Jove
Visualize
Contact Us

Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K
Mismatch Repair01:20

Mismatch Repair

4.8K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.8K
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
Tumor Progression02:07

Tumor Progression

6.3K
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...
6.3K
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
  1. Home
  2. Characterizing M6a Modification Factors And Their Interactions In Colorectal Cancer: Implications For Tumor Subtypes And Clinical Outcomes.
  1. Home
  2. Characterizing M6a Modification Factors And Their Interactions In Colorectal Cancer: Implications For Tumor Subtypes And Clinical Outcomes.

Related Experiment Video

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.3K

Characterizing m6A modification factors and their interactions in colorectal cancer: implications for tumor subtypes

Weidong Sun1, Yingchao Su2, Zhiqiang Zhang3

  • 1Department of Colorectal Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150000, China.

Discover Oncology
|September 18, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

This study reveals how N6-methyladenosine (m6A) regulators impact colorectal cancer (CRC) by analyzing gene expression and mutations. Findings offer insights into CRC molecular mechanisms and potential therapeutic targets.

Keywords:
CNV variation frequencyColorectal cancer (CRC)Differential expressionM6A modificationMutation frequency

More Related Videos

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

638
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

6.5K

Related Experiment Videos

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.3K
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

638
Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
06:52

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

Published on: July 22, 2020

6.5K

Area of Science:

  • Oncology
  • Epigenetics
  • Bioinformatics

Background:

  • Colorectal cancer (CRC) has high incidence and mortality with limited advanced treatment options.
  • DNA methylation is a key epigenetic regulator in tumor molecular mechanisms.
  • Understanding m6A regulators' role in CRC is crucial for developing effective therapies.

Purpose of the Study:

  • To comprehensively analyze the impact of N6-methyladenosine (m6A) modification-related genes in colorectal cancer.
  • To construct molecular typing and prognostic models based on m6A regulators.
  • To identify potential drug sensitivities and immune cell interactions associated with m6A methylation in CRC.

Main Methods:

  • Integrated analysis of multiple single-cell and transcriptome cohorts (GSE166555, GSE146771, EMTAB8107, TCGA-CRC, etc.).
  • Utilized 20 m6A regulators (erasers, writers, readers) for molecular typing and prognostic model construction.
  • Employed ConsensusClusterPlus for pattern identification and drug sensitivity analysis; TISCH2 for immune cell infiltration assessment.
  • Main Results:

    • Analyzed mutation and copy number variation frequencies of 20 m6A regulators in 583 CRC patients.
    • Identified distinct molecular subtypes based on m6A modification patterns, revealing differences in clinicopathological characteristics and prognosis.
    • Developed and validated an m6A-associated gene signature for CRC prognosis, confirming elevated m6A regulator expression in tumor cells via single-cell data.

    Conclusions:

    • Elucidated the mutation frequency, expression patterns, interactions, and prognostic significance of m6A regulators in CRC.
    • Validated findings at the single-cell level, highlighting the spatial explanation of m6A methylation-driven immunosuppression.
    • Provided crucial insights into m6A alterations in CRC, aiding molecular recognition and therapeutic strategies.