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Journal articles on the topic 'BRAF isoforms'

Author: Grafiati

Published: 14 March 2023

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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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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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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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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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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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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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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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Duggan, Megan C., Andrew R. Stiff, Maryam Bainazar, et al. "Identification of NRAS isoform 2 overexpression as a mechanism facilitating BRAF inhibitor resistance in malignant melanoma." Proceedings of the National Academy of Sciences 114, no. 36 (2017): 9629–34. http://dx.doi.org/10.1073/pnas.1704371114.

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Activating mutations in BRAF are found in 50% of melanomas and although treatment with BRAF inhibitors (BRAFi) is effective, resistance often develops. We now show that recently discovered NRAS isoform 2 is up-regulated in the setting of BRAF inhibitor resistance in melanoma, in both cell lines and patient tumor tissues. When isoform 2 was overexpressed in BRAF mutant melanoma cell lines, melanoma cell proliferation and in vivo tumor growth were significantly increased in the presence of BRAFi treatment. shRNA-mediated knockdown of isoform 2 in BRAFi resistant cells restored sensitivity to BRA

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12

Wagner, Michael, Melinda Wuest, Ana Lopez-Campistrous, et al. "Tyrosine kinase inhibitor therapy and metabolic remodelling in papillary thyroid cancer." Endocrine-Related Cancer 27, no. 9 (2020): 495–507. http://dx.doi.org/10.1530/erc-20-0135.

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Targeted therapy is increasingly used to manage metastatic papillary thyroid cancer. The focus of the present study was to examine glucose metabolism and tumor responses for thyroid cancer xenografts expressing the glycolytic pathway modulators platelet-derived growth factor receptor (PDGFR) and BRAFV600E. Radiolabelled glucose derivative [18F]FDG was used to analyze the effects of PDGFR blockade with imatinib, BRAF blockade with vemurafenib, as well as combined PDGFR and BRAF blockade in vitro and in vivo with PET. Dynamic PET data was correlated with immunohistochemistry staining and kinetic

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13

Wang, Bi-Dar, and Norman Lee. "Aberrant RNA Splicing in Cancer and Drug Resistance." Cancers 10, no. 11 (2018): 458. http://dx.doi.org/10.3390/cancers10110458.

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More than 95% of the 20,000 to 25,000 transcribed human genes undergo alternative RNA splicing, which increases the diversity of the proteome. Isoforms derived from the same gene can have distinct and, in some cases, opposing functions. Accumulating evidence suggests that aberrant RNA splicing is a common and driving event in cancer development and progression. Moreover, aberrant splicing events conferring drug/therapy resistance in cancer is far more common than previously envisioned. In this review, aberrant splicing events in cancer-associated genes, namely BCL2L1, FAS, HRAS, CD44, Cyclin D

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Albers, Corinna, Anna Lena Illert, Hannes Leischner, et al. "A Single Retroviral Vector Design for the Simultaneous Expression of a Mir30 Based Shrna with An Oncogene – Identification of Raf-1 but Not BRAF as a Crucial Mediator for BCR-ABL Mediated Leukemogenesis." Blood 116, no. 21 (2010): 3392. http://dx.doi.org/10.1182/blood.v116.21.3392.3392.

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Abstract Abstract 3392 Introduction: Chronic myelogenous leukemia (CML) is characterized by the t(9;22)(q34;q11) chromosomal translocation and the expression of BCR-ABL, a fusion protein with tyrosine kinase activity. BCR-ABL activates various signaling cascades mediating signals for proliferation, transformation and anti-apoptosis. The BCR-ABL inhibitor imatinib is the standard therapy for CML. However, this treatment is assumed to be not curative since leukemia initiating cells cannot be completely eradicated by solely BCR-ABL inhibition. Identification of key mediators within the BCR-ABL si

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15

Hwang, Kwangwoo, SeoHyun Jo, Jieun Choi, et al. "Abstract LB521: Antitumor activity of potent RAF inhibitors in solid tumors with activated RAS-RAF axis." Cancer Research 82, no. 12_Supplement (2022): LB521. http://dx.doi.org/10.1158/1538-7445.am2022-lb521.

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Abstract FDA approved three RAF inhibitors for the treatment of tumors containing BRAFV600 mutations, but one of the major drawbacks of these type I RAF inhibitors is to activate MAPK signaling pathway, instead of inhibiting signaling, which is referred to as paradoxical activation. Such undesired paradoxical activation not only leads to renewed tumor growth but also spurs additional cancer growth in non-cancerous wild-type BRAF tissue. Plus, these first-generation RAF inhibitors targeting BRAFV600 mutants are unable to inhibit oncogenic RAF dimers. This has led to the development of type II R

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Peng, Sheng-Bin, James R. Henry, Michael D. Kaufman, et al. "Inhibition of RAF Isoforms and Active Dimers by LY3009120 Leads to Anti-tumor Activities in RAS or BRAF Mutant Cancers." Cancer Cell 28, no. 3 (2015): 384–98. http://dx.doi.org/10.1016/j.ccell.2015.08.002.

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17

Bhatia, Ankush, Vaios Hatzoglou, Gary Ulaner, et al. "Neurologic and oncologic features of Erdheim–Chester disease: a 30-patient series." Neuro-Oncology 22, no. 7 (2020): 979–92. http://dx.doi.org/10.1093/neuonc/noaa008.

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Abstract Background Erdheim–Chester disease (ECD) is a rare histiocytic neoplasm characterized by recurrent alterations in the MAPK (mitogen-activating protein kinase) pathway. The existing literature about the neuro-oncological spectrum of ECD is limited. Methods We present retrospective clinical, radiographic, pathologic, molecular, and treatment data from 30 patients with ECD neurohistiocytic involvement treated at a tertiary center. Results Median age was 52 years (range, 7–77), and 20 (67%) patients were male. Presenting symptoms included ataxia in 19 patients (63%), dysarthria in 14 (47%

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18

De Roock, W., M. Janssens, B. Biesmans, et al. "DUSPs as markers of MEK/Erk activation in primary colorectal cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): 4064. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4064.

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4064 Background: DUSPs dephosphorylate P-MAPK and are activated as a negative feedback loop upon RTK signaling. Higher expression of DUSP 4 & 6 is also found in cells with constitutive Erk activation like KRAS mutant (MUT) cells (Bild et al. Nature 2005). We correlated DUSP1, 4, 6 (isoforms a & b) & 8 mRNA expression level in FFPE primary colorectal cancer (CRC) of 186 chemorefractory patients treated with cetuximab (CTX) with KRAS MUT state and progression-free survival (PFS) and overall survival (OS). Methods: KRAS codon 12,13, 61&146, BRAF V600E and NRAS codon 12&13 MUT

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Nastasă, Cristina, Radu Tamaian, Ovidiu Oniga, and Brîndușa Tiperciuc. "5-Arylidene(chromenyl-methylene)-thiazolidinediones: Potential New Agents against Mutant Oncoproteins K-Ras, N-Ras and B-Raf in Colorectal Cancer and Melanoma." Medicina 55, no. 4 (2019): 85. http://dx.doi.org/10.3390/medicina55040085.

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Background and objectives: Cancer represents the miscommunication between and within the body cells. The mutations of the oncogenes encoding the MAPK pathways play an important role in the development of tumoral diseases. The mutations of KRAS and BRAF oncogenes are involved in colorectal cancer and melanoma, while the NRAS mutations are associated with melanoma. Thiazolidine-2,4-dione is a versatile scaffold in medicinal chemistry and a useful tool in the development of new antitumoral compounds. The aim of our study was to predict the pharmacokinetic/pharmacodynamic properties, the drug-like

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20

Carvalho, Larissa A. C., Rodrigo G. Queijo, Alexandre L. B. Baccaro, et al. "Redox-Related Proteins in Melanoma Progression." Antioxidants 11, no. 3 (2022): 438. http://dx.doi.org/10.3390/antiox11030438.

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Melanoma is the most aggressive type of skin cancer. Despite the available therapies, the minimum residual disease is still refractory. Reactive oxygen and nitrogen species (ROS and RNS) play a dual role in melanoma, where redox imbalance is involved from initiation to metastasis and resistance. Redox proteins modulate the disease by controlling ROS/RNS levels in immune response, proliferation, invasion, and relapse. Chemotherapeutics such as BRAF and MEK inhibitors promote oxidative stress, but high ROS/RNS amounts with a robust antioxidant system allow cells to be adaptive and cooperate to n

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Yaktapour, Niuscha, Christine Dierks, Dietmar Pfeifer, et al. "Combination Of Kinase Inhibitors Overcomes B-Raf Inhibitor-Induced Paradoxical ERK Activation In CLL Cells In Vitro – Potential Implications For CLL Treatment." Blood 122, no. 21 (2013): 4121. http://dx.doi.org/10.1182/blood.v122.21.4121.4121.

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Abstract Chronic lymphocytic leukemia (CLL) remains incurable with current state of the art therapy creating the need for novel therapeutic concepts. Kinase inhibitors represent a promising strategy in the treatment of various malignancies including CLL. However, based on the recent experience with other targeted therapy compounds used as single agents, it appears important to identify additional targets and to evaluate therapeutic combinations targeting two or more critical signaling hubs in CLL cells. This strategy is likely to counteract the development of drug resistance more efficiently.

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22

Barceló, Carla, Pol Sisó, Oscar Maiques, Inés de la Rosa, Rosa M. Martí, and Anna Macià. "T-Type Calcium Channels: A Potential Novel Target in Melanoma." Cancers 12, no. 2 (2020): 391. http://dx.doi.org/10.3390/cancers12020391.

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T-type calcium channels (TTCCs) are overexpressed in several cancers. In this review, we summarize the recent advances and new insights into TTCC biology, tumor progression, and prognosis biomarker and therapeutic potential in the melanoma field. We describe a novel correlation between the Cav3.1 isoform and the increased basal autophagy in BRAFV600E-mutant melanomas and after acquired resistance to BRAF inhibitors. Indeed, TTCC blockers reduce melanoma cell viability and migration/invasion in vitro and tumor growth in mice xenografts in both BRAF-inhibitor-sensitive and -resistant scenarios.

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Lin, Tong, Yuqin Qiu, Wenya Peng, and Lisheng Peng. "Heat Shock Protein 90 Family Isoforms as Prognostic Biomarkers and Their Correlations with Immune Infiltration in Breast Cancer." BioMed Research International 2020 (October 21, 2020): 1–15. http://dx.doi.org/10.1155/2020/2148253.

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Background. The heat shock protein 90 (HSP90s) family is composed of molecular chaperones composed of four isoforms in humans, which has been widely reported as unregulated in various kinds of cancers. Nevertheless, the role of each HSP90s isoform in prognosis and immune infiltration in distinct subtypes of breast cancer (BRAC) remains unclear. Methods. Public online databases including the Oncomine, UALCAN, Kaplan-Meier Plotter, Tumor IMmune Estimation Resource (TIMER), Gene Expression Profiling Interactive Analysis (GEPIA), GeneMANIA, and Database for Annotation, Visualization, and Integrate

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Titov, K. S., A. A. Markin, A. M. Kazakov, and S. V. Chulkova. "The role of a new <i>ALK</i> isoform in the diagnosis and targeted therapy of skin melanoma." Russian Journal of Biotherapy 20, no. 4 (2021): 33–41. http://dx.doi.org/10.17650/1726-9784-2021-20-4-33-41.

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Contemporary discoveries of fundamental science in recent decades in the field of oncology have led to the emergence of new highly effective anticancer drugs: targeted drugs and immune checkpoint inhibitors, use of which has made a breakthrough in the treatment of oncological diseases, including skin melanoma. Melanoma is still one of the most cancerous tumors. The number of patients resistant to targeted therapy and immunotherapy increases in the world every year. Oncologists have practically no leverage to influence the disease after the development of resistance to this type of therapy. In

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Morgan, TE, RO Lockerbie, LS Minamide, MD Browning, and JR Bamburg. "Isolation and characterization of a regulated form of actin depolymerizing factor." Journal of Cell Biology 122, no. 3 (1993): 623–33. http://dx.doi.org/10.1083/jcb.122.3.623.

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Actin depolymerizing factor (ADF) is an 18.5-kD protein with pH-dependent reciprocal F-actin binding and severing/depolymerizing activities. We previously showed developing muscle down-regulates ADF (J. R. Bamburg and D. Bray. 1987. J. Cell Biol. 105: 2817-2825). To further study this process, we examined ADF expression in chick myocytes cultured in vitro. Surprisingly, ADF immunoreactivity increases during the first 7-10 d in culture. This increase is due to the presence of a new ADF species with higher relative molecular weight which reacts identically to brain ADF with antisera raised again

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Lonial, Sagar, Venkata D. Yellapantula, Winnie Liang, et al. "Interim Analysis of the Mmrf Commpass Trial: Identification of Novel Rearrangements Potentially Associated with Disease Initiation and Progression." Blood 124, no. 21 (2014): 722. http://dx.doi.org/10.1182/blood.v124.21.722.722.

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Abstract The Multiple Myeloma Research Foundation (MMRF) CoMMpass trial (NCT0145429) is a longitudinal study of 1000 patients with newly-diagnosed multiple myeloma. The study opened July 2011 and now includes over 650 patients from 91 sites in the United States, Canada and European Union. Each patient is required to receive an approved proteasome inhibitor, immunumodulatory agent, or both. Enriched tumor and matched constitutional samples are comprehensively analyzed using Long-Insert Whole Genome Sequencing (WGS), Whole Exome Sequencing (WES) and RNA sequencing (RNAseq). Clinical parameters,

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Naffa, Randa, Lisa Vogel, Luca Hegedűs, et al. "P38 MAPK Promotes Migration and Metastatic Activity of BRAF Mutant Melanoma Cells by Inducing Degradation of PMCA4b." Cells 9, no. 5 (2020): 1209. http://dx.doi.org/10.3390/cells9051209.

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Metastatic melanoma is the most aggressive type of skin cancer. Previously, we identified the plasma membrane Ca2+ pump isoform 4b (PMCA4b or ATP2B4) as a putative metastasis suppressor in BRAF mutant melanoma cells. Metastasis suppressors are often downregulated in cancer, therefore, it is important to identify the pathways involved in their degradation. Here, we studied the role of p38 MAPK in PMCA4b degradation and its effect on melanoma metastasis. We found that activation of p38 MAPK induces internalization and subsequent degradation of PMCA4b through the endo/lysosomal system that contri

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Gregory, Matthew D., Pablo E. Puente, Nadine L. Belony, et al. "Abstract C022: Treatment of a Black American lung cancer cell line harboring KRAS mutations with polyisoprenylated cysteinyl amide inhibitors reveals effects on the MAP kinase signaling pathway, cell migration and apoptosis." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (2023): C022. http://dx.doi.org/10.1158/1538-7755.disp22-c022.

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Abstract KRAS mutations are the most common oncogenic mutations in lung adenocarcinoma in Black Americans. Polyisoprenylated cysteinyl amide inhibitors (PCAIs) constitute a group of cancer therapy agents designed to specifically disrupt and suppress hyperactive G protein signaling, such as that triggered by RAS mutations. Here we determine the effects of PCAIs on the viability, G-proteins levels, downstream mediators, and apoptosis-related proteins on the KRAS-mutant, Black American-derived lung adenocarcinoma cell line, NCI-H23. Of the 17 PCAIs tested, compounds NSL-YHJ-2-27 and NSL-YHJ-2-46

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Gnoni, Antonio, Antonella Licchetta, Riccardo Memeo, et al. "Role of BRAF in Hepatocellular Carcinoma: A Rationale for Future Targeted Cancer Therapies." Medicina 55, no. 12 (2019): 754. http://dx.doi.org/10.3390/medicina55120754.

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The few therapeutic strategies for advance hepatocellular carcinoma (HCC) on poor knowledge of its biology. For several years, sorafenib, a tyrosine kinase inhibitors (TKI) inhibitor, has been the approved treatment option, to date, for advanced HCC patients. Its activity is the inhibition of the retrovirus-associated DNA sequences protein (RAS)/Rapidly Accelerated Fibrosarcoma protein (RAF)/mitogen-activated and extracellular-signal regulated kinase (MEK)/extracellular-signal regulated kinases (ERK) signaling pathway. However, the efficacy of sorafenib is limited by the development of drug re

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Miller, Nichol L. G., Tim S. Wang, Paul Severson, et al. "Abstract 2674: Antitumor activity of KIN-2787, a next-generation pan-RAF inhibitor, in preclinical models of human RAF/RAS mutant melanoma." Cancer Research 82, no. 12_Supplement (2022): 2674. http://dx.doi.org/10.1158/1538-7445.am2022-2674.

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Abstract Background: In the US in 2021, invasive melanoma will account for an estimated 106,000 new cases and &gt; 7,000 deaths. Somatic mutations that activate the MAPK signaling pathway are a leading cause of melanoma with 50% harboring oncogenic BRAF alterations and another 20% with activating NRAS mutations. Of note, NRAS mutant melanoma has been shown to be dependent upon RAF signaling via CRAF dimers for downstream activation of MEK/ERK. While targeted therapies are approved for V600 (Class I, monomer-driven) BRAF mutant melanoma, no approved targeted therapy exists for patients with

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Zhang, Bo, Prajish Iyer, Meiling Jin, et al. "Expression of Sf3b1-K700E accelerates the Development of Chronic Lymphocytic Leukemia in a Del(13q) Murine Model." Blood 136, Supplement 1 (2020): 4–5. http://dx.doi.org/10.1182/blood-2020-139096.

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RNA splicing factor SF3B1 is one of the most recurrently mutated genes in chronic lymphocytic leukemia (CLL), but expression of this mutation alone in murine B cells does not result in CLL. This gene mutation is often subclonal and associated with poor survival. How this mutation impacts CLL progression remains elusive. Since SF3B1 mutation frequently co-occurs with chromosome 13q deletion (del(13q)), and mice with deletion of the Minimal Deleted Region (MDR) of del(13q) develop indolent CLL, we therefore asked whether co-expression of Sf3b1 mutation can accelerate the onset of CLL in this mur

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Wagle, Nikhil, Eliezer Mendel Van Allen, Dennie T. Frederick, et al. "Whole exome and whole transcriptome sequencing in melanoma patients to identify mechanisms of resistance to combined RAF/MEK inhibition." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9015. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9015.

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9015 Background: The RAF inhibitors vemurafenib and dabrafenib (D) and the MEK inhibitor trametinib (T) improve survival as monotherapies in BRAF-mutant melanoma. Since clinical mechanisms of resistance (MoR) result in MAPK pathway reactivation, recent efforts have focused on combined targeting of RAF and MEK. The combination of D and T (D/T) increased progression-free survival and response rate compared with D alone (Flaherty et al, NEJM, 2012). The MoR to this combination remain unknown. Methods: To look for clinical MoR to combined RAF/MEK inhibition, we performed whole exome (WES) and whol

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Miller, Nichol, Tim Sen Wang, Catherine Lee, et al. "Antitumor activity of KIN-2787, a next-generation pan-RAF inhibitor, in combination with MEK inhibition in preclinical models of human NRAS mutant melanoma." Journal of Clinical Oncology 40, no. 16_suppl (2022): e15099-e15099. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e15099.

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e15099 Background: NRAS mutations which activate MAPK signaling represent oncogenic driver alterations in approximately 20% melanoma cases in the US. NRAS mutant melanomas are uniquely dependent upon CRAF rather than BRAF for activation of downstream MEK/ERK signaling. In BRAF mutant melanoma, approved RAF-targeted therapies are commonly used in combination with a MEK inhibitor which provides clinical benefit by inhibition of two targets within the oncogenic MAPK signaling pathway. Emerging data with pan-RAF inhibitors in early clinical development suggests benefit with and without combined ME

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Miller, Nichol, Tim Sen Wang, Catherine Lee, et al. "Antitumor activity of KIN-2787, a next-generation pan-RAF inhibitor, in combination with MEK inhibition in preclinical models of human NRAS mutant melanoma." Journal of Clinical Oncology 40, no. 16_suppl (2022): e15099-e15099. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e15099.

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e15099 Background: NRAS mutations which activate MAPK signaling represent oncogenic driver alterations in approximately 20% melanoma cases in the US. NRAS mutant melanomas are uniquely dependent upon CRAF rather than BRAF for activation of downstream MEK/ERK signaling. In BRAF mutant melanoma, approved RAF-targeted therapies are commonly used in combination with a MEK inhibitor which provides clinical benefit by inhibition of two targets within the oncogenic MAPK signaling pathway. Emerging data with pan-RAF inhibitors in early clinical development suggests benefit with and without combined ME

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Capocchi, Antonella, Debora Fontanini, Vera Muccilli, et al. "NsLTP1 and NsLTP2 Isoforms in Soft Wheat (Triticum aestivumCv. Centauro) and Farro (Triticum dicocconSchrank) Bran." Journal of Agricultural and Food Chemistry 53, no. 20 (2005): 7976–84. http://dx.doi.org/10.1021/jf0580465.

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Vats, Arpita, and Saroj Mishra. "Identification and evaluation of bioremediation potential of laccase isoforms produced by Cyathus bulleri on wheat bran." Journal of Hazardous Materials 344 (February 2018): 466–79. http://dx.doi.org/10.1016/j.jhazmat.2017.10.043.

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Teixeira da Silva, Vanessa de Cássia, Amanda Lais de Souza Coto, Rafael de Carvalho Souza, Marcello Bertoldi Sanchez Neves, Eleni Gomes та Gustavo Orlando Bonilla-Rodriguez. "Effect of pH, Temperature, and Chemicals on the Endoglucanases andβ-Glucosidases from the Thermophilic FungusMyceliophthora heterothallicaF.2.1.4. Obtained by Solid-State and Submerged Cultivation". Biochemistry Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9781216.

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This work reports endoglucanase and beta-glucosidase production by the thermophilic fungusMyceliophthora heterothallicain solid-state (SSC) and submerged (SmC) cultivation. Wheat bran and sugarcane bagasse were used for SSC and cardboard for SmC. Highest endoglucanase production in SSC occurred after 192 hours: 1,170.6 ± 0.8 U/g, and in SmC after 168 hours: 2,642 ± 561 U/g. The endoglucanases and beta-glucosidases produced by both cultivation systems showed slight differences concerning their optimal pH and temperature. The number of endoglucanases was also different: six isoforms in SSC and t

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Vidal, Anna, and Torben Redmer. "Decoding the Role of CD271 in Melanoma." Cancers 12, no. 9 (2020): 2460. http://dx.doi.org/10.3390/cancers12092460.

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The evolution of melanoma, the most aggressive type of skin cancer, is triggered by driver mutations that are acquired in the coding regions of particularly BRAF (rat fibrosarcoma serine/threonine kinase, isoform B) or NRAS (neuroblastoma-type ras sarcoma virus) in melanocytes. Although driver mutations strongly determine tumor progression, additional factors are likely required and prerequisite for melanoma formation. Melanocytes are formed during vertebrate development in a well-controlled differentiation process of multipotent neural crest stem cells (NCSCs). However, mechanisms determining

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Del Re, Marzia, Stefania Crucitta, Giulia Gianfilippo, et al. "Understanding the Mechanisms of Resistance in EGFR-Positive NSCLC: From Tissue to Liquid Biopsy to Guide Treatment Strategy." International Journal of Molecular Sciences 20, no. 16 (2019): 3951. http://dx.doi.org/10.3390/ijms20163951.

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Liquid biopsy has emerged as an alternative source of nucleic acids for the management of Epidermal Growth Factor Receptor (EGFR)-mutant non-Small Cell Lung Cancer (NSCLC). The use of circulating cell-free DNA (cfDNA) has been recently introduced in clinical practice, resulting in the improvement of the identification of druggable EGFR mutations for the diagnosis and monitoring of response to targeted therapy. EGFR-dependent (T790M and C797S mutations) and independent (Mesenchymal Epithelial Transition [MET] gene amplification, Kirsten Rat Sarcoma [KRAS], Phosphatidyl-Inositol 4,5-bisphosphate

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Papadaki, Chara, Maria Sfakianaki, Zacharenia Saridaki, et al. "PKM2 mRNA expression to predict disease recurrence in patients with stage II or III colon cancer treated with oxaliplatin in combination with fluoropyrimidines." Journal of Clinical Oncology 30, no. 4_suppl (2012): 468. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.468.

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468 Background: Tumor cells have been shown to express exclusively the embryonic M2 isoform of pyruvate kinase (PKM2), which is a key enzyme that regulates aerobic glycolysis in tumor cells. Use of RNA interfering (RNAi) targeting PKM2 significantly inhibits tumor growth when combined with cisplatin in xenograft models. We evaluated the predictive significance of PKM2 in patients with “high” risk stage II or stage III colon cancer treated with oxaliplatin-fluoropyrimidines chemotherapy adjuvant treatment. Methods: FFPE primary tumours from 261 patients with stage II or III colon cancer with co

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Guglielmelli, Paola, Tiziana Fanelli, Valentina Ariu, et al. "Comparative Genomic and Expression Analysis of Chronic and Blast-Phase Cells in Patients with Myeloproliferative Neoplasms." Blood 132, Supplement 1 (2018): 1777. http://dx.doi.org/10.1182/blood-2018-99-112894.

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Abstract Background. Progression to acute myeloid leukemia (sAML) occurs in 20% of myelofibrosis (MF) and 10% of polycythemia vera (PV) or essential thrombocythemia (ET). sAML has dismal outcome with median survival of <6 months. We recently reported that a restricted set of mutations predict for leukemic transformation in MPN (Vannucchi AM, Leukemia 2013; Tefferi A, Blood Adv. 2016). However, the molecular mechanisms underlying transformation to sAML are poorly characterized, in particular the relationships between the clones establishing the chronic phase and the one dominating the leukem

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Prasad Asija, Aakanksha, Alina E. Dulau Florea, Xianguo Kong, Douglass A. Drelich, Srikanth Nagalla, and Steven E. McKenzie. "Molecular Characterization Of a Patient With Thrombocytopenia-Absent Radii (TAR) Syndrome and Diffuse Langerhans Cell Histiocytosis (LCH): Novel Genetic Findings." Blood 122, no. 21 (2013): 2326. http://dx.doi.org/10.1182/blood.v122.21.2326.2326.

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Abstract TAR is a rare bone marrow failure syndrome comprised of thrombocytopenia and a spectrum of bony abnormalities, the most common being bilateral radial aplasia in the presence of thumbs. Recent research has implicated alterations in the RBM8A gene in the pathogenesis of this disorder. Diffuse LCH is a neoplasm of mature Langerhans cells, a subset of dendritic cells, that has now been demonstrated to be clonal in nature. The co-occurrence of these two rare disorders has only been reported twice (Ingram, BMT 2006; Guastadisegni EJMG 2012). We report the third case of a patient with TAR an

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Ciudad-Mulero, María, Lillian Barros, Ângela Fernandes, et al. "Potential Health Claims of Durum and Bread Wheat Flours as Functional Ingredients." Nutrients 12, no. 2 (2020): 504. http://dx.doi.org/10.3390/nu12020504.

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Wheat is an important cereal with a key role in human nutrition. In this study, dietary fiber (DF) and arabinoxylans of different durum (Triticum turgidum ssp. Durum L.) and bread (Triticum aestivum L.) wheat flours were analyzed in order to point out their potential nutritional and health claims allege according to the current European regulation (Regulation (EU) No 432/2012). Moreover, other bioactive compounds (phenolics and tocopherols) were quantified as a first approach to their phytochemical composition in the analyzed wheat varieties. DF was analyzed following AOAC enzymatic-gravimetri

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Menyhárt, Otília, Virag Vas, Balázs Győrffy, and László Buday. "A személyre szabott terápia legújabb lehetőségei a molekuláris onkológiában." Scientia et Securitas 2, no. 2 (2021): 191–99. http://dx.doi.org/10.1556/112.2021.00035.

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Összefoglaló. A molekuláris onkológia térnyerésével számos új lehetőség érhető el a daganatos betegek hatékonyabb kezelésére. Ilyen a klinikai vizsgálatokban alkalmazott, a valóban személyre szabott kezelést elősegítő génpanelelemzés, illetve a célzott kezelés szövettípustól független alkalmazása. A személyre szabott terápiák jelentős hányada valamelyik kinázt gátolja. Az összefoglalónkban bemutatjuk a RAS jelátviteli út sejten belüli komplex szabályozását, valamint ismertetjük az útvonal további farmakológiai szempontból kiaknázható célpontjait nemzetközi és saját eredményeink alapján. A kiná

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Fischer, John, Karyn Bouhana, Mark J. Chicarelli, et al. "Abstract 167: Pre-clinical characterization of a novel series of FGFR2 selective inhibitors with potency against clinically relevant mutations." Cancer Research 82, no. 12_Supplement (2022): 167. http://dx.doi.org/10.1158/1538-7445.am2022-167.

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Abstract The fibroblast growth factor receptor (FGFR) family of protein tyrosine kinases plays a role in many physiological processes including angiogenesis and wound healing. FGFR mutations, fusions, rearrangements, and amplifications have been linked to the pathogenesis of multiple tumor types. For example, approximately 10-15% of patients with intrahepatic cholangiocarcinoma have FGFR2 fusions, and amplification of FGFR2 is prevalent in gastric cancer and implicated in tumor growth. Approved FGFR inhibitors produce responses in patients that harbor FGFR genetic alterations but show reduced

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Thaijongrak, Prawporn, Charoonroj Chotwiwatthanakun, Phaivit Laphyai, et al. "Molecular characterization and expression profiling of transformer 2 and fruitless-like homologs in the black tiger shrimp, Penaeus monodon." PeerJ 10 (February 17, 2022): e12980. http://dx.doi.org/10.7717/peerj.12980.

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Transformer 2 (tra 2) and fruitless (fru) genes have been proven to play a key role in sex determination pathways in many Arthropods, including insects and crustaceans. In this study, a paralog of P. monodon tra 2 (Pmtra 2), P. monodon ovarian associated transformer 2 (PmOvtra 2) and 2 isoforms of P. monodon fruitless-like gene (Pmfru-1 and Pmfru-2) were identified and characterized. The full cDNA sequence of PmOvtra 2 consisted of 1,774 bp with the longest open reading frame (ORF) of 744 bp encoding for 247 amino acids. The PmOvtra 2 exhibited a predicted RNA-recognition motif (RRM) domain an

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Gillard, G., J. Proctor, S. Hyzy, et al. "OP0307 A NOVEL TARGETED APPROACH TO ACHIEVE IMMUNE SYSTEM RESET: CD45-TARGETED ANTIBODY DRUG CONJUGATES AMELIORATE DISEASE IN PRECLINICAL AUTOIMMUNE DISEASE MODELS AND ENABLE AUTO-HSCT." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 190–91. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5744.

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Background:Resetting the immune system through autologous hematopoietic stem cell transplant (autoHSCT) is a highly effective treatment in selected patients with autoimmune diseases. AutoHSCT can induce long-term remission with 80% progression free survival in multiple sclerosis patients (Muraro 2017, Burt 2019). Use of autoHSCT in scleroderma patients has achieved superior outcomes in two randomized studies compared to standard of care (Tyndall 2014, Sullivan 2018). These impressive results are achieved by a combination of the eradication of autoreactive immune effector cells and re-establish

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Screnci, Brad, Trevor Barnes, Kristen Shema, et al. "Abstract 317: Isolation of highly selective antibodies against claudin 18.2 for the treatment of solid tumors." Cancer Research 82, no. 12_Supplement (2022): 317. http://dx.doi.org/10.1158/1538-7445.am2022-317.

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Abstract Monoclonal antibodies (MAbs) are a well-established treatment approach in oncology and other diseases. Nevertheless, many multipass membrane proteins are largely inaccessible as antibody targets due to their poor expression, membrane-dependent structure, small extracellular regions, and high sequence conservation between humans and rodents. Integral Molecular’s MPS Antibody Discovery platform specifically addresses each of these challenges. A key enabling feature of MPS is the use of chickens as an evolutionarily divergent host species for immunization, allowing a more robust immune r

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Rico-Fontalvo, Jorge, Rodrigo Daza-Arnedo, Tomas Rodríguez-Yanez, et al. "Obesidad y enfermedad renal crónica. Una mirada desde los mecanismos fisiopatológicos." Revista de la Sociedad Ecuatoriana de Nefrología, Diálisis y Trasplante 10, no. 2 (2022): 97–107. http://dx.doi.org/10.56867/32.

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Introducción: La enfermedad renal crónica asociada a la obesidad (ERC-AO) es una enfermedad con aumento en la prevalencia en las últimas décadas. Se caracteriza por un exceso de desequilibrios hormonales adipocíticos (adipoquinas), desregulación del sistema de equilibrio energético y desequilibrios en la homeostasis metabólica. Propósito de la revisión: El objetivo de la revisión es delinear el papel de los diferentes mecanismos fisiopatológicos para el desarrollo de enfermedad renal funcional o anatómica en pacientes con obesidad. Buscamos reportes actualizados en donde se incluye los resulta

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Tran, Khanh B., Sharada Kolekar, Anower Jabed, et al. "Diverse mechanisms activate the PI 3-kinase/mTOR pathway in melanomas: implications for the use of PI 3-kinase inhibitors to overcome resistance to inhibitors of BRAF and MEK." BMC Cancer 21, no. 1 (2021). http://dx.doi.org/10.1186/s12885-021-07826-4.

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Abstract Background The PI 3-kinase (PI3K) pathway has been implicated as a target for melanoma therapy. Methods Given the high degree of genetic heterogeneity in melanoma, we sought to understand the breadth of variation in PI3K signalling in the large NZM panel of early passage cell lines developed from metastatic melanomas. Results We find the vast majority of lines show upregulation of this pathway, and this upregulation is achieved by a wide range of mechanisms. Expression of all class-IA PI3K isoforms was readily detected in these cell lines. A range of genetic changes in different compo

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