KVOKAČKOVÁ, Barbora, Ján REMŠÍK, Mohit Kumar JOLLY and Karel SOUČEK. Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity. Cancers. Basel: MDPI, 2021, vol. 13, No 9, p. "2188", 20 pp. ISSN 2072-6694. Available from: https://dx.doi.org/10.3390/cancers13092188.
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Basic information
Original name Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity
Authors KVOKAČKOVÁ, Barbora (703 Slovakia, belonging to the institution), Ján REMŠÍK, Mohit Kumar JOLLY and Karel SOUČEK (203 Czech Republic, guarantor, belonging to the institution).
Edition Cancers, Basel, MDPI, 2021, 2072-6694.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30204 Oncology
Country of publisher Switzerland
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 6.575
RIV identification code RIV/00216224:14310/21:00121663
Organization unit Faculty of Science
Doi http://dx.doi.org/10.3390/cancers13092188
UT WoS 000649879200001
Keywords in English triple-negative breast cancer; plasticity; epithelial– mesenchymal transition; mesenchymal– epithelial transition; metastasis
Tags rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Marie Šípková, DiS., učo 437722. Changed: 28/5/2021 11:48.
Abstract
Triple-negative breast cancer (TNBC) is a subtype of breast carcinoma known for its unusually aggressive behavior and poor clinical outcome. Besides the lack of molecular targets for therapy and profound intratumoral heterogeneity, the relatively quick overt metastatic spread remains a major obstacle in effective clinical management. The metastatic colonization of distant sites by primary tumor cells is affected by the microenvironment, epigenetic state of particular subclones, and numerous other factors. One of the most prominent processes contributing to the intratumoral heterogeneity is an epithelial–mesenchymal transition (EMT), an evolutionarily conserved developmental program frequently hijacked by tumor cells, strengthening their motile and invasive features. In response to various intrinsic and extrinsic stimuli, malignant cells can revert the EMT state through the mesenchymal–epithelial transition (MET), a process that is believed to be critical for the establishment of macrometastasis at secondary sites. Notably, cancer cells rarely undergo complete EMT and rather exist in a continuum of E/M intermediate states, preserving high levels of plasticity, as demonstrated in primary tumors and, ultimately, in circulating tumor cells, representing a simplified element of the metastatic cascade. In this review, we focus on cellular drivers underlying EMT/MET phenotypic plasticity and its detrimental consequences in the context of TNBC cancer.
Links
EF16_025/0007381, research and development projectName: Preklinická progrese nových organických sloučenin s cílenou biologickou aktivitou
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