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Статті в журналах з теми "Plasmacytoid dendritic cell, metastatic melanoma"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Monti, Matilde, Raffaella Vescovi, Francesca Consoli, Davide Farina, Daniele Moratto, Alfredo Berruti, Claudia Specchia, and William Vermi. "Plasmacytoid Dendritic Cell Impairment in Metastatic Melanoma by Lactic Acidosis." Cancers 12, no. 8 (July 28, 2020): 2085. http://dx.doi.org/10.3390/cancers12082085.

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The introduction of targeted therapies and immunotherapies has significantly improved the outcome of metastatic melanoma (MM) patients. These approaches rely on immune functions for their anti-melanoma response. Plasmacytoid dendritic cells (pDCs) exhibit anti-tumor function by production of effector molecules, type I interferons (I-IFNs), and cytokines. Tissue and blood pDCs result compromised in MM, although these findings are still partially conflicting. This study reports that blood pDCs were dramatically depleted in MM, particularly in patients with high lactate dehydrogenase (LDH) and high tumor burden; the reduced pDC frequency was associated with poor overall survival. Circulating pDCs resulted also in significant impairment in interferon alpha (IFN-α) and C-X-C motif chemokine 10 (CXCL10) production in response to toll-like receptor (TLR)-7/8 agonists; on the contrary, the response to TLR-9 agonist remained intact. In the BRAFV600+ subgroup, no recovery of pDC frequency could be obtained by BRAF and MEK inhibitors (BRAFi; MEKi), whereas their function was partially rescued. Mechanistically, in vitro exposure to lactic acidosis impaired both pDC viability and function. In conclusion, pDCs from MM patients were found to be severely impaired, with a potential role for lactic acidosis. Short-term responses to treatments were not associated with pDC recovery, suggesting long-lasting effects on their compartment.

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Monti, Matilde, Francesca Consoli, Raffaella Vescovi, Mattia Bugatti, and William Vermi. "Human Plasmacytoid Dendritic Cells and Cutaneous Melanoma." Cells 9, no. 2 (February 11, 2020): 417. http://dx.doi.org/10.3390/cells9020417.

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The prognosis of metastatic melanoma (MM) patients has remained poor for a long time. However, the recent introduction of effective target therapies (BRAF and MEK inhibitors for BRAFV600-mutated MM) and immunotherapies (anti-CTLA-4 and anti-PD-1) has significantly improved the survival of MM patients. Notably, all these responses are highly dependent on the fitness of the host immune system, including the innate compartment. Among immune cells involved in cancer immunity, properly activated plasmacytoid dendritic cells (pDCs) exert an important role, bridging the innate and adaptive immune responses and directly eliminating cancer cells. A distinctive feature of pDCs is the production of high amount of type I Interferon (I-IFN), through the Toll-like receptor (TLR) 7 and 9 signaling pathway activation. However, published data indicate that melanoma-associated escape mechanisms are in place to hijack pDC functions. We have recently reported that pDC recruitment is recurrent in the early phases of melanoma, but the entire pDC compartment collapses over melanoma progression. Here, we summarize recent advances on pDC biology and function within the context of melanoma immunity.

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Gerlini, Gianni, Carmelo Urso, Giulia Mariotti, Paola Di Gennaro, Domenico Palli, Paola Brandani, Adriana Salvadori, Nicola Pimpinelli, Umberto Maria Reali, and Lorenzo Borgognoni. "Plasmacytoid dendritic cells represent a major dendritic cell subset in sentinel lymph nodes of melanoma patients and accumulate in metastatic nodes." Clinical Immunology 125, no. 2 (November 2007): 184–93. http://dx.doi.org/10.1016/j.clim.2007.07.018.

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4

Pashenkov, Mikhail, Gerda Goëss, Christine Wagner, Markus Hörmann, Tamara Jandl, Anna Moser, Cedrik M. Britten, et al. "Phase II Trial of a Toll-Like Receptor 9–Activating Oligonucleotide in Patients With Metastatic Melanoma." Journal of Clinical Oncology 24, no. 36 (December 20, 2006): 5716–24. http://dx.doi.org/10.1200/jco.2006.07.9129.

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Purpose The recent identification of toll-like receptors (TLRs) and respective ligands allows the evaluation of novel dendritic cell (DC) –activating strategies. Stimulation of TLR9 directly activates human plasmacytoid DCs (PDCs) and indirectly induces potent innate immune responses in preclinical tumor models. We performed an open-label, multicenter, single-arm, phase II pilot trial with a TLR9-stimulating oligodeoxynucleotide in melanoma patients. Patients and Methods Patients with unresectable stage IIIb/c or stage IV melanoma received 6 mg PF-3512676 weekly by subcutaneous injection for 24 weeks or until disease progression to evaluate safety as well as clinical and immunologic activity. Clinical and laboratory safety assessments were performed weekly; blood samples for immunological measurements were taken every 8 weeks. Tumor measurements were performed according to Response Evaluation Criteria in Solid Tumors. Results Twenty patients received PF-3512676 for a mean of 10.9 weeks with a mean of 10.7 injections. Laboratory and nonlaboratory adverse events were limited, transient, and did not result in any withdrawals. Two patients experienced a confirmed partial response; one response is ongoing for 140+ weeks. Three patients experienced stable disease. Immunologic measurements revealed induction of an activated phenotype of PDC, elevation of serum levels of 2′,5′-oligoadenylate, a surrogate marker of type I interferon production, and significant stimulation of natural killer cell cytotoxicity (the latter was associated with clinical benefit). Conclusion These results indicate that TLR9-targeted therapy can stimulate innate immune responses in cancer patients, identify biomarkers that may be associated with TLR9-induced tumor regression, and encourage the design of follow-up studies to evaluate the ability of this therapeutic approach to target human cancer.

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Royal, Richard Eldon, Luis M. Vence, Tara Wray, Janice N. Cormier, Jeffrey Edwin Lee, Jeffrey E. Gershenwald, Merrick I. Ross, et al. "A toll-like receptor agonist to drive melanoma regression as a vaccination adjuvant or by direct tumor application." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 9582. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.9582.

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9582 Background: Toll like receptor (TLR) agonists may enhance vaccination or direct immune activation at the tumor microenvironment. This trial evaluates the biologic and clinical effects of Resiquimod, a TLR 7/8 agonist that can activate both myeloid (mDC, TLR 8) and plasmacytoid (pDC, TLR 7) dendritic cells, in patients with advanced stage melanoma. Methods: Class I HLA-A0201+ subjects with in-transit melanoma metastases or high risk for recurrence were vaccinated weekly with peptide vaccination (class I restricted peptide GP100209-2m and, if HLA-DP4+, also with class II restricted peptide MAGE-3243-258). Subjects were randomized 1:1 to receive Resiquimod as an adjuvant applied to the GP100 vaccination site. Subjects with in-transit disease were thereafter treated with resiquimod topically on half of the target lesions. Results: All patients (n = 47) underwent GP100209-2m vaccination, a majority (39) also received the MAGE-3243-258 peptide. The type I interferon-inducible genes (Mx A and IRF7), IFNg, and IP-10 RNA expression were up-regulated only in vaccination sites treated with Resiquimod (each p < 0.01) , demonstrating pDC activation (Type I interferon) and possibly T and NK cell activation (IFNg and IP-10). Nineteen subjects had in-transit disease at entry into the trial. In response to peptide vaccination alone, tumor regression was more likely in patients who received Resiquimod at the vaccination site (group A) compared to those who did not (group B). (4/9 vs 0/10, p = 0.033). In group A, 5 patients continued treatment with Resiquimod topically on the tumors, and all had tumor response (4PR, 1CR). In group B, 5 continued to tumoral resiquimod and 3 had regression (3 PR). Conclusions: Resiquimod increases Type I interferon and IFNg at the peptide vaccination site by activation of pDC/mDC and increases the antitumor response sufficiently to mediate regression of in-transit melanoma metastasis. Resiquimod on in-transit melanoma, in vaccinated hosts, drives regression of metastases, regardless of previous exposure at vaccination. Clinical trial information: NCT00960752.

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Hanks, Brent Allen, Alisha Holtzhausen, Petra Gimpel, Rebekah Jamieson, Olivia M. Campbell, Lihong Sun, Christina K. Augustine та ін. "Effect of the loss of the type III TGFβ receptor during tumor progression on tumor microenvironment: Preclinical development of TGFβ inhibition and TGFβ-related biomarkers to enhance immunotherapy efficacy." Journal of Clinical Oncology 30, № 15_suppl (20 травня 2012): 10563. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10563.

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10563 Background: Overall, the clinical efficacy of tumor immunotherapy has been limited. Our incomplete understanding of the complex interplay between tumors and the immune microenvironment has contributed to these modest outcomes. Our work has revealed that several tumors downregulate the expression of the type III TGFβ receptor (TβRIII) with progression. TβRIII is shed from the cell surface to generate soluble TβRIII (sTβRIII) which is capable of sequestering TGFβ. Methods and Results: Using both breast cancer and melanoma tumor models we have demonstrated that the loss of TβRIII expression is associated with diminished tumor infiltrating CD8+ T cells and increased regulatory T cells (Tregs) within the tumor microenvironment. Our data implies that these alterations correlate with suppressed tumor antigen-specific T cell responses and more rapid disease progression. We show that these changes are due to enhanced TGFβ signaling within the immune compartment of the tumor microenvironment resulting in enhanced expression of the indoleamine 2,3-dioxygenase immunoregulatory enzyme by local plasmacytoid dendritic cells (DCs) as well as increased expression of the Treg-recruiting CCL22 chemokine by local myeloid DCs. Microarray analysis indicates that these same gene expression associations also exist in human breast cancers. Consistent with these studies, we have demonstrated that TGF-β inhibition synergistically enhances the efficacy of a Her2/neu vaccine in a breast cancer model and that plasma levels of sTβRIII correlate with clinical response and overall survival in stage III melanoma patients. Conclusions: We have elucidated a novel mechanism that tumors utilize to suppress the generation of anti-tumor immunity by establishing a link between the loss of an endogenous suppressor of tumor metastasis, TβRIII, and the generation of an immunotolerant tumor microenvironment. We are pursuing a phase I clinical trial to investigate the efficacy of combining a TGF-β inhibitor with a tumor vaccine while also determining if sTβRIII may function as a predictive biomarker for this approach.

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Wong, Deborah J. L., Aru Panwar, Ari Rosenberg, Vidhya Karivedu, Douglas Earl Laux, Dan Paul Zandberg, Dmitri Bobilev, et al. "CMP-001-007: Open-label, phase 2 study of intratumoral CMP-001 + pembrolizumab in patients with recurrent or metastatic head and neck squamous cell carcinoma." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): TPS6089. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.tps6089.

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TPS6089 Background: PD-1 blockade ± chemotherapy has recently become a primary systemic therapy recommended by NCCN guidelines for patients (pts) with recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC). However, most pts still do not respond to treatment, indicating a large unmet need for pts with unresectable disease. CMP-001 is a toll-like receptor 9 (TLR9) agonist comprising a CpG-A oligodeoxynucleotide packaged in a virus-like particle that can induce type I interferon secretion from tumor-associated plasmacytoid dendritic cells, promoting a Th1-like chemokine milieu in the tumor microenvironment and inducing an antitumor CD8+ T-cell response. In a phase (ph) 1b study in pts with metastatic melanoma, intratumoral (IT) injection of CMP-001 + intravenous (IV) pembrolizumab (pembro) reversed PD-1 blockade resistance, induced responses in injected and noninjected lesions, and had an acceptable safety profile (Milhem et al, SITC 2020). This combination is therefore being tested in pts with HNSCC. Methods: CMP-001-007 (NCT04633278) is an open-label, multicenter, ph 2 study designed to investigate the efficacy and safety of CMP-001 + IV pembro in adult pts with histologically or cytologically confirmed R/M HNSCC considered incurable by local therapies. Eligible pts have undergone a pretreatment tumor biopsy, received no prior systemic therapy in the R/M setting, and have primary tumor locations of oropharynx, oral cavity, hypopharynx, or larynx. In addition, pts must have PD-L1-positive tumors (combined positive score ≥1), known tumor human papillomavirus (HPV) status (for oropharyngeal cancer), and measurable disease per RECIST v1.1 with ≥1 lesion amenable to IT injection. Pts with primary tumors in the nasopharynx are excluded. Enrolled pts will receive CMP-001 10 mg once weekly for 7 doses and every 3 weeks (Q3W) thereafter. The first dose may be administered subcutaneously or via IT injection, with all subsequent doses administered IT. All pts will also receive pembro 200 mg IV Q3W after the CMP-001 injection. Treatment continues until unacceptable toxicity or disease progression. The primary endpoint is investigator-assessed objective response rate (ORR) per RECIST v1.1. Secondary endpoints include safety, duration of response (DOR), progression-free survival (PFS), overall survival, and effects of HPV infection and PD-L1 expression on ORR, DOR, and PFS. Exploratory endpoints include analyses of baseline and changes from baseline in tumor or serum biomarkers related to TLR9, immune checkpoints, and potential predictors of response, as well as serum concentrations of CXCL10 and CMP-001. Refer to clinicaltrials.gov/ct2/show/NCT04633278 for the most current information on enrolling sites. Clinical trial information: NCT04633278.

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Davar, Diwakar, Arivarasan Karunamurthy, Douglas Hartman, Richelle DeBlasio, Joe-Marc Chauvin, Quanquan Ding, Ornella Pagliano, Amy Rose, John Kirkwood, and Hassane Zarour. "303 Phase II trial of neoadjuvant nivolumab (Nivo) and intra-tumoral (IT) CMP-001 in high-risk resectable melanoma (Neo-C-Nivo): final results." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A330. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0303.

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BackgroundNeoadjuvant PD-1 blockade produces major pathological responses (MPR) in ~30% of patients (pts) with high-risk resectable melanoma (MEL) with durable relapse-free benefit, and increased circulating activated CD8+ T cells.1 2 CMP-001 is a type A CpG packaged within a virus-like particle that activates tumor-associated plasmacytoid dendritic cells (pDC) via TLR9 inducing type I interferons and anti-tumor CD8+ T cells. CMP-001/pembrolizumab produces durable anti-tumor responses in PD-1 refractory melanoma.3 We previously reported preliminary evidence of efficacy of neoadjuvant IT CMP/Nivo in high-risk resectable MEL; and herein present final results on 30 evaluable patients.Methods30 pts with stage III B/C/D MEL were enrolled. Pre-operatively, CMP-001 was dosed at 5 mg subcutaneous (SC, 1st), then 10 mg IT (2nd-7th) weekly; Nivo was dosed 240 mg q2 weeks for 3 doses – both agents given for 7 weeks. Post-operatively, Nivo was dosed 480 mg q4 weeks with CMP-001 5 mg q4 weeks SC for 48 weeks. Primary endpoints included major pathologic response rate (MPR), and incidence of dose-limiting toxicities (DLT). Secondary endpoints were radiographic response, relapse-free survival (RFS) and overall survival (OS). Pathological response was scored blinded by pathologists based on residual volume of tumor (RVT) using prior specified cutoffs:4 60% (complete response, pCR); 0%<rvt<rvt50% (non-response, pNR). Radiographic response was assessed using RECIST v1.1. Sequential blood draws and tumor biopsies were collected and analyzed for CD8+ T cell infiltrate (TIL), multiparameter flow cytometry (MFC) and multiplex immunofluorescence (mIF).Results30 pts with regionally advanced MEL were enrolled, of stages IIIB (57%), IIIC (37%), IIID (7%). 29/30 (97%) of pts completed 7 weeks of neoadjuvant Nivo/CMP; while 1 pt had a delay in surgery related to a pre-operative infection unrelated to therapy. No DLTs were reported; grade 3/4 irAE were reported in 3 pts (11%) leading to CMP-001 discontinuation in 2 pts (7%). Radiographic responses were seen in 13 pts (43%), while 9 pts (30%) had stable disease and 8 pts (27%) had progressive disease. Pathological responses (RVT <50%) were seen in 70% of pts: pCR 15 (50%), pMR 3 (10%), 3 pPR (10%); only 9 (30%) had pNR. Pathological responders (pCR/pMR) had increased CD8+ TIL and CD303+ pDC intra-tumorally by mIF; and peripherally activated PD1+/Ki67+ CD8+ T cells by MFC.ConclusionsNeoadjuvant CMP/Nivo has acceptable toxicity and promising efficacy. MPR is 60% in 30 pts. 1-year RFS was 82% (all pts) and 89% (among those with pCR/pMR); median RFS is 9 months (among pNR/pPR) and not reached (among pCR/pMR). Response is associated with evidence of immune activation intra-tumorally and peripherally. IT CMP001 increases clinical efficacy of PD-1 blockade with minimal additional toxicity in pts with regionally advanced MEL. Further study of this combination in high-risk resectable MEL is planned.AcknowledgementsWe thank Dr. Jagjit Singh and the pathology grossing room staff for their assistance and Checkmate Pharmaceuticals for funding and CMP-001.Trial RegistrationClinical trial information: NCT03618641Ethics ApprovalThe study was approved by University of Pittsburgh’s Institutional Review Board, approval number MOD19040237-002.ConsentWritten informed consent was obtained from the patient for publication of this abstract and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.ReferencesAmaria RN, Reddy SM, Tawbi HA, et al. Neoadjuvant immune checkpoint blockade in high-risk resectable melanoma. Nat Med 2018. Nov;24(11):1649–1654.Huang AC, Orlowski RJ, Xu X, et al. A single dose of neoadjuvant PD-1 blockade predicts clinical outcomes in resectable melanoma. Nat Med 2019. Mar;25(3):454–461. doi: 10.1038/s41591-019-0357-y.Milhem M, Gonzales R, Medina T, et al. Abstract CT144: Intratumoral toll-like receptor 9 (TLR9) agonist, CMP-001, in combination with pembrolizumab can reverse resistance to PD-1 inhibition in a phase Ib trial in subjects with advanced melanoma. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14–18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract CT144.Tetzlaff MT, Messina JL, Stein JE, et al. Pathological assessment of resection specimens after neoadjuvant therapy for metastatic melanoma. Ann Oncol 2018. Aug 1;29(8):1861–1868.Cottrell TR, Thompson ED, Forde PM, et al. Pathologic features of response to neoadjuvant anti-PD-1 in resected non-small-cell lung carcinoma: a proposal for quantitative immune-related pathologic response criteria (irPRC). Ann Oncol 2018 Aug 1;29(8):1853–1860. doi: 10.1093/annonc/mdy218.Stein JE, Soni A, Danilova L, et al. Major pathologic response on biopsy (MPRbx) in patients with advanced melanoma treated with anti-PD-1: evidence for an early, on-therapy biomarker of response. Ann Oncol 2019 Apr 1;30(4):589–596. doi: 10.1093/annonc/mdz019.

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de Rosa, Francesco, Laura Ridolfi, Laura Fiammenghi, Massimiliano Petrini, Anna M. Granato, Valentina Ancarani, Elena Pancisi, et al. "Dendritic cell vaccination for metastatic melanoma." Melanoma Research 27, no. 4 (August 2017): 351–57. http://dx.doi.org/10.1097/cmr.0000000000000356.

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10

Chen, Vivien. "Dendritic-cell vaccination for metastatic melanoma?" Lancet Oncology 7, no. 5 (May 2006): 368. http://dx.doi.org/10.1016/s1470-2045(06)70678-7.

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11

Damiano, J. J., C. C. Patrone, L. D. Falo, L. H. Butterfield, J. M. Kirkwood, and L. J. Geskin. "361 Dendritic cell vaccines for metastatic melanoma." Journal of Investigative Dermatology 137, no. 5 (May 2017): S62. http://dx.doi.org/10.1016/j.jid.2017.02.378.

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12

Charfi, Slim, Sameh Ellouze, Hela Mnif, Ali Amouri, Abdelmajid Khabir, and Tahya Sellami-Boudawara. "Plasmacytoid Melanoma of the Urinary Bladder and Lymph Nodes with Immunohistochemical Expression of Plasma Cell Markers Revealing Primary Esophageal Melanoma." Case Reports in Pathology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/916256.

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Plasmacytoid variant of melanoma is reported in only rare cases. We present the case of a 54-years-old man admitted for enlarged lymph nodes in the lumbar region. Initial diagnosis of plasmablastic lymphoma/plasma cell myeloma was considered. At our institute, a bladder polyp was removed. Microscopic exam demonstrated dense plasmacytoid cells infiltration with pigment deposits. Immunohistochemical study showed strong expression of HMB45, Melan A, and vimentin. There was focal positivity with S100 protein and CD138/syndecan-1. The diagnosis of metastatic plasmacytoid melanoma was finally established. Clinical exam revealed an esophageal melanoma with melanosis supporting its primary location. Although rarely, melanoma especially plasmacytoid variant may express plasma cell markers which may lead to erroneous diagnosis of plasma cell proliferation. Careful morphological examination for melanin pigment and the use of panel of melanocytic markers are helpful for diagnosis.

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13

Dillman, Robert O., Senthamil R. Selvan, and Patric M. Schiltz. "Patient-Specific Dendritic-Cell Vaccines for Metastatic Melanoma." New England Journal of Medicine 355, no. 11 (September 14, 2006): 1179–81. http://dx.doi.org/10.1056/nejmc061667.

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Nesselhut, Jan, Dagmar Marx, Raymond Y. Chang, and Thomas Nesselhut. "Dendritic cell based immunotherapy in metastatic uveal melanoma." Journal of Clinical Oncology 36, no. 15_suppl (May 20, 2018): e21526-e21526. http://dx.doi.org/10.1200/jco.2018.36.15_suppl.e21526.

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15

Di Domizio, Jeremy, Olivier Demaria, and Michel Gilliet. "Plasmacytoid Dendritic Cells in Melanoma: Can We Revert Bad into Good?" Journal of Investigative Dermatology 134, no. 7 (July 2014): 1797–800. http://dx.doi.org/10.1038/jid.2014.155.

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16

Wilson, Natalie, Catherine Mikol, Anna Donaldson, Daniel Fowler, and Angus Dalgleish. "Dendritic Cell Immunotherapy for Advanced Metastatic Melanoma: Interim Report." Journal of Immunotherapy 28, no. 6 (November 2005): 661. http://dx.doi.org/10.1097/01.cji.0000191106.88690.e1.

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17

Tel, Jurjen, Erik H. J. G. Aarntzen, Tetsuro Baba, Gerty Schreibelt, Barbara M. Schulte, Daniel Benitez-Ribas, Otto C. Boerman, et al. "Natural Human Plasmacytoid Dendritic Cells Induce Antigen-Specific T-Cell Responses in Melanoma Patients." Cancer Research 73, no. 3 (January 23, 2013): 1063–75. http://dx.doi.org/10.1158/0008-5472.can-12-2583.

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Aspord, Caroline, Marie-Therese Leccia, Dimitri Salameire, David Laurin, Laurence Chaperot, Julie Charles, and Joel Plumas. "HLA-A*0201 + Plasmacytoid Dendritic Cells Provide a Cell-Based Immunotherapy for Melanoma Patients." Journal of Investigative Dermatology 132, no. 10 (October 2012): 2395–406. http://dx.doi.org/10.1038/jid.2012.152.

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Charles, Julie, Jérémy Di Domizio, Dimitri Salameire, Nathalie Bendriss-Vermare, Caroline Aspord, Ramzan Muhammad, Christine Lefebvre, Joël Plumas, Marie-Thérèse Leccia, and Laurence Chaperot. "Characterization of Circulating Dendritic Cells in Melanoma: Role of CCR6 in Plasmacytoid Dendritic Cell Recruitment to the Tumor." Journal of Investigative Dermatology 130, no. 6 (June 2010): 1646–56. http://dx.doi.org/10.1038/jid.2010.24.

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Geskin, Larisa J., James J. Damiano, Christina C. Patrone, Lisa H. Butterfield, John M. Kirkwood, and Louis D. Falo. "Three antigen-loading methods in dendritic cell vaccines for metastatic melanoma." Melanoma Research 28, no. 3 (June 2018): 211–21. http://dx.doi.org/10.1097/cmr.0000000000000441.

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Butterfield, Lisa H., Begonya Comin-Anduix, Lazar Vujanovic, Yohan Lee, Vivian B. Dissette, Jin-Quan Yang, Hong T. Vu, et al. "Adenovirus MART-1–engineered Autologous Dendritic Cell Vaccine for Metastatic Melanoma." Journal of Immunotherapy 31, no. 3 (April 2008): 294–309. http://dx.doi.org/10.1097/cji.0b013e31816a8910.

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Nesselhut, J., D. Marx, R. Y. Chang, C. Matthes, D. Lorenzen, B. Hildenbrand, J. Peters, and T. Nesselhut. "Immunotherapy with dendritic cells primed with an allogenic melanoma cell line in advanced metastatic melanoma." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 20026. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.20026.

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Huijts, Charlotte M., Saskia J. Santegoets, Tamarah D. de Jong, Henk M. Verheul, Tanja D. de Gruijl, and Hans J. van der Vliet. "Immunological effects of everolimus in patients with metastatic renal cell cancer." International Journal of Immunopathology and Pharmacology 30, no. 4 (October 9, 2017): 341–52. http://dx.doi.org/10.1177/0394632017734459.

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The mammalian target of rapamycin (mTOR) is a crucial kinase present in all cells. Besides its role in the regulation of cell-growth, proliferation, angiogenesis, and survival of malignant tumors, mTOR additionally plays an important role in immune regulation by controlling the balance between effector T cells and regulatory T cells (Tregs). This critically affects the suppressive state of the immune system. Here, the systemic immunological effects of everolimus treatment were comprehensively investigated in five patients with metastatic renal cell cancer. In this hypothesis generating study, the immunological alterations in circulating immune subsets induced by everolimus included a (non-significant) increase in the frequency of Tregs, a significant increase in monocytic myeloid-derived suppressor cells, a significant decrease in the frequency of immunoregulatory natural killer cells, classical CD141+ (cDC1) and CD1c+ (cDC2) dendritic cell subsets, as well as a decrease in the activation status of plasmacytoid dendritic cells and cDC1. These date indicate that the immunological effects of everolimus affect multiple immune cell subsets and altogether tip the balance in favor of immunosuppression, which can be considered a detrimental effect in the treatment of cancer, and may require combination treatment with agents able to negate immune suppression and boost T cell immunity.

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OSHITA, CHIE, MASAKO TAKIKAWA, AKIKO KUME, HARUO MIYATA, TADASHI ASHIZAWA, AKIRA IIZUKA, YOSHIO KIYOHARA, et al. "Dendritic cell-based vaccination in metastatic melanoma patients: Phase II clinical trial." Oncology Reports 28, no. 4 (August 7, 2012): 1131–38. http://dx.doi.org/10.3892/or.2012.1956.

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Markov, Oleg V., Nadezhda L. Mironova, Sergey V. Sennikov, Valentin V. Vlassov, and Marina A. Zenkova. "Prophylactic Dendritic Cell-Based Vaccines Efficiently Inhibit Metastases in Murine Metastatic Melanoma." PLOS ONE 10, no. 9 (September 1, 2015): e0136911. http://dx.doi.org/10.1371/journal.pone.0136911.

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Boudewijns, Steve, Rutger H. T. Koornstra, Harm Westdorp, Gerty Schreibelt, Alfons J. M. van den Eertwegh, Marnix H. Geukes Foppen, John B. Haanen, et al. "Ipilimumab administered to metastatic melanoma patients who progressed after dendritic cell vaccination." OncoImmunology 5, no. 8 (June 17, 2016): e1201625. http://dx.doi.org/10.1080/2162402x.2016.1201625.

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Bol, Kalijn F., Hanneke W. Mensink, Erik H. J. G. Aarntzen, Gerty Schreibelt, Jan E. E. Keunen, Pierre G. Coulie, Annelies de Klein, et al. "Long Overall Survival After Dendritic Cell Vaccination in Metastatic Uveal Melanoma Patients." American Journal of Ophthalmology 158, no. 5 (November 2014): 939–47. http://dx.doi.org/10.1016/j.ajo.2014.07.014.

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Ribas, Antoni, Begoña Comin-Anduix, Bartosz Chmielowski, Jason Jalil, Pilar de la Rocha, Tara A. McCannel, Maria Teresa Ochoa, et al. "Dendritic Cell Vaccination Combined with CTLA4 Blockade in Patients with Metastatic Melanoma." Clinical Cancer Research 15, no. 19 (September 29, 2009): 6267–76. http://dx.doi.org/10.1158/1078-0432.ccr-09-1254.

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Gerlini, Gianni, Paola Di Gennaro, Giulia Mariotti, Carmelo Urso, Alberto Chiarugi, Nicola Pimpinelli, and Lorenzo Borgognoni. "Indoleamine 2,3-Dioxygenase+ Cells Correspond to the BDCA2+ Plasmacytoid Dendritic Cells in Human Melanoma Sentinel Nodes." Journal of Investigative Dermatology 130, no. 3 (March 2010): 898–901. http://dx.doi.org/10.1038/jid.2009.307.

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Nguyen, Xuan Duc, Hermann Eichler, Antje Sucker, Udo Hofmann, Dirk Schadendorf, and Harald Kluter. "Collection of autologous monocytes for dendritic cell vaccination therapy in metastatic melanoma patients." Transfusion 42, no. 4 (April 2002): 428–32. http://dx.doi.org/10.1046/j.1525-1438.2002.00067.x.

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Benitez-Ribas, Daniel, Gosse J. Adema, Gregor Winkels, Ina S. Klasen, Cornelis J. A. Punt, Carl G. Figdor та I. Jolanda M. de Vries. "Plasmacytoid dendritic cells of melanoma patients present exogenous proteins to CD4+ T cells after FcγRII-mediated uptake". Journal of Experimental Medicine 203, № 7 (19 червня 2006): 1629–35. http://dx.doi.org/10.1084/jem.20052364.

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Plasmacytoid dendritic cells (pDCs) contribute to innate antiviral immune responses by producing type I interferons. Although human pDCs can induce T cell responses upon viral infection, it remains unclear if pDCs can present exogenous antigens. Here, we show that human pDCs exploit FcγRII (CD32) to internalize antigen–antibody complexes, resulting in the presentation of exogenous antigen to T cells. pDCs isolated from melanoma patients vaccinated with autologous monocyte-derived peptide- and keyhold limpet hemocyanin (KLH)–loaded dendritic cells, but not from nonvaccinated patients or patients that lack a humoral response against KLH, were able to stimulate KLH-specific T cell proliferation. Interestingly, we observed that internalization of KLH by pDCs depended on the presence of serum from vaccinated patients that developed an anti-KLH antibody response. Anti-CD32 antibodies inhibited antigen uptake and presentation, demonstrating that circulating anti-KLH antibodies binding to CD32 mediate KLH internalization. We conclude that CD32 is an antigen uptake receptor on pDCs and that antigen presentation by pDCs is of particular relevance when circulating antibodies are present. Antigen presentation by pDCs may thus modulate the strength and quality of the secondary phase of an immune response.

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Yang, De, Xiao-Qing Li, Md Masud Alam, Øystein Rekdal, and Joost J. Oppenheim. "Oncolytic peptide LTX-315 enhances anti-melanoma immunity by inducing MyD88-dependent maturation of dendritic cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 91.5. http://dx.doi.org/10.4049/jimmunol.204.supp.91.5.

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Abstract LTX-315 is a synthetic cationic oncolytic peptide with potent anticancer cytotoxicity. LTX-315 induces both immunogenic tumor cell death and the generation of tumor-specific immune response. Given the central role of dendritic cell (DC) maturation in the induction of antigen-specific immune responses, we investigated the effect of LTX-315 treatment on the maturation of tumor-infiltrating DCs (TiDCs) and the generation of anti-melanoma immunity. The results reveal that LTX-315 induces the maturation of DCs through three distinct mechanisms: 1) release of DAMPs/alarmins; 2) complexes of LTX-315 with nucleic acids that act immunostimulatory; and 3) direct induction of the maturation of both conventional and plasmacytoid DCs by triggering TLR7. Importantly, LTX-315-induced maturation of DCs in vitro and in vivo was dependent on the presence of the signal transducer MyD88 as well as distinct TLRs. Our data also substantiate the notion that reagents like LTX-315 with both tumor cell cytotoxic and immunostimulaing capacities are more effective immunotherapeutics.

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Thomas, R., J. Padmanabha, M. Chambers, S. McFadyen, E. Walpole, G. Nielssen, and M. Smithers. "Metastatic lesions in the joint associated with acute inflammatory arthritis after dendritic cell immunotherapy for metastatic melanoma." Melanoma Research 11, no. 2 (April 2001): 167–73. http://dx.doi.org/10.1097/00008390-200104000-00012.

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Pachynski, Russell K., Brian A. Zabel, Holbrook E. Kohrt, Nicole M. Tejeda, Justin Monnier, Christina D. Swanson, Alison K. Holzer, et al. "The chemoattractant chemerin suppresses melanoma by recruiting natural killer cell antitumor defenses." Journal of Experimental Medicine 209, no. 8 (July 2, 2012): 1427–35. http://dx.doi.org/10.1084/jem.20112124.

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Infiltration of specialized immune cells regulates the growth and survival of neoplasia. Here, in a survey of public whole genome expression datasets we found that the gene for chemerin, a widely expressed endogenous chemoattractant protein, is down-regulated in melanoma as well as other human tumors. Moreover, high chemerin messenger RNA expression in tumors correlated with improved outcome in human melanoma. In experiments using the B16 transplantable mouse melanoma, tumor-expressed chemerin inhibited in vivo tumor growth without altering in vitro proliferation. Growth inhibition was associated with an altered profile of tumor-infiltrating cells with an increase in natural killer (NK) cells and a relative reduction in myeloid-derived suppressor cells and putative immune inhibitory plasmacytoid dendritic cells. Tumor inhibition required host expression of CMKLR1 (chemokine-like receptor 1), the chemoattractant receptor for chemerin, and was abrogated by NK cell depletion. Intratumoral injection of chemerin also inhibited tumor growth, suggesting the potential for therapeutic application. These results show that chemerin, whether expressed by tumor cells or within the tumor environment, can recruit host immune defenses that inhibit tumorigenesis and suggest that down-regulation of chemerin may be an important mechanism of tumor immune evasion.

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Gajewski, T., Y. Zha, B. Thurner, and G. Schuler. "Association of gene expression profile in metastatic melanoma and survival to a dendritic cell-based vaccine." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 9002. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.9002.

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9002 Background: Emerging data suggests that features of the melanoma tumor microenvironment may determine the clinical outcome to immunotherapies. We recently have observed a gene expression signature that correlated with a favorable clinical outcome in response to an IL-12-based melanoma vaccine. Increased expression of chemokine genes and T cell transcripts, and decreased expression of genes associated with aggressive tumor biology, were observed in the favorable group. To determine whether these patterns were reproducible, gene expression profiling was performed from an independent vaccine clinical trial. Methods: Patients with advanced melanoma were treated with autologous, mature monocyte-derived dendritic cells loaded with a combination of melanoma antigen peptides. Pretreatment biopsies were cryopreserved for RNA extraction and gene expression profiling. Patients were categorized into “long survival” (> 24 months) or “short survival” outcomes. Supervised hierarchical clustering was performed to identify genes differentially expressed in the two outcome groups. Results: RNA that passed quality control was obtained from 17 stage IV patients, 5 with a short survival and 12 with a long survival. 408 genes were differentially at least 2- fold. Consistent with previous observations, tumors from favorable outcome patients expressed higher levels of several T cell-specific genes, including Thy1 and CD28; chemokines, including CCL19, CXCL12, and CXCL14; and other immune genes, including LTβ, IL-1R, IFNαR2, IL27R, CD69, and FcRs. Conversely, tumors from unfavorable outcome patients expressed higher levels of pro- angiogeneic genes, including Flt1; anti-apoptotic genes, including SerpinH1 and Serpine1; and multiple collagens. Conclusions: Our results confirm that a subset of transcripts expressed in melanoma metastases may be useful as a predictive biomarker for response to melanoma vaccines. The categories of genes identified point toward new opportunities for overcoming resistance mechanisms. Future studies should integrate gene expression profiling of pre-treatment biopsies as a stratification or enrichment factor in immunotherapy trials. No significant financial relationships to disclose.

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Barbour, Angela H., and Brendon J. Coventry. "Dendritic cell density and activation status of tumour-infiltrating lymphocytes in metastatic human melanoma." Melanoma Research 13, no. 3 (June 2003): 263–69. http://dx.doi.org/10.1097/00008390-200306000-00007.

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Moreira, Alvaro, Stefanie Gross, Ugur Uslu, Jan Doerrie, Mirko Kummer, Stefan Schliep, Felix Sponagl, et al. "Dendritic cell vaccination in metastatic uveal melanoma as compassionate treatment: Immunological and clinical responses." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e21024-e21024. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e21024.

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e21024 Background: Other than cutaneous melanoma, metastatic uveal melanoma (UM) is minimally responsive to checkpoint inhibitors. The prognosis remains very poor with mortality rates nearly unchanged over the last decades. The recently growing insight that immunotherapy significantly improves outcomes for cancer patients led to a re-emergence of vaccines including dendritic cell (DC) vaccines. Methods: We vaccinated an UM patient in a compassionate use setting and assessed the immunological and clinical responses. Based on this experience we performed individual compassionate treatments in other UM patients using DC loaded by peptide pulsing and/or mRNA transfection (autologous tumor RNA or RNA coding for tumor antigens). Results: The first patient was vaccinated in 2013 after a liver metastasis was resected and checkpoint blockade with ipilimumab was started. In 2014 the patient showed progression in the liver. We continued DC vaccination in shorter intervals and adapted antigen loading (with mRNA coding for an individual GNAQ driver mutation) accompanied by a further cycle of ipilimumab. Therapy resulted in complete remission of liver metastases, but the patient developed new skin metastases. Again the loading of DC was adapted (peptides of passenger mutations predicted after Next-Generation Sequencing) and infusions with pembrolizumab were started. Pathology from some regressing lesions showed a massive T cell infiltration and in parallel GNAQ mutation-specific T cells could be found in the patient’s blood. Skin metastases regressed and the patient is now free of detectable tumor after 65 months. Immune monitoring in the patient’s blood showed a vaccine-induced functional T cell response against the QNAQ-driver mutation. Three of other four patients are also still alive, one in complete remission under DC vaccination in combination with pembrolizumab, two of them showing measurable disease, and one deceased disease related after 28 months, resulting in a median OS of the five patients of 36.4 months. Immune monitoring in one of those patients showed a CD4+ and CD8+ INF-gamma T cell response against the autologous tumor RNA vaccine. No grade 3 or 4 toxicity occurred. Conclusions: The observed prolonged median OS and the fact that 2/5 patients remain disease-free is definitely encouraging. Vaccination immunotherapy with antigen-laden DC is a potential therapeutic option for patients with metastatic uveal melanoma. Combinations with checkpoint inhibitors proved promising, and should be further evaluated in clinical trials.

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Fay, J. W., H. Ueno, J. Connolly, J. Banchereau, and K. Palucka. "Durable clinical responses in patients with metastatic melanoma vaccinated with dendritic cells loaded with killed allogeneic melanoma cells." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 2576. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.2576.

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2576 Background: We demonstrated that DCs loaded with killed allogeneic tumors can cross-prime tumor-specific naïve CD8+T cells in vitro. Clinically this approach would overcome HLA restriction inherent to peptide vaccines and allow diversification of immune responses including priming of many clones of CD8+ and CD4+ T cells. Methods: Twenty (20) patients with metastatic melanoma were vaccinated with autologous monocyte-derived DCs loaded with killed allogeneic Colo829 melanoma cell line. A total of 8 vaccines were administered at monthly intervals. DCs were generated from monocytes by culturing with GM-CSF and IL-4 and activated by additional culture with TNFα and CD40 ligand. KLH was used as a control antigen. The first patient was accrued December, 2002 and the last November, 2003. Results: DC vaccinations induced durable objective clinical responses in two patients who had progressive metastatic disease after previous cytotoxic chemotherapy. One patient experienced a CR and one patient a PR both remissions have lasted ≥ 20 months. Fourteen patients were alive at 12 months and 9 patients are alive at the end of 2005. The estimated median overall survival is 22 months with a range of 2–31 months. DC vaccination led to elicitation of CD8+T cell immunity specific to MART-1 tissue differentiation antigen, suggesting that cross-priming/presentation of melanoma antigens by the DC vaccines had occurred in vivo. Vaccinations were safe and tolerable. There were no significant adverse events. Conclusions: The present results justify the design of larger follow-up studies to assess the immunological and clinical response to DC vaccines in patients with metastatic melanoma and other malignant diseases. No significant financial relationships to disclose.

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Lenogue, Kevin, Alexandre Walencik, Karine Laulagnier, Jean-Paul Molens, Houssem Benlalam, Brigitte Dreno, Pierre Coulie, Martin Pule, Laurence Chaperot, and Joël Plumas. "Engineering a Human Plasmacytoid Dendritic Cell-Based Vaccine to Prime and Expand Multispecific Viral and Tumor Antigen-Specific T-Cells." Vaccines 9, no. 2 (February 10, 2021): 141. http://dx.doi.org/10.3390/vaccines9020141.

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Because dendritic cells are crucial to prime and expand antigen-specific CD8+ T-cells, several strategies are designed to use them in therapeutic vaccines against infectious diseases or cancer. In this context, off-the-shelf allogeneic dendritic cell-based platforms are more attractive than individualized autologous vaccines tailored to each patient. In the present study, a unique dendritic cell line (PDC*line) platform of plasmacytoid origin, already used to prime and expand antitumor immunity in melanoma patients, was improved thanks to retroviral engineering. We demonstrated that the clinical-grade PDC*line, transduced with genes encoding viral or tumoral whole proteins, efficiently processed and stably presented the transduced antigens in different human leukocyte antigen (HLA) class I contexts. Moreover, the use of polyepitope constructs allowed the presentation of immunogenic peptides and the expansion of specific cytotoxic effectors. We also demonstrated that the addition of the Lysosome-associated membrane protein-1 (LAMP-1) sequence greatly improved the presentation of some peptides. Lastly, thanks to transduction of new HLA molecules, the PDC platform can benefit many patients through the easy addition of matched HLA-I molecules. The demonstration of the effective retroviral transduction of PDC*line cells strengthens and broadens the scope of the PDC*line platform, which can be used in adoptive or active immunotherapy for the treatment of infectious diseases or cancer.

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Samoylenko, Igor, Tatiana Zabotina, Irina N. Mikhaylova, George Z. Chkadua, Olga V. Korotkova, Anastasia S. Vikhrova, Valery V. Nazarova, Galina Kharkevich, and Lev V. Demidov. "Biochemical and immunologic markers in patients with metastatic melanoma treated with chemotherapy and dendritic cell vaccine." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e20042-e20042. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e20042.

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e20042 Background: The purpose of this sub study was to identify peripheral blood biomarkers associated with the therapeutic effect of immunotherapy with dendritic cell vaccine in patients with metastatic melanoma (MM). Methods: Patients (pts) with low disease burden achieved disease control after two cycles of chemo (cisplatine, vinbalstie, DTIC) were randomized dendritic cell vaccine (DC) or three cycles of chemo. Vaccination schedule consisted of 5 subcutaneous injections of dendritic cell (DC) vaccine (2×106 cells pulsed with autologous lysate) with 14 days intervals. S100B level, LDH level, and peripheral blood lymphocytes immune phenotype were assessed before treatment, after two cycles of chemo and after each vaccination cycle. Results: 104 pts were included in the study, 30 pts were randomized to DC arm, 29 pts were randomized to continue chemo. In pts with rapid disease progression baseline serum S100b level was significantly higher compared to patients with objective response or stable disease (0.874±1.15 mcg/L vs. 0.361±0.66 mcg/L, P=0.002). Similar results were found for baseline serum LDH level (559.8±469.7 U/L vs. 412.5±184.4 U/L, P=0.005) and serum S100b level after 2 cycles of chemo (0.688±0.855 mcg/L vs. 0.187±0,29 mcg/L, P<0.001). Contrary, baseline CD3+HLA-DR+ and CD4+CD25+ lymphocytes levels after 2 cycles of chemo were significantly higher in pts with disease control (11.9±8.9% vs. 8.9±5.3%, P=0.047 and 14.4±8.3% vs. 11.3±5.5%, P=0.036 respectively).In pts randomized to DC arm following markers were associated with long lasting objective response or stable disease course (>6 months): lower baseline S100b level (0.133±0.120 mcg/L vs. 0.445±0.406 mcg/L, P=0.014), lower S100b level after 2 cycles of chemo (0.105±0.095 mcg/L vs. 0.255±0.154 mcg/L, P=0.048), higher proportion of active CD8+lymphocytes prior to vaccination (74.7±3.6% vs. 51.7±14.2%, P=0.05); and more prominent increase of NK-cells CD3-CD16+CD56+ from baseline (increase in 76.5%±41.12% vs. 4.5±28.8%, P=0.01). Conclusions: Biochemical and immunological markers may be helpful when selecting patients with metastatic melanoma for immunotherapy with dendritic cell vaccine.

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Paczesny, Sophie, Jacques Banchereau, Knut M. Wittkowski, Giovanna Saracino, Joseph Fay, and A. Karolina Palucka. "Expansion of Melanoma-specific Cytolytic CD8+ T Cell Precursors in Patients with Metastatic Melanoma Vaccinated with CD34+ Progenitor-derived Dendritic Cells." Journal of Experimental Medicine 199, no. 11 (June 1, 2004): 1503–11. http://dx.doi.org/10.1084/jem.20032118.

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Cancer vaccines aim at inducing (a) tumor-specific effector T cells able to reduce/eliminate the tumor mass, and (b) long-lasting tumor-specific memory T cells able to control tumor relapse. We have shown earlier, in 18 human histocompatibility leukocyte antigen (HLA)-A*0201 patients with metastatic melanoma, that vaccination with peptide-loaded CD34–dendritic cells (DCs) leads to expansion of melanoma-specific interferon γ–producing CD8+ T cells in the blood. Here, we show in 9 out of 12 analyzed patients the expansion of cytolytic CD8+ T cell precursors specific for melanoma differentiation antigens. These precursors yield, upon single restimulation with melanoma peptide–pulsed DCs, cytotoxic T lymphocytes (CTLs) able to kill melanoma cells. Melanoma-specific CTLs can be grown in vitro and can be detected in three assays: (a) melanoma tetramer binding, (b) killing of melanoma peptide–pulsed T2 cells, and (c) killing of HLA-A*0201 melanoma cells. The cytolytic activity of expanded CTLs correlates with the frequency of melanoma tetramer binding CD8+ T cells. Thus, CD34-DC vaccines can expand melanoma-specific CTL precursors that can kill melanoma antigen–expressing targets. These results justify the design of larger follow-up studies to assess the immunological and clinical response to peptide-pulsed CD34-DC vaccines.

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Dillman, Robert O., Andrew N. Cornforth, Edward F. McClay, and Carol Depriest. "Patient-specific dendritic cell vaccines with autologous tumor antigens in 72 patients with metastatic melanoma." Melanoma Management 6, no. 2 (June 2019): MMT20. http://dx.doi.org/10.2217/mmt-2018-0010.

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Dillman, Robert O., Gary B. Fogel, Andrew N. Cornforth, Senthamil R. Selvan, Patric M. Schiltz, and Carol DePriest. "Features Associated with Survival in Metastatic Melanoma Patients Treated with Patient-Specific Dendritic Cell Vaccines." Cancer Biotherapy and Radiopharmaceuticals 26, no. 4 (August 2011): 407–15. http://dx.doi.org/10.1089/cbr.2011.0973.

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44

Ridolfi, L., I. Vannini, F. Fanini, L. Fiammenghi, M. Petrini, V. Ancarani, A. M. Granato, et al. "Use of microRNA signature to predict patient sensitivity to dendritic cell vaccination in metastatic melanoma." Journal of Clinical Oncology 29, no. 15_suppl (May 20, 2011): 8591. http://dx.doi.org/10.1200/jco.2011.29.15_suppl.8591.

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45

Stucci, Stefania, Marco Tucci, Paolo Ascierto, Anna Passarelli, Capone Mariaelena, Gabriele Madonna, Simeone Ester, Antonio Grimaldi, and Franco Silvestris. "Dendritic cell-derived exosomes (Dex) are potential biomarkers of response to Ipilimumab in metastatic melanoma." Journal of Translational Medicine 13, Suppl 1 (2015): P15. http://dx.doi.org/10.1186/1479-5876-13-s1-p15.

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46

Samoylenko, I. V., T. N. Zabotina, I. N. Mikhaylova, G. Z. Chkadua, O. V. Korotkova, K. Baryshnikov, and L. V. Demidov. "Chemotherpay and Dendritic Cell Vaccine in Patient with Metastatic Melanoma: Phase II Prospective Randomized Trial." Annals of Oncology 23 (September 2012): ix371. http://dx.doi.org/10.1016/s0923-7534(20)33693-0.

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47

Bol, K., E. Aarntzen, W. R. Gerritsen, G. Schreibelt, J. Jacobs, W. J. Lesterhuis, M. van Rossum, C. J. A. Punt, C. Figdor, and J. De Vries. "Skin-Test Infiltrating Lymphocytes Predict Clinical Outcome of Dendritic Cell Based Vaccination in Metastatic Melanoma." Annals of Oncology 23 (September 2012): ix363. http://dx.doi.org/10.1016/s0923-7534(20)33710-8.

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Meyer, Christiane, Laurene Cagnon, Nicole Montandon, Grégoire Berthod, Loredana Leyvraz, Olivier Michielin, Emanuela Romano, and Daniel E. Speiser. "Preferential enrichment of myeloid-derived suppressor cell subsets in patients with metastatic melanoma." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e19050-e19050. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e19050.

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e19050 Background: Myeloid derived suppressor cells (MDSC) are key immunosuppressive cells enriched in peripheral blood during chronic inflammation. While these cells have been extensively studied in mice, their human counterparts are less well characterized. Several MDSC populations have been identified in cancer patients, depending on tumor type and experimental settings. MDSC include immature macrophages, granulocytes and dendritic cells, at different degree of maturation, from immature CD33+, to mature CD14+ and CD15+HLA-DR- cells. The goal of this study was to characterize myeloid cells in melanoma patients compared with healthy donors (HD) to identify inflammation-mediated alterations involved in melanoma progression. Methods: PBMC were isolated by Lymphoprep gradient centrifugation from fresh blood samples of patients with malignant melanoma. We performed 9-color FACS staining of the freshly isolated cells. Results: CD15+ granulocytic MDSC are enriched in the mononuclear cell layer after gradient centrifugation, together with the CD14+ monocytic MDSCs. They display significantly different sedimentation abilities compared with neutrophils. Furthermore, CD14 and CD15 were partially co-expressed by the monocytic and granulocytic MDSC subsets, respectively. Our data show that CD14+HLA-DR- monocytic and CD15+HLA-DR- granulocytic MDSC were significantly enriched in peripheral blood of metastatic melanoma patients, regardless of whether or not they received any prior therapy for metastatic melanoma. The more immature CD33+CD11b- subset was found at significantly lower frequencies in melanoma patients compared with HD. We found a trend for accumulation of non-classical CD14+CD16+ monocytes. However, the increased percentages did not differ significantly from HD. The frequencies of classical CD14+CD16- monocytes were unchanged. Conclusions: Melanoma is associated with increased frequencies of CD14+ monocytic and CD15+ granulocytic MDSC, and decreased frequencies of the more immature CD33+CD11b- cells. This finding demonstrates tumor-mediated changes in the composition of myeloid cells, which could influence response to treatment and clinical behavior of the disease.

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Dillman, Robert O., Andrew N. Cornforth, Edward Francis McClay, and Carol DePriest. "Survival by stage and tumor measurability in metastatic melanoma patients treated with autologous dendritic cell tumor cell vaccines." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 2637. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2637.

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2637 Background: Survival of cancer patients is greatly affected by stage and tumor burden. The purpose of this study was to determine survival for melanoma patients who were treated with patient specific vaccines in the context of prospective clinical trials, by cohorts defined by stage and tumor measurability. Methods: Metastatic melanoma patients were treated with autologous dendritic cells loaded with antigens from irradiated cells from short-term autologous tumor cell lines (DCV). All patients had a metastatic melanoma lesion surgically resected, from which a tumor cell line was established. Irradiated tumor cells (ITC) were incubated with autologous dendritic cells (DC) to produce the DCV, which were injected s.c. in 500 micrograms GM-CSF weekly x 3 weeks, then monthly for 5 months. Data was pooled for DCV-treated patients enrolled in either of two phase II trials: one single-arm (NCT00948480), one randomized (NCT00436930). Patients were assigned to one of three cohorts based on their most advanced stage of disease prior to treatment, and whether they had measurable disease at the time of treatment. Survival was determined per Kaplan and Meier. Results: The final therapeutic products consisted of autologous DC with non-phagocytosed ITC making up 0% to 20% of cells in the final product. There were 45 men and 27 women. Median age was 52 years (range 17 to 83). Tumor sources were 37-lymph node, 20-viscera, and 15-soft tissue. No patients were lost to follow up; all surviving patients were followed 5 years. Toxicity was minimal. Median overall survival (OS) for all 72 patients was 49.4 mos; 5-year OS 46%. There was no correlation between survival and the number of DC or ITC in the first three injections. Patients with recurrent stage 3 disease that had not recurred (n=18) had a 72% 5-year OS; patients with non-measurable stage 4 (n=30) had a 53% 5-year OS. Patients with measurable stage 4 (n=18) had received an average of four prior therapies. They had a median OS of 18.5 months, and 2-year OS of 46%. Conclusions: This patient-specific DCV was associated with encouraging survival in all three clinical subsets. Because of its mechanism of action and absence of toxicity, it should be evaluated further. Clinical trial information: NCT00948480, NCT00436930.

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Meredith, Matthew M., Kang Liu, Guillaume Darrasse-Jeze, Alice O. Kamphorst, Heidi A. Schreiber, Pierre Guermonprez, Juliana Idoyaga, et al. "Expression of the zinc finger transcription factor zDC (Zbtb46, Btbd4) defines the classical dendritic cell lineage." Journal of Experimental Medicine 209, no. 6 (May 21, 2012): 1153–65. http://dx.doi.org/10.1084/jem.20112675.

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Classical dendritic cells (cDCs), monocytes, and plasmacytoid DCs (pDCs) arise from a common bone marrow precursor (macrophage and DC progenitors [MDPs]) and express many of the same surface markers, including CD11c. We describe a previously uncharacterized zinc finger transcription factor, zDC (Zbtb46, Btbd4), which is specifically expressed by cDCs and committed cDC precursors but not by monocytes, pDCs, or other immune cell populations. We inserted diphtheria toxin (DT) receptor (DTR) cDNA into the 3′ UTR of the zDC locus to serve as an indicator of zDC expression and as a means to specifically deplete cDCs. Mice bearing this knockin express DTR in cDCs but not other immune cell populations, and DT injection into zDC-DTR bone marrow chimeras results in cDC depletion. In contrast to previously characterized CD11c-DTR mice, non-cDCs, including pDCs, monocytes, macrophages, and NK cells, were spared after DT injection in zDC-DTR mice. We compared immune responses to Toxoplasma gondii and MO4 melanoma in DT-treated zDC- and CD11c-DTR mice and found that immunity was only partially impaired in zDC-DTR mice. Our results indicate that CD11c-expressing non-cDCs make significant contributions to initiating immunity to parasites and tumors.

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