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Posted On: 11/03/2024 12:07:28 AM
Post# of 147996
LL / CCL4: Jan. 2021. "Leronlimab blocks CCL5, CCL3, and CCL4 induced calcium signaling in breast cancer cells"
* The current studies showed that leronlimab blocks CCR5 signaling, assessed by calcium release in response to several distinct ligands. Upon binding of the ligand, the conformational change in CCR5 dissociates the Gαi and the Gβγ subunits, inducing downstream signaling. The activation of Ca2+ signaling and cellular migration by CCR5 is preserved in both immune cells [23] and cancer cells [12, 13]. CCR5 binds many ligands which are overexpressed in the tumor microenvironment including CXCL13 (BCA-1), CCL3 (MIP1α), CCL3L1, CCL4 (MP-1β), CCL8 (MCP2), CCL11 (eotaxin), CCL13 (MCP-4), and CCL16 (HCC-4). Elevated levels of CCL5 indicate poor prognosis in breast cancer [33, 34], pancreatic cancer [35], cervical cancer [34], prostate cancer, ovarian cancer [36], and gastric cancer [14, 37].
https://pmc.ncbi.nlm.nih.gov/articles/PMC7825185/
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Non medical knowledge post.
Only going by this trial CCL4 mention & from Dr. Palmer press release:
"...as well as a second model of liver fibrosis driven by CCL4 toxicity that is independent of fat deposition."
& my broad assumption, liver fat fibrosis & breast tumors are fundamentaly different.
Yet both CCL4 is associated.
With LL already having shown affective against CCL4 in non-fat deposition.
* The current studies showed that leronlimab blocks CCR5 signaling, assessed by calcium release in response to several distinct ligands. Upon binding of the ligand, the conformational change in CCR5 dissociates the Gαi and the Gβγ subunits, inducing downstream signaling. The activation of Ca2+ signaling and cellular migration by CCR5 is preserved in both immune cells [23] and cancer cells [12, 13]. CCR5 binds many ligands which are overexpressed in the tumor microenvironment including CXCL13 (BCA-1), CCL3 (MIP1α), CCL3L1, CCL4 (MP-1β), CCL8 (MCP2), CCL11 (eotaxin), CCL13 (MCP-4), and CCL16 (HCC-4). Elevated levels of CCL5 indicate poor prognosis in breast cancer [33, 34], pancreatic cancer [35], cervical cancer [34], prostate cancer, ovarian cancer [36], and gastric cancer [14, 37].
https://pmc.ncbi.nlm.nih.gov/articles/PMC7825185/
___
Non medical knowledge post.
Only going by this trial CCL4 mention & from Dr. Palmer press release:
"...as well as a second model of liver fibrosis driven by CCL4 toxicity that is independent of fat deposition."
& my broad assumption, liver fat fibrosis & breast tumors are fundamentaly different.
Yet both CCL4 is associated.
With LL already having shown affective against CCL4 in non-fat deposition.
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