I have always been drawn to this board for the immense knowledge base, I am trying to keep up and want to believe we are all (most) here for the same purpose. The CCL5/CCR5 issues regarding a whole host of cancer types is very real. Especially considering I am going to see a surgical oncologist tomorrow for a look at the chunk of melanoma cancer I had cut off my ear and the inflamed scaly issues remaining at said. I am sure it will be just fine, I am a positive person anyway.
And whats up with the 15 min presentation tomorrow? Seems oddly short and
at the exact time I see the doc who I mentioned CYDY to back in mid Feb (his nurse lit up when I mentioned the breast cancer connection, covid was but a twinkle at that time).
Something raises the level and over expression of CCR5 receptor sites on cells in many patients with various types of cancers, that is a fact not subject to debate. Mouse models have proven tumor metastasis can be induced by increasing the CCR5 receptors. Some suggest the increase with cancer is the result of the mutated cancer cells releasing abnormal levels of CCL5 (RANTES) that helps in self preservation and ultimate metastasis that kills. Something is raising the number of CCR5 receptors and CCL5 signaling is the easy culprit for many immunology researchers. Of course we believe leron will help stop the signaling by blocking the CCR5 receptor, allowing other chemokines to pass thru the door, and slow or stop metastasis (spreading and killing).
High expression of CCR5 in melanoma enhances epithelial-to-mesenchymal transition and metastasis via TGFβ1: CCR5 enhances melanoma EMT and metastasis via TGFβ1
Chemokine receptors are highly expressed in various cancers and play crucial roles in tumor progression. However, their expression patterns and functions in melanoma are unclear. The present study aimed to identify the chemokine receptors that play critical roles in melanoma progression and unravel the underlying molecular mechanisms. We found that the C‐C chemokine receptor 5 (CCR5) was more abundant in melanoma cells than normal cells and was positively associated with tumor malignancy in clinical patients. Animal experiments suggested that CCR5 deficiency in B16/F10 or A375 cells suppressed primary tumor growth and lung metastasis, while CCR5overexpression in B16/F0 cells enhanced primary tumor growth and lung metastasis. CCR5 played a critical role in proliferation and migration of melanoma cells in vitro. Importantly, CCR5 was required for maintenance of the mesenchymal phenotype of metastatic melanoma cells. Mechanistically, CCR5 positively regulated expression of Transforming Growth Factor β1 (TGFβ1), which in turn induced epithelial‐mesenchymal transition (EMT) and migration via PI3K/AKT/GSK3β signaling. Collectively, our results establish a critical role of CCR5 expressed by melanoma cells in cancer progression and reveal the novel mechanisms controlling this process, which suggests the prognostic value of CCR5 in melanoma patients and provides novel insights into CCR5‐targeted strategies for melanoma treatment.
https://www.researchgate.net/publication/3291..._via_TGFb1
And whats up with the 15 min presentation tomorrow? Seems oddly short and
at the exact time I see the doc who I mentioned CYDY to back in mid Feb (his nurse lit up when I mentioned the breast cancer connection, covid was but a twinkle at that time).
Something raises the level and over expression of CCR5 receptor sites on cells in many patients with various types of cancers, that is a fact not subject to debate. Mouse models have proven tumor metastasis can be induced by increasing the CCR5 receptors. Some suggest the increase with cancer is the result of the mutated cancer cells releasing abnormal levels of CCL5 (RANTES) that helps in self preservation and ultimate metastasis that kills. Something is raising the number of CCR5 receptors and CCL5 signaling is the easy culprit for many immunology researchers. Of course we believe leron will help stop the signaling by blocking the CCR5 receptor, allowing other chemokines to pass thru the door, and slow or stop metastasis (spreading and killing).
High expression of CCR5 in melanoma enhances epithelial-to-mesenchymal transition and metastasis via TGFβ1: CCR5 enhances melanoma EMT and metastasis via TGFβ1
Chemokine receptors are highly expressed in various cancers and play crucial roles in tumor progression. However, their expression patterns and functions in melanoma are unclear. The present study aimed to identify the chemokine receptors that play critical roles in melanoma progression and unravel the underlying molecular mechanisms. We found that the C‐C chemokine receptor 5 (CCR5) was more abundant in melanoma cells than normal cells and was positively associated with tumor malignancy in clinical patients. Animal experiments suggested that CCR5 deficiency in B16/F10 or A375 cells suppressed primary tumor growth and lung metastasis, while CCR5overexpression in B16/F0 cells enhanced primary tumor growth and lung metastasis. CCR5 played a critical role in proliferation and migration of melanoma cells in vitro. Importantly, CCR5 was required for maintenance of the mesenchymal phenotype of metastatic melanoma cells. Mechanistically, CCR5 positively regulated expression of Transforming Growth Factor β1 (TGFβ1), which in turn induced epithelial‐mesenchymal transition (EMT) and migration via PI3K/AKT/GSK3β signaling. Collectively, our results establish a critical role of CCR5 expressed by melanoma cells in cancer progression and reveal the novel mechanisms controlling this process, which suggests the prognostic value of CCR5 in melanoma patients and provides novel insights into CCR5‐targeted strategies for melanoma treatment.
https://www.researchgate.net/publication/3291..._via_TGFb1
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