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

Tumor Progression02:07

Tumor Progression

7.1K
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...
7.1K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.7K
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...
5.7K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

14.4K
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...
14.4K
Abnormal Proliferation02:23

Abnormal Proliferation

5.0K
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...
5.0K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

11.0K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
11.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.5K
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...
4.5K

You might also read

Related Articles

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

Sort by
Same author

IL1RAP antibody-drug conjugates potently target primary and metastatic disease in multiple oncofusion-driven cancers.

Cancer discovery·2026
Same author

Androgen activity in the male embryonic hindbrain drives lethal PFA ependymoma.

Nature·2026
Same author

Spatial transcriptomics reveals the molecular signatures of prodromal and advanced α-synucleinopathy.

iScience·2026
Same author

MIF-CD74 signaling drives immune modulation in medulloblastoma.

Neuro-oncology·2026
Same author

Surgical management of sellar arachnoid cyst: state of the art and systematic review.

Frontiers in neurology·2026
Same author

Endoglin-Directed CAR T Cells Comprehensively Target Tumors in Advanced Sarcomas.

Cancer immunology research·2025

Related Experiment Video

Updated: Dec 22, 2025

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

13.8K

RNA modifications in brain tumorigenesis.

Albert Z Huang1, Alberto Delaidelli2,3, Poul H Sorensen4,5

  • 1Department of Molecular Oncology, British Columbia Cancer Research Centre, Vancouver, BC, V5Z 1L3, Canada.

Acta Neuropathologica Communications
|May 8, 2020
PubMed
Summary
This summary is machine-generated.

RNA modifications like m6A regulate gene expression in cancer. This review explores how these RNA changes contribute to brain tumor development and potential therapeutic targets.

Keywords:
Alternative polyadenylation (APA)Alternative splicingBrain tumorsGliomaInosineN6-methyladenosine (m6A)Post-translational modificationsmRNA modifications

More Related Videos

Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells
05:02

Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells

Published on: February 4, 2021

3.7K
Processing of Primary Brain Tumor Tissue for Stem Cell Assays and Flow Sorting
08:14

Processing of Primary Brain Tumor Tissue for Stem Cell Assays and Flow Sorting

Published on: September 25, 2012

18.5K

Related Experiment Videos

Last Updated: Dec 22, 2025

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

13.8K
Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells
05:02

Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells

Published on: February 4, 2021

3.7K
Processing of Primary Brain Tumor Tissue for Stem Cell Assays and Flow Sorting
08:14

Processing of Primary Brain Tumor Tissue for Stem Cell Assays and Flow Sorting

Published on: September 25, 2012

18.5K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • RNA modifications are dynamic regulators of gene expression and protein isoforms.
  • Their deregulation is linked to various diseases, including cancer.
  • Post-transcriptional RNA modifications play crucial roles in cell proliferation and migration.

Purpose of the Study:

  • To review the role of four key RNA modifications in brain tumor pathogenesis.
  • To discuss the potential of targeting these modifications for brain tumor treatment.

Main Methods:

  • Literature review focusing on m6A, alternative polyadenylation, alternative splicing, and adenosine to inosine modifications.
  • Analysis of current research on RNA modifications in brain tumor progression.

Main Results:

  • m6A, alternative polyadenylation, alternative splicing, and adenosine to inosine modifications are implicated in brain tumor development.
  • These modifications influence gene expression and protein isoforms relevant to oncogenic properties.

Conclusions:

  • RNA modifications are critical in brain tumor progression.
  • Targeting these RNA processes offers potential therapeutic strategies for improving brain tumor prognosis.