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Article ; Online: Observations on the use of Bruton's tyrosine kinase inhibitors in SAR-CoV-2 and cancer.

Benner, Brooke / Carson, William E

2021 Volume 14, Issue 1, Page(s) 15

Abstract: Bruton's tyrosine kinase (BTK) inhibitors, drugs utilized in cancer, are being repurposed for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) (COVID-19). Recently, BTK inhibitors acalabrutinib and ibrutinib have been found to protect against ...

Abstract	Bruton's tyrosine kinase (BTK) inhibitors, drugs utilized in cancer, are being repurposed for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) (COVID-19). Recently, BTK inhibitors acalabrutinib and ibrutinib have been found to protect against pulmonary injury in a small group of patients infected with SARS-CoV-2. The high levels of pro-inflammatory cytokines found in the circulation of COVID-19 patients with severe lung disease suggest the involvement of the innate immune system in this process. Understanding the potential mechanism of action of BTK inhibition in SARS-CoV-2 is clearly of importance to determine how acalabrutinib, ibrutinib and possibly other BTK inhibitors may provide protection against lung injury.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/therapeutic use ; Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors ; Benzamides/therapeutic use ; COVID-19/drug therapy ; COVID-19/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Drug Repositioning ; Gene Expression Regulation/drug effects ; Humans ; Piperidines/therapeutic use ; Pyrazines/therapeutic use ; SARS-CoV-2
Chemical Substances	Benzamides ; Cytokines ; Piperidines ; Pyrazines ; ibrutinib (1X70OSD4VX) ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; BTK protein, human (EC 2.7.10.2) ; acalabrutinib (I42748ELQW) ; Adenine (JAC85A2161)
Language	English
Publishing date	2021-01-13
Publishing country	England
Document type	Letter ; Research Support, N.I.H., Extramural
ZDB-ID	2429631-4
ISSN	1756-8722 ; 1756-8722
ISSN (online)	1756-8722
ISSN	1756-8722
DOI	10.1186/s13045-020-00999-8
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Article ; Online: Analysis of Changes in Plasma Cytokine Levels in Response to IL12 Therapy in Three Clinical Trials.

Schwarz, Emily / Benner, Brooke / Yu, Lianbo / Tounkara, Fode / Carson, William E

Cancer research communications

2023 Volume 4, Issue 1, Page(s) 81–91

Abstract: The ability of IL12 to stimulate natural killer (NK) cell and T-cell antitumor activity makes it an attractive candidate for the immune therapy of cancer. Our group has demonstrated that IL12 enhances the NK cell response to antibody-coated tumor cells ... ...

Abstract	The ability of IL12 to stimulate natural killer (NK) cell and T-cell antitumor activity makes it an attractive candidate for the immune therapy of cancer. Our group has demonstrated that IL12 enhances the NK cell response to antibody-coated tumor cells and conducted three clinical trials utilizing IL12 with mAbs (OSU-9968, OSU-0167, and OSU-11010). To better characterize IL12-induced immunity, plasma cytokine levels were measured in 21 patients from these trials with favorable and unfavorable responses. t-statistics and linear modeling were used to test for differences within and between response groups by examining levels at baseline and post-IL12 administration. Patients exhibited significant increases in 11 cytokines post-IL12 administration when analyzed collectively. However, several cytokines were differentially induced by IL12 depending on response. GMCSF was significantly increased in complete/partially responding patients, while stable disease patients had significant increases in IL10 and decreases in VEGF-C. Patients who experienced progressive disease had significant increases in CCL3, CCL4, IL18, TNFα, CXCL10, CCL8, CCL2, IL6, and IFNγ. The increases in CCL3, CCL4, and IL6 in progressive disease patients were significantly higher than in clinically benefitting patients and most prominent within the first two cycles of IL12 therapy. This correlative pilot study has identified changes that occur in levels of circulating cytokines following IL12 administration to patients with cancer, but this report must be viewed as exploratory in nature. It is meant to spark further inquiry into the topic via the analysis of additional cohorts of patients with similar characteristics who have received IL12 in a uniform fashion. Significance: IL12 activates immune cells and is used to treat cancer. The profile of circulating cytokines was measured in an exploratory fashion in patients with cancer that received IL12 in combination with mAbs. This correlative pilot study could serve as the basis for additional studies of IL12 effects on the production of immune cytokines.
MeSH term(s)	Humans ; Cytokines ; Interleukin-12 ; Interleukin-6 ; Neoplasms/drug therapy ; Pilot Projects
Chemical Substances	Cytokines ; Interleukin-12 (187348-17-0) ; Interleukin-6
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, N.I.H., Extramural
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0122
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Article ; Online: Bruton's tyrosine kinase: an emerging targeted therapy in myeloid cells within the tumor microenvironment.

Good, Logan / Benner, Brooke / Carson, William E

Cancer immunology, immunotherapy : CII

2021 Volume 70, Issue 9, Page(s) 2439–2451

Abstract: Bruton's tyrosine kinase (BTK) is a non-receptor kinase belonging to the Tec family of kinases. The role of BTK in B cell receptor signaling is well defined and is known to play a key role in the proliferation and survival of malignant B cells. Moreover, ...

Abstract	Bruton's tyrosine kinase (BTK) is a non-receptor kinase belonging to the Tec family of kinases. The role of BTK in B cell receptor signaling is well defined and is known to play a key role in the proliferation and survival of malignant B cells. Moreover, BTK has been found to be expressed in cells of the myeloid lineage. BTK has been shown to contribute to a variety of cellular pathways in myeloid cells including signaling in the NLRP3 inflammasome, receptor activation of nuclear factor-κβ and inflammation, chemokine receptor activation affecting migration, and phagocytosis. Myeloid cells are crucial components of the tumor microenvironment and suppressive myeloid cells contribute to cancer progression, highlighting a potential role for BTK inhibition in the treatment of malignancy. The increased interest in BTK inhibition in cancer has resulted in many preclinical studies that are testing the efficacy of using single-agent BTK inhibitors. Moreover, the ability of tumor cells to develop resistance to single-agent checkpoint inhibitors has resulted in clinical studies utilizing BTK inhibitors in combination with these agents to improve clinical responses. Furthermore, BTK regulates the immune response in microbial and viral infections through B cells and myeloid cells such as monocytes and macrophages. In this review, we describe the role that BTK plays in supporting suppressive myeloid cells, including myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM), while also discussing the anticancer effects of BTK inhibition and briefly describe the role of BTK signaling and BTK inhibition in microbial and viral infections.
MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors ; Agammaglobulinaemia Tyrosine Kinase/genetics ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Humans ; Molecular Targeted Therapy/methods ; Myeloid Cells/drug effects ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Myeloid Cells/pathology ; Myeloid-Derived Suppressor Cells/immunology ; Myeloid-Derived Suppressor Cells/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Receptors, Antigen, B-Cell/metabolism ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology ; Tumor-Associated Macrophages/drug effects ; Tumor-Associated Macrophages/immunology ; Tumor-Associated Macrophages/metabolism
Chemical Substances	Protein Kinase Inhibitors ; Receptors, Antigen, B-Cell ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2)
Language	English
Publishing date	2021-04-05
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-021-02908-5
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Article ; Online: Pexidartinib, a Novel Small Molecule CSF-1R Inhibitor in Use for Tenosynovial Giant Cell Tumor: A Systematic Review of Pre-Clinical and Clinical Development.

Benner, Brooke / Good, Logan / Quiroga, Dionisia / Schultz, Thomas E / Kassem, Mahmoud / Carson, William E / Cherian, Mathew A / Sardesai, Sagar / Wesolowski, Robert

Drug design, development and therapy

2020 Volume 14, Page(s) 1693–1704

Abstract: Tenosynovial giant cell tumor (TGCT) is a rare benign tumor that involves the synovium, bursa, and tendon sheath, resulting in reduced mobility of the affected joint or limb. The current standard of care for TGCT is surgical resection. However, some ... ...

Abstract	Tenosynovial giant cell tumor (TGCT) is a rare benign tumor that involves the synovium, bursa, and tendon sheath, resulting in reduced mobility of the affected joint or limb. The current standard of care for TGCT is surgical resection. However, some patients have tumor recurrence, present with unresectable tumors, or have tumors that are in locations where resection could result in amputations or significant debility. Therefore, the development of systemic agents with activity against TGCT to expand treatment options is a highly unmet medical need. Pathologically, TGCT is characterized by the overexpression of colony-stimulating factor 1 (CSF-1), which leads to the recruitment of colony-stimulating factor-1 receptor (CSF-1R) expressing macrophages that make up the primary cell type within these giant cell tumors. The binding of CSF-1 and CSF-1R controls cell survival and proliferation of monocytes and the switch from a monocytic to macrophage phenotype contributing to the growth and inflammation within these tumors. Therefore, molecules that target CSF-1/CSF-1R have emerged as potential systemic agents for the treatment of TGCT. Given the role of macrophages in regulating tumorigenesis, CSF1/CSF1R-targeting agents have emerged as attractive therapeutic targets for solid tumors. Pexidartinib is an orally bioavailable and potent inhibitor of CSF-1R which is one of the most clinically used agents. In this review, we discuss the biology of TGCT and review the pre-clinical and clinical development of pexidartinib which ultimately led to the FDA approval of this agent for the treatment of TGCT as well as ongoing clinical studies utilizing pexidartinib in the setting of cancer.
MeSH term(s)	Aminopyridines/pharmacology ; Antineoplastic Agents/pharmacology ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Giant Cell Tumor of Tendon Sheath/drug therapy ; Giant Cell Tumor of Tendon Sheath/metabolism ; Humans ; Molecular Structure ; Pyrroles/pharmacology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Structure-Activity Relationship
Chemical Substances	Aminopyridines ; Antineoplastic Agents ; CSF1R protein, human ; Pyrroles ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor ; pexidartinib (6783M2LV5X)
Language	English
Publishing date	2020-05-04
Publishing country	New Zealand
Document type	Journal Article ; Systematic Review
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S253232
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Article: Evidence for interaction of the NLRP3 inflammasome and Bruton's tyrosine kinase in tumor-associated macrophages: implications for myeloid cell production of interleukin-1beta.

Benner, Brooke / Scarberry, Luke / Stiff, Andrew / Duggan, Megan C / Good, Logan / Lapurga, Gabriella / Butchar, Jonathan P / Tridandapani, Susheela / Carson, William E

Oncoimmunology

2019 Volume 8, Issue 11, Page(s) 1659704

Abstract: An inflammatory microenvironment has been shown to play an important role in the growth and metastasis of tumors. The NLRP3 inflammasome is a multi-protein complex of the innate immune system that is responsible for the production of the potent ... ...

Abstract	An inflammatory microenvironment has been shown to play an important role in the growth and metastasis of tumors. The NLRP3 inflammasome is a multi-protein complex of the innate immune system that is responsible for the production of the potent inflammatory cytokine IL-1β. Tumor- associated macrophages (TAM) are an expanded population of immune cells found in the tumor microenvironment that can promote the initiation and metastasis of tumor cells. Their presence has been correlated with disease burden, highlighting the therapeutic potential of targeting this population. However, to date clinically relevant pharmacologic strategies to target TAM remain elusive. Here, we show that
Language	English
Publishing date	2019-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2019.1659704
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Article ; Online: BTK inhibition potentiates anti-PD-L1 treatment in murine melanoma: potential role for MDSC modulation in immunotherapy.

Cancer immunology, immunotherapy : CII

2023 Volume 72, Issue 11, Page(s) 3461–3474

Abstract: Myeloid-derived suppressor cells (MDSC) have been linked to loss of immune effector cell function through a variety of mechanisms such as the generation of reactive oxygen and nitrogen species and the production of inhibitory cytokines. Our group has ... ...

Abstract	Myeloid-derived suppressor cells (MDSC) have been linked to loss of immune effector cell function through a variety of mechanisms such as the generation of reactive oxygen and nitrogen species and the production of inhibitory cytokines. Our group has shown that signaling through Bruton's tyrosine kinase (BTK) is important for MDSC function. Ibrutinib is an orally administered targeted agent that inhibits BTK activation and is currently used for the treatment of B cell malignancies. Using a syngeneic murine model of melanoma, the effect of BTK inhibition with ibrutinib on the therapeutic response to systemic PD-L1 blockade was studied. BTK was expressed by murine MDSC and their activation was inhibited by ibrutinib. Ibrutinib was not directly cytotoxic to cancer cells in vitro, but it inhibited BTK activation in MDSC and reduced expression of inducible nitric oxide synthase (NOS2) and production of nitric oxide. Ibrutinib treatments decreased the levels of circulating MDSC in vivo and increased the therapeutic efficacy of anti-PD-L1 antibody treatment. Gene expression profiling showed that ibrutinib decreased Cybb (NOX2) signaling, and increased IL-17 signaling (upregulating downstream targets Mmp9, Ptgs2, and S100a8). These results suggest that further exploration of MDSC inhibition could enhance the immunotherapy of advanced melanoma.PrécisInhibition of Bruton's tyrosine kinase, a key enzyme in myeloid cellular function, improves therapeutic response to an anti-PD-L1 antibody in an otherwise fairly resistant murine melanoma model.
MeSH term(s)	Humans ; Mice ; Animals ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Protein-Tyrosine Kinases ; Myeloid-Derived Suppressor Cells/metabolism ; B7-H1 Antigen ; Immunotherapy ; Antineoplastic Agents/therapeutic use ; Melanoma/drug therapy
Chemical Substances	Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; B7-H1 Antigen ; Antineoplastic Agents
Language	English
Publishing date	2023-08-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-023-03497-1
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Article ; Online: Deep and Durable Response to Nivolumab and Temozolomide in Small-Cell Lung Cancer Associated With an Early Decrease in Myeloid-Derived Suppressor Cells.

Owen, Dwight H / Benner, Brooke / Pilcher, Carly / Good, Logan / Savardekar, Himanshu / Norman, Ruthann / Ghattas, Christian / Shah, Manisha / Konda, Bhavana / Verschraegen, Claire F / Wesolowski, Robert / Behbehani, Gregory K / Carson, William E / Otterson, Gregory A

Clinical lung cancer

2020 Volume 22, Issue 4, Page(s) e487–e497

MeSH term(s)	Aged ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Male ; Myeloid-Derived Suppressor Cells/metabolism ; Nivolumab/administration & dosage ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/pathology ; Temozolomide/administration & dosage ; Treatment Outcome
Chemical Substances	Nivolumab (31YO63LBSN) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2020-11-02
Publishing country	United States
Document type	Case Reports ; Research Support, N.I.H., Extramural
ZDB-ID	2145146-1
ISSN	1938-0690 ; 1525-7304
ISSN (online)	1938-0690
ISSN	1525-7304
DOI	10.1016/j.cllc.2020.10.018
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Zs.A 5893: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 440: Show issues

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Article: Reciprocal Signaling between Myeloid Derived Suppressor and Tumor Cells Enhances Cellular Motility and is Mediated by Structural Cues in the Microenvironment.

Shukla, Vasudha C / Duarte-Sanmiguel, Silvia / Panic, Ana / Senthilvelan, Abirami / Moore, Jordan / Bobba, Christopher / Benner, Brooke / Carson, William E / Ghadiali, Samir N / Gallego-Perez, Daniel

Advanced biosystems

2020 Volume 4, Issue 6, Page(s) e2000049

Abstract: Myeloid derived suppressor cells (MDSCs) have gained significant attention for their immunosuppressive role in cancer and their ability to contribute to tumor progression and metastasis. Understanding the role of MDSCs in driving cancer cell migration, a ...

Abstract	Myeloid derived suppressor cells (MDSCs) have gained significant attention for their immunosuppressive role in cancer and their ability to contribute to tumor progression and metastasis. Understanding the role of MDSCs in driving cancer cell migration, a process fundamental to metastasis, is essential to fully comprehend and target MDSC-tumor cell interactions. This study employs microfabricated platforms, which simulate the structural cues present in the tumor microenvironment (TME) to elucidate the effects of MDSCs on the migratory phenotype of cancer cells at the single cell level. The results indicate that the presence of MDSCs enhances the motility of cancer-epithelial cells when directional cues (either topographical or spatial) are present. This behavior appears to be independent of cell-cell contact and driven by soluble byproducts from heterotypic interactions between MDSCs and cancer cells. Moreover, MDSC cell-motility is also impacted by the presence of cancer cells and the cancer cell secretome in the presence of directional cues. Epithelial dedifferentiation is the likely mechanism for changes in cancer cell motility in response to MDSCs. These results highlight the biochemical and biostructural conditions under which MDSCs can support cancer cell migration, and could therefore provide new avenues of research and therapy aimed at stemming cancer progression.
MeSH term(s)	Animals ; Cell Communication ; Cell Line, Tumor ; Cell Movement ; Female ; Mice ; Myeloid-Derived Suppressor Cells/metabolism ; Myeloid-Derived Suppressor Cells/pathology ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Tumor Microenvironment
Language	English
Publishing date	2020-05-18
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2366-7478
ISSN	2366-7478
DOI	10.1002/adbi.202000049
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Article ; Online: A Phase II Clinical Trial of Nivolumab and Temozolomide for Neuroendocrine Neoplasms.

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 29, Issue 4, Page(s) 731–741

Abstract: Purpose: Treatment options are limited in patients with metastatic neuroendocrine neoplasms (NEN). We present the results for a phase II trial of combination nivolumab and temozolomide in patients with advanced NEN along with results of immune changes ... ...

Abstract	Purpose: Treatment options are limited in patients with metastatic neuroendocrine neoplasms (NEN). We present the results for a phase II trial of combination nivolumab and temozolomide in patients with advanced NEN along with results of immune changes in peripheral blood. Patients and methods: NCT03728361 is a nonrandomized, phase II study of nivolumab and temozolomide in patients with NEN. The primary endpoint was response rate using RECIST 1.1. Secondary endpoints included progression-free survival (PFS), overall survival (OS), and safety. Immune profiling was performed by mass cytometry to evaluate the effect on peripheral blood immune cell subsets. Results: Among all 28 patients with NEN, the confirmed response rate was 9/28 [32.1%, 95% confidence interval (CI): 15.9-52.4]. Of 11 patients with lung NEN, the response rate was 64% (n = 7); there was a significant difference in responses by primary tumor location (lung vs. others, P = 0.020). The median PFS was 8.8 months (95% CI: 3.9-11.1 months), and median OS was 32.3 months (95% CI: 20.7-not reached months). Exploratory blood immune cell profiling revealed an increase in circulating CD8+ T cells (27.9% ± 13.4% vs. 31.7% ± 14.6%, P = 0.03) and a decrease in CD4+ T cells (59.6% ± 13.1% vs. 56.5% ± 13.0%, P = 0.001) after 2 weeks of treatment. LAG-3-expressing total T cells were lower in patients experiencing a partial response (0.18% ± 0.24% vs. 0.83% ± 0.55%, P = 0.028). Myeloid-derived suppressor cell levels increased during the study and did not correlate with response. Conclusions: Combination nivolumab and temozolomide demonstrated promising activity in NEN. See related commentary by Velez and Garon, p. 691.
MeSH term(s)	Humans ; Nivolumab/therapeutic use ; Temozolomide/therapeutic use ; Lung Neoplasms/drug therapy ; Neuroendocrine Tumors/drug therapy ; Progression-Free Survival
Chemical Substances	Nivolumab (31YO63LBSN) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2022-10-18
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-1552
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Article ; Online: Effect of Immune Checkpoint Blockade on Myeloid-Derived Suppressor Cell Populations in Patients With Melanoma.

Sun, Steven H / Benner, Brooke / Savardekar, Himanshu / Lapurga, Gabriella / Good, Logan / Abood, David / Nagle, Erin / Duggan, Megan / Stiff, Andrew / DiVincenzo, Mallory J / Suarez-Kelly, Lorena P / Campbell, Amanda / Yu, Lianbo / Wesolowski, Robert / Howard, Harrison / Shah, Hiral / Kendra, Kari / Carson, William E

Frontiers in immunology

2021 Volume 12, Page(s) 740890

Abstract: Introduction: Myeloid-derived suppressor cells (MDSC) are a subset of immature myeloid cells that inhibit anti-tumor immunity and contribute to immune therapy resistance. MDSC populations were measured in melanoma patients receiving immune checkpoint ... ...

Abstract	Introduction: Myeloid-derived suppressor cells (MDSC) are a subset of immature myeloid cells that inhibit anti-tumor immunity and contribute to immune therapy resistance. MDSC populations were measured in melanoma patients receiving immune checkpoint inhibitors (ICI). Methods: Patients with melanoma (n=128) provided blood samples at baseline (BL), and before cycles 2 and 3 (BC2, BC3). Peripheral blood mononuclear cells (PBMC) were analyzed for MDSC (CD33 Results: Levels of MDSC as a percentage of PBMC increased during ICI (BL: 9.2 ± 1.0% to BC3: 23.6 ± 1.9%, p<0.0001), and patients who developed progressive disease (PD) had higher baseline MDSC. In patients who had a complete or partial response (CR, PR), total MDSC levels rose dramatically and plateaued (BL: 6.4 ± 1.4%, BC2: 26.2 ± 4.2%, BC3: 27.5 ± 4.4%; p<0.0001), whereas MDSC rose less sharply in PD patients (BL: 11.7 ± 2.1%, BC2: 18.3 ± 3.1%, BC3: 19.0 ± 3.2%; p=0.1952). Subset analysis showed that within the expanding MDSC population, PMN-MDSC and E-MDSC levels decreased, while the proportion of M-MDSC remained constant during ICI. In PD patients, the proportion of PMN-MDSC (as a percentage of total MDSC) decreased (BL: 25.1 ± 4.7%, BC2: 16.1 ± 5.2%, BC3: 8.6 ± 1.8%; p=0.0105), whereas a heretofore under-characterized CD14+/CD15+ double positive MDSC subpopulation increased significantly (BL: 8.7 ± 1.4% to BC3: 26.9 ± 4.9%; p=0.0425). Conclusions: MDSC levels initially increased significantly in responders. PMN-MDSC decreased and CD14+CD15+ MDSC increased significantly in PD patients. Changes in MDSC levels may have prognostic value in ICI.
MeSH term(s)	Adult ; Aged ; Antibodies, Monoclonal, Humanized/therapeutic use ; Cell Count ; Female ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Ipilimumab/therapeutic use ; Male ; Melanoma/drug therapy ; Middle Aged ; Myeloid-Derived Suppressor Cells/immunology ; Nivolumab/therapeutic use ; Prospective Studies ; Skin Neoplasms/drug therapy
Chemical Substances	Antibodies, Monoclonal, Humanized ; Immune Checkpoint Inhibitors ; Ipilimumab ; Nivolumab (31YO63LBSN) ; pembrolizumab (DPT0O3T46P)
Language	English
Publishing date	2021-10-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.740890
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