CD200 mimetic aptamer PEG-M49 markedly increases the therapeutic effects of pegylated liposomal doxorubicin in a mouse model of metastatic breast carcinoma: an effect independent of CD200 receptor 1

Erin, Nuray; Dilmaç, Sayra; Curry, Anna; Duymuş, Özlem; Tanrıöver, Gamze; Prodeus, Aaron; Gariépy, Jean; Gorczynski, Reginald M.

doi:10.1007/s00262-019-02444-3

Cited by 10 publications

(5 citation statements)

References 42 publications

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“…Lenalidomide alone decreased the number of systemic MDSCs and regulatory T cell in tumorbearing but not in naive mice (Sakamaki et al, 2014). Lenalidomide also induced strong antiinflammatory effects (Yamamoto et al, 2019), which may have been responsible for the suppression of MDSCs, since inhibition of inflammation using CD200 mimetics also decreased MDSCs (Erin et al, 2015;Erin et al, 2018b) and increased the therapeutic potential of doxorubicin (Erin et al, 2020).…”

Section: Therapeutic Approaches Targeting Mdscsmentioning

confidence: 99%

Tumor microenvironment and epithelial mesenchymal transition as targets to overcome tumor multidrug resistance

Erin

Grahovac

Brozović

et al. 2020

Drug Resistance Updates

Self Cite

316

187

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Therapeutic Approaches Targeting Mdscsmentioning

confidence: 99%

Tumor microenvironment and epithelial mesenchymal transition as targets to overcome tumor multidrug resistance

Erin

Grahovac

Brozović

et al. 2020

Drug Resistance Updates

Self Cite

316

187

View full text Add to dashboard Cite

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“…Collectively the associations between CD200R1 and these diverse immune-related proteins suggest that CD200R1 is involved in a variety of immune mechanisms and may explain why HNSCC with high CD200R1 expression is related to an 'immune-rich' microenvironment with high immune cell estimates. Thus, our findings suggest that modulation of the CD200R1 pathway could be used as an immunotherapeutic strategy in patients with HNSCC [22,35,36].…”

Section: Discussionmentioning

confidence: 70%

Prognostic Value of CD200R1 mRNA Expression in Head and Neck Squamous Cell Carcinoma

Chang

Lee

et al. 2020

Cancers

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Immune system dysfunction is associated with head and neck squamous cell carcinoma (HNSCC) development and progression and immune checkpoint inhibitors have demonstrated substantial survival benefits in platinum-refractory HNSCC; therefore, we examined the prognostic value of immune-related gene (IRG) expression in HNSCC. We analyzed the expression of 82 IRGs in 71 patients with HNSCC enrolled in a feasibility study for a prospective HNSCC biomarker-driven umbrella trial (Korean Cancer Study Group TRIUMPH study, NCT03292250). CD200R1 was identified as an independent prognostic factor and validated in GEO and TCGA database. CD2000R1 mRNA expression was found to be an independent favorable prognostic factor in patients with HNSCC. Moreover, CD200R1 was found to affect genes and pathways associated with the immune response, while seven differentially expressed genes (CD8A, DOK2, CX3CR1, TYROBP, CXCL9, CD300LF, IFNG) were associated with CD200R1 expression. Samples with higher CD200R1 expression displayed higher tumor-infiltrating immune cell counts both in silico and in histological analysis. These findings will help in the development of more accurate prognostic tools and suggest CD200R1 modulation as a HNSCC immunotherapy.

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“…Indeed, CD11b+ myeloid cells, isolated from the tumors of mice receiving combined treatment inhibited tumor outgrowth on adoptive transfer suggesting that administration of agonistic anti-CD200R improved the antitumor effects of TLR7 signaling and altered the local TME to become one less supportive of tumor progression [110]. More recently an intriguing effect of a CD200 mimetic aptamer given in conjunction with pegylated doxorubicin was reported in regulation of growth of breast cancer cells in a mouse model [111]. PEG-M49 and Peg-Dox co-treatment induced complete tumor regression and loss of macroscopic lung metastasis in four out of seven BALB/c mice [111].…”

Section: Regulation Of Solid Tumor Growth By Cd200:cd200rmentioning

confidence: 99%

“…More recently an intriguing effect of a CD200 mimetic aptamer given in conjunction with pegylated doxorubicin was reported in regulation of growth of breast cancer cells in a mouse model [111]. PEG-M49 and Peg-Dox co-treatment induced complete tumor regression and loss of macroscopic lung metastasis in four out of seven BALB/c mice [111]. Synergism was associated with Peg-M49-induced inhibition of Gr1+CD11b+ cells and Peg-Dox-induced increases in tumorinfiltrating CD8+ and CD8+CD4+ cells.…”

Section: Regulation Of Solid Tumor Growth By Cd200:cd200rmentioning

confidence: 99%

Updates on the Importance of CD200:CD200R Checkpoint Blockade in Solid Tumors and B cell Malignancies

2023

J Oncol Res Ther

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The last several years have seen the introduction into clinical medicine of a family of reagents directed towards so-called "checkpoint inhibitors", which act at gateways in a developing immune response to regulate unwanted and/or harmful selfdirected activation responses. The molecules involved at such gateways generally belong to an extended immunoglobulin supergene family, and contribute inhibitory signals to dampen over-exuberant responses. They include, but are not limited to, molecules of the CD28/cytotoxic T-lymphocyte antigen-4 (CTLA-4):B7.1/B7.2 receptor/ligand family; PD-1 and PDL-1; CD200 and CD200R; TIGIT and VISTA and their respective ligands (VSIG-3/IGSF11, Nectin), all of which are presumed to play a physiological role in maintaining natural self-tolerance. In the field of cancer immunotherapy, where the ultimate clinical goal is to improve immuno-targeting of cancer cells, triggering these checkpoint inhibitory signaling pathways, has the potential to thwart effective tumor immunity. This in turn has led to the characterization and application of multiple reagents, including antibodies and other designed inhibitory molecules, which can act as checkpoint blockade agents. Such reagents have had a dramatic effect on human cancer treatment, with marked success for anti-CTLA-4 and PD-1 in particular in clinical trials. This review elaborates on the promise on other more under-appreciated target molecules for checkpoint blockade in human B cell malignancies and solid tumors, particularly CD200:CD200R, and describes both the background, and newer studies, which highlight the potential importance of targeting the CD200:CD200R dyad in cancer immunobiology/therapy.

show abstract

CD200 mimetic aptamer PEG-M49 markedly increases the therapeutic effects of pegylated liposomal doxorubicin in a mouse model of metastatic breast carcinoma: an effect independent of CD200 receptor 1

Cited by 10 publications

References 42 publications

Tumor microenvironment and epithelial mesenchymal transition as targets to overcome tumor multidrug resistance

Tumor microenvironment and epithelial mesenchymal transition as targets to overcome tumor multidrug resistance

Prognostic Value of CD200R1 mRNA Expression in Head and Neck Squamous Cell Carcinoma

Updates on the Importance of CD200:CD200R Checkpoint Blockade in Solid Tumors and B cell Malignancies

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