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

Oogenesis02:07

Oogenesis

58.3K
In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
58.3K
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

157
Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
157
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

31
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
31
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

81
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
81
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

2.0K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
2.0K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.1K
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...
9.1K

You might also read

Related Articles

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

Sort by
Same author

Accelerated Biological Aging Increases the Risk of Head and Neck Cancer: Insights From Genetic Instruments of Epigenetic Clocks.

Molecular carcinogenesis·2026
Same author

Exploring the Contribution of Interleukin-12A Genetic Polymorphisms to Pterygium Risk.

In vivo (Athens, Greece)·2026
Same author

Genetic Insights into Interleukin-13 Polymorphisms in Colorectal Cancer Risk and Progression.

Cancer genomics & proteomics·2026
Same author

Insights into Matrix Metalloproteinase-2 Genotypes, Smoking, Alcohol Drinking, Hypertension and Renal Cell Carcinoma in Taiwan.

Anticancer research·2026
Same author

8-Gingerol Mitigates MPP<sup>+</sup>-Induced α-Synuclein Aggregation and NLRP3 Inflammasome Activation by Inducing the Insulin Signaling Pathway in SH-SY5Y Cells.

Neurochemical research·2026
Same author

MMP-9 Genotypes Serve as Oral Cancer Predictive Marker for Smokers.

Anticancer research·2026

Related Experiment Video

Updated: Apr 30, 2026

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

6.3K

Inflammatory Cytokine Genotypic Markers and Ovarian Cancer Risk.

Wen-Shin Chang1,2, Chia-Wen Tsai1,2, Jaw-Chyun Chen3

  • 1Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.

Anticancer Research
|April 28, 2026
PubMed
Summary

Genetic variations in inflammatory cytokine pathways influence ovarian cancer risk and progression. Certain gene polymorphisms increase risk by promoting inflammation, while others offer protection by dampening it, impacting diagnosis and treatment.

Keywords:
Genotypesinterleukinovarian cancerpolymorphismreview

More Related Videos

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

3.2K
Characterization and Functional Prediction of Bacteria in Ovarian Tissues
10:12

Characterization and Functional Prediction of Bacteria in Ovarian Tissues

Published on: October 23, 2021

2.3K

Related Experiment Videos

Last Updated: Apr 30, 2026

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

6.3K
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
09:40

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

3.2K
Characterization and Functional Prediction of Bacteria in Ovarian Tissues
10:12

Characterization and Functional Prediction of Bacteria in Ovarian Tissues

Published on: October 23, 2021

2.3K

Area of Science:

  • Genetics and Oncology
  • Immunology
  • Molecular Biology

Background:

  • Ovarian cancer is a leading cause of gynecological cancer mortality globally.
  • Late diagnosis and lack of screening hinder effective treatment.
  • Inflammatory cytokines play crucial roles in cancer development, making their genetic variations potential determinants of ovarian cancer risk.

Purpose of the Study:

  • To review and summarize evidence on inherited variations in inflammatory cytokine pathways and their association with ovarian cancer.
  • To provide an overview of genetic markers that influence susceptibility and progression.
  • To highlight the role of genetically modulated inflammation in epithelial ovarian carcinogenesis.

Main Methods:

  • Systematic review of candidate-gene studies published since the early 2000s.
  • Analysis of polymorphisms in genes encoding interleukins (IL), tumor necrosis factor alpha (TNFA), transforming growth factor beta 1 (TGFB1), and nuclear factor kappa B (NFKB) pathway components.
  • Examination of associations between specific genotypes and ovarian cancer risk, clinical features, and prognosis.

Main Results:

  • Identified specific genotypes associated with increased risk (e.g., IL1B rs16944 CC, TNFA rs1800629 GA/AA) and protective effects (e.g., IL1A rs17561 GT/TT, TGFB1 rs1800469 CT/TT).
  • Observed that certain polymorphisms correlate with clinical features like tumor stage and recurrence, suggesting prognostic relevance.
  • Noted significant population-specific differences in allelic frequencies and linkage disequilibrium, necessitating cross-ethnic validation.

Conclusions:

  • Genetically modulated inflammation is a key driver of epithelial ovarian carcinogenesis.
  • Specific cytokine gene polymorphisms can increase or decrease ovarian cancer risk and influence clinical outcomes.
  • Further research and cross-ethnic replication are crucial for developing targeted prevention and personalized management strategies for ovarian cancer.