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  4. Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.
 
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Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.

Journal
Journal of hematology & oncology
Journal Volume
18
Journal Issue
1
Start Page
6
ISSN
1756-8722
Date Issued
2025-01-13
Author(s)
Glaviano, Antonino
Lau, Hannah Si-Hui
Carter, Lukas M
Lee, E Hui Clarissa
Lam, Hiu Yan
Okina, Elena
Tan, Donavan Jia Jie
Tan, Wency
Ang, Hui Li
Carbone, Daniela
Yee, Michelle Yi-Hui
Shanmugam, Muthu K
Huang, Xiao Zi
Sethi, Gautam
Tan, Tuan Zea
Lim, Lina H K
RUBY YUN-JU HUANG  
Ungefroren, Hendrik
Giovannetti, Elisa
Tang, Dean G
Bruno, Tullia C
Luo, Peng
Andersen, Mads Hald
Qian, Bin-Zhi
Ishihara, Jun
Radisky, Derek C
Elias, Salem
Yadav, Saurabh
Kim, Minah
Robert, Caroline
Diana, Patrizia
Schalper, Kurt A
Shi, Tao
Merghoub, Taha
Krebs, Simone
Kusumbe, Anjali P
Davids, Matthew S
Brown, Jennifer R
Kumar, Alan Prem
DOI
10.1186/s13045-024-01634-6
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/725143
Abstract
The tumor microenvironment (TME) is integral to cancer progression, impacting metastasis and treatment response. It consists of diverse cell types, extracellular matrix components, and signaling molecules that interact to promote tumor growth and therapeutic resistance. Elucidating the intricate interactions between cancer cells and the TME is crucial in understanding cancer progression and therapeutic challenges. A critical process induced by TME signaling is the epithelial-mesenchymal transition (EMT), wherein epithelial cells acquire mesenchymal traits, which enhance their motility and invasiveness and promote metastasis and cancer progression. By targeting various components of the TME, novel investigational strategies aim to disrupt the TME's contribution to the EMT, thereby improving treatment efficacy, addressing therapeutic resistance, and offering a nuanced approach to cancer therapy. This review scrutinizes the key players in the TME and the TME's contribution to the EMT, emphasizing avenues to therapeutically disrupt the interactions between the various TME components. Moreover, the article discusses the TME's implications for resistance mechanisms and highlights the current therapeutic strategies toward TME modulation along with potential caveats.
Subjects
Cancer
Cancer-associated fibroblasts (CAFs)
Chimeric antigen-receptor (CAR) T-cell therapy
Dendritic cells (DCs)
Epithelial-mesenchymal transition (EMT)
Extracellular matrix (ECM)
Metastasis
Myeloid-derived suppressor cells (MDSCs)
Natural killer (NK) cells
T-cell receptor (TCR) therapy
T-cells, B-cells, tumor-associated macrophages (TAMs)
Theranostics
Tumor microenvironment (TME)
Tumor-associated neutrophils (TANs)
SDGs

[SDGs]SDG3

Type
review article

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