Relevant bibliographies by topics / AKT1 E17K mutation

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  3. Conference papers

Academic literature on the topic 'AKT1 E17K mutation'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "AKT1 E17K mutation"

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Tolcher, Anthony, Andreas Varkaris, Jordi Rodón, et al. "Abstract P4-08-24: AKTive-001: A Phase 1/1b Multiple Cohort Trial of ALTA2618 in Patients with Advanced Solid Tumors with AKT1 E17K Mutation (Trial in Progress)." Clinical Cancer Research 31, no. 12_Supplement (2025): P4–08–24—P4–08–24. https://doi.org/10.1158/1557-3265.sabcs24-p4-08-24.

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Abstract Background: AKT1 E17K is an activating driver mutation with a prevalence of 4-8% in breast cancer, with the vast majority found in HR+/HER2-negative breast cancer. Approximately 90% of AKT driver mutations are AKT1 E17K, and half of AKT1 E17K-mutant breast and gynecologic cancers are homozygous for the AKT1 E17K oncogene with concurrent loss of the wildtype (WT) AKT1 allele. These genomic features suggest AKT1 E17K exhibits uniquely potent oncogene addiction in these tumor types. Non mutant-selective AKT inhibitors have demonstrated clinical activity in patients with AKT1 E17K-mutant
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Alasmar, Ala’a, Zina Al-Alami, Sima Zein, et al. "Novel Mutations in AKT1 Gene in Prostate Cancer Patients in Jordan." Current Issues in Molecular Biology 46, no. 9 (2024): 9856–66. http://dx.doi.org/10.3390/cimb46090586.

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The AKT1 oncogene is related to various cancers due to its critical role in the PIC3CA/AKT1 pathway; however, most of the studies screened the hotspot mutation AKT1 (E17K) with various incidences. Low frequency or lack of AKT1 (E17K) mutation was reported in prostate cancer (PC) patients. This study aims to explore genetic alterations in the AKT1 PH domain by extending the sequencing to include AKT1 gene exons 3 and 4. Genomic DNA was extracted from 84 Formalin-Fixed Paraffin-Embedded samples of PC patients in Jordan, and then subjected to PCR and sequencing for the targeted exons. This study
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Rudolph, Marion, Tobias Anzeneder, Anke Schulz, et al. "AKT1 E17K mutation profiling in breast cancer: prevalence, concurrent oncogenic alterations, and blood-based detection." BMC Cancer 16, no. 1 (2016): 622. https://doi.org/10.1186/s12885-016-2626-1.

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<strong>Background: </strong>The single hotspot mutation <i>AKT1</i> [G49A:E17K] has been described in several cancers, with the highest incidence observed in breast cancer. However, its precise role in disease etiology remains unknown.<strong>Methods: </strong>We analyzed more than 600 breast cancer tumor samples and circulating tumor DNA for <i>AKT1</i> <sup>E17K</sup> and alterations in other cancer-associated genes using Beads, Emulsions, Amplification, and Magnetics digital polymerase chain reaction technology and targeted exome sequencing.<strong>Results: </strong>Overall <i>AKT1</i> <su
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He, Yanli, Jine Zheng, Yanjie Hu, et al. "Chronic Myeloid Leukemia and BCR/ABL Signal Pathway Are Not Associated with AKT1 Pleckstrin Homology Domain(E17K) Mutations." Blood 114, no. 22 (2009): 4262. http://dx.doi.org/10.1182/blood.v114.22.4262.4262.

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Abstract Abstract 4262 AKT1 E17K mutation was recently found in several human cancers. PI3K/AKT is one of major downstream signal pathways of BCR-ABL oncogene and essential for CML leukemogenesis and IM resistance. More recently, it has been shown that increased PI3K/AKT activity in CML contributes to the development of drug resistance of malignant cells and combination of PI3K/AKT pathway inhibitor and rapamycin can efficiently kill imatinib-resistant BCR-ABL-expressing cells, highlighting the potential of PI3K/AKT as the new targets for CML therapy. Considering the central role of AKT in CML
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Hyman, David M., Lillian M. Smyth, Mark T. A. Donoghue, et al. "AKT Inhibition in Solid Tumors With AKT1 Mutations." Journal of Clinical Oncology 35, no. 20 (2017): 2251–59. http://dx.doi.org/10.1200/jco.2017.73.0143.

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Purpose AKT1 E17K mutations are oncogenic and occur in many cancers at a low prevalence. We performed a multihistology basket study of AZD5363, an ATP-competitive pan-AKT kinase inhibitor, to determine the preliminary activity of AKT inhibition in AKT-mutant cancers. Patients and Methods Fifty-eight patients with advanced solid tumors were treated. The primary end point was safety; secondary end points were progression-free survival (PFS) and response according to Response Evaluation Criteria in Solid Tumors (RECIST). Tumor biopsies and plasma cell-free DNA (cfDNA) were collected in the majori
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Alkhatib, Majd, Gabriele Schackert, and Tareq Juratli. "PATH-35. AKT1(E17K) MUTATIONS ARE FREQUENT GENOMIC EVENTS IN CERVICAL SPINAL MENINGIOMAS." Neuro-Oncology 23, Supplement_6 (2021): vi122—vi123. http://dx.doi.org/10.1093/neuonc/noab196.487.

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Abstract INTRODUCTION Spinal meningiomas represent about one-third of all spine tumors. To date, little is known about the molecular profile of spinal meningiomas and their clinical impact. In this study, we correlate clinical parameters with targeted sequencing findings in a well-characterized cohort of 42 patients with spinal meningiomas. METHODS Samples from 42 spinal meningiomas (31 females and 11 males) were collected. Targeted sequencing for AKT1 E17K hot spot mutations was performed. Furthermore, clinical and imaging data were collected and correlated with the AKT1 mutation status. RESU
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Mohamedali, Azim, Nicholas C. Lea, Roger M. Feakins, Kavita Raj, Ghulam J. Mufti, and Hemant M. Kocher. "AKT1 (E17K) Mutation in Pancreatic Cancer." Technology in Cancer Research & Treatment 7, no. 5 (2008): 407–8. http://dx.doi.org/10.1177/153303460800700509.

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The prevalence of a novel somatic mutation (E17K) in the pleckstrin homology domain of AKT1 was investigated in pancreatic cancer using a quantitative pyrosequencing assay. This mutation was un-detectable in pancreatic cancer tissue samples (n=65) and pancreatic cell line (n=10) DNA suggesting that pancreatic cancer progression is mainly dependent on the K-Ras mutation.
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Williams, Sally R., Tareq A. Juratli, Brandyn A. Castro, et al. "Genomic Analysis of Posterior Fossa Meningioma Demonstrates Frequent AKT1 E17K Mutations in Foramen Magnum Meningiomas." Journal of Neurological Surgery Part B: Skull Base 80, no. 06 (2019): 562–67. http://dx.doi.org/10.1055/s-0038-1676821.

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Objective Posterior fossa meningiomas are surgically challenging tumors that are associated with high morbidity and mortality. We sought to investigate the anatomical distribution of clinically actionable mutations in posterior fossa meningioma to facilitate identifying patients amenable for systemic targeted therapy trials. Methods Targeted sequencing of clinically targetable AKT1, SMO, and PIK3CA mutations was performed in 61 posterior fossa meningioma using Illumina NextSeq 500 to a target depth of &gt;500 × . Samples were further interrogated for 53 cancer-relevant RNA fusions by the Arche
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Gan, PingPing, Yi Lu, Xiaomin Li, et al. "AKT1 in Asia: A landscape analysis of 11,813 Chinese tumor samples." Journal of Clinical Oncology 39, no. 15_suppl (2021): e15076-e15076. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15076.

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e15076 Background: AKT1 is a key gene of the PI3K/AKT/mTOR signalling pathway. The recent development of ATK1 targeting drug has shown great promise. It is thus important to understand the genomic landscape of AKT1 in a specific population. Methods: Sequencing data of 11,813 tumor samples collected in China were analyzed for AKT1 mutation status. Concomitant genomic aberrations were further analyzed in tumors with AKT1 mutations. Results: AKT1 mutations were observed in 173 of 11,813 tumor samples (1.46%). The most common cancer types in our study included cervical (5.17%), breast (5.15%), ost
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Hua, Lingyang, Majd Alkhatib, Matthias Meinhardt, et al. "SURG-11. AKT1 E17K AND NF2 MUTATIONS DOMINATE SPINAL MENINGIOMAS WHO GRADE 1 AND PRESENT DISTINCT TUMOR FEATURES." Neuro-Oncology 24, Supplement_7 (2022): vii253. http://dx.doi.org/10.1093/neuonc/noac209.977.

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Abstract INTRODUCTION While the mutational landscape of intracranial meningiomas has been extensively studied, our understanding of the molecular profile of spinal meningiomas (SM) remains incomplete. In this study, we correlate the molecular status with tumor features in a clinically well-characterized cohort. METHODS Samples from 50 patients (38 females and 12 males) with WHO grade 1 SM were collected. We performed next-generation sequencing (NGS) using an assay covering frequently mutated genes in meningiomas including AKT1, KLF4, NF2, PIK3CA, POLR2A, SMARCB1, SMARCE1, SMO, SUFU, and TRAF7.
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Dissertations / Theses on the topic "AKT1 E17K mutation"

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Deyle, Kaycie Marie. "Development of Protein-Catalyzed Capture (PCC) Agents with Application to the Specific Targeting of the E17K Point Mutation of AKt1." Thesis, 2014. https://thesis.library.caltech.edu/8398/43/Deyle_Kaycie_2014_Thesis_Ch2.pdf.

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<p>This thesis describes the expansion and improvement of the iterative in situ click chemistry OBOC peptide library screening technology. Previous work provided a proof-of-concept demonstration that this technique was advantageous for the production of protein-catalyzed capture (PCC) agents that could be used as drop-in replacements for antibodies in a variety of applications. Chapter 2 describes the technology development that was undertaken to optimize this screening process and make it readily available for a wide variety of targets. This optimization is what has allowed for the explosi
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Conference papers on the topic "AKT1 E17K mutation"

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Rudolph, Marion, Tobias Anzeneder, Matthias Ocker, et al. "Abstract 569: AKT1 (E17K) mutation: coexistence with oncogenic alterations, prevalence, and correlation to clinical parameter in a large series of breast cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-569.

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