High VCAM-1 Predicts Poor Prognosis and is Associated with Chemotherapy Resistance in Nasopharyngeal Carcinoma

Huang, Yu; Miao, Hongbin; Xia, Chenxi; Feng, Huajun; Xu, Shengen; Zeng, Liang; Wang, Yuanyuan; Zhao, Chong; Qin, Gang; Ou, Xiaoyi; Zhao, Fei

doi:10.2147/ott.s292259

Cited by 1 publication

(1 citation statement)

References 38 publications

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“…Targeted increases in VCAM1 and MAdCAM1 expression have been considered a potential strategy to manage brain and colon tumor metastasis, respectively ( 166 , 167 ). However, high expression of VCAM1 correlated with poor prognosis and increased tumor invasion in colorectal cancer (CRC) ( 168 , 169 ). The double-edged functions of these molecules limit their applicability for therapy.…”

Section: Induction Of Tls: Current and Potential Strategiesmentioning

confidence: 99%

Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures

Omotesho,

Escamilla,

Pérez-Ruiz

et al. 2024

Front. Immunol.

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Tertiary lymphoid structures (TLS) are ectopic lymphoid aggregates found in sites of chronic inflammation such as tumors and autoimmune diseases. The discovery that TLS formation at tumor sites correlated with good patient prognosis has triggered extensive research into various techniques to induce their formation at the tumor microenvironment (TME). One strategy is the exogenous induction of specific cytokines and chemokine expression in murine models. However, applying such systemic chemokine expression can result in significant toxicity and damage to healthy tissues. Also, the TLS formed from exogenous chemokine induction is heterogeneous and different from the ones associated with favorable prognosis. Therefore, there is a need to optimize additional approaches like immune cell engineering with lentiviral transduction to improve the TLS formation in vivo. Similarly, the genetic and epigenetic regulation of the different phases of TLS neogenesis are still unknown. Understanding these molecular regulations could help identify novel targets to induce tissue-specific TLS in the TME. This review offers a unique insight into the molecular checkpoints of the different stages and mechanisms involved in TLS formation. This review also highlights potential epigenetic targets to induce TLS neogenesis. The review further explores epigenetic therapies (epi-therapy) and ongoing clinical trials using epi-therapy in cancers. In addition, it builds upon the current knowledge of tools to generate TLS and TLS phenotyping biomarkers with predictive and prognostic clinical potential.

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