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Relevant bibliographies by topics / Melanoma, BRAF, target therapy, melanoma acrale

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Journal articles

Academic literature on the topic 'Melanoma, BRAF, target therapy, melanoma acrale'

Author: Grafiati

Published: 9 March 2023

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

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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2

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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3

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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4

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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5

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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7

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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8

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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9

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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10

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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