2024
DOI: 10.1016/j.critrevonc.2023.104226
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Cancer-associated fibroblasts in neoadjuvant setting for solid cancers

Yanan Gu,
Qiangda Chen,
Hanlin Yin
et al.
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Cited by 3 publications
(4 citation statements)
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“…Another important clinical feature of both HY-oAd and 9-ING-41 for cancer therapy is that they are capable of degrading aberrant tumor ECM ( Figure 5A ), which is a well-known barrier against intratumoral penetration and dispersion of various cancer therapeutics and immune cells ( 52 54 ). In line with this literature, effective degradation of tumor ECM by HY-oAd and 9-ING-41 was shown to facilitate CD4 + and CD8 + T-cell infiltration into the tumor tissues ( Figures 6B, C , 7B ), as well as simultaneously improving HY-oAd dispersion and accumulation throughout the bladder tumor tissues in a viral replication-independent manner ( Figures 5B , Supplementary Figure S2 ).…”
Section: Discussionmentioning
confidence: 99%
“…Another important clinical feature of both HY-oAd and 9-ING-41 for cancer therapy is that they are capable of degrading aberrant tumor ECM ( Figure 5A ), which is a well-known barrier against intratumoral penetration and dispersion of various cancer therapeutics and immune cells ( 52 54 ). In line with this literature, effective degradation of tumor ECM by HY-oAd and 9-ING-41 was shown to facilitate CD4 + and CD8 + T-cell infiltration into the tumor tissues ( Figures 6B, C , 7B ), as well as simultaneously improving HY-oAd dispersion and accumulation throughout the bladder tumor tissues in a viral replication-independent manner ( Figures 5B , Supplementary Figure S2 ).…”
Section: Discussionmentioning
confidence: 99%
“…A significant consequence of CAFs interaction with cancer cells, either through direct contact or indirect paracrine communication, is induced therapy resistance. Particularly, ECM produced by CAFs prevents immune cell infiltration into the TME, hampers drug penetration, and diminishes therapeutic efficacy ( Gu et al, 2024 ). Therefore, therapeutic strategies targeting the communication between cancer cells and their TME are actively explored.…”
Section: Therapeutic Implications and Challengesmentioning
confidence: 99%
“…Therefore, therapeutic strategies targeting the communication between cancer cells and their TME are actively explored. Previous reviews have described in detail the interplay between CAFs and TME and CAFs and immune cells and their role in chemotherapy resistance ( Raskov et al, 2021 ; Gu et al, 2024 ; Piwocka et al, 2024 ). Novel therapeutic approaches include: 1) modulators of gap junctions, 2) integrins blocking antibodies, 3) suppressors of tunnel nanotubes, 4) inhibitors of exosome biogenesis, 5) inhibition of TGFβ and other growth factors cascade, 6) inhibitors of chemokine receptors, and 7) modulators of metabolites ( Dominiak et al, 2020 ).…”
Section: Therapeutic Implications and Challengesmentioning
confidence: 99%
“…Apart from key genetic factors, desmoplasia and the tumor microenvironment (TME) have been recognized as key contributors to PDAC chemoresistance [ 19 , 20 ], and Gregori et al integrated biomechanical and pharmacological approaches to investigate the role of the cell-adhesion molecule Integrin Subunit Alpha 2 (ITGA2), a crucial regulator of the extracellular matrix [ 21 ], in PDAC resistance to gemcitabine [ 22 ]. Notably, high ITGA2 expression was correlated with shorter progression-free and overall survival, indicating its prognostic significance and association with gemcitabine treatment ineffectiveness.…”
mentioning
confidence: 99%