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

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
Metastasis02:30

Metastasis

5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Tumor Progression02:07

Tumor Progression

6.2K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.2K
Cancer02:18

Cancer

47.4K
Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
47.4K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

11.4K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
11.4K
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

You might also read

Related Articles

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

Sort by
Same author

The structural basis of RanGAP1 regulation and catalysis in nuclear transport.

bioRxiv : the preprint server for biology·2026
Same author

ERK autoinhibition mechanism informs a drug combination strategy.

Protein science : a publication of the Protein Society·2026
Same author

How Functional Variants Reconfigure the Rac2 Conformational Landscape.

bioRxiv : the preprint server for biology·2026
Same author

Energy landscapes in molecular biology: History, principles, and perspectives.

Quarterly reviews of biophysics·2026
Same author

Cyclin-E/A/CDK1/2 Kinetic Landscapes Drive Cell Cycle Phase-Specific Progression and Guide Cyclin-E Degradation Strategy.

Journal of chemical information and modeling·2026
Same author

Oncogenic PI3Kα variants reveal graded conformational spectrum with mutation-specific cryptic pockets.

Communications chemistry·2026

Related Experiment Video

Updated: May 27, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

19.5K

Molecular principles underlying aggressive cancers.

Ruth Nussinov1,2,3, Bengi Ruken Yavuz4, Hyunbum Jang5,4

  • 1Computational Structural Biology Section, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA. NussinoR@mail.nih.gov.

Signal Transduction and Targeted Therapy
|February 16, 2025
PubMed
Summary

Aggressive cancers exhibit overexpressed signaling proteins driving rapid growth and drug resistance. Understanding these molecular drivers is key to developing effective cancer treatments and overcoming resistance mechanisms.

More Related Videos

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
07:41

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

2.4K
Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma
09:06

Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma

Published on: November 11, 2021

2.5K

Related Experiment Videos

Last Updated: May 27, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

19.5K
A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
07:41

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

2.4K
Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma
09:06

Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma

Published on: November 11, 2021

2.5K

Area of Science:

  • Molecular oncology
  • Quantitative biophysics
  • Cancer cell signaling

Background:

  • Aggressive cancers present significant challenges in drug resistance and treatment efficacy.
  • Current single-cell technologies have not yet overcome drug resistance mechanisms.
  • The National Cancer Institute defines aggressive cancers by rapid spread despite treatment.

Purpose of the Study:

  • To explore highly aggressive cancers at the molecular and cell signaling levels.
  • To differentiate aggressive cancers from more treatable ones based on molecular underpinnings.
  • To formulate principles of cancer aggressiveness at the molecular level.

Main Methods:

  • Review of molecular and cell signaling characteristics of aggressive cancers.
  • Analysis of oncogenic protein overexpression and activation in proliferation pathways.
  • Examination of chromatin dysfunction, signaling crosstalk, and epigenetic dysregulation.

Main Results:

  • Aggressive tumors harbor massive, activated oncogenic proteins, particularly through overexpression.
  • Observed strong activation of ERK1/2 and other oncogenic proteins via chromatin and signaling defects.
  • Identified increased cancer heterogeneity, plasticity, and drug resistance in aggressive types.

Conclusions:

  • Aggressiveness is linked to massive, catalysis-primed oncogenic proteins and signaling pathway activation.
  • Overexpression of master transcription factors, gene fusions, and copy number alterations are common.
  • High mutation loads in signaling regulators (e.g., EGFR, c-MET, K-Ras) and epigenetic dysregulation contribute to aggressiveness.