Inflammatory Mediators in Breast Cancer and Their Role in Disease Progression
Author Information
Author(s): Soria Gali, Ofri-Shahak Maya, Haas Ilana, Yaal-Hahoshen Neora, Leider-Trejo Leonor, Leibovich-Rivkin Tal, Weitzenfeld Polina, Meshel Tsipi, Shabtai Esther, Gutman Mordechai, Ben-Baruch Adit
Primary Institution: Tel Aviv University, Israel
Hypothesis
Are there associations between inflammatory chemokines CCL2 & CCL5 and cytokines TNFα & IL-1β in breast cancer progression?
Conclusion
The coordinated expression of CCL2 & CCL5 and TNFα & IL-1β may be important for disease course, and TNFα & IL-1β may promote disease relapse.
Supporting Evidence
- CCL2, CCL5, TNFα, and IL-1β were expressed at very low incidence in normal breast epithelial cells.
- Significant associations were found between CCL2 & CCL5 and TNFα & IL-1β in tumor cells of DCIS and IDC-no-relapse patients.
- In the IDC-with-relapse group, the expression of CCL2 & CCL5 was accompanied by further elevated incidence of TNFα & IL-1β expression.
- Continuous stimulation of tumor cells by TNFα led to epithelial-to-mesenchymal transition (EMT).
- IL-1β acts jointly with other pro-malignancy factors to promote disease relapse.
Takeaway
This study found that certain proteins related to inflammation are more common in breast cancer than in healthy tissue, and they might help the cancer grow and spread.
Methodology
The study used immunohistochemistry to analyze the expression of inflammatory mediators in breast cancer patients at different disease stages.
Potential Biases
Potential biases may arise from the retrospective nature of the study and the reliance on archived data.
Limitations
The study is retrospective and based on archived patient data, which may limit the ability to draw causal conclusions.
Participant Demographics
The study included 38 healthy individuals and 88 breast cancer patients, categorized into DCIS, IDC-no-relapse, and IDC-with-relapse groups.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
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