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Related Concept Videos

Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Tumor Progression02:07

Tumor Progression

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...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...

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Related Experiment Video

Updated: May 14, 2026

Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
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Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer

Published on: March 26, 2014

A Developmental Lectin-Glycan Program Enables Early Breast Cancer Dissemination and Metastatic Onset.

Ramiro M Perrotta, Magalí Berton, Luis Valencia Salazar

    Biorxiv : the Preprint Server for Biology
    |May 13, 2026
    PubMed
    Summary

    A conserved galectin-1 (GAL1)-glycan checkpoint links normal mammary gland development to breast cancer metastasis. Targeting GAL1 inhibits tumor spread and progression, offering a new therapeutic strategy for early-stage breast cancer.

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    A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer
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    A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

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    Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
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    07:35

    A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

    Published on: December 26, 2016

    Area of Science:

    • Cell biology
    • Developmental biology
    • Cancer research

    Background:

    • Early breast cancer cell dissemination precedes detectable tumor growth.
    • Molecular mechanisms driving early metastasis are not well understood.
    • Mammary gland development involves complex morphogenetic programs.

    Purpose of the Study:

    • To identify molecular programs linking normal mammary gland morphogenesis to early breast cancer dissemination.
    • To investigate the role of the galectin-1 (GAL1)-glycan axis in breast cancer metastasis.
    • To evaluate GAL1 as a potential therapeutic target for early-stage breast cancer.

    Main Methods:

    • Utilized mouse models (MMTV-PyMT, MMTV-HER2) with genetic ablation and pharmacological inhibition of GAL1.
    • Analyzed patient-derived data to correlate GAL1 expression with clinical outcomes.
    • Investigated the impact of GAL1 on epithelial-to-mesenchymal transition and stem-like traits.

    Main Results:

    • Identified a conserved GAL1-glycan checkpoint regulating mammary gland development and cancer metastasis.
    • Demonstrated that GAL1 drives epithelial-to-mesenchymal transition and metastatic competence in breast cancer.
    • Therapeutic targeting of GAL1 reduced tumor progression, circulating tumor cells, and lung metastasis.
    • High GAL1 and low ST6GAL1 expression correlated with poor clinical outcomes in breast cancer patients.

    Conclusions:

    • Early breast cancer dissemination hijacks a GAL1-glycan morphogenetic program.
    • GAL1 represents a direct link between mammary development and metastatic progression.
    • GAL1 is a promising therapeutic vulnerability for early-stage breast cancer.