Bibliographies thématiques / Targeted therapies, RAS, MEK, PI3K

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Littérature scientifique sur le sujet « Targeted therapies, RAS, MEK, PI3K »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Targeted therapies, RAS, MEK, PI3K"

LaRue, Rebecca S., Hanh Nguyen, Karen Sachs, et al. "Ras-Pathway Inhibition With Targeted Therapies Abrogates Self-Renewal In Acute Myelogenous Leukemia." Blood 122, no. 21 (2013): 819. http://dx.doi.org/10.1182/blood.v122.21.819.819.

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Abstract Hyperactivated Ras-pathways serve as oncogenic drivers in multiple human tumors including acute myelogenous leukemia (AML) (Ahearn et al. Nat Rev Mol Cell Biol 2011). The specific functions of these pathways in AML are unclear, thwarting the rational application of targeted therapeutics. Recently, we have shown that NRASG12V–activated signaling pathways are critical to leukemia stem cell maintenance (Sachs et al. submitted). To elucidate which Ras-activated signaling molecules mediate self-renewal in AML, we employed a murine model that harbors Mll-AF9 and a tetracycline repressible,

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Huang, Tannie, Jon Akutagawa, Inbal Epstein, Charisa Cottonham, Maricel Quirindongo-Crespo, and Benjamin S. Braun. "Inhibition of Akt Signaling Alleviates MDS/MPN Driven By KrasD12 or Nf1 Loss." Blood 126, no. 23 (2015): 360. http://dx.doi.org/10.1182/blood.v126.23.360.360.

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Abstract Juvenile and chronic myelomonocytic leukemias (JMML and CMML) are aggressive myeloid malignancies categorized as myelodysplastic syndromes/myeloproliferative neoplasms (MDS/MPN). Chemotherapy has little benefit for MDS/MPN patients, and new therapies are needed. We have used mouse models investigate the potential of signal transduction inhibitors in MDS/MPN, as JMML and CMML are associated with mutations in NRAS, KRAS, PTPN11, CBL, or NF1 that activate Ras signaling. Conditional Mx1-Cre, KrasLSL-D12 (designated KrasD12) mice develop an aggressive and fully penetrant MDS/MPN characteri

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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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Tamura, Ryota, and Masahiro Toda. "A Critical Overview of Targeted Therapies for Vestibular Schwannoma." International Journal of Molecular Sciences 23, no. 10 (2022): 5462. http://dx.doi.org/10.3390/ijms23105462.

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Vestibular schwannoma (VS) is a benign tumor that originates from Schwann cells in the vestibular component. Surgical treatment for VS has gradually declined over the past few decades, especially for small tumors. Gamma knife radiosurgery has become an accepted treatment for VS, with a high rate of tumor control. For neurofibromatosis type 2 (NF2)-associated VS resistant to radiotherapy, vascular endothelial growth factor (VEGF)-A/VEGF receptor (VEGFR)-targeted therapy (e.g., bevacizumab) may become the first-line therapy. Recently, a clinical trial using a VEGFR1/2 peptide vaccine was also co

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Yoko, Yoshikawa1. "RAS Inhibition Suppresses the Progression and Metastasis of Triple-Negative Breast Cancer." Mega Journal of Case Reports 7, no. 5 (2024): 2001–15. https://doi.org/10.5281/zenodo.11236631.

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<strong>Abstract</strong> Triple<strong>-</strong>negative breast cancer (TNBC) is the most lethal subtype of breast cancer and currently lacks effective targeted therapies. Therefore, there is an urgent need to develop new therapeutic strategies for patients with TNBC; the poor prognosis of TNBC patients is linked to the overexpression of epidermal growth factor receptor (EGFR), which is involved in tumor progression, and lysyl oxidase (LOX), which is associated with metastasis. We previously reported that RAS inhibition with small-molecule pan-RAS inhibitors, such as Kobe0065, exerts antitum

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Patel, Meet, Adam Eckburg, Shahina Gantiwala, et al. "Resistance to Molecularly Targeted Therapies in Melanoma." Cancers 13, no. 5 (2021): 1115. http://dx.doi.org/10.3390/cancers13051115.

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Malignant melanoma is the most aggressive type of skin cancer with invasive growth patterns. In 2021, 106,110 patients are projected to be diagnosed with melanoma, out of which 7180 are expected to die. Traditional methods like surgery, radiation therapy, and chemotherapy are not effective in the treatment of metastatic and advanced melanoma. Recent approaches to treat melanoma have focused on biomarkers that play significant roles in cell growth, proliferation, migration, and survival. Several FDA-approved molecular targeted therapies such as tyrosine kinase inhibitors (TKIs) have been develo

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Giraud, Jean-Stephane, Doriane Gorret, Manuela Ye, et al. "Abstract 6709: NF1 mutations in lung adenocarcinoma preclinical models and potential targeted therapies: The crucial role of the RAS-MAPK pathway." Cancer Research 85, no. 8_Supplement_1 (2025): 6709. https://doi.org/10.1158/1538-7445.am2025-6709.

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Targeting tumor suppressor genes, such as NF1, is a major challenge in cancer. Somatic NF1 mutations are found in ∼15% of lung adenocarcinoma (LUAD) cases. Still, the molecular vulnerabilities and cellular adaptations associated with these mutations remain unclear. Therefore, we aimed to study the functional consequences of NF1 loss in LUAD and its impact on the RAS/MAPK pathway, as well as potential therapeutic strategies. We established isogenic NF1-mutated cellular models (mono- and bi-allelic NF1 mutations) using CRISPR-Cas9 technology on the HBE4-E6/E7-C1 human bronchial epithelial cell l

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Derwich, Aleksandra, Monika Sykutera, Barbara Bromińska, Błażej Rubiś, Marek Ruchała, and Nadia Sawicka-Gutaj. "The Role of Activation of PI3K/AKT/mTOR and RAF/MEK/ERK Pathways in Aggressive Pituitary Adenomas—New Potential Therapeutic Approach—A Systematic Review." International Journal of Molecular Sciences 24, no. 13 (2023): 10952. http://dx.doi.org/10.3390/ijms241310952.

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Pituitary tumors (PT) are mostly benign, although occasionally they demonstrate aggressive behavior, invasion of surrounding tissues, rapid growth, resistance to conventional treatments, and multiple recurrences. The pathogenesis of PT is still not fully understood, and the factors responsible for its invasiveness, aggressiveness, and potential for metastasis are unknown. RAF/MEK/ERK and mTOR signaling are significant pathways in the regulation of cell growth, proliferation, and survival, its importance in tumorigenesis has been highlighted. The aim of our review is to determine the role of th

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Przestrzelska, Magda, Iga Ślesicka, Natalia Zozula, et al. "Advances in Targeted Therapies and Combination Approaches for Melanoma: A Comprehensive Review." Quality in Sport 23 (October 3, 2024): 54869. http://dx.doi.org/10.12775/qs.2024.23.54869.

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Introduction and Purpose: Melanoma, an aggressive malignancy from melanocytes, has a poor prognosis. Despite advances in targeted therapies and immunotherapies, drug resistance remains a challenge. This review examines the molecular pathways involved in melanoma and therapeutic strategies targeting them, aiming to improve patient outcomes and overcome treatment resistance by understanding genetic alterations and signaling cascades driving melanoma progression. State of Knowledge: Melanoma arises from genetic predisposition and UV radiation exposure, involving mutations in pathways like RAS/RAF

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Afonso, Mariana, and Maria Alexandra Brito. "Therapeutic Options in Neuro-Oncology." International Journal of Molecular Sciences 23, no. 10 (2022): 5351. http://dx.doi.org/10.3390/ijms23105351.

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One of the biggest challenges in neuro-oncology is understanding the complexity of central nervous system tumors, such as gliomas, in order to develop suitable therapeutics. Conventional therapies in malignant gliomas reconcile surgery and radiotherapy with the use of chemotherapeutic options such as temozolomide, chloroethyl nitrosoureas and the combination therapy of procarbazine, lomustine and vincristine. With the unraveling of deregulated cancer cell signaling pathways, targeted therapies have been developed. The most affected signaling pathways in glioma cells involve tyrosine kinase rec

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Thèses sur le sujet "Targeted therapies, RAS, MEK, PI3K"

CONTINO, GIANMARCO. "Rational design of targeted therapies for Pancreatic adenocarcinoma in K-ras GEMMs." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/55465.

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L’adenocarcinoma pancreatico e’ una delle neoplasie con piu’ alta mortalita’ nei paesi occidentali, con una sopravvivenza media di 6 mesi e una percentuale estremamente bassa di sopravvivenza a lungo termine. L’evento principale nello sviluppo dell’adenocarcinoma pancreatico e’ la mutazione del gene KRAS, che tuttavia e’ particolarmente difficile da colpire a livello molecolare. Strategie terapeutiche piu’ efficaci per l’adenocarcinoma pancreatico possono derivare dall’impiego di terapie molecolari. L'obiettivo di questo lavoro e’ quello di identificare nuovi meccanismi e molecolari e strateg

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Chapitres de livres sur le sujet "Targeted therapies, RAS, MEK, PI3K"

Kursunluoglu, Gizem, Duygu Erdogan, Elcin Cagatay, et al. "The Role of Kinase Inhibitors in Cancer Therapies." In Protein Kinases - Promising Targets for Anticancer Drug Research. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99070.

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Protein kinases are enzymes that transfer a phosphate group to the threonine, serine, or tyrosine residues of the target protein, regulating its activity. The activity of these enzymes are very important and strictly regulated in the cell as they promote cell proliferation, survival, and migration. In the case of any dysregulation of these enzymes, they can be associated with cancer initiation and progression. Small-molecule kinase inhibitors approved by the FDA for their improved clinical benefits are currently used in targeted therapy for the treatment of various cancers. So far, there are 6

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Babu, Geethu, R. Rejnish Ravi Kumar, Malu Rafi, et al. "Systemic Therapy in Thyroid Cancer." In Thyroid Cancer - The Road From Genes to Successful Treatment [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106462.

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The standard treatment for patients with differentiated thyroid cancer (DTC) is a combination of surgery, radioactive iodine (RAI), and long-term thyroid hormone–suppression therapy. Treatment of patients whose diseases persist, recur, or metastasize remains a challenge. The role of cytotoxic chemotherapy in the treatment of thyroid cancer is limited. The key signaling pathways involved in the pathogenesis of thyroid cancers are the RAS/RAF/MEK & PI3K/Akt/mTOR pathways. Systemic therapy in thyroid cancer involves the use of tyrosine kinase inhibitors targeting the above mentioned pathways

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Actes de conférences sur le sujet "Targeted therapies, RAS, MEK, PI3K"

Carlson, JH, P. De, N. Dey, and B. Leyland-Jones. "Abstract P2-03-11: Genetic background determines the algorithm of effectiveness of targeted drugs of RAS and PI3K pathways in TNBC: Testing a combination of MEK 1/2 inhibitor with mTOR kinase inhibitor or AKT inhibitor." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p2-03-11.

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