reconstruct Human Retinoblastoma In Vitro
06:52

Reconstruct Human Retinoblastoma In Vitro

Published on: October 11, 2022

Main Results:

  • TSC2 inactivation in Rb-mutant cancer cells triggers synergistic cell death.
  • This cell death is mediated by increased cellular stress, including metabolic, ER, and oxidative stress.
  • Combined inactivation of TSC2 and induction of cellular stress demonstrates a significant effect.

Conclusions:

  • Targeting TSC2 inactivation presents a potential therapeutic strategy for Rb-mutant cancers.
  • Therapeutics that induce cellular stress may be effective in treating cancers with inactivated Rb.
  • This research opens new avenues for developing targeted cancer therapies.