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Molecular mediators of breast cancer metastasis
Author(s) -
Ragini Yeeravalli,
Amitava Das
Publication year - 2021
Publication title -
hematology/oncology and stem cell therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 22
eISSN - 1658-3876
pISSN - 2589-0646
DOI - 10.1016/j.hemonc.2021.02.002
Subject(s) - breast cancer , metastasis , malignancy , medicine , metastasis suppressor gene , cancer research , cancer stem cell , cancer , oncology , population , epithelial–mesenchymal transition , ca15 3 , gene silencing , pathology , biology , gene , biochemistry , environmental health
Breast cancer has the highest incidence rate of malignancy in women worldwide. A major clinical challenge faced by patients with breast cancer treated by conventional therapies is frequent relapse. This relapse has been attributed to the cancer stem cell (CSC) population that resides within the tumor and possess stemness properties. Breast CSCs are generated when breast cancer cells undergo epithelial-mesenchymal transition resulting in aggressive, highly metastatic, and invasive phenotypes that exhibit resistance towards chemotherapeutics. Metastasis, a phenomenon that aids in the migration of breast CSCs, occurs through any of three different routes: hematogenous, lymphatic, and transcoelomic. Hematogenous dissemination of breast CSCs leads to metastasis towards distant unrelated organs like lungs, liver, bone, and brain causing secondary tumor generation. Activation of metastasis genes or silencing of metastasis suppressor genes often leads to the advancement of metastasis. This review focuses on various genes and molecular factors that have been implicated to regulate organ-specific breast cancer metastasis by defying the available therapeutic interventions.

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