Related Experiment Video For CCL11
Updated: Dec 20, 2025

Non-invasive Assessment of the Efficacy of New Therapeutics for Intestinal Pathologies Using Serial Endoscopic Imaging of Live Mice
Published on: March 10, 2015
Eotaxins and Their Receptor in Colorectal Cancer-A Literature Review
Monika Zajkowska1, Barbara Mroczko1,2
1Department of Neurodegeneration Diagnostics, Medical University of Bialystok, 15-269 Bialystok, Poland.
Abstract:
Colorectal cancer (CRC) is one of the most common malignancies in the world, with a global incidence of almost 2 million new cases every year. Despite the availability of many diagnostic tests, including laboratory tests and molecular diagnostics, an increasing number of new cases is observed. Thus, it is very important to search new markers that would show high diagnostic sensitivity and specificity in the detection of colorectal cancer in early stages of the disease. Eotaxins are proteins that belong to the cytokine group-small molecules with a variety of applications. Their main role is the activation of basophils and eosinophils involved in inflammatory processes. Therefore, we performed an extensive search of the literature pertaining to our investigation via the MEDLINE/PubMed database. On the basis of available literature, we can assume that eotaxins accumulate in cancer cells in the course of CRC. This leads to a decrease in the chemotaxis of eosinophils, which are effector immune cells with anti-tumor activity. This may explain a decrease in their number as a defense mechanism of cancer cells against their destruction and may be useful when attempting anti-tumor therapy with the use of chemokines.
Related Concept Videos
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
Mitogens and the Cell Cycle
Canonical Wnt Signaling Pathway
Non-Canonical Wnt Signaling Pathways
Selectins
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

