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Journal articles on the topic 'AKT1 E17K mutation'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

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 >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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Wang, Guoqian, Yao Tang, Jingxiao Xu, et al. "Abstract 6917: Ba/F3 AKT engineering cell lines, a useful platform for novel drug discovery." Cancer Research 84, no. 6_Supplement (2024): 6917. http://dx.doi.org/10.1158/1538-7445.am2024-6917.

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Abstract AKT, also known as phosphoinositide 3-kinase (PI3K), plays a key role in various signaling cascades involved in cell growth and division, apoptosis inhibition, and angiogenesis. For AKT, which is at the central node of the PI3K/AKT/mTOR signaling pathway, the loss of PTEN, mutation, or amplification of AKT/PIK3CA can lead to the overactivation of the AKT signaling pathway, resulting in the occurrence and development of tumors. Recent studies have also found that AKT activation is associated with drug resistance in tumor therapy. Therefore, AKT has become a hot target for tumor therapy

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Mearns, Sarah, Alex Pearson, Ros Cutts, et al. "Abstract P1-01-19: Predicting response to capivasertib in AKT1 mutant advanced breast cancer." Clinical Cancer Research 31, no. 12_Supplement (2025): P1–01–19—P1–01–19. https://doi.org/10.1158/1557-3265.sabcs24-p1-01-19.

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Abstract Introduction: Activation of the PI3K-AKT and mTOR pathways is a major feature of the biology of breast cancer (BC), with these pathways altered or dysregulated in most BC. Oncogenic mutations in AKT1, most frequently E17K, are found in ∼5% of advanced BC and are targetable by the approved AKT inhibitor capivasertib. We conducted genomic and transcriptomic analysis of a cohort of AKT1 mutant metastatic BCs with the aim to identify determinants of response to capivasertib. Methods: We identified 39 AKT1 mutant BC from the plasmaMATCH clinical trial (18/39; NCT03182634), the FAKTION clin

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Cohen, Yoram, Bruria Shalmon, Jacob Korach, Iris Barshack, Eddie Fridman, and Gideon Rechavi. "AKT1 pleckstrin homology domain E17K activating mutation in endometrial carcinoma." Gynecologic Oncology 116, no. 1 (2010): 88–91. http://dx.doi.org/10.1016/j.ygyno.2009.09.038.

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Thomas, David Morgan, Gennaro Daniele, Jeong Eun Kim, et al. "Ipatasertib in patients with AKT1/2/3 mutation-positive (AKTmut) tumors: TAPISTRY study." Journal of Clinical Oncology 42, no. 16_suppl (2024): 3092. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.3092.

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3092 Background: AKT1/2/3 point mutations are found in ~1% of all solid tumors, with varying prevalence across different tumor types. Ipatasertib is an inhibitor of the AKT kinase, but its antitumor activity as monotherapy in patients with AKTmut tumors is unknown. We present efficacy and safety data of ipatasertib in patients with advanced/metastatic AKTmut solid tumors from Cohort E of the TAPISTRY trial (NCT04589845). Methods: TAPISTRY is a phase II, global, open-label, multi-cohort trial evaluating the efficacy and safety of different therapies in patients with advanced/metastatic solid tu

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Akther, Yeasmin, Jemma Dunn, Claire Adams, Vikram Sharma, Matthew Banton, and Clemens Hanemann. "CSIG-27. PROTEOMIC ANALYSIS OF GENETICALLY STRATIFIED MENINGIOMA." Neuro-Oncology 23, Supplement_6 (2021): vi39. http://dx.doi.org/10.1093/neuonc/noab196.153.

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Abstract WHO grade II and III as well as some WHO grade I meningioma are clinically aggressive. Approximately 60% sporadic meningiomas harbour mutations in the NF2 gene, others in genes including TRAF7, KLF4, AKT1, SMO and PIK3CA . However, the molecular mechanisms behind meningioma tumourigenesis are still unclear. We aim to identify novel biomarkers and therapeutic targets of meningioma by characterising the proteomic landscape. We performed (phosho)proteomic profiling of grade I, II and III meningiomas and three different mutational groups: AKT1 E17K /TRAF7, KLF4 K409Q /TRAF7 and NF2 -/-. W

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Mancini, Maria L., Evan C. Lien, and Alex Toker. "Oncogenic AKT1(E17K) mutation induces mammary hyperplasia but prevents HER2-driven tumorigenesis." Oncotarget 7, no. 14 (2016): 17301–13. http://dx.doi.org/10.18632/oncotarget.8191.

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Rajput, Sanjna, and Karthik V. Giridhar. "Abstract P1-12-17: A case of sequential alpelisib and capivasertib in a patient with metastatic breast cancer harboring both a PIK3CA and AKT mutations." Clinical Cancer Research 31, no. 12_Supplement (2025): P1–12–17—P1–12–17. https://doi.org/10.1158/1557-3265.sabcs24-p1-12-17.

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Abstract Introduction: Somatic mutations in the PIK3CA/AKT/mTOR pathway are associated with resistance to first-line endocrine therapy in hormone-receptor positive (HR+) breast cancer (BC). PIK3CA and AKT1 mutations are reported in 35-40% and 4-7% of HR+ BC respectively, with less published about the rates of co-occurrence (PMID: 32983983). Therapies targeting mutations in this pathway approved in conjunction with endocrine therapy include alpelisib, everolimus and capivasertib. Prior cohort data showed limited benefit of alpelisib after everolimus (PMID:36292649). Recent data notes that AKT e

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Smilkou, Stavroula, Aliki Ntzifa, Dimitra Stergiopoulou, et al. "Abstract 6701: 6-color Crystal Digital PCR for the high-plex detection of 10 ESR1 mutations in breast cancer." Cancer Research 83, no. 7_Supplement (2023): 6701. http://dx.doi.org/10.1158/1538-7445.am2023-6701.

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Abstract Introduction. ESR1 mutations have emerged as a key mechanism of resistance to endocrine therapy in estrogen-receptor-positive (ER+) breast cancer, thus detection of ESR1 mutations is crucial to monitor during patient treatment. We evaluated a novel 12plex breast cancer assay for the detection of 10 ESR1 mutations and AKT1 E17K in plasma cell-free DNA (cfDNA) using 6-color Crystal Digital PCRTM (naica® system, Stilla Technologies, France). We further compared the results with our previously reported ESR1 NAPA assay for D538G, Y537S, Y537C and Y537N mutations (Stergiopoulou et al, Cance

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Askham, J. M., F. Platt, P. A. Chambers, H. Snowden, C. F. Taylor, and M. A. Knowles. "AKT1 mutations in bladder cancer: identification of a novel oncogenic mutation that can co-operate with E17K." Oncogene 29, no. 1 (2009): 150–55. http://dx.doi.org/10.1038/onc.2009.315.

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Kumar, Ambuj, and Rituraj Purohit. "Cancer Associated E17K Mutation Causes Rapid Conformational Drift in AKT1 Pleckstrin Homology (PH) Domain." PLoS ONE 8, no. 5 (2013): e64364. http://dx.doi.org/10.1371/journal.pone.0064364.

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Lauring, J., D. P. Cosgrove, S. Fontana, et al. "Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations." Oncogene 29, no. 16 (2010): 2337–45. http://dx.doi.org/10.1038/onc.2009.516.

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Trivedi, Harsha, Omar Hamdani, Brittani Thomas, et al. "Patient with Lobular Carcinoma of the Breast and Activating AKT1 E17K Variant." Acta Medica Academica 50, no. 1 (2021): 209. http://dx.doi.org/10.5644/ama2006-124.336.

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<p><strong>Objective</strong>. To present the characteristics of the AKT1E117K gene variant and a description of the clinical application in a patient with metastatic breast cancer.</p><p><strong>Results</strong>. 63 y/o woman with Stage IV Invasive lobular carcinoma at diagnosis was treated with Palbociclib and aromatase inhibitors (AI). At progression, tissue was sent for comprehensive genomic profiling to Foundation Medicine (FM) which revealed AKT1E17K mutation. In lieu of available clinical data within the patient’s tumor type (HR+ HER2- breast ca

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Sengupta, Shomit, Aaron Coffin, Anna C. Schinzel, et al. "Abstract LB008: ATV-1601, a potent and selective allosteric inhibitor of AKT1E17K, demonstrates profound and durable regressions in multiple patient and cell derived xenograft models." Cancer Research 85, no. 8_Supplement_2 (2025): LB008. https://doi.org/10.1158/1538-7445.am2025-lb008.

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Abstract Background: Hyperactive AKT signaling drives tumorigenesis across a wide swath of solid tumors. Of the three AKT isoforms, multiple lines of evidence point to AKT1 as the key isoform that drives tumorigenesis including genetic screens in PIK3CA/PTEN mutant cancer cell lines identifying AKT1 as a dependency, and an oncogenic gain-of-function mutation in the AKT1 Pleckstrin-Homology domain from glutamic acid to lysine (E17K). AKT1E17K driver mutations are predominantly found in ER+/HER2- breast cancer and also occur as a mechanism of acquired resistance to PIK3CAi treatment in these tum

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Tao, Jacqueline, Saumya Sisoudiya, Smruthy Sivakumar, Ethan Sokol, and Neil Vasan. "Abstract P5-02-20: Clinicogenomic landscape and function of PIK3CA, AKT1, and PTEN mutations in breast cancer." Clinical Cancer Research 31, no. 12_Supplement (2025): P5–02–20—P5–02–20. https://doi.org/10.1158/1557-3265.sabcs24-p5-02-20.

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Abstract Background: The AKT inhibitor capivasertib was recently approved in the 2L+ setting for patients (pts) with hormone receptor-positive metastatic breast cancer with alterations in PIK3CA, AKT1, and/or PTEN. There is a need to further characterize the landscape of PIK3CA, AKT1, and PTEN mutations in breast cancer and their functions, to improve our understanding and therapeutic targeting of PI3K-driven breast cancer. Methods: 51,767 pts with breast cancer who underwent tumor sequencing using FoundationOne®CDx or FoundationOne® were included in this analysis. We assessed the frequency, t

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Franken, André, Bianca Behrens, Florian Reinhardt, et al. "Multiparametric Circulating Tumor Cell Analysis to Select Targeted Therapies for Breast Cancer Patients." Cancers 13, no. 23 (2021): 6004. http://dx.doi.org/10.3390/cancers13236004.

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Background: The analysis of liquid biopsies, e.g., circulating tumor cells (CTCs) is an appealing diagnostic concept for targeted therapy selection. In this proof-of-concept study, we aimed to perform multiparametric analyses of CTCs to select targeted therapies for metastatic breast cancer patients. Methods: First, CTCs of five metastatic breast cancer patients were analyzed by whole exome sequencing (WES). Based on the results, one patient was selected and monitored by longitudinal and multiparametric liquid biopsy analyses over more than three years, including WES, RNA profiling, and in vit

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de Bruin, Elza C., Jessica L. Whiteley, Claire Corcoran, et al. "Accurate detection of low prevalence AKT1 E17K mutation in tissue or plasma from advanced cancer patients." PLOS ONE 12, no. 5 (2017): e0175779. http://dx.doi.org/10.1371/journal.pone.0175779.

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Mahmoud, I. S., M. A. Sughayer, H. A. Mohammad, et al. "The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias." British Journal of Cancer 99, no. 3 (2008): 488–90. http://dx.doi.org/10.1038/sj.bjc.6604512.

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Do, Hongdo, Benjamin Solomon, Paul L. Mitchell, Stephen B. Fox, and Alexander Dobrovic. "Detection of the transforming AKT1 mutation E17K in non-small cell lung cancer by high resolution melting." BMC Research Notes 1, no. 1 (2008): 14. http://dx.doi.org/10.1186/1756-0500-1-14.

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Perkins, G., J. Dukes, T. A. Yap, et al. "Prospective study of genetic mutations in matched tumor and plasma specimens in colorectal cancer patients." Journal of Clinical Oncology 29, no. 4_suppl (2011): 356. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.356.

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356 Background: Circulating free DNA (cfDNA) represents a minimally-invasive resource for detecting mutations in advanced cancer patients. The primary objective of this study was to determine if cfDNA is representative of tumor tissue for multiplex mutation detection utilizing Sequenom MassARRAY. Methods: Samples were spiked with dilutions (10ng/μl to 0.01ng/μl) of HCT116 DNA containing KRAS G13D mutations to determine assay sensitivity and specificity. Metastatic colorectal cancer patients referred to the Drug Development Unit at the Royal Marsden Hospital between 9/09-8/10 gave their consent

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Behl, Deepti, Michael Rothe, Pam K. Mangat, et al. "Abstract CT267: Temsirolimus (T) in patients (pts) with solid tumors with AKT1/3 amplification (amp) or mutation (mut): Results from the Targeted Agent and Profiling Utilization Registry (TAPUR) Study." Cancer Research 84, no. 7_Supplement (2024): CT267. http://dx.doi.org/10.1158/1538-7445.am2024-ct267.

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Abstract Background: TAPUR is a phase II basket study evaluating antitumor activity of commercially available targeted agents in pts with advanced cancers with specific genomic alterations. Results in a cohort of pts with solid tumors with AKT1/3 amp or mut treated with T are reported. Methods: Eligible pts had solid tumors, measurable disease, ECOG performance status (PS) 0-2, adequate organ function, and no standard treatment (tx) options. Genomic testing was performed in CLIA-certified, CAP-accredited site selected labs. After antihistamine pretreatment, 25 mg T was infused over 30-60 minut

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Eom, Hyeon Seok, Min Sung Kim, Soo Young Hur, Nam Jin Yoo, and Sug Hyung Lee. "Absence of oncogenic AKT1 E17K mutation in prostate, esophageal, laryngeal and urothelial carcinomas, hepatoblastomas, gastrointestinal stromal tumors and malignant meningiomas." Acta Oncologica 48, no. 7 (2009): 1084–85. http://dx.doi.org/10.1080/02841860902878152.

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Deyle, Kaycie M., Blake Farrow, Ying Qiao Hee, et al. "A protein-targeting strategy used to develop a selective inhibitor of the E17K point mutation in the PH domain of Akt1." Nature Chemistry 7, no. 5 (2015): 455–62. http://dx.doi.org/10.1038/nchem.2223.

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Jones, Robert Hugh, Angela Claire Casbard, Margherita Carucci, et al. "Fulvestrant plus capivasertib versus fulvestrant plus placebo after relapse or progression on an aromatase inhibitor in metastatic, estrogen receptor–positive breast cancer (FAKTION): Overall survival and updated progression-free survival data with enhanced biomarker analysis." Journal of Clinical Oncology 40, no. 16_suppl (2022): 1005. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.1005.

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1005 Background: Previous results from the Phase 2 FAKTION trial (NCT01992952) showed progression free survival (PFS) in patients with aromatase inhibitor (AI) resistant ER+/HER2− advanced breast cancer was significantly longer with fulvestrant plus capivasertib vs fulvestrant plus placebo. At the time of analysis, PFS benefit associated with capivasertib was not restricted to patients with activating mutations in PIK3CA (E542K, E545K, H1047R or H1047L) or PTEN protein null. We report now mature overall survival (OS) data with enhanced biomarker analysis. Methods: For the enhanced analysis, av

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Thirumal Kumar, D., Nikita Jain, Judith Evangeline, et al. "A computational approach for investigating the mutational landscape of RAC-alpha serine/threonine-protein kinase (AKT1) and screening inhibitors against the oncogenic E17K mutation causing breast cancer." Computers in Biology and Medicine 115 (December 2019): 103513. http://dx.doi.org/10.1016/j.compbiomed.2019.103513.

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Guo, G., X. Qiu, S. Wang, et al. "Oncogenic E17K mutation in the pleckstrin homology domain of AKT1 promotes v-Abl-mediated pre-B-cell transformation and survival of Pim-deficient cells." Oncogene 29, no. 26 (2010): 3845–53. http://dx.doi.org/10.1038/onc.2010.149.

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Sengupta, Shomit, Anna C. Schinzel, Aaron Coffin, et al. "Abstract P5-04-24: ATV-1601 is a Potent and Selective Allosteric Inhibitor of AKT1E17K and Shows Profound and Durable Regressions in AKT1E17K-Driven Patient Derived Xenograft Models." Clinical Cancer Research 31, no. 12_Supplement (2025): P5–04–24—P5–04–24. https://doi.org/10.1158/1557-3265.sabcs24-p5-04-24.

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Abstract Background: The AKT pathway modulates cell survival and proliferation in response to insulin and growth factor signaling. A gain-of-function mutation in the AKT1 Pleckstrin-Homology domain from glutamic acid to lysine (E17K) leads to constitutive activation resulting in tumorigenesis. AKT1E17K driver mutations are predominantly found in ER+/HER2- breast cancer and occur as a mechanism of acquired resistance to PIK3CAi treatment in these tumors. Additionally, AKT1E17K mutations are found in triple negative breast cancer, endometrial cancer, prostate cancer and meningiomas among other s

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Murphy, Eric A., Michael D. Bartberger, Maureen Ibanez, et al. "Abstract LB173: Discovery of ALTA-2618, the first allosteric, mutant-selective targeted therapy for AKT1 E17K driven cancers." Cancer Research 84, no. 7_Supplement (2024): LB173. http://dx.doi.org/10.1158/1538-7445.am2024-lb173.

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Abstract BACKGROUND: AKT1 E17K is a clinically validated oncogenic driver mutated in ~1-2% of all cancers and is enriched in several solid tumors including breast (~5%), endometrial (~3%) and prostate (~1.5%) cancer. Over half of AKT1 E17K mutant breast and gynecologic cancers are homozygous for the mutant oncogene with loss of the wildtype (WT) AKT1 allele via copy-neutral loss-of-heterozygosity (CN-LOH), suggesting uniquely potent oncogene addiction in these tumor types. While inhibitors of WT PI3K or AKT have demonstrated clinical efficacy in HR+/HER2- metastatic breast cancers with PI3K/AK

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Singh, Neeraj, and Smita Agrawal. "Abstract 3829: Identifying the genetic basis for resistance to aromatase inhibitors (AIs) in metastatic breast cancer (mBC) patients." Cancer Research 84, no. 6_Supplement (2024): 3829. http://dx.doi.org/10.1158/1538-7445.am2024-3829.

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Abstract Background: AIs, such as letrozole, anastrozole, and exemestane, are used to treat hormonal receptor positive (HR+) breast cancer (BC) patients. Many patients either respond poorly or relapse on AIs. A comprehensive view of the underlying genomic landscape of such patients may aid in a better understanding of the resistance mechanisms and the development of new targeted therapies. This study leveraged a real-world clinico-genomic dataset of BC patients to identify key biomarkers and the corresponding high frequency mutations in this relapse/refractory patient population. Methods: This

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Harb, Wael, Mansoor N. Saleh, Kyriakos P. Papadopoulos, et al. "Clinical Trial Results from the Subgroup of Lymphoma/CLL in a Phase 1 Study of ARQ 092, a Novel Pan AKT-Inhibitor." Blood 126, no. 23 (2015): 5116. http://dx.doi.org/10.1182/blood.v126.23.5116.5116.

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Abstract Background: ARQ 092 is an oral allosteric, potent and selective AKT inhibitor with in vitro and in vivo activity in solid and hematological tumors. ARQ 092-101, the first clinical trial of ARQ 092, has enrolled more than 100 subjects with advanced solid tumors or recurrent malignant lymphoma. As reported previously, the dose escalation portion of the study has been completed and two dosing schedules (intermittent and weekly), are recommended for phase 2 studies. The recommended phase 2 dose (RP2D) for the intermittent dosing schedule is 200 mg once daily (QD) (one week on, one week of

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Smyth, Lillian M., Jonathan B. Reichel, Jiabin Tang, et al. "Utility of Serial cfDNA NGS for Prospective Genomic Analysis of Patients on a Phase I Basket Study." JCO Precision Oncology, no. 5 (January 2021): 6–16. http://dx.doi.org/10.1200/po.20.00184.

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PURPOSE Cell-free DNA (cfDNA) analysis offers a noninvasive means to access the tumor genome. Despite limited sensitivity of broad-panel sequencing for detecting low-frequency mutations in cfDNA, it may enable more comprehensive genomic characterization in patients with sufficiently high disease burden. We investigated the utility of large-panel cfDNA sequencing in patients enrolled to a Phase I AKT1-mutant solid tumor basket study. METHODS Patients had AKT1 E17K-mutant solid tumors and were treated on the multicenter basket study (ClinicalTrials.gov identifier: NCT01226316 ) of capivasertib,

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Smyth, Lillian M., Jonathan B. Reichel, Jiabin Tang, et al. "Utility of Serial cfDNA NGS for Prospective Genomic Analysis of Patients on a Phase I Basket Study." JCO Precision Oncology, no. 5 (January 2021): 6–16. http://dx.doi.org/10.1200/po.20.00184.

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PURPOSE Cell-free DNA (cfDNA) analysis offers a noninvasive means to access the tumor genome. Despite limited sensitivity of broad-panel sequencing for detecting low-frequency mutations in cfDNA, it may enable more comprehensive genomic characterization in patients with sufficiently high disease burden. We investigated the utility of large-panel cfDNA sequencing in patients enrolled to a Phase I AKT1-mutant solid tumor basket study. METHODS Patients had AKT1 E17K-mutant solid tumors and were treated on the multicenter basket study (ClinicalTrials.gov identifier: NCT01226316 ) of capivasertib,

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Hua, Lingyang, Shingo Fujio, Majd Alkhatib, et al. "PATH-51. GENETIC CHARACTERIZATION AND MUTATIONAL PROFILING OF FORAMEN MAGNUM MENINGIOMAS: A MULTI-INSTITUTIONAL STUDY." Neuro-Oncology 25, Supplement_5 (2023): v180. http://dx.doi.org/10.1093/neuonc/noad179.0681.

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Abstract OBJECTIVE Foramen magnum (FM) meningiomas pose significant surgical challenges and have high morbidity and mortality rates. This study aims to investigate the distribution of clinically actionable mutations in FM meningiomas and identify clinical characteristics associated with specific mutational profiles. METHODS We conducted targeted next-generation sequencing of 62 FM meningiomas from three international institutions, covering all relevant meningioma genes (AKT1, KLF4, NF2, POLR2A, PIK3CA, SMO, and TRAF7). Additionally, we retrospectively collected and evaluated patient and tumor

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Shafer, Paul, Wingchi K. Leung, Mae L. Woods, et al. "Abstract P6-10-11: Engineered neoantigen-specific T cell receptors to treat metastatic breast cancer." Cancer Research 83, no. 5_Supplement (2023): P6–10–11—P6–10–11. http://dx.doi.org/10.1158/1538-7445.sabcs22-p6-10-11.

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Abstract T cell receptor engineered T cell (TCR T) therapy has emerged as a promising therapeutic modality for solid cancer following recent trials demonstrating the safety and efficacy of TCR T therapies against some types of metastatic solid cancers. However, the broader application of TCR T towards many solid tumors, including metastatic breast cancer (MBC), has been limited by several factors, chiefly among them the current scarcity of tumor selective target antigens. Neoantigens, which are expressed exclusively in cancer cells, are currently underrepresented in TCR T development, being ta

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Roudnicky, Filip, Yanjun Lan, Max Friesen, et al. "Modeling the Effects of Severe Metabolic Disease by Genome Editing of hPSC-Derived Endothelial Cells Reveals an Inflammatory Phenotype." International Journal of Molecular Sciences 20, no. 24 (2019): 6201. http://dx.doi.org/10.3390/ijms20246201.

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The kinase AKT2 (PKB) is an important mediator of insulin signaling, for which loss-of-function knockout (KO) mutants lead to early onset diabetes mellitus, and dominant active mutations lead to early development of obesity and endothelial cell (EC) dysfunction. To model EC dysfunction, we used edited human pluripotent stem cells (hPSCs) that carried either a homozygous deletion of AKT2 (AKT2 KO) or a dominant active mutation (AKT2 E17K), which, along with the parental wild type (WT), were differentiated into ECs. Profiling of EC lines indicated an increase in proinflammatory and a reduction i

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Gallay, Nathalie, Cédric Dos Santos, Lise Cuzin, et al. "The Level of AKT Phosphorylation on Threonine 308 but Not on Serine 473 Is Associated with High-Risk Cytogenetics and Predicts Poor Overall Survival in Acute Myeloid Leukemia." Blood 112, no. 11 (2008): 1503. http://dx.doi.org/10.1182/blood.v112.11.1503.1503.

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Abstract The PI3K/Akt pathway is an important signaling pathway governing cell survival, proliferation and drug resistance in AML. However, the prognosis impact of Akt phosphorylation in AML has yielded some controversies as far as the phosphorylation on Ser473 is concerned. Because full activation of Akt requires phosphorylation on both Thr308 and Ser473, the assessment of these two sites would allow a more complete analysis of Akt activation in AML cells. We have studied the level of phosphorylation on both sites in primary AML samples by flow cytometry. We retrospectively assessed samples f

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Adams, Claire L., Emanuela Ercolano, Sara Ferluga, et al. "A Rapid Robust Method for Subgrouping Non-NF2 Meningiomas According to Genotype and Detection of Lower Levels of M2 Macrophages in AKT1 E17K Mutated Tumours." International Journal of Molecular Sciences 21, no. 4 (2020): 1273. http://dx.doi.org/10.3390/ijms21041273.

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The majority of meningiomas are grade I, but some grade I tumours are clinically more aggressive. Recent advances in the genetic study of meningiomas has allowed investigation into the influence of genetics on the tumour microenvironment, which is important for tumorigenesis. We have established that the endpoint genotyping method Kompetitive Allele Specific PCR (KASP™) is a fast, reliable method for the screening of meningioma samples into different non-NF2 mutational groups using a standard real-time PCR instrument. This genotyping method and four-colour flow cytometry has enabled us to asse

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Kim, M. S., E. G. Jeong, N. J. Yoo, and S. H. Lee. "Mutational analysis of oncogenic AKT E17K mutation in common solid cancers and acute leukaemias." British Journal of Cancer 98, no. 9 (2008): 1533–35. http://dx.doi.org/10.1038/sj.bjc.6604212.

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Rooper, Lisa M., Prokopios P. Argyris, Lester D. R. Thompson, et al. "Salivary Mucinous Adenocarcinoma Is a Histologically Diverse Single Entity With Recurrent AKT1 E17K Mutations." American Journal of Surgical Pathology 45, no. 10 (2021): 1337–47. http://dx.doi.org/10.1097/pas.0000000000001688.

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Zilberman, Dorit E., Yoram Cohen, Ninette Amariglio, Edward Fridman, Jacob Ramon, and Gideon Rechavi. "AKT1 E17 K pleckstrin homology domain mutation in urothelial carcinoma." Cancer Genetics and Cytogenetics 191, no. 1 (2009): 34–37. http://dx.doi.org/10.1016/j.cancergencyto.2009.01.009.

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Pant, Asmita, Yue Chen, Annapurna Kuppa, Xiaomeng Du, Brian D. Halligan, and Elizabeth K. Speliotes. "Perturbation of TM6SF2 Expression Alters Lipid Metabolism in a Human Liver Cell Line." International Journal of Molecular Sciences 22, no. 18 (2021): 9758. http://dx.doi.org/10.3390/ijms22189758.

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Non-alcoholic fatty liver disease (NAFLD) is caused by excess lipid accumulation in hepatocytes. Genome-wide association studies have identified a strong association of NAFLD with non-synonymous E167K amino acid mutation in the transmembrane 6 superfamily member 2 (TM6SF2) protein. The E167K mutation reduces TM6SF2 stability, and its carriers display increased hepatic lipids and lower serum triglycerides. However, the effects of TM6SF2 on hepatic lipid metabolism are not completely understood. We overexpressed wild-type or E167K variant of TM6SF2 or knocked down TM6SF2 expression in lipid-trea

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