Related Experiment Video
Updated: Jun 3, 2026

09:20
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
Inflammatory talk: linking obesity, NF-κB, and Aromatase
1Department of Nutritional Sciences, University of Texas at Austin, Dell Pediatric Research Institute, Austin, TX 78723, USA. shursting@austin.utexas.edu
Cancer Prevention Research (Philadelphia, Pa.)
|March 5, 2011
Summary
Obesity increases postmenopausal breast cancer risk and worsens prognosis. New research reveals obesity, inflammation, and aromatase interact via cell cross-talk, offering potential therapeutic targets.
Area of Science:
- Oncology
- Endocrinology
- Immunology
Background:
- Obesity is a known risk factor for postmenopausal breast cancer, yet the specific mechanisms driving this association are not fully understood.
- Previous research indicates a link between obesity and increased breast cancer risk and poorer outcomes.
Discussion:
- This study elucidates the intricate interplay between obesity, chronic inflammation, and aromatase activity in breast cancer.
- It highlights the crucial cross-talk between adipocytes, macrophages, and epithelial cells in mediating these effects.
Key Insights:
- The research identifies novel molecular pathways connecting obesity, inflammation, and aromatase in the context of breast cancer.
- Specific cellular interactions (adipocyte-macrophage-epithelial cell cross-talk) are implicated in promoting obesity-related breast cancer.
Outlook:
- Findings suggest new molecular targets and preventative strategies for obesity-related breast cancer.
- This work provides a foundational framework for further investigation into the complex mechanisms underlying the obesity-cancer relationship.
Related Concept Videos
NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Obesity
The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...
NF-kB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
The JAK-STAT Signaling Pathway
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
Inflammation
Overview
