Relevant bibliographies by topics / Melanoma – Immunotherapy

Academic literature on the topic 'Melanoma – Immunotherapy'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Melanoma – Immunotherapy"

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Rebegea, Laura, Dorel Firescu, Gabriela Stoleriu, Manuela Arbune, Rodica Anghel, Mihaela Dumitru, Raul Mihailov, Anca Iulia Neagu, and Xenia Bacinschi. "Radiotherapy and Immunotherapy, Combined Treatment for Unresectable Mucosal Melanoma with Vaginal Origin." Applied Sciences 12, no. 15 (August 1, 2022): 7734. http://dx.doi.org/10.3390/app12157734.

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Gynecologic melanomas are uncommon and malignant mucosal melanomas with vaginal origin are extremely rare, treatment strategies are limited and extrapolated from those of cutaneous melanoma. A better understanding of the vulvovaginal melanoma’s biology and its risk factors is needed. Therapeutic strategies include surgery, systemic therapy and radiotherapy. For vulvovaginal melanoma, surgery is selected as the primary treatment. Immunotherapy and target treatment have recently enhanced the systemic therapy for cutaneous melanoma (CM). Immunotherapy and new target agents demonstrated a better survival of melanoma and might be considered as treatment of vulvovaginal melanoma. Radiotherapy is included in the therapeutic arsenal for mucosal melanoma and may be performed on selected patients who may receive concurrent checkpoints and inhibition neoadjuvant radiotherapy with the purpose of reducing morbidity and mortality.
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Sanlorenzo, Martina, Igor Vujic, Christian Posch, Akshay Dajee, Adam Yen, Sarasa Kim, Michelle Ashworth, et al. "Melanoma immunotherapy." Cancer Biology & Therapy 15, no. 6 (March 20, 2014): 665–74. http://dx.doi.org/10.4161/cbt.28555.

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Garg, Abhishek D., Aleksandra M. Dudek-Peric, and Patrizia Agostinis. "Melanoma immunotherapy." Oncoscience 2, no. 10 (August 31, 2015): 845–46. http://dx.doi.org/10.18632/oncoscience.228.

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OʼDonnell-Tormey, Jill. "Melanoma Immunotherapy." Oncology Times 38, no. 8 (April 2016): 1. http://dx.doi.org/10.1097/01.cot.0000482915.84819.6e.

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Sivendran, Shanthi, Bradley Glodny, Michael Pan, Miriam Merad, and Yvonne Saenger. "Melanoma Immunotherapy." Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine 77, no. 6 (November 2010): 620–42. http://dx.doi.org/10.1002/msj.20215.

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Eggermont, Alexander M. M., Marka Crittenden, and Jennifer Wargo. "Combination Immunotherapy Development in Melanoma." American Society of Clinical Oncology Educational Book, no. 38 (May 2018): 197–207. http://dx.doi.org/10.1200/edbk_201131.

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Melanoma has been the most important cancer to drive immunotherapy development of solid tumors. Since 2010, immunotherapy has been revolutionized by the concept of breaking tolerance. It represents a major paradigm shift and marks the beginning of a new era. The impact of the first immune checkpoint inhibitors, anti–CTLA-4 and anti–PD-1/anti–PD-L1, is unprecedented. In 7 years, it transformed advanced-stage melanoma into a curable disease in over 50% of patients. Another major step has been the development of the combination of BRAF inhibitors plus MEK inhibitors in the treatment of BRAF-mutant melanomas. For the treatment of advanced disease, approvals were obtained for the immune checkpoint inhibitors ipilimumab (2011), nivolumab (2014), pembrolizumab (2014), the combination ipilimumab plus nivolumab (2015), and the oncolytic virus vaccine laherparepvec (2015). The combination dabrafenib plus trametinib for BRAF-mutant melanoma was approved in 2014, with similar success for other BRAF plus MEK inhibitor combinations. Because of its unique therapeutic index (high efficacy and low toxicity) anti–PD-1 agents (nivolumab and pembrolizumab) have now been placed at the center of practically all combination therapy development strategies in melanoma. Anti–PD-1 agents are the central molecule for combinations with a great variety of other immunotherapeutics such as immune checkpoint inhibitors, agonists, IDO inhibitors, macrophage polarizing agents, monoclonal antibodies, vaccines, targeted agents, chemotherapeutics, radiation therapy, and even microbiome modulators.
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Anko, Mayuka, Yusuke Kobayashi, Kouji Banno, and Daisuke Aoki. "Current Status and Prospects of Immunotherapy for Gynecologic Melanoma." Journal of Personalized Medicine 11, no. 5 (May 12, 2021): 403. http://dx.doi.org/10.3390/jpm11050403.

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Gynecologic melanomas are rare and have a poor prognosis. Although immunotherapy (immune checkpoint inhibitors) and targeted therapy has greatly improved the systemic treatment of cutaneous melanoma (CM) in recent years, its efficacy in gynecologic melanomas remains uncertain because of the rarity of this malignancy and its scarce literature. This review aimed to evaluate the literature of gynecologic melanomas treated with immunotherapy and targeted therapy through a PubMed search. We identified one study focusing on the overall survival of gynecologic melanomas separately and five case series and nine case reports concentrating on gynecologic melanomas treated with an immune checkpoint inhibitor and/or targeted therapy. Furthermore, the KIT mutation has the highest rate among all mutations in mucosal melanoma types. The KIT inhibitors (Tyrosine kinase inhibitors: TKIs) imatinib and nilotinib could be the treatment options. Moreover, immune checkpoint inhibitors combined with KIT inhibitors may potentially treat cases of resistance to immune checkpoint inhibitors. However, because of the different conditions and a small number of cases, it is difficult to evaluate the efficacy of immunotherapy and targeted therapy for gynecologic melanoma rigorously at this time. Further prospective cohort or randomized trials of gynecologic melanoma alone are needed to assess the treatment with solid evidence.
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Helgadottir, Hildur, Paola Ghiorzo, Remco van Doorn, Susana Puig, Max Levin, Richard Kefford, Martin Lauss, et al. "Efficacy of novel immunotherapy regimens in patients with metastatic melanoma with germline CDKN2A mutations." Journal of Medical Genetics 57, no. 5 (October 5, 2018): 316–21. http://dx.doi.org/10.1136/jmedgenet-2018-105610.

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BackgroundInherited CDKN2A mutation is a strong risk factor for cutaneous melanoma. Moreover, carriers have been found to have poor melanoma-specific survival. In this study, responses to novel immunotherapy agents in CDKN2A mutation carriers with metastatic melanoma were evaluated.MethodsCDKN2A mutation carriers that have developed metastatic melanoma and undergone immunotherapy treatments were identified among carriers enrolled in follow-up studies for familial melanoma. The carriers’ responses were compared with responses reported in phase III clinical trials for CTLA-4 and PD-1 inhibitors. From publicly available data sets, melanomas with somatic CDKN2A mutation were analysed for association with tumour mutational load.ResultsEleven of 19 carriers (58%) responded to the therapy, a significantly higher frequency than observed in clinical trials (p=0.03, binomial test against an expected rate of 37%). Further, 6 of the 19 carriers (32%) had complete response, a significantly higher frequency than observed in clinical trials (p=0.01, binomial test against an expected rate of 7%). In 118 melanomas with somatic CDKN2A mutations, significantly higher total numbers of mutations were observed compared with 761 melanomas without CDKN2A mutation (Wilcoxon test, p<0.001).ConclusionPatients with CDKN2A mutated melanoma may have improved immunotherapy responses due to increased tumour mutational load, resulting in more neoantigens and stronger antitumorous immune responses.
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Saraceni, Megan M., Nikhil I. Khushalani, and Anthony Jarkowski. "Immunotherapy in Melanoma." Journal of Pharmacy Practice 28, no. 2 (March 27, 2014): 193–203. http://dx.doi.org/10.1177/0897190014527317.

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The incidence and mortality of melanoma are on the rise. Historically, patients diagnosed with metastatic melanoma were faced with a grim prognosis, with survival rates of 15% at 5 years. Prior to 2011, no drug or therapeutic regimen had been shown to improve overall survival (OS) in metastatic melanoma. Chemotherapeutic agents, such as dacarbazine or temozolomide, are often given to patients for palliative purposes; high-dose interleukin 2 and biochemotherapy are immunotherapeutic options that could be offered to patients with a good performance status at specialized centers. Neither has been shown to impact OS, but durable complete responses are seen in a minority of patients. Since 2011, 4 new drugs have been approved by the US Food and Drug Administration for the treatment of metastatic melanoma, all of which improve survival. Three of these agents (vemurafenib, dabrafenib, and trametinib) are targeted therapies, with ipilimumab being the only new immunotherapy. With a focus on immunotherapeutic agents, this review seeks to summarize the treatment options currently available for metastatic melanoma and to examine those on the near horizon.
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Buchbinder, Elizabeth Iannotti, Jason L. Weirather, Michael P. Manos, Ryan C. Brennick, Patrick Alexander Ott, Rizwan Haq, Benjamin Izar, and F. Stephen Hodi. "Characterization of the genetics of mucosal melanoma in patients treated with immunotherapy." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 9556. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.9556.

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9556 Background: Mucosal melanomas can be effectively treated with checkpoint inhibitors, although the response rates are lower than those observed for melanomas arising in cutaneous sites. The mechanistic basis for the lower efficacy of immunotherapies in mucosal melanoma has been suggested to be related to their lower mutational burden. However, there has been limited characterization of the genetics in this melanoma subtype. Methods: Tumor genotyping was performed on all mucosal melanoma patients seen within the Dana Farber Cancer Institute from 2011 until the present by Oncopanel analysis. Results: We identified a total of 57 mucosal melanoma patients whose tumors had been genotyped. Of these 42 received immunotherapy and had response data available. Within the cohort of mucosal melanoma patients, 37.3% had durable clinical benefit (DCB) to their first line of IO therapy. These patients had an average mutational burden/megabase of 6.41 (95% CI 3.53-11.01) but tumor mutational burden did not correlate with response in this cohort. The pattern of mutations in mucosal melanomas was distinct from cutaneous melanomas, as the most frequent mutations were in SF3B1, ATRX, KIT and NF1 genes. Patients with KIT aberrations had a higher DCB rate compared patients with wildtype KIT (73 vs. 33%). In addition, there were several genetic differences observed based upon the site of origin of the mucosal melanoma. A higher rate of SF3B1 mutations was observed in patients with melanoma of anal/rectal origin while patients with vulvar/vaginal melanoma had higher rates of ATRX mutations, which frequently correlated with p53 ( TP53) mutations. Conclusions: This analysis is one of the first to look at genetic patterns in a large cohort of a relatively rare type of melanoma and correlate with response. Our findings confirm the low mutational burden observed in mucosal melanoma despite the high response rate observed in these patients. In addition, this study uncovered a higher rate of response to immunotherapy in mucosal melanoma patients with a KIT mutation.
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Dissertations / Theses on the topic "Melanoma – Immunotherapy"

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Woods, David Michael. "Histone Deacetylases as Targets for Melanoma Immunotherapy." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4856.

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Cancer represents the second leading cause of death in the United States. For many malignancies, currently available treatment options offer little long-lasting survival benefits to patients. However, recent studies have shown immunotherapeutic approaches to be an attractive strategy to cancer treatment. While many current immunotherapeutic strategies convey durable responses, such responses are only seen in a minority of patients. An increased understanding of the mechanisms governing tumor immunogenicity and the biology of immune responses is crucial to improving upon the efficacy of current and future cancer immunotherapies. Histone deacetylases (HDACs), enzymes classically associated with regulation of gene expression, have been therapeutic targets in various cancers for several years due to their involvement in cell growth. However, it has become increasingly clear that HDACs are intimately involved in regulating both the immunogenicity of tumor cells and immune response of leukocytes and lymphocytes. In order to expand upon this growing knowledge, the therapeutic efficacy of the pan-HDAC inhibitor LBH589 in the treatment of melanoma was studied. The results presented here demonstrate that LBH589 is a potent inhibitor of growth in a wide variety of melanomas through induction of cell cycle arrest and apoptosis. Additionally, LBH589 increases the immune visibility of melanoma cells by increasing expression of several immune associated cell surface markers (e.g. MHC I, MHC II, CD80, CD86) in addition to upregulating expression of melanoma differentiation antigens. Furthermore, LBH589 treatment of immune cells results in an enhanced pro-inflammatory phenotype of both APCs and T-cells. These combined effects result in better activation of T-cells and ultimately prolonged survival in LBH589 treated, melanoma-baring mice. To further the understanding of the role of individual HDACs in the T-cell response, the biology of the newest HDAC, HDAC11, was further assessed. To this end, it is shown that HDAC11 is differentially expressed in T-cell populations, and expression is rapidly decreased following activation. Utilizing an HDAC11 knockout (HDAC11KO) mouse strain, it is found that both CD4+ and CD8+ T-cells lacking HDAC11 have an enhanced type 1 effector function characterized by increased proliferation and secretion of IL-2, TNF and IFN-γ. Additionally, HDAC11KO CD8+ T-cells have increased expression of both granzyme B and perforin. HDAC11KO T-cells also demonstrate enhanced resistance to inhibition by Tregs and anergy formation. As a possible mechanism for the observed phenotype, it is also demonstrated that HDAC11KO T-cells produce elevated levels of the transcription factors Eomes and T-bet, both at the basal state and post-activation. In vivo, T-cells lacking HDAC11 have a more potent and robust ability to cause GvHD and mediate an enhanced anti-tumor response. Collectively, these results demonstrate that targeting of HDACs is a viable approach to cancer immunotherapy, and that targeting of specific HDACs may be an attractive strategy for optimizing immunotherapy efficacy while minimizing side effects.
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Barnard, Amanda Louise. "A murine model for immunotherapy of melanoma." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298460.

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Lo, Jennifer Alys. "Regulation of the Inflamed Tumor Phenotype in Melanoma Immunotherapy." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493467.

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Immune checkpoint inhibitors targeting cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) and programmed cell death-1 (PD-1) pathways can deliver durable anti-tumor effects. However, a major fraction of metastatic cancer patients fail to respond to checkpoint blockade. Recent studies suggest that efficacy of checkpoint inhibitors is associated with inflammation in the tumor microenvironment. In this thesis, I demonstrate using genetically-defined murine models that sterile melanomas can be converted into inflamed tumors with improved responses to checkpoint blockade via two independent approaches: introduction of neoantigens and a novel combinatorial therapeutic strategy. In addition to tumor inflammation, genomic studies have identified elevated numbers of neoantigens, mutated proteins that can serve as targets of immune responses, as potential predictors of clinical benefit. The preponderance of UVR-associated somatic mutations in melanoma has been proposed to play a role in mediating responses to immunotherapy, but model systems to study the contribution of such mutations to anti-melanoma immunity have been lacking. In chapter 2, I present a BrafV600E/Pten-/- syngeneic tumor graft murine model in which melanomas bearing numerous non-synonymous UVB-induced mutations were markedly more inflamed and responsive to PD-1 inhibition than matched parental melanomas. For the treatment of neoantigen-deficient, poorly-inflamed tumors, in chapter 3 I tested the novel combination of imiquimod, ablative fractional photothermolysis (aFP), and checkpoint inhibitors. In anti-PD-1 resistant models of melanoma and pancreatic adenocarcinoma, addition of imiquimod and aFP produced abscopal tumor regressions with long-term survival in 50-60% of cases. Combination therapy stimulated autoimmunity against wildtype tumor-lineage antigens, suggesting that therapeutic strategies which enhance inflammation and responses against self-antigens may bypass a need for neoantigens and produce major regressions of cancers that are currently refractory to checkpoint blockade in the clinic. In chapter 4 I show that PD-L1 expression is transcriptionally regulated by the melanocyte lineage factor and oncogene microphthalmia-associated transcription factor (MITF). PD-L1 expression is significantly correlated with MITF copy number in patient melanomas and is induced in skin as part of the MITF-dependent tanning response pathway. Our data suggest that loss of PD-L1 predisposes mice to apparent vitiligo after chronic UVR, suggesting that the UVR-MITF-PD-L1 axis represents a melanocyte lineage-specific mechanism of immune tolerance.
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Thomas, Myles Duncan. "Production and characterisation of novel human monoclonal antibodies against malignant melanoma." Thesis, University of East London, 1995. http://roar.uel.ac.uk/1275/.

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Malignant melanoma is an immunogenic tumour capable of inducing a humoral immune response, as shown by tumour-reactive serum antibody in patients. Lack of effective chemotherapy in association with the immunogenic nature of the malignancy, has stimulated interest in the immunological management of the malignancy by antibody. Many mouse monoclonal antibodies against melanoma antigens have been developed, and some have been shown to induce tumour regression. However, a limitation on the use of mouse monoclonal antibodies in patients is the induction of an immune response against the immunising xenogeneic protein. The employment of human monoclonal antibodies, may be expected to reduce the patient's immune response against the allogeneic protein. Although more difficult to produce than mouse monoclonal antibodies, several human monoclonal antibodies have been established which induce tumour regression. Here I describe the establishment of mouse/human heterohybridomas producing human monoclonal antibody, from tumour-draining lymph nodes. A series of novel assay systems, initially developed and characterised using melanoma reactive mouse monoclonal antibodies, were sequentially employed for the selection of human antibody exhibiting high tumour specificity. Several clones producing melanoma reactive human antibody were established. Clone MDT. 1 was selected for further characterisation, because of its highly selective reactivity against viable melanoma and other neuroectodermal cell lines, but lack of reactivity against other common malignant and non-malignant cell lines. Such restricted cell reactivity is characteristic of reactivity with class 2 tumour associated antigens. MDT. 1 was shown, in ELISA, to exhibit reactivity to ganglioside antigens GD3, GD2, GD1b, GM3 and GM2. These antigens are commonly associatedw ith the malignant transformation of melanocytes and other neuroectodermal cells. Enzymatic modification of GM3, with neuraminidase, identified the reactive minimal essential epitope as Neua2- 3Galß1-4GIc-. Reactivity with rat monoclonal antibody 9G4 and molecular analysis showed MDT. 1 is encoded by the highly conserved VH4 gene, VH4-21. Like other VH4-21 encoded autoantibodies MDT. 1 exhibits reactivity with the cold agglutinin T. Analysis of the structures of `i' and sialogangliosides has identified similar structural epitopes, which may confer MDT. 1 reactivity. VH4-21 encoded autoantibody 216 exhibits similar reactivity with tumour associated ganglioside antigens as MDT. 1. Sialo-ganglioside/`i' reactive VH4-21 encoded antibodies, could therefore represent an important aspect of autoantibodies in the overall host immune response to tumour.
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Sodre, De Castro Laino Andressa. "Targeting Histone Deacetylases in Melanoma and T-cells to Improve Cancer Immunotherapy." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6144.

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Histone deacetylases (HDACs) are key mediators of gene expression and, thus, major regulators of cell function. As such, HDACs play a role in orchestrating tumor biology, and the use of small inhibitors targeting theses proteins is attractive for the field of cancer therapy. Indeed, several HDAC inhibitors have received FDA-approval for the treatment of malignancies, while a myriad of these compounds continue to be evaluated in clinical trials. Besides their direct impact on tumor growth, HDAC inhibitors have been shown to increase immunogenicity of cancer cells, facilitating generation of a productive immune response against tumors. Immunotherapeutic approaches take advantage of the intrinsic ability of the immune system to manifest an anti-tumor response. Mechanisms of immune escape are often developed by cancer cells, neutralizing activity of the immune system. For example, upregulation of the PD1 ligands PDL1 and PDL2 by tumor cells negatively regulates the anti-tumor functions of PD1-expressing infiltrating T-cells. Importantly, strategies targeting this inhibitory axis have shown outstanding clinical benefit for the treatment of solid and hematological malignancies. The mechanisms by which HDAC inhibitors modulate tumor and immune cells biology were explored herein. Initially, treatment of melanoma cells with pan- and class I-selective HDAC inhibitors resulted in upregulation of PDL1 and PDL2 molecules. These effects were observed in mouse and human cell lines, as well as in tumor cells resected from metastatic melanoma patients. This upregulation was robust and sustained, lasting at least 96 hours in vitro, and validated in vivo using a B16F10 syngeneic mouse model. Enhanced expression of PDL1 mediated by HDAC inhibitors was found to result from enhanced histone acetylation at the PDL1 gene promoter region. Combination therapy of HDAC inhibition and PD1 blockade was explored in the tumor setting, leading to synergistic effects in terms of reducing melanoma progression and increasing survival of B16F10 melanoma-bearing mice. These data provide a clinical rationale for combination therapy of epigenetic modifiers (e.g. HDAC inhibitors) and PD1 blockade as means to augment cancer immunotherapy, improving patient outcomes. As a second pillar of this research, the impacts of HDAC-selective inhibition were explored on immune cell biology, since the broad nature of pan-HDAC inhibitors was shown to be detrimental to T-cells in vitro and in vivo. Based on screening assay results, novel implications of treating melanoma patient T-cells ex vivo with the HDAC6-selective inhibitor ACY1215 were investigated. Treatment with this compound was unique among pan- and isotype-selective HDAC inhibitors in modulating T-cell cytokine production and showing minimal impact of T-cell viability. ACY1215 tempered Th2 cytokine production (i.e. IL-4, IL-6 and IL-10), and maintained Th1 effector cytokines (e.g. IFNγ and IL-2). Furthermore, ACY1215 increased expression of surface markers, including CD69 activation marker and ICOS co-stimulatory molecule. In addition, ACY1215 treatment enhanced accumulation of central memory T-cells during ex vivo expansion of tumor infiltrating T-cells harvested from resected tumors of metastatic melanoma patients. Importantly, ACY1215-mediated inhibition improved tumor-killing capacity of T-cells. These results highlight an unexplored ability of selective HDAC inhibitor ACY1215 to augment T-cell expansion during protocols of adoptive cell therapy. While the discoveries presented here warrant further investigation of cellular and molecular mechanisms associated with ACY1215-treated T-cells, the clinic implications are clear and rapidly translatable.
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Shridhar, Naveen [Verfasser]. "Novel vaccination strategies for CD4+ T cell immunotherapy of melanoma / Naveen Shridhar." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/119893378X/34.

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Karagiannis, Panagiotis. "Dissecting humoral immune responses in melanoma and the design of antibody immunotherapy." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/dissecting-humoral-immune-responses-in-melanoma-and-the-design-of-antibody-immunotherapy(1b263e41-dedd-4d98-a045-97bfd6fa6f0b).html.

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Antibodies against melanoma antigens have been detected in patients but, despite known regulatory and activatory functions attributed to humoral immunity, the roles of B cells in solid tumours such as melanoma are inadequately understood. Insights into humoral responses and mechanisms of tumour-induced immune escape may in-form the design of more effective antibodies. The aims of this thesis are three-fold: a) to gain insights into regulatory mechanisms in tumour microenvironments that influence antibody expression; b) to examine whether humoral immune responses are associated with clinical outcomes with a view of defining biomarkers for melanoma; and c) to design antibody therapeutic strategies that may be less prone to tumour-induced immunomodulatory mechanisms. Th2-biased microenvironments favour production of IgG4 subclass antibodies, mainly through local expression of IL-10. Since IL-10 is expressed locally in melanoma tu-mours, B cell infiltration, IgG expression, cytokine production and IgG subclass distribution in melanoma tissues (n=57) were investigated and compared to samples from health volunteers (n=26). Consistent with Th2-biased inflammation, CD22+ and IgG4+ B cells infiltrated melanoma lesions. When cultured together ex vivo, B cells secreted increased VEGF and IgG4, while tumour cells enhanced IL-10 secre-tion. Two antibodies (IgG1, IgG4) against the tumour-associated antigen CSPG4 were engineered to examine the functional significance of IgG4 subclass. Despite ac-cumulation in tumours, anti-CSPG4 IgG4, in contrast to anti-CSPG4 IgG1, did not trigger effector cells to kill tumours in vitro and in vivo. IgG4 mediated IgG1 block-ade through the reduction of FcγRI activatory signalling, reducing immune effector cell capacity, and significantly impairing the potency of IgG1 in a humanised mouse model of cutaneous melanoma. Since IgG4 may impair anti-tumoural immunity, correlations between IgG4 serum levels and clinical outcomes were studied. Increased IgG4/IgGtotal ratios (G4-levels) in melanoma patient sera (n=173) were seen compared to those of healthy volun-teers (n=104). G4-levels were predictive of disease progression (ROC Curve analysis z=0.62; p=0.0065). Using 0.034 as a cut-off for G4-levels (Youden Index) higher ex-pression correlated with decreased progression-free survival (median 694 days; hazard ratio 2.559; 95% CI 1.555 to 4.211; p=0.0004) and overall survival (median 879 days; hazard ratio 1.871; 95% CI 1.0.45 to 3.349; P=0.035). These findings suggest that IgG4 may be further evaluated as a putative biomarker in sera of patients with melanoma. Tumour immune evasion may be overcome by employing antibodies less prone to Fcγ-mediated blockade, such as those of the IgE class. Two antibodies, anti-CSPG4 IgG1 and anti-CSPG4 IgE induced significant tumor cell death by differential mecha-nisms: antibody-dependent cell-mediated phagocytosis and antibody-dependent cell-mediated cytotoxicity, respectively, by human monocytes in vitro. Anti-CSPG4 IgE was however superior to IgG1 (p < 0.05) in restricting subcutaneous human melanoma tumour growth in a humanized mouse model. IgE efficacy was confirmed in an or-thotropic patient tumour in mice populated with autologous patient PBMCs. In summary, this thesis reports a novel pathway of tumour evasion through melanoma favouring production of IgG4 subclass antibodies; provides evidence that IgG4 can be considered as a putative biomarker in melanoma and demonstrates a possible strategy to overcome Fcγ-mediated blockade by designing an IgE antibody against a melanoma-associated antigen and demonstrating its superiority to IgG1.
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Riding, Rebecca L. "The Role of Type I Interferon in Vitiligo Pathogenesis and Melanoma Immunotherapy." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1065.

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Vitiligo is an autoimmune skin disease in which the pigment producing cells of the epidermis, melanocytes, are targeted for destruction by CD8+ T cells specific for melanocyte/melanoma-shared antigens. Previous work has identified IFNg as the central cytokine driving disease pathogenesis in both human patients and in our mouse model of vitiligo. IFNg signaling induces production of the chemokines CXCL9 and CXCL10, which trigger autoreactive T cell migration into the epidermis where effector T cells can target and destroy melanocytes. However, both IFNg and type I IFN signaling through activation of STAT1 proteins can induce transcription of the chemokines CXCL9 and CXCL10. Therefore, it seems reasonable that type I IFN signaling may also contribute to disease pathogenesis. The role of type I IFN in vitiligo is still unclear. Genome wide association studies identified multiple genes within the type I IFN pathway including TICAM1 and IFIH1 as susceptibility loci in vitiligo. One additional study reported increased epidermal staining of CD123, a marker expressed by pDCs, and the type I IFN induced gene MX1 in vitiligo patient skin. However, this study did not show any functional data to support the role of type I IFN signaling in vitiligo pathogenesis. Since the role of type I IFN in vitiligo is ill-defined, we used two different mouse models of vitiligo to functionally determine the role of type I IFN in disease by inducing vitiligo in hosts which lack the type I IFN receptor (IFNaR). In the first model, we induced vitiligo by adoptive transfer of melanocyte-specific CD8 T cells, which are activated in vivo by infection with recombinant vaccinia virus (VACV) expressing their cognate antigen. Vitiligo induction in IFNaR-deficient mice led to the development of severe disease compared to wild type mice. Acceleration and severity of disease was characterized by increased early recruitment of melanocyte-specific CD8 T cells to the skin, increased production of effector cytokines TNFa and IFNg, and reduced PD-1 expression. Increased production of IFNg by CD8 T cells in the skin of IFNaR-deficient mice led to increased expression of the chemokines CXCL9 and CXCL10 driving disease progression. IFNaR-deficient mice also displayed significantly increased VACV titters compared to wild type hosts. This data reveals a role of type I IFN in the clearance of recombinant VACV. This data also suggests that persistent VACV infection and prolonged antigen exposure in IFNaR deficient hosts is likely driving enhanced activation of melanocyte specific CD8 T cells and the subsequent development of severe vitiligo. Since melanocytes and melanoma cells express shared antigens that can be recognized by CD8 T cells, and because the development of vitiligo after melanoma immunotherapy is a positive prognostic factor for patients, we asked whether VACV vaccine therapy in IFNaR deficient mice would enhance the anti-tumor response to melanoma. B16-F10 inoculated wild type and IFNaR-deficient mice received adoptive transfer of melanocyte-specific CD8 T cells in combination with vaccinia virus expressing their cognate antigen to activate the cells in vivo. Treatment of adoptive T cell transfer and infection with VACV in IFNaR-deficient mice revealed significantly reduced tumor burden compared to wild type mice. Improved tumor regression in IFNaR-deficient hosts was characterized by increased infiltrating cytotoxic T lymphocytes and reduced PD-1 expression. These results further demonstrate that in the absence of type I IFN, hosts mount a robust cytotoxic CD8 T cell response against melanocyte/melanoma antigens and this is likely a result of persistent VACV that leads to prolonged CD8 T cell priming. As a result, IFNaR deficient hosts kill tumor cells more efficiently. To determine whether type I IFN regulates disease pathogenesis in the absence of virus infection, we generated a model of vitiligo in which bone marrow derived dendritic cells (BMDCs) pulsed with the cognate antigen were used to prime melanocyte-specific T cells in place of the viral vector. Induction of vitiligo in IFNaR-deficient hosts using BMDCs revealed no significant differences in disease score compared to wild type hosts. This data clearly demonstrates that type I IFN, in contrast to IFNg, is not required during the effector stage of vitiligo pathogenesis in mice. However, since we intentionally activate transferred melanocyte-specific CD8 T cells with VACV or BMDCs expressing their cognate antigen, our mouse models may circumvent the role of type I IFNs in initiating activation of autoreactive cells and driving autoimmunity. Type I IFN is critical for providing innate immune signals that drive the priming of autoreactive T cells through maturation of DCs by inducing antigen presentation, co-stimulatory molecule expression, and migration to the lymph nodes to encounter naïve T cells. Our mouse models of vitiligo may not capture this process. We have addressed this question by using a TLR ligand to activate BMDCs before transfer into hosts. In fact, activation of BMDCs before transfer leads to significantly enhanced vitiligo in mice and this is partially a result of type I IFN signaling on host cells. Thus, we provide evidence that type I IFNs can enhance the activation of melanocyte-specific CD8 T cells and drive autoimmunity. Collectively, our results show that type I IFN signaling has disparate effects on autoreactive T cell priming in a context dependent manner. We reveal that although type I IFN is not required for the effector phase of vitiligo in mice, maturation of DCs and subsequent type I IFN production can enhance the priming of autoreactive T cells and enhance vitiligo severity. Our studies also reveal that type I IFN is required to clear recombinant attenuated VACV infection and vaccine administration in IFNaR deficient hosts led to a robust autoreactive and anti-tumor response. These insights describing the role of type I IFN in autoimmunity and tumor immunology could have important implications for T cell dependent tumor immunotherapy.
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Engel, Christina [Verfasser]. "The influence of hypoxia on RIG-I-mediated melanoma immunotherapy / Christina Engel." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1122193920/34.

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Guan, Xiangnan. "The Effects of Stromal and T cell Senescence on Melanoma." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1528720866526502.

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Books on the topic "Melanoma – Immunotherapy"

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Rotte, Anand, and Madhuri Bhandaru. Immunotherapy of Melanoma. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48066-4.

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Wolf, John E. Malignant melanoma: Clinical immunology, immunodiagnosis and immunotherapy. Bethesda, MD (Bldg. 82, Rm. 103, Bethesda 20892): U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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Rotte, Anand, and Madhuri Bhandaru. Immunotherapy of Melanoma. Springer, 2018.

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Rotte, Anand, and Madhuri Bhandaru. Immunotherapy of Melanoma. Springer International Publishing AG, 2017.

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Rotte, Anand, and Madhuri Bhandaru. Immunotherapy of Melanoma. Springer, 2017.

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Immunotherapy of malignant melanoma. Austin, Tex: R.G. Landes Co., 1996.

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Malignant melanoma: Clinical immunology, immunodiagnosis and immunotherapy. Bethesda, MD (Bldg. 82, Rm. 103, Bethesda 20892): U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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Michele, Maio, ed. Immunology of human melanoma: Tumor-host interaction and immunotherapy. Armsterdam: IOS Press, 1996.

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Melanoma Emerging Cancer Therapeutics. Demos Medical Publishing, 2012.

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Guida, Michele, Paola Queirolo, and Pietro Quaglino, eds. The Evolving Role of Immunotherapy in Non-Melanoma Skin Cancers. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-326-9.

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Book chapters on the topic "Melanoma – Immunotherapy"

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Block, Matthew S. "Melanoma Immunotherapy." In The Basics of Cancer Immunotherapy, 39–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70622-1_3.

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Daniels, Gregory A. "Melanoma Immunotherapy." In Early Phase Cancer Immunotherapy, 307–31. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-63757-0_11.

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Loo, Kimberly, Clinton Wu, and Adil Daud. "Current Immunotherapy of Melanoma." In Melanoma, 567–76. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78310-9_35.

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Sullivan, Ryan J., and F. Stephen Hodi. "Melanoma Immunology and Immunotherapy." In Melanoma, 651–65. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-7147-9_36.

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Sullivan, Ryan J., and F. Stephen Hodi. "Melanoma Immunology and Immunotherapy." In Melanoma, 1–15. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-7322-0_36-2.

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Rotte, Anand, and Madhuri Bhandaru. "Melanoma—Treatment." In Immunotherapy of Melanoma, 79–109. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48066-4_4.

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Bystryn, J. C. "Vaccine Immunotherapy of Melanoma." In Human Melanoma, 513–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74496-9_35.

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Trinh, Van A., Yeorim Ahn, and Wen-Jen Hwu. "Immunotherapy in Melanoma." In Genetics of Melanoma, 207–36. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3554-3_10.

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Rotte, Anand, and Madhuri Bhandaru. "Challenges of Immunotherapy." In Immunotherapy of Melanoma, 419–34. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48066-4_16.

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Albittar, Aya A., Omar Alhalabi, and Isabella C. Glitza Oliva. "Immunotherapy for Melanoma." In Advances in Experimental Medicine and Biology, 51–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41008-7_3.

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Conference papers on the topic "Melanoma – Immunotherapy"

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Kandolf Sekulović, Lidija. "TOXICITIES OF TARGETED THERAPY AND IMMUNE-RELATED ADVERSE DRUG REACTIONS OF IMMUNOTHERAPY IN THE TREATMENT OF METASTATIC MELANOMA." In Okrugli sto s međunarodnim učešćem "Melanom". Akademija nauka i umjetnosti Bosne i Hercegovine, 2018. http://dx.doi.org/10.5644/pi2019.180.04.

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Targeted therapy and immunotherapy changed the treatment landscape for metastatic melanoma, which is chemotherapy resistant cancer. In pre-innovation era, the overall survival of patients with metastatic melanoma was 6 months, while today 5-year overall survival rate of 34% (and 50% in good prognostic groups) is evident. However, both treatments have their side effects, and cutaneous are the most frequent. Treating physicians in oncology centres, but also primary care specialists, need to be aware of their spectrum which differs for each class of drug: BRAF inhibitors, MEK inhibitors and immunotherapy with anti-PD1 and anti-CTLA4. While BRAF inhibitors have the most prominent adverse effects which are class specific, there are also drug-specific adverse effects. For example, vemurafenib causes photosensitivity, which is not specific for dabrafenib, while dabrafenib induces pyrexia, that occurs much less frequently with other BRAF inhibitors. Cutaneous rash and cutaneous neoplasms which develop due to paradoxical activation of RAS signalling are described with BRAF inhibitor monotherapy. These side-effects are much less common in combination therapy with BRAF and MEK inhibitor, but MEK inhibitor itself causes characteristic acneiform eruption, and serous retinopathy. Immune related adverse drug reactions are a hallmark of the immune checkpoint inhibitor immunotherapy, which can affect every organ system, and most commonly skin, lungs and gastrointestinal system, with differential frequencies recorded with anti-CTLA4 therapy and anti PD-1 therapy. Skin reactions most frequently include pruritus and eczematous reactions, as well as vitiligo-like hypopigmentation, which is linked Melanom 45 to the better response to treatment. In this review, frequent and rare side effects are presented, as well as the current algorithms for their treatment.
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Wolchok, Jedd D. "Abstract IA27: Combination immunotherapy for melanoma." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-ia27.

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Sachett, Mariana Linhares, GIANCARLLO DANEZI FELIN, GIULLIANO DANEZI FELIN, CAROLLINA DANEZI FELIN, and FELLIPE DANEZI FELIN. "GENÉTICA MOLECULAR DO MELANOMA MALÍGNO: UM ALVO TERAPÊUTICO." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/9012.

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Introdução: O melanoma maligno corresponde a 4% das neoplasias malignas da pele e é responsável por 90% dos óbitos por câncer nesse sítio primário. A alta mortalidade torna seu estudo altamente relevante. Até por volta de 2011, as estratégias antineoplásicas disponíveis para o melanoma avançado eram limitadas. Objetivos: Elucidar a importância da genética molecular na escolha do tratamento antineoplásico do melanoma maligno. Metodologia: Revisão de literatura através de pesquisa de artigos realizada na base de dados MEDLINE, via PubMed, utilizando-se os seguintes termos DeCS/ MeHS: "melanoma" [AND] “molecular targeted therapy" [AND] "immunotherapy”. Ao usar os filtros “textos completos” e “1 ano” foram encontrados 36 resultados. Após aplicados os critérios de inclusão (texto completo, 1 ano e adequação a temática proposta) e de exclusão (todos que não atendessem aos critérios de inclusão e artigos duplicados), foram selecionados 9 artigos para compor essa revisão. Realizada a extração dos dados e análise para redação da revisão. Resultados: Aproximadamente 50% dos melanomas malignos exibem mutação BRAF, enquanto que 20% apresentam mutação NRAS e mais raramente, mutação cKit. A identificação do tipo de mutação associada ao melanoma é de extremo valor, pois é capaz de direcionar para uma forma distinta de terapia alvo molecular (TAM) e ou imunoterapia (IMT), em especial nos casos avançados. Melanomas metastáticos com mutação BRAF tem indicação terapêutica do uso de TAM combinada com utilização de inibidores BRAF e inibidores MEK, devendo ainda ser associada a IMT através dos inibidores do checkpoint imunológico (anti-PD-1 e anti-CTLA-4). Conclusão: Através dessa revisão de literatura foi possível identificar que as bases genéticas e moleculares que compõem o genótipo maligno do melanoma, determinam novas promissoras terapias adjuvantes, o que inclui a TAM e a IMT para casos avançados. Portanto, foi possível elucidar a importância da genética molecular do melanoma para o seu tratamento oncológico adequado. Adicionalmente, foi possível reconhecer que a TAM e a IMT são indicações limitadas ao melanoma metastático com mutação BRAF detectada, permanecendo as incertezas em relação aos casos que não são avançados e que exibem mutações detectadas.
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Hersey, Peter, Stuart Gallagher, Jessamy Tiffen, Elena Shklovskaya, Stephen Wilson, and Fabian Filipp. "Abstract 1676: EZH2 inhibitors in immunotherapy of melanoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1676.

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Wolchok, Jedd D. "Abstract IA22: Immunotherapy for melanoma: Checkpoint blockade combinations." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-ia22.

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Jaiswal, Ashvin R., Shivanand Pudakalakatti, Prasanta Dutta, Arthur Liu, Todd Bartkowiak, Casey Ager, Cristina Ivan, et al. "Abstract PR08: Metabolic adaptations establish immunotherapy resistance in melanoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-pr08.

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Hodi, F. Stephen, Jedd D. Wolchok, Dirk Schadendorf, James Larkin, Max Qian, Abdel Saci, Tina C. Young, et al. "Abstract CT037: Genomic analyses and immunotherapy in advanced melanoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-ct037.

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Jaiswal, Ashvin R., Shivanand Pudakalakatti, Dutta Prasanta, Arthur Liu, Todd Bartkowiak, Casey Ager, Michael A. Davies, et al. "Abstract 1700: Metabolic adaptations confer immunotherapy resistance in melanoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1700.

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Hodi, F. Stephen, Jedd D. Wolchok, Dirk Schadendorf, James Larkin, Max Qian, Abdel Saci, Tina C. Young, et al. "Abstract CT037: Genomic analyses and immunotherapy in advanced melanoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-ct037.

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Andtbacka, Robert H., Darren R. Shafren, Mark Grose, Len Post, and Jeffrey Weisberg. "Abstract 2939: CAVATAK-mediated oncolytic immunotherapy in advanced melanoma patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2939.

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Reports on the topic "Melanoma – Immunotherapy"

1

Biggs, M. W., and J. E. Eiselein. Immunotherapy of metastatic melanoma by reversal of immune suppression. Office of Scientific and Technical Information (OSTI), January 1997. http://dx.doi.org/10.2172/454026.

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Callahan, Margaret, and Taha Merghoub. Evaluation of the Immunologic Impact of RAF Inhibitors to Guide Optimal Combination of RAF Inhibitors and Immunotherapy for the Treatment of Advanced Melanoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada612829.

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Callahan, Margaret, and Taha Merghoub. Evaluation of the Immunologic Impact of RAF Inhibitors to Guide Optimal Combination of RAF Inhibitors and Immunotherapy for the Treatment of Advanced Melanoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada621079.

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