Institution
Hebron University
Education•Hebron, Palestinian Territory•
About: Hebron University is a education organization based out in Hebron, Palestinian Territory. It is known for research contribution in the topics: Population & Cancer. The organization has 2714 authors who have published 4180 publications receiving 163736 citations.
Papers published on a yearly basis
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TL;DR: The IMpower110 trial as mentioned in this paper showed significant overall survival (OS) benefit with atezolizumab versus chemotherapy in patients with treatment-naive EGFR-and ALK-negative (wild type [WT]) metastatic NSCLC with high-programmed death-ligand 1 (PD-L1) expression (≥50% on tumor cells [TCs] or ≥10% on cancer-infiltrating immune cells [ICs), per SP142 immunohistochemistry assay; p = 0.0106).
50 citations
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Hebron University1, University of Manchester2, Institute of Cancer Research3, University of Oxford4, University of Glasgow5, University Medical Center Groningen6, Radboud University Nijmegen7, Ghent University Hospital8, Netherlands Cancer Institute9, Erasmus University Rotterdam10, Université libre de Bruxelles11
TL;DR: SYD985, (vic-)trastuzumab duocarmazine, is a HER2-targeting antibody-drug conjugate with a cleavable linker-duocarmycin payload that causes irreversible alkylation of the DNA in tum...
Abstract: 1014Background: SYD985, (vic-)trastuzumab duocarmazine, is a HER2-targeting antibody-drug conjugate with a cleavable linker-duocarmycin payload that causes irreversible alkylation of the DNA in tum...
49 citations
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Harvard University1, Sarah Cannon Research Institute2, University of California, San Francisco3, Netherlands Cancer Institute4, Institut Gustave Roussy5, University of North Carolina at Chapel Hill6, University of Milan7, University of Birmingham8, Pinnacle Financial Partners9, Hebron University10, Memorial Sloan Kettering Cancer Center11, Amgen12, Novartis13, Katholieke Universiteit Leuven14
49 citations
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TL;DR: Next-generation sequencing may help identify patients with lung squamous cell carcinoma who would derive additional benefit from treatment with afatinib, and the role of ERBB mutations, particularly HER2 mutations, as predictive biomarkers for afatinIB treatment in this setting warrants further evaluation.
Abstract: Importance Treatment choice for lung squamous cell carcinoma could be aided by identifying predictive biomarkers. Objective To assess whether patient outcomes in the LUX-Lung 8 trial were associated withERBBgene family member aberrations in tumor specimens. Design, Setting, and Participants Ad hoc secondary analysis of the LUX-Lung 8 trial conducted at 183 centers in 23 countries from March 30, 2012, to January 30, 2014. Eligible patients had stage IIIB or IV lung squamous cell carcinoma with progressive disease after 4 or more cycles of platinum-based chemotherapy. Tumor genetic analysis (TGA) was performed using next-generation sequencing in a cohort enriched for patients with progression-free survival (PFS) of more than 2 months. Epidermal growth factor receptor (EGFR) expression levels were assessed by immunohistochemistry in a separate cohort of patients from the LUX-Lung 8 population. Associations of PFS and overall survival (OS) withERBBgene alterations and EGFR expression levels were assessed. This analysis was conducted from February 26, 2015, to June 12, 2017. Interventions Patients were randomized 1:1 to treatment with afatinib dimaleate (40 mg/d; n = 398) or erlotinib hydrochloride (150 mg/d; n = 397). Main Outcomes and Measures Overall survival, PFS, pooled and individualERBBgene mutations,ERBBcopy number alterations, and EGFR expression. Results Tumor specimens from 245 patients were eligible for next-generation sequencing (TGA subset: 132 patients treated with afatinib; 113 patients treated with erlotinib). In this population, outcomes were improved with afatinib vs erlotinib treatment (PFS: median, 3.5 vs 2.5 months; hazard ratio [HR], 0.69; 95% CI, 0.51-0.92;P = .01; OS: median, 8.4 vs 6.6 months; HR, 0.81; 95% CI, 0.62-1.05;P = .12). Of 245 patients in the TGA subset, 53 (21.6%) had tumors with 1 or moreERBBmutations. Among afatinib-treated patients, PFS (median, 4.9 vs 3.0 months; HR, 0.62; 95% CI, 0.37-1.02;P = .06) and OS (median, 10.6 vs 8.1 months; HR, 0.75; 95% CI, 0.47-1.17;P = .21) were longer among those withERBBmutation–positive disease than among those without. The presence ofHER2mutations was associated with favorable PFS and OS following afatinib vs erlotinib treatment. There was no apparent association between copy number alteration or EGFR expression level and outcome. Conclusions and Relevance Next-generation sequencing may help identify patients with lung squamous cell carcinoma who would derive additional benefit from treatment with afatinib. The role ofERBBmutations, particularlyHER2mutations, as predictive biomarkers for afatinib treatment in this setting warrants further evaluation. Trial Registration ClinicalTrials.gov Identifier:NCT01523587
49 citations
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TL;DR: Capivasertib demonstrated clinically meaningful activity in heavily pretreated patients with AKT1E17K-mutant ER+ MBC, including those with prior disease progression on fulvestrant, including the latter group may have had more aggressive disease at baseline.
Abstract: Purpose: The activating mutation AKT1E17K occurs in approximately 7% of estrogen receptor–positive (ER+) metastatic breast cancer (MBC). We report, from a multipart, first-in-human, phase I study (NCT01226316), tolerability and activity of capivasertib, an oral AKT inhibitor, as monotherapy or combined with fulvestrant in expansion cohorts of patients with AKT1E17K-mutant ER+ MBC. Patients and Methods: Patients with an AKT1E17K mutation, detected by local (next-generation sequencing) or central (plasma-based BEAMing) testing, received capivasertib 480 mg twice daily, 4 days on, 3 days off, weekly or 400 mg twice daily combined with fulvestrant at the labeled dose. Study endpoints included safety, objective response rate (ORR; RECIST v1.1), progression-free survival (PFS), and clinical benefit rate at 24 weeks (CBR24). Biomarker analyses were conducted in the combination cohort. Results: From October 2013 to August 2018, 63 heavily pretreated patients received capivasertib (20 monotherapy, 43 combination). ORR was 20% with monotherapy, and within the combination cohort was 36% in fulvestrant-pretreated and 20% in fulvestrant-naive patients, although the latter group may have had more aggressive disease at baseline. AKT1E17K mutations were detectable in plasma by BEAMing (95%, 41/43), droplet digital PCR (80%, 33/41), and next-generation sequencing (76%, 31/41). A ≥50% decrease in AKT1E17K at cycle 2 day 1 was associated with improved PFS. Combination therapy appeared more tolerable than monotherapy [most frequent grade ≥3 adverse events: rash (9% vs. 20%), hyperglycemia (5% vs. 30%), diarrhea (5% vs. 10%)]. Conclusions: Capivasertib demonstrated clinically meaningful activity in heavily pretreated patients with AKT1E17K-mutant ER+ MBC, including those with prior disease progression on fulvestrant. Tolerability and activity appeared improved by the combination.
49 citations
Authors
Showing all 2723 results
Name | H-index | Papers | Citations |
---|---|---|---|
José Baselga | 156 | 707 | 122498 |
M. I. Martínez | 134 | 1251 | 79885 |
Josep Tabernero | 111 | 803 | 68982 |
Jordi Rello | 103 | 694 | 35994 |
Xavier Montalban | 95 | 762 | 52842 |
James M. Downey | 91 | 381 | 29506 |
Enriqueta Felip | 83 | 622 | 53364 |
Joaquim Bellmunt | 82 | 660 | 41472 |
Joan Montaner | 80 | 489 | 22413 |
Marc Miravitlles | 76 | 651 | 25671 |
David H. Salat | 75 | 241 | 36779 |
Eduard Gratacós | 75 | 531 | 20178 |
Alex Rovira | 74 | 356 | 19586 |
Ramon Bataller | 72 | 283 | 19316 |
Maria Buti | 71 | 493 | 26596 |