Very favorable LL science and MoA overview. Thank
Post# of 157598
(Total Views: 385)
Posted On: 09/19/2025 12:48:32 PM
Very favorable LL science and MoA overview. Thanks Brentie.
... the CCL5/CCR5 axis has been extensively studied in the context of tumorigenesis. The CCL5/CCR5 axis always aims to create a more favorable microenvironment for tumor cell survival, as tumor cells can “hijack” chemokine networks to support tumor progression.18 In this context, the CCL5/CCR5 axis is gaining increasing attention, as abnormal expression and activity of CCL5 and its receptor CCR5 have been reported in tumors.18 CCR5 expression has been found to be preferentially expressed on regulatory T cells (Tregs). Intra tumoral injection of CCL5 led to an increase in tumor infiltrating Tregs.19 Elevated levels of CCL5 and its receptor CCR5 were found in more than 58% of patients with basal BC.20
Deactivation of CCL5/CCR5 Axis Inhibits Epistemology of BC Tumor Growth
If we consider CCL5/CCR5 as a contributor and potential trigger in the development of BC, the impact of anti-CCL5/CCR5 treatments on the immune integrity of the patient should also be evaluated. The optimal therapeutic modalities would need to address two conflicting needs: the need to prevent the deleterious involvement of CCL5 and activated CCR5 in BC, and the need to protect their potentially beneficial activities in immunity, including anti-cancer immune responses.21 CCL5/CCR5 also recruits Tregs, MDSCs and TAM to induce immunosuppression of the tumor.21 Research suggests that CCR5 antagonists could be used as adjuvant therapy to reduce the risk of metastasis in patients with basal BC.22 In addition, CCR5 secreted by the tumor microenvironment is highly sensitive to drug blockade, particularly in BC.23 Due to the interactions between CCR5 signaling and immune checkpoint function, research into blocking the CCL5/CCR5 axis in tumor therapy has gained a broad application perspective.23–26 Attenuation of tumor promoting inflammation in tumor tissue and objective tumor responses were observed.26 Studies therefore suggest that the myeloid CCL5-CCR5 axis is an excellent target for cancer immunotherapy.27 CCR5 promotes the invasiveness and metastatic potential of BC, while CCR5 inhibition abolishes them.
Therefore, CCR5 antagonists may represent an alternative therapeutic approach for patients with metastatic basal BC.28 BC cells stimulate de novo secretion of the chemokine CCL5/RANTES from mesenchymal stem cells, which then acts in a paracrine manner on cancer cells to promote their motility, invasion and metastasis
... the CCL5/CCR5 axis has been extensively studied in the context of tumorigenesis. The CCL5/CCR5 axis always aims to create a more favorable microenvironment for tumor cell survival, as tumor cells can “hijack” chemokine networks to support tumor progression.18 In this context, the CCL5/CCR5 axis is gaining increasing attention, as abnormal expression and activity of CCL5 and its receptor CCR5 have been reported in tumors.18 CCR5 expression has been found to be preferentially expressed on regulatory T cells (Tregs). Intra tumoral injection of CCL5 led to an increase in tumor infiltrating Tregs.19 Elevated levels of CCL5 and its receptor CCR5 were found in more than 58% of patients with basal BC.20
Deactivation of CCL5/CCR5 Axis Inhibits Epistemology of BC Tumor Growth
If we consider CCL5/CCR5 as a contributor and potential trigger in the development of BC, the impact of anti-CCL5/CCR5 treatments on the immune integrity of the patient should also be evaluated. The optimal therapeutic modalities would need to address two conflicting needs: the need to prevent the deleterious involvement of CCL5 and activated CCR5 in BC, and the need to protect their potentially beneficial activities in immunity, including anti-cancer immune responses.21 CCL5/CCR5 also recruits Tregs, MDSCs and TAM to induce immunosuppression of the tumor.21 Research suggests that CCR5 antagonists could be used as adjuvant therapy to reduce the risk of metastasis in patients with basal BC.22 In addition, CCR5 secreted by the tumor microenvironment is highly sensitive to drug blockade, particularly in BC.23 Due to the interactions between CCR5 signaling and immune checkpoint function, research into blocking the CCL5/CCR5 axis in tumor therapy has gained a broad application perspective.23–26 Attenuation of tumor promoting inflammation in tumor tissue and objective tumor responses were observed.26 Studies therefore suggest that the myeloid CCL5-CCR5 axis is an excellent target for cancer immunotherapy.27 CCR5 promotes the invasiveness and metastatic potential of BC, while CCR5 inhibition abolishes them.
Therefore, CCR5 antagonists may represent an alternative therapeutic approach for patients with metastatic basal BC.28 BC cells stimulate de novo secretion of the chemokine CCL5/RANTES from mesenchymal stem cells, which then acts in a paracrine manner on cancer cells to promote their motility, invasion and metastasis
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