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Artículos de revistas

Literatura académica sobre el tema "BRAF isoforms"

Autor: Grafiati

Publicado: 14 de marzo de 2023

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Artículos de revistas sobre el tema "BRAF isoforms"

1

Marranci, Andrea, Andrea Tuccoli, Marianna Vitiello, et al. "Identification of BRAF 3′UTR Isoforms in Melanoma." Journal of Investigative Dermatology 135, no. 6 (2015): 1694–97. http://dx.doi.org/10.1038/jid.2015.47.

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2

Bayer, Abraham L., Jodie Pietruska, Jaymes Farrell, Siobhan McRee, Pilar Alcaide, and Philip W. Hinds. "AKT1 Is Required for a Complete Palbociclib-Induced Senescence Phenotype in BRAF-V600E-Driven Human Melanoma." Cancers 14, no. 3 (2022): 572. http://dx.doi.org/10.3390/cancers14030572.

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Cellular senescence is a carefully regulated process of proliferative arrest accompanied by functional and morphologic changes. Senescence allows damaged cells to avoid neoplastic proliferation; however, the induction of the senescence-associated secretory phenotype (SASP) can promote tumor growth. The complexity of senescence may limit the efficacy of anti-neoplastic agents, such as CDK4/6 inhibitors (Cdk4/6i), that induce a senescence-like state in tumor cells. The AKT kinase family, which contains three isoforms that play both unique and redundant roles in cancer progression, is commonly hy

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3

Tadijan, Ana, Francesca Precazzini, Nikolina Hanžić, et al. "Altered Expression of Shorter p53 Family Isoforms Can Impact Melanoma Aggressiveness." Cancers 13, no. 20 (2021): 5231. http://dx.doi.org/10.3390/cancers13205231.

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Cutaneous melanoma is the most aggressive form of skin cancer. Despite the significant advances in the management of melanoma in recent decades, it still represents a challenge for clinicians. The TP53 gene, the guardian of the genome, which is altered in more than 50% of human cancers, is rarely mutated in melanoma. More recently, researchers started to appreciate the importance of shorter p53 isoforms as potential modifiers of the p53-dependent responses. We analyzed the expression of p53 and p73 isoforms both at the RNA and protein level in a panel of melanoma-derived cell lines with differ

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4

Vlašić, Ignacija, Anđela Horvat, Ana Tadijan, and Neda Slade. "p53 Family in Resistance to Targeted Therapy of Melanoma." International Journal of Molecular Sciences 24, no. 1 (2022): 65. http://dx.doi.org/10.3390/ijms24010065.

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Metastatic melanoma is one of the most aggressive tumors, with frequent mutations affecting components of the MAPK pathway, mainly protein kinase BRAF. Despite promising initial response to BRAF inhibitors, melanoma progresses due to development of resistance. In addition to frequent reactivation of MAPK or activation of PI3K/AKT signaling pathways, recently, the p53 pathway has been shown to contribute to acquired resistance to targeted MAPK inhibitor therapy. Canonical tumor suppressor p53 is inactivated in melanoma by diverse mechanisms. The TP53 gene and two other family members, TP63 and

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5

Dillon, Martha, Antonio Lopez, Edward Lin, Dominic Sales, Ron Perets, and Pooja Jain. "Progress on Ras/MAPK Signaling Research and Targeting in Blood and Solid Cancers." Cancers 13, no. 20 (2021): 5059. http://dx.doi.org/10.3390/cancers13205059.

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The mitogen-activated protein kinase (MAPK) pathway, consisting of the Ras-Raf-MEK-ERK signaling cascade, regulates genes that control cellular development, differentiation, proliferation, and apoptosis. Within the cascade, multiple isoforms of Ras and Raf each display differences in functionality, efficiency, and, critically, oncogenic potential. According to the NCI, over 30% of all human cancers are driven by Ras genes. This dysfunctional signaling is implicated in a wide variety of leukemias and solid tumors, both with and without viral etiology. Due to the strong evidence of Ras-Raf invol

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6

Sorokin, Alex, Lea Bitner, Ji Wu, David Menter, Scott Kopetz, and Van Karlyle Morris. "Antitumor activity of panRAF inhibition in BRAF V600E metastatic colorectal cancer." Journal of Clinical Oncology 35, no. 4_suppl (2017): 616. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.616.

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616 Background: BRAF V600E mutations, present in <10% of patients with metastatic colorectal cancer (mCRC), are associated with low responses to chemotherapy and poor survival outcomes. Targeted therapies against BRAF and EGFR have shown promising clinical activity. The panRAF inhibitor (PRI) LSN3074753 inhibits dimerization of all RAF isoforms to impede downstream MEK activation, with no reflexive MAPK reactivation common with other BRAF inhibitors. Anti-tumor activity of PRI has not been compared to BRAF + EGFR inhibition in patient-derived xenograft (PDX) models of BRAF V600E mCRC. Metho

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7

Broseghini, Elisabetta, Emi Dika, Eric Londin, and Manuela Ferracin. "MicroRNA Isoforms Contribution to Melanoma Pathogenesis." Non-Coding RNA 7, no. 4 (2021): 63. http://dx.doi.org/10.3390/ncrna7040063.

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Cutaneous melanoma (CM) is the most lethal tumor among skin cancers, and its incidence is constantly increasing. A deeper understanding of the molecular processes guiding melanoma pathogenesis could improve diagnosis, treatment and prognosis. MicroRNAs play a key role in melanoma biology. Recently, next generation sequencing (NGS) experiments, designed to assess small-RNA expression, revealed the existence of microRNA variants with different length and sequence. These microRNA isoforms are known as isomiRs and provide an additional layer to the complex non-coding RNA world. Here, we collected

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8

Ngeow, Kao Chin, Hans J. Friedrichsen, Linxin Li, et al. "BRAF/MAPK and GSK3 signaling converges to control MITF nuclear export." Proceedings of the National Academy of Sciences 115, no. 37 (2018): E8668—E8677. http://dx.doi.org/10.1073/pnas.1810498115.

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The close integration of the MAPK, PI3K, and WNT signaling pathways underpins much of development and is deregulated in cancer. In principle, combinatorial posttranslational modification of key lineage-specific transcription factors would be an effective means to integrate critical signaling events. Understanding how this might be achieved is central to deciphering the impact of microenvironmental cues in development and disease. The microphthalmia-associated transcription factor MITF plays a crucial role in the development of melanocytes, the retinal pigment epithelium, osteoclasts, and mast

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9

Farrell, Jaymes, Jodie Pietruska, Siobhan McRee, Philip Tsichlis, and Philip Hinds. "Abstract PR14: Defining isoform-specific roles for AKTs in BRAFV600E-driven melanoma." Cancer Research 80, no. 19_Supplement (2020): PR14. http://dx.doi.org/10.1158/1538-7445.mel2019-pr14.

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Abstract The PI3K/AKT pathway is frequently dysregulated in cutaneous melanoma and impacts both tumor aggression and resistance to BRAFV600E/K inhibitors. While current clinical approaches to AKT inhibition are severely limited by the toxicity of pan-AKT inhibitors, selective inhibition of individual AKT isoforms (AKT1, AKT2, or AKT3) remains an attractive, if yet unattainable, approach. A critical gap in our understanding concerns how the three highly homologous yet functionally distinct AKT isoforms contribute to melanomagenesis and treatment response. To address this question, we are employ

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10

Journal, Baghdad Science. "Detection of RAF fusion transcripts in FFPE samples of Medullablastoma and Ependymom in Iraqi children with RT-RQPCR assays." Baghdad Science Journal 11, no. 3 (2014): 1411–19. http://dx.doi.org/10.21123/bsj.11.3.1411-1419.

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Medulloblastomas and ependymomas are the most common malignant brain tumors in children. However genetic abnormalities associated with their development and prognosis remain unclear. Recently two gene fusions, KIAA1549–BRAF and SRGAP3–RAF1 have been detected in a number of brain tumours. We report here our development and validation of RT-RQPCR assays to detect various isoforms of these two fusion genes in formalin fixed paraffin embedded (FFPE) tissues of medulloblastoma and ependymoma. We examined these fusion genes in 44 paediatric brain tumours, 33 medulloblastomas and 11 ependymomas. We d

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