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Journal articles on the topic 'Melanoma, BRAF, target therapy, melanoma acrale'

Author: Grafiati

Published: 9 March 2023

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1

Gams, Polona, Zvezdana Dolenc Stražar, Maja Šoštarič, Matic Bošnjak, and Juš Kšela. "Cardiac Melanoma Metastasis with ERBB2 Gene Amplification: A Potential for Future Targeted Therapy." Case Reports in Oncology 14, no. 1 (2021): 622–27. http://dx.doi.org/10.1159/000514981.

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Cardiac tumors are rare, and their treatment differs interindividually regarding the histopathological proprieties and the stage of disease. Authors present a case of symptomatic cardiac melanoma metastasis that expressed an <i>ERBB2</i> (<i>HER2</i>) gene amplification in a course of the disease that has not yet been reported. The frail patient with a history of pulmonary and renal carcinoma, was admitted to the hospital due to a symptomatic left atrial tumor mass. The patient underwent a tumor-resecting cardiac surgery. At first mistaken for myxoma on echocardiography

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Tsai, Katy K., Iwei Yeh, Adil Daud, and Ari Oglesby. "Phase II study of binimetinib with imatinib in patients with unresectable KIT-mutant melanoma." Journal of Clinical Oncology 39, no. 15_suppl (2021): TPS9594. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.tps9594.

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TPS9594 Background: Immune checkpoint inhibitors (ICI) have transformed treatment for patients (pts) with advanced melanoma, as have BRAF/MEK inhibitors for pts with BRAF V600-mutant melanoma. However, pts with acral or mucosal melanomas are in particular need of more options given a lower objective response rate (ORR) to ICI, and lower incidence of BRAF V600 driver mutation. Such BRAF mutations are found in only 5-10% of acral/mucosal melanomas, while KIT mutations/amplifications are found in 10-20%. Even when present, a KIT alteration does not guarantee response to KIT inhibition, with only

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Yeh, Iwei, Eric Jorgenson, Ling Shen, et al. "Targeted Genomic Profiling of Acral Melanoma." JNCI: Journal of the National Cancer Institute 111, no. 10 (2019): 1068–77. http://dx.doi.org/10.1093/jnci/djz005.

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Abstract Background Acral melanoma is a rare type of melanoma that affects world populations irrespective of skin color and has worse survival than other cutaneous melanomas. It has relatively few single nucleotide mutations without the UV signature of cutaneous melanomas, but instead has a genetic landscape characterized by structural rearrangements and amplifications. BRAF mutations are less common than in other cutaneous melanomas, and knowledge about alternative therapeutic targets is incomplete. Methods To identify alternative therapeutic targets, we performed targeted deep-sequencing on

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Teixido, Cristina, Paola Castillo, Clara Martinez-Vila, Ana Arance, and Llucia Alos. "Molecular Markers and Targets in Melanoma." Cells 10, no. 9 (2021): 2320. http://dx.doi.org/10.3390/cells10092320.

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Melanoma develops as a result of several genetic alterations, with UV radiation often acting as a mutagenic risk factor. Deep knowledge of the molecular signaling pathways of different types of melanoma allows better characterization and provides tools for the development of therapies based on the intervention of signals promoted by these cascades. The latest World Health Organization classification acknowledged the specific genetic drivers leading to melanoma and classifies melanocytic lesions into nine distinct categories according to the associate cumulative sun damage (CSD), which correlat

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Rodrigues, Ana Sofia, and Ana Brinca. "Treatment of BRAF-Mutated Metastatic Melanoma: Immunotherapy or Target Therapy?" Journal of the Portuguese Society of Dermatology and Venereology 79, no. 2 (2021): 103–11. http://dx.doi.org/10.29021/spdv.79.2.1342.

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Metastatic melanoma has been associated with a poor prognosis, with overall survival rates at 5 years of 10%. Until 2011, the only treatments available for metastatic melanoma were chemotherapy and immunotherapy with interleukin-2. The more in-depth knowledge about the molecular biology of melanoma and the identification of BRAF mutations, which are the most frequently found, allowed us to find new therapeutic targets that came to modify the prognosis of these patients. Currently, the treatments available for metastatic melanoma with BRAF mutation are immunotherapy with immunological checkpoin

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Jebali, Ahlem, Maxime Battistella, Céleste Lebbé, and Nicolas Dumaz. "RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy." Biomedicines 9, no. 10 (2021): 1498. http://dx.doi.org/10.3390/biomedicines9101498.

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The network defined by phosphatidylinositol-3-kinase (PI3K), AKT, and mammalian target of rapamycin (mTOR) plays a major role in melanoma oncogenesis and has been implicated in BRAF inhibitor resistance. The central role of RICTOR (rapamycin-insensitive companion of mTOR) in this pathway has only recently begun to be unraveled. In the present study, we assessed the role of mTORC2/RICTOR in BRAF-mutated melanomas and their resistance to BRAF inhibition. We showed that RICTOR was significantly overexpressed in melanoma and associated with bad prognoses. RICTOR overexpression stimulated melanoma-

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Fattore, Luigi, Rita Mancini, Mario Acunzo, et al. "miR-579-3p controls melanoma progression and resistance to target therapy." Proceedings of the National Academy of Sciences 113, no. 34 (2016): E5005—E5013. http://dx.doi.org/10.1073/pnas.1607753113.

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Therapy of melanoma patients harboring activating mutations in the BRAF (V-raf murine sarcoma viral oncogene homolog B1) oncogene with a combination of BRAF and MEK inhibitors is plagued by the development of drug resistance. Mutational events, as well as adaptive mechanisms, contribute to the development of drug resistance. In this context we uncover here the role of a miRNA, miR-579-3p. We first show that low expression of miR-579-3p is a negative prognostic factor correlating with poor survival. Expression levels of miR-579-3p decrease from nevi to stage III/IV melanoma samples and even fur

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Pizzimenti, Stefania, Simone Ribero, Marie Angele Cucci, et al. "Oxidative Stress-Related Mechanisms in Melanoma and in the Acquired Resistance to Targeted Therapies." Antioxidants 10, no. 12 (2021): 1942. http://dx.doi.org/10.3390/antiox10121942.

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Melanoma is a highly aggressive cancer with the poorest prognosis, representing the deadliest form of skin cancer. Activating mutations in BRAF are the most frequent genetic alterations, present in approximately 50% of all melanoma cases. The use of specific inhibitors towards mutant BRAF variants and MEK, a downstream signaling target of BRAF in the MAPK pathway, has significantly improved progression-free and overall survival in advanced melanoma patients carrying BRAF mutations. Nevertheless, despite these improvements, resistance still develops within the first year of therapy in around 50

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Rossi, Ernesto, Giovanni Schinzari, Francesco Cellini, et al. "Dabrafenib-Trametinib and Radiotherapy for Oligoprogressive BRAF Mutant Advanced Melanoma." Biomedicines 11, no. 2 (2023): 394. http://dx.doi.org/10.3390/biomedicines11020394.

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The clinical management of metastatic melanoma has been changed by BRAF (BRAFi) and MEK inhibitors (MEKi), which represent a standard treatment for BRAF-mutant melanoma. In oligoprogressive melanoma patients with BRAF mutations, target therapy can be combined with loco-regional radiotherapy (RT). However, the association of BRAF/MEK inhibitors and RT needs to be carefully monitored for potential increased toxicity. Despite the availability of some reports regarding the tolerability of RT + target therapy, data on simultaneous RT and BRAFi/MEKi are limited and mostly focused on the BRAFi vemura

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Pavlick, Anna C., Leslie Fecher, Paolo A. Ascierto, and Ryan J. Sullivan. "Frontline Therapy forBRAF-Mutated Metastatic Melanoma: How Do You Choose, and Is There One Correct Answer?" American Society of Clinical Oncology Educational Book, no. 39 (May 2019): 564–71. http://dx.doi.org/10.1200/edbk_243071.

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Genetic analysis of melanoma has allowed us to identify a population of patients who have more aggressive disease and harbor the driver mutation BRAF. This mutation is found in approximately 50% of metastatic disease and provides a target for focused therapies to control this disease. These responses are usually brisk; however, they lack the durability of immunotherapy. Frontline therapy for patients with BRAF-mutated melanoma is not as straightforward as prescribing BRAF/MEK inhibitors. Prior trials of combination immunotherapy demonstrate similar responses and durability of responses in pati

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Ice, Ryan J., Michelle Chen, Max Sidorov, et al. "Drug responses are conserved across patient-derived xenograft models of melanoma leading to identification of novel drug combination therapies." British Journal of Cancer 122, no. 5 (2019): 648–57. http://dx.doi.org/10.1038/s41416-019-0696-y.

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Abstract Background Patient-derived xenograft (PDX) mouse tumour models can predict response to therapy in patients. Predictions made from PDX cultures (PDXC) would allow for more rapid and comprehensive evaluation of potential treatment options for patients, including drug combinations. Methods We developed a PDX library of BRAF-mutant metastatic melanoma, and a high-throughput drug-screening (HTDS) platform utilising clinically relevant drug exposures. We then evaluated 34 antitumor agents across eight melanoma PDXCs, compared drug response to BRAF and MEK inhibitors alone or in combination

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Andronova, N. V., L. F. Morozova, I. N. Mikhailova, et al. "MODELING OF A SUBCUTANEOUS XENOGRAFT OF HUMAN SKIN MELANOMA MEL CHER WITH V600E BRAF MUTATION IN IMMUNODEFICIENT MICE FOR PRECLINICAL STUDY THE TARGETING ANTICANCER DRUGS." Russian Journal of Biotherapy 15, no. 4 (2016): 65–71. http://dx.doi.org/10.17650/1726-9784-2016-15-4-65-71.

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Introduction. Development of new models of a human disseminated skin melanoma of the with molecular-genetic targets for specific therapy increases productivity of the preclinical researches new the anti-melanoma drugs or their combinations in vitro and in vivo. Such opportunity is realized by adaptation in vivo of the original human pigmented skin melanoma cell line mel Cher and receiving subcutaneous (s. c.) xenograft under monitoring of transplant, morphological, molecular-genetic (V600E BRAF mutation) and chemotherapeutic (sensitivity for the inhibitor of BRAF kinases to a vemurafenib) char

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Moiseyenko, Fedor V., Vitaliy V. Egorenkov, Mikhail M. Kramchaninov, et al. "Lack of Response to Vemurafenib in Melanoma Carrying BRAF K601E Mutation." Case Reports in Oncology 12, no. 2 (2019): 339–43. http://dx.doi.org/10.1159/000500481.

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Vemurafenib has been developed to target common BRAF mutation V600E. It also exerts activity towards some but not all rare BRAF substitutions. Proper cataloguing of drug-sensitive and -insensitive rare mutations remains a challenge, due to low occurrence of these events and inability of commercial PCR-based diagnostic kits to detect the full spectrum of BRAF gene lesions. We considered the results of BRAF exon 15 testing in 1872 consecutive melanoma patients. BRAF mutation was identified in 1,090 (58.2%) cases. While drug-sensitive codon 600 substitutions constituted the majority of BRAF gene

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Porumb-Andrese, Elena, Ramona Gabriela Ursu, Iuliu Ivanov, et al. "The BRAF V600E Mutation Detection by quasa Sensitive Real-Time PCR Assay in Northeast Romania Melanoma Patients." Applied Sciences 11, no. 20 (2021): 9511. http://dx.doi.org/10.3390/app11209511.

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Background: The prevalence of melanoma in Romanian patients is underestimated. There is a need to identify the BRAF V600E mutation to accurately treat patients with the newest approved BRAF inhibitor therapy. This is a pilot study in which we first aimed to choose the optimal DNA purification method from formalin fixation and paraffin embedding (FFPE) malignant melanoma skin samples to assess the BRAF mutation prevalence and correlate it with clinical pathological parameters. Methods: 30 FFPE samples were purified in parallel with two DNA extraction kits, a manual and a semi-automated kit. The

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McKenna, Stephanie, and Lucía García-Gutiérrez. "Resistance to Targeted Therapy and RASSF1A Loss in Melanoma: What Are We Missing?" International Journal of Molecular Sciences 22, no. 10 (2021): 5115. http://dx.doi.org/10.3390/ijms22105115.

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Melanoma is one of the most aggressive forms of skin cancer and is therapeutically challenging, considering its high mutation rate. Following the development of therapies to target BRAF, the most frequently found mutation in melanoma, promising therapeutic responses were observed. While mono- and combination therapies to target the MAPK cascade did induce a therapeutic response in BRAF-mutated melanomas, the development of resistance to MAPK-targeted therapies remains a challenge for a high proportion of patients. Resistance mechanisms are varied and can be categorised as intrinsic, acquired,

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Hu-Lieskovan, Siwen, Lidia Robert, Blanca Homet Moreno, and Antoni Ribas. "Combining Targeted Therapy With Immunotherapy in BRAF-Mutant Melanoma: Promise and Challenges." Journal of Clinical Oncology 32, no. 21 (2014): 2248–54. http://dx.doi.org/10.1200/jco.2013.52.1377.

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Recent breakthroughs in the treatment of advanced melanoma are based on scientific advances in understanding oncogenic signaling and the immunobiology of this cancer. Targeted therapy can successfully block oncogenic signaling in BRAFV600-mutant melanoma with high initial clinical responses, but relapse rates are also high. Activation of an immune response by releasing inhibitory check points can induce durable responses in a subset of patients with melanoma. These advances have driven interest in combining both modes of therapy with the goal of achieving high response rates with prolonged dur

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Tímár, József, and Andrea Ladányi. "Molecular Pathology of Skin Melanoma: Epidemiology, Differential Diagnostics, Prognosis and Therapy Prediction." International Journal of Molecular Sciences 23, no. 10 (2022): 5384. http://dx.doi.org/10.3390/ijms23105384.

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Similar to other malignancies, TCGA network efforts identified the detailed genomic picture of skin melanoma, laying down the basis of molecular classification. On the other hand, genome-wide association studies discovered the genetic background of the hereditary melanomas and the susceptibility genes. These genetic studies helped to fine-tune the differential diagnostics of malignant melanocytic lesions, using either FISH tests or the myPath gene expression signature. Although the original genomic studies on skin melanoma were mostly based on primary tumors, data started to accumulate on the

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Yilmaz, Mesut, and Şermin Güven Meşe. "Treatment exceeds expectations with vemurafenib monotherapy in a patient with BRAFV600E-mutant metastatic melanoma." Journal of Oncology Pharmacy Practice 26, no. 7 (2020): 1754–58. http://dx.doi.org/10.1177/1078155220906011.

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Introduction Patients with distant metastatic melanoma has a poor prognosis, with a reported median survival time of six to eight months. In modern era, survival has prolonged with the immunotherapy and targeted therapy options. Potent and selective BRAF inhibitors have been developed that specifically inhibit mutated BRAF over other RAF kinases. Vemurafenib was the first selective tyrosine kinase inhibitor developed to target the V600E allele of BRAF-mutant melanoma. Case Report In this report, we present a case of BRAFV600E-mutant metastatic melanoma, which is being treated with vemurafenib

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Ruggiero, Ciro Francesco, Debora Malpicci, Luigi Fattore, et al. "ErbB3 Phosphorylation as Central Event in Adaptive Resistance to Targeted Therapy in Metastatic Melanoma: Early Detection in CTCs during Therapy and Insights into Regulation by Autocrine Neuregulin." Cancers 11, no. 10 (2019): 1425. http://dx.doi.org/10.3390/cancers11101425.

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In recent years the introduction of target therapies with BRAF and MEK inhibitors (MAPKi) and of immunotherapy with anti-CTLA-4 and anti-PD-1 monoclonal antibodies have dramatically improved survival of metastatic melanoma patients. Despite these changes drug resistance remains a major hurdle. Several mechanisms are at the basis of drug resistance. Particular attention has been devoted over the last years to unravel mechanisms at the basis of adaptive/non genetic resistance occurring in BRAF mutated melanomas upon treatment with to MAPKi. In this paper we focus on the involvement of activation

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Lau, Peter Kar Han, Carleen Cullinane, Susan Jackson, et al. "Enhancing Adoptive Cell Transfer with Combination BRAF-MEK and CDK4/6 Inhibitors in Melanoma." Cancers 13, no. 24 (2021): 6342. http://dx.doi.org/10.3390/cancers13246342.

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Despite the success of immune checkpoint inhibitors that target cytotoxic lymphocyte antigen-4 (CTLA-4) and programmed-cell-death-1 (PD-1) in the treatment of metastatic melanoma, there is still great need to develop robust options for patients who are refractory to first line immunotherapy. As such there has been a resurgence in interest of adoptive cell transfer (ACT) particularly derived from tumor infiltrating lymphocytes. Moreover, the addition of cyclin dependent kinase 4/6 inhibitors (CDK4/6i) have been shown to greatly extend duration of response in combination with BRAF-MEK inhibitors

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Becco, Paolo, Susanna Gallo, Stefano Poletto, et al. "Melanoma Brain Metastases in the Era of Target Therapies: An Overview." Cancers 12, no. 6 (2020): 1640. http://dx.doi.org/10.3390/cancers12061640.

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Malignant melanoma is the third most common type of tumor that causes brain metastases. Patients with cerebral involvement have a dismal prognosis and their treatment is an unmet medical need. Brain involvement is a multistep process involving several signaling pathways such as Janus kinase/signal Transducer and Activator of Transcription (JAK/STAT), Phosphoinositide 3-kinase/Protein Kinase B (PI3K/AKT), Vascular Endothelial Growth Factor and Phosphatase and Tensin Homolog (PTEN). Recently therapy that targets the MAPK signaling (BRAF/MEK inhibitors) and immunotherapy (anti-CTLA4 and anti-PD1

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Karki, Prashant, Shayne Sensenbach, Vahideh Angardi, and Mehmet A. Orman. "BRAF-Inhibitor-Induced Metabolic Alterations in A375 Melanoma Cells." Metabolites 11, no. 11 (2021): 777. http://dx.doi.org/10.3390/metabo11110777.

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Acquired drug tolerance has been a major challenge in cancer therapy. Recent evidence has revealed the existence of slow-cycling persister cells that survive drug treatments and give rise to multi-drug-tolerant mutants in cancer. Cells in this dynamic persister state can escape drug treatment by undergoing various epigenetic changes, which may result in a transient metabolic rewiring. In this study, with the use of untargeted metabolomics and phenotype microarrays, we characterize the metabolic profiles of melanoma persister cells mediated by treatment with vemurafenib, a BRAF inhibitor. Our f

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Nepote, Alessandro, Gianluca Avallone, Simone Ribero, et al. "Current Controversies and Challenges on BRAF V600K-Mutant Cutaneous Melanoma." Journal of Clinical Medicine 11, no. 3 (2022): 828. http://dx.doi.org/10.3390/jcm11030828.

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About 50% of melanomas harbour a BRAF mutation. Of these 50%, 10% have a V600K mutation. Although it is the second most common driver mutation after V600E, no specific studies have been conducted to identify a clinical and therapeutic gold standard for this patient subgroup. We analysed articles, including registrative clinical trials, to identify common clinical and biological traits of the V600K melanoma population, including different adopted therapeutic strategies. Melanoma V600K seems to be more frequent in Caucasian, male and elderly populations with a history of chronic sun damage and e

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Testori, Alessandro A. E., Silvia Chiellino, and Alexander C. J. van Akkooi. "Adjuvant Therapy for Melanoma: Past, Current, and Future Developments." Cancers 12, no. 7 (2020): 1994. http://dx.doi.org/10.3390/cancers12071994.

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This review describes the progress that the concept of adjuvant therapies has undergone in the last 50 years and focuses on the most recent development where an adjuvant approach has been scientifically evaluated in melanoma clinical trials. Over the past decade the development of immunotherapies and targeted therapies has drastically changed the treatment of stage IV melanoma patients. These successes led to trials studying the same therapies in the adjuvant setting, in high risk resected stage III and IV melanoma patients. Adjuvant immune checkpoint blockade with anti-CTLA-4 antibody ipilimu

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Fattore, Luigi, Virginia Campani, Ciro Francesco Ruggiero, et al. "In Vitro Biophysical and Biological Characterization of Lipid Nanoparticles Co-Encapsulating Oncosuppressors miR-199b-5p and miR-204-5p as Potentiators of Target Therapy in Metastatic Melanoma." International Journal of Molecular Sciences 21, no. 6 (2020): 1930. http://dx.doi.org/10.3390/ijms21061930.

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Uncontrolled MAPK signaling is the main oncogenic driver in metastatic melanomas bearing mutations in BRAF kinase. These tumors are currently treated with the combination of BRAF/MEK inhibitors (MAPKi), but this therapy is plagued by drug resistance. In this context we recently discovered that several microRNAs are involved in the development of drug resistance. In particular miR-204-5p and miR-199b-5p were found to function as antagonists of resistance because their enforced overexpression is able to inhibit melanoma cell growth in vitro either alone or in combination with MAPKi. However, the

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Valpione, Sara, Luca G. Campana, Jacopo Pigozzo, and Vanna Chiarion-Sileni. "Consolidation electrochemotherapy with bleomycin in metastatic melanoma during treatment with dabrafenib." Radiology and Oncology 49, no. 1 (2015): 71–74. http://dx.doi.org/10.2478/raon-2014-0035.

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Abstract Background. Small molecules that inhibit V600 mutated BRAF protein, such as vemurafenib and dabrafenib, are effective in treatment of metastatic melanoma. Case report. We here describe the clinical course of a V600E BRAF mutated metastatic melanoma patient with systemic disease, who developed tumor progression on superficial soft-tissue metastases during treatment with dabrafenib. Bleomycin electrochemotherapy during dabrafenib treatment was administered to control the soft-tissue progressing metastases and ensured sustained local control without significant toxicity. Conclusions. The

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Sarnaik, Amod, Sajeve Samuel Thomas, Diwakar Davar, et al. "Safety and efficacy of cryopreserved autologous tumor infiltrating lymphocyte therapy (LN-144, lifileucel) in advanced metastatic melanoma patients previously treated with at least one prior systemic therapy." Journal of Clinical Oncology 37, no. 8_suppl (2019): 136. http://dx.doi.org/10.1200/jco.2019.37.8_suppl.136.

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136 Background: While immunotherapies including checkpoint inhibitors and targeted therapies (BRAF/MEK inhibitors) are options for patients with metastatic melanoma, many patients still develop progressive disease. These patients have few treatment options available including high dose IL-2 and chemotherapy with reported second line response rates of 4-10%. Adoptive cell therapy utilizing tumor-infiltrating lymphocytes (TIL) is recognized as an effective treatment in metastatic melanoma, able to elicit durable and complete responses in even heavily pretreated patients. We provide preliminary d

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Sarnaik, Amod, Nikhil I. Khushalani, Jason Alan Chesney, et al. "Safety and efficacy of cryopreserved autologous tumor infiltrating lymphocyte therapy (LN-144, lifileucel) in advanced metastatic melanoma patients who progressed on multiple prior therapies including anti-PD-1." Journal of Clinical Oncology 37, no. 15_suppl (2019): 2518. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2518.

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2518 Background: Treatment options are limited for patients with advanced melanoma who have progressed on checkpoint inhibitors and targeted therapies such as BRAF/MEK inhibitors (if BRAF-V600E mutated). Adoptive cell therapy utilizing tumor-infiltrating lymphocytes (TIL) has shown antitumor efficacy with durable long-term responses in heavily pretreated melanoma patients. Safety and efficacy of lifileucel (LN-144), a centrally manufactured autologous TIL therapy are presented. Methods: C-144-01 is a global Phase 2 open-label, multicenter study of the efficacy and safety of lifileucel in patie

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Dzienis, Marcin Radoslaw, and Victoria Atkinson. "Response rate to vemurafenib in BRAF-positive melanoma brain metastases." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9081. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9081.

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9081 Background: Brain is a common site for melanoma metastases. Responses to dabrafenib have already been reported in over 50% of patients. We aimed at assessing response rate (RR) to vemurafenib (Vem). Methods: Patients with BRAF positive melanoma and asymptomatic brain metastases at initiation of Vem were eligible. Records were analysed retrospectively to calculate RR (at least 30% decrease in the sum of diameters of target lesions), duration of response and time to CNS progression (TTP). Results: 18 patients with CNS metastasis received Vem (M/F=8/10; median age 50); 9 received no prior th

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Algazi, Alain Patrick, Christian Posch, Susana Ortiz-Urda, Alyson Cockerill, Pamela N. Munster, and Adil Daud. "BKM120 combined with vemurafenib in vemurafenib-refractory BRAF mutant metastatic melanoma: Two cases." Journal of Clinical Oncology 31, no. 15_suppl (2013): e20010-e20010. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e20010.

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e20010 Background: PTEN loss and PI3K activation are common in BRAF mutant metastatic melanoma, and PI3K activation has been implicated as a cause of acquired resistance to BRAF inhibitors. Two vemurafenib refractory were treated with the potent BRAF inhibitor, vemurafenib, and the pan-class I PI3K inhibitor BKM120. Methods: The study enrolled BRAF-V600E/K mutant metastatic melanoma patients with an ECOG PS ≥ 2 and adequate organ function. Vemurafenib refractory BRAF-V600E/K mutant melanoma patients started both vemurafenib twice daily and BKM120 daily on cycle 1, day 1 after a vemurafenib was

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Bernocchi, Ottavia, Marianna Sirico, Silvia Paola Corona, et al. "Tumor Type Agnostic Therapy Carrying BRAF Mutation: Case Reports and Review of Literature." Pharmaceuticals 14, no. 2 (2021): 159. http://dx.doi.org/10.3390/ph14020159.

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Background: Precision medicine is based on molecular and genotypic patient characterization to define specific target treatment. BRAF mutation is an oncogenic driver, and the Cancer Genome Atlas has identified BRAF mutations in different cancer types. Tumor type agnostic therapy is based on targeting genomic alterations, regardless of tumor origin. In this context, novel therapeutic agents including BRAF and MEK inhibitors based on the molecular landscape in solid tumors have been investigated. Case presentation, Case 1: The first case is chemotherapy-refractory, BRAF V600E mutated intrahepati

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Homicsko, Krisztian Gyuta, Veronica Aedo, Edoardo Missiaglia, Bettina Bisig, and Olivier Michielin. "Targeting MAP2K1 mutation with trametinib in a triple wild-type melanoma patient." Journal of Clinical Oncology 37, no. 15_suppl (2019): e21027-e21027. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e21027.

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e21027 Background: MAP2K1 inhibitors combined with BRAF inhibitors provide a prolonged progression-free survival for BRAF mutant patients. However, the impact of MEK inhibition of MAP2K1 mutant and BRAF/NRAS/NF1 wild type melanoma patients remains elusive. Methods: We performed next-generation sequencing using an in-house developed 400 full exon panel for one of our triple wild type (BRAF/NRAS/NF1) melanoma patient. The patient received off-label, trametinib at a dose of 2 mg o.d. We performed additional sequencing at progression. After progression, the patient was treated off-label with combi

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Fattore, Luigi, Rita Mancini, and Gennaro Ciliberto. "Cancer Stem Cells and the Slow Cycling Phenotype: How to Cut the Gordian Knot Driving Resistance to Therapy in Melanoma." Cancers 12, no. 11 (2020): 3368. http://dx.doi.org/10.3390/cancers12113368.

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Cancer stem cells (CSCs) have historically been defined as slow cycling elements that are able to differentiate into mature cells but without dedifferentiation in the opposite direction. Thanks to advances in genomic and non-genomic technologies, the CSC theory has more recently been reconsidered in a dynamic manner according to a “phenotype switching” plastic model. Transcriptional reprogramming rewires this plasticity and enables heterogeneous tumors to influence cancer progression and to adapt themselves to drug exposure by selecting a subpopulation of slow cycling cells, similar in nature

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Jamme, Philippe, Guillaume Delzenne, Laurent Mortier, Olivier Farchi, and Marie Boileau. "Relevance of detection of RAF fusion in pan-negative melanoma in routine practice." Journal of Clinical Oncology 40, no. 16_suppl (2022): e21500-e21500. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21500.

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e21500 Background: Pan-negative melanomas (i.e. without MAPK kinase pathway alteration and C-kit wild type) account for 30% of melanomas (according to the AACR GENIE database). In case of immunotherapy failure, therapeutic options are limited. Oncogene fusions represent a target of interest in many solid cancers (NSCLC, Cholangiocarcinoma, Glioma, GIST, pancreatic acinar carcinoma, thyroid, and prostate cancers). In melanoma, the frequency of oncogene fusion is not well documented and not routinely investigated. Methods: We conducted a single-center retrospective study. The objective was to de

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Tawbi, Hussein A., Celine Boutros, David Kok, Caroline Robert, and Grant McArthur. "New Era in the Management of Melanoma Brain Metastases." American Society of Clinical Oncology Educational Book, no. 38 (May 2018): 741–50. http://dx.doi.org/10.1200/edbk_200819.

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The remarkable advances in the systemic therapy of metastatic melanoma have now extended the 1-year overall survival rate from 25% to nearing 85%. Systemic treatment in the form of BRAF-targeted therapy and immunotherapy is slowly but surely proving its efficacy in the treatment of metatstatic brain metastases (MBM). Single-agent BRAF inhibitors provide an intracranial response rate of 25% to 40%, whereas the combination of BRAFi/MEKi leads to responses in up to 58%. However, the durability of responses induced by BRAFi/MEKi seems to be even shorter than in extracranial disease. On the other h

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Rager, Taylor, Adam Eckburg, Meet Patel, et al. "Treatment of Metastatic Melanoma with a Combination of Immunotherapies and Molecularly Targeted Therapies." Cancers 14, no. 15 (2022): 3779. http://dx.doi.org/10.3390/cancers14153779.

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Melanoma possesses invasive metastatic growth patterns and is one of the most aggressive types of skin cancer. In 2021, it is estimated that 7180 deaths were attributed to melanoma in the United States alone. Once melanoma metastasizes, traditional therapies are no longer effective. Instead, immunotherapies, such as ipilimumab, pembrolizumab, and nivolumab, are the treatment options for malignant melanoma. Several biomarkers involved in tumorigenesis have been identified as potential targets for molecularly targeted melanoma therapy, such as tyrosine kinase inhibitors (TKIs). Unfortunately, me

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Comunanza, Valentina, Chiara Gigliotti, Gabriella Doronzo, et al. "Abstract B17: VEGF removal delays the onset of acquired resistance to target therapy and increases the efficacy of immune checkpoint inhibitors in BRAF-mutated melanoma." Cancer Research 80, no. 19_Supplement (2020): B17. http://dx.doi.org/10.1158/1538-7445.mel2019-b17.

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Abstract The introduction of BRAF inhibitors (BRAFi) has improved response rate and overall survival of metastatic melanoma patients compared to standard chemotherapy. However, acquired drug resistance occurs in nearly all patients. The comprehension of cellular and molecular mechanisms underlying BRAFi resistance could help to identify novel actionable pathways in the treatment of BRAF-dependent tumors. VEGFA is an attractive target for combinatorial cancer therapy, and we have recently demonstrated in melanoma and CRC xenografts that targeting VEGFA enhanced the antitumor effect of BRAFi by

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Musi, Alice, and Laura Bongiovanni. "Extracellular Vesicles in Cancer Drug Resistance: Implications on Melanoma Therapy." Cancers 15, no. 4 (2023): 1074. http://dx.doi.org/10.3390/cancers15041074.

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Extracellular vesicles (EVs) are involved in the pathogenesis of neoplastic diseases. Their role in mediating drug resistance has been widely described in several types of cancers, including melanoma. EVs can mediate drug resistance through several different mechanisms, such as drug-sequestration, transfer of pro-survival proteins and RNA, induction of cancer stem cell-like features and interaction with cells of the tumor microenvironment and immune-system. Melanoma is a highly immunogenic tumor originating from the malignant transformation of melanocytes. Several therapeutic strategies curren

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Sosman, Jeffrey A. "Abstract IA24: Are there nonimmune targets in the BRAFV600 WT melanoma patient?" Cancer Research 80, no. 19_Supplement (2020): IA24. http://dx.doi.org/10.1158/1538-7445.mel2019-ia24.

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Abstract Molecular targeting of melanoma beyond the BRAFV600 mutation has been a frustrating and largely unsuccessful pursuit. The dominant driver in many of these cases is the gain of function NRAS mutations, while a smaller subset are in part driven by NF1 loss of function genetic alterations, and lastly a subset (WT) with a variety of mutations, most of which activate the MAPK pathway such as mutations in c-Kit, MEK, KRAS, HRAS, and alternate non-V600 BRAF mutations. This effort has concentrated on the inhibition of the activated MAPK pathway with MEK inhibitors and targeted NRAS tumors, wh

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Gatalica, Zoran, Kathleen D. Danenberg, Matthew Jerome McGinniss, et al. "Molecular profiling of uveal melanoma patients." Journal of Clinical Oncology 30, no. 15_suppl (2012): 10630. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10630.

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10630 Background: Although uveal melanoma represents only 5% of all melanomas, it is the most common primary intraocular malignancy of the adult eye. Approximately 50% of patients will develop metastases which are resistant to medical interventions. There is a great need for improved therapy as the prognosis is poor for advanced stages. Our study was undertaken to investigate the presence of novel therapeutic targets. Methods: We analyzed 49 uveal melanoma patients with immunohistochemistry for 16 markers including cKIT, PDGFR, cMET, PTEN and IGF1R. Further, microarray analysis was performed o

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Mikhaylova, I. N., E. M. Treshalina, L. F. Morozova, N. V. Andronova, I. Zh Shubina, and A. A. Lushnikova. "Cell lines of human melanoma and their xenograft with braf or nras mutations a targets for targeted therapy. Reviews." Russian Journal of Biotherapy 17, no. 4 (2019): 27–35. http://dx.doi.org/10.17650/1726-9784-2018-17-4-27-35.

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The review presents a discussion on articles and patents, describing new in vitro and in vivo models of pigmented or non-pigmented human cutaneous melanoma, received in NMRCO from the patients» metastases. Molecular genetic characteristics of the new models is supported by the arguments in addition to the given data and visual materials. The subjects of the discussed publications are 3 polyclonal cell lines, 2 subclones and 4 subcutaneous (s/c) xenografts in immunodeficient mice Balb/c nude. All the models are stored in Cryo Collection with xenografts at N.N. Blokhin NMRCO as well as in the Ru

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Sarnaik, Amod, Nikhil Khushalani, Jason Chesney, et al. "P865 Safety & efficacy of lifileucel (LN-144) tumor infiltrating lymphocyte therapy in metastatic melanoma patients after progression on multiple therapies – independent review committee data update." Journal for ImmunoTherapy of Cancer 8, Suppl 1 (2020): A12. http://dx.doi.org/10.1136/lba2019.18.

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BackgroundTreatment options are limited for patients with advanced melanoma who have progressed on checkpoint inhibitors and targeted therapies such as BRAF/MEK inhibitors (if BRAF-V600E mutated). Adoptive cell therapy utilizing tumor-infiltrating lymphocytes (TIL) has shown antitumor efficacy with durable responses in heavily pretreated melanoma patients. Safety and efficacy of lifileucel, a centrally manufactured cryopreserved autologous TIL therapy assessed by both investigator and an independent review committee (IRC), are presented.MethodsC-144-01 is a global Phase 2 open-label, multicent

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Kendra, Kari Lynn, Ryan Watson, and Gregory B. Lesinski. "Selinexor, a selective inhibitor of nuclear export (SINE), in patients with unresectable melanoma." Journal of Clinical Oncology 35, no. 15_suppl (2017): e21014-e21014. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e21014.

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e21014 Background: Limited effective therapies exist for patients with melanoma after progression on immune- and targeted-therapies. Treatment with selinexor, a potent small molecule inhibitor of exportin-1 (CRM/XPO1), results in nuclear retention of major tumor suppressor proteins and cell cycle regulators, leads to growth arrest and apoptosis in vitro, in xenograft models (BRAF +/-), and Phase I solid tumor trial. (Yang et al PLOS One, 2014, Razak et al JCO, 2016). Methods: Objectives of this single institution trial were to determine: the safety in melanoma patients, the clinical benefit ra

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Sarnaik, Amod, Nikhil I. Khushalani, Jason Alan Chesney, et al. "Long-term follow up of lifileucel (LN-144) cryopreserved autologous tumor infiltrating lymphocyte therapy in patients with advanced melanoma progressed on multiple prior therapies." Journal of Clinical Oncology 38, no. 15_suppl (2020): 10006. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.10006.

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10006 Background: Treatment options are limited for patients with advanced melanoma who have progressed on checkpoint inhibitors and targeted therapies. Adoptive cell therapy using tumor-infiltrating lymphocytes (TIL) leverages and enhances the body’s natural defense against cancer and has shown durable responses in heavily pretreated melanoma patients. Methods: C-144-01 is a global Phase 2 open-label, multicenter study of efficacy & safety of lifileucel in patients with unresectable metastatic melanoma who have progressed on checkpoint inhibitors and BRAF/MEK inhibitors, if BRAFv600 mutan

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Rebecca, Vito W., Jianglan Liu, Thomas Connelly, Keith Flaherty, Ze’ev Ronai, and Meenhard Herlyn. "Abstract PR18: Comparative screening of skin-derived NCSCs, melanocytes, and melanoma developmental programs reveals LPAR1 in MAPKi resistance." Cancer Research 80, no. 19_Supplement (2020): PR18. http://dx.doi.org/10.1158/1538-7445.mel2019-pr18.

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Abstract Despite the high efficacy of BRAFi/MEKi in BRAF-MT melanomas, resistance arises in the majority of cases. Melanoma hijacks developmental pathways that drive aggressiveness; however, gene signatures shared by melanocyte progenitor cells and melanoma cells remain poorly understood. Here, we define common dependencies in neural crest stem cells (NCSCs) and melanoma cells not present in melanocytes through computational transcriptome analyses and targeted siRNA screens against shared developmental genes. Secondary validation coupled with Ingenuity Pathway Analysis identified the LPAR1-RAP

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Betoff, Allison, Jonathan Zippin, Taha Merghoub, Paul B. Chapman, and Jedd Wolchok. "Abstract IA10: Targeting melanoma metabolism to overcome resistance to treatment." Cancer Research 80, no. 19_Supplement (2020): IA10. http://dx.doi.org/10.1158/1538-7445.mel2019-ia10.

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Abstract Despite adequate oxygen levels, cancer cells undergo anaerobic glycolysis converting glucose to lactate (the Warburg effect). It is now thought that the advantage of this for the cancer cell is that it provides the carbon and nitrogen precursors critical for macromolecule synthesis (amino acids, nucleotides, fatty acids) while still providing an adequate supply of ATP needed for growth. Understanding this metabolic landscape may provide strategies to overcome mechanisms of resistance to therapy in melanoma. AMP-activated protein kinase (AMPK) has been shown to inactivate BRAF by phosp

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Zhai, Zili, Prasanna K. Vaddi, Jenny Mae Samson, Tomoya Takegami, and Mayumi Fujita. "NLRP1 Functions Downstream of the MAPK/ERK Signaling via ATF4 and Contributes to Acquired Targeted Therapy Resistance in Human Metastatic Melanoma." Pharmaceuticals 14, no. 1 (2020): 23. http://dx.doi.org/10.3390/ph14010023.

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The BRAF V600E mutation leads to constitutive activation of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and its downstream effector responses. Uncovering the hidden downstream effectors can aid in understanding melanoma biology and improve targeted therapy efficacy. The inflammasome sensor, NACHT, LRR, and PYD domains-containing protein 1 (NLRP1), is responsible for IL-1β maturation and itself is a melanoma tumor promoter. Here, we report that NLRP1 is a downstream effector of MAPK/ERK signaling through the activating transcription factor 4 (

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Madhusudanannair, Vinu, Filip Janku, Gerald Steven Falchook, et al. "NRAS mutations in patients with advanced cancers treated with target-based therapies in early-phase clinical trials." Journal of Clinical Oncology 30, no. 15_suppl (2012): 3106. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.3106.

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3106 Background: NRAS mutations in cancers increase MAPK signaling. It is plausible that NRAS mutations may be associated with sensitivity to drugs targeting the MAPK pathway. Methods: Tumors from 689 patients with advanced cancers referred to the Clinical Center for Targeted Therapy (phase I program) were screened in a CLIA-certified laboratory for NRAS mutations and if feasible, for PIK3CA, KRAS, BRAF mutations and PTEN aberrations. Whenever possible, patients with NRAS mutations were treated with agents targeting the RAF-MEK pathway. Results: Of the 689 patients, 58 (8%) had NRAS mutations.

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Wagenseller, Aubrey G., Amber L. Shada, Kevin D'Auria, et al. "MicroRNAs induced in melanoma treated with combination targeted therapy of temsirolimus and bevacizumab." Journal of Clinical Oncology 30, no. 15_suppl (2012): 8597. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.8597.

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8597 Background: Targeted therapies directed at commonly overexpressed pathways in melanoma have clinical activity in numerous trials. Little is known about how these therapies influence microRNA expression, particularly with combination regimens. A better understanding of how microRNAs are altered with treatment may contribute to understanding mechanisms of therapeutic effects as well as mechanisms of tumor escape from therapy. Methods: Using microRNA arrays, we analyzed microRNA expression levels in melanoma samples from a Cancer Therapy Evaluation Program-sponsored phase II trial of combina

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Vosganian, Gregory S., Rinke Bos, and Linda Sherman. "Immunologic Effects of An Oral BRAF Inhibitor in a BRAF Wild-Type Murine Model." Blood 118, no. 21 (2011): 4935. http://dx.doi.org/10.1182/blood.v118.21.4935.4935.

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Abstract Abstract 4935 Introduction: Metastatic melanoma represents a clinical challenge as aggressive therapy often results in unacceptable toxicity and less intensive therapy results in suboptimal clinical outcomes. PLX-4032 is an orally available small molecule which targets constitutively activated BRAFV600E in melanoma cells. BRAF is an important regulator of cell growth, proliferation and migration. We examined the effect of PLX-4032 on the immune system in two BRAF wild type murine systems: the first to determine the effect of PLX-4032 on cytokine production and the second to determine

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