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
Papers
More filters
••
Harvard University1, University of California, Los Angeles2, Curie Institute3, Université libre de Bruxelles4, Hebron University5, University of Pittsburgh6, Ohio State University7, Memorial Sloan Kettering Cancer Center8, Northside Hospital9, Georgetown University10, Baylor University Medical Center11, Jewish General Hospital12, Queen Mary University of London13, University of North Carolina at Chapel Hill14, University of California, San Francisco15
TL;DR: The Sacituzumab govitecan (SgoVitecan) is an antibody-drug conjugate composed of an antibody targeting the human tro... as mentioned in this paper.
Abstract: Background Patients with metastatic triple-negative breast cancer have a poor prognosis. Sacituzumab govitecan is an antibody–drug conjugate composed of an antibody targeting the human tro...
387 citations
••
University of Ioannina1, Sun Yat-sen University2, University of Ulsan3, National University of Malaysia4, National Taiwan University5, Mayo Clinic6, Zhejiang University7, Yonsei University8, Hospital Kuala Lumpur9, National Health Research Institutes10, University of Texas MD Anderson Cancer Center11, St. Marianna University School of Medicine12, Kanazawa University13, University of Valencia14, Hebron University15, Kobe University16
TL;DR: These guidelines represent the consensus opinions reached by experts in the treatment of patients with mCRC identified by the Presidents of the oncological societies of Japan (JSMO), China, Korea, Malaysia, Singapore, Singapore and Taiwan.
386 citations
••
TL;DR: This study demonstrates a good correlation between the degree of inhibition of EGFR in skin and in breast tumors, and the lack of significant clinical activity of gefitinib in the study population is not due to lack of receptor inhibition in these tumors but rather to lackof EGFR dependence in the tested population.
Abstract: Purpose To evaluate the antitumor activity and pharmacodynamic/biologic effect of gefitinib 500 mg/day monotherapy in patients with previously treated, advanced breast cancer. Methods In this phase II multicenter trial, the primary objective was assessment of the tumor response rate with gefitinib; secondary objectives included analysis of the pharmacodynamic and biologic profiles in healthy and tumor tissue. Results Of 31 assessable patients, 12 (38.7%) had stable disease, including 3 (9.7%) with recurrent breast cancer that stabilized for ≥ 6 months. No complete or partial responses were observed. Pretreatment tumor samples were available in all patients. In addition, paired baseline and on-treatment (day 28) assessable skin and tumor biopsies were available in 27 and 16 patients, respectively. Sequential immunohistochemical studies in skin and tumor biopsies demonstrated complete inhibition of epidermal growth factor receptor (EGFR) phosphorylation in both healthy and malignant tissues. The downstream ...
385 citations
••
TL;DR: Lapatinib-induced accumulation of HER2 at the cell surface by lapatinib enhanced immune-mediated trastuzumab-dependent cytotoxicity is proposed that may be clinically relevant and exploitable in the therapy of patients with HER2-positive tumors.
Abstract: Lapatinib is a human epidermal growth factor receptor 2 (HER2) tyrosine kinase inhibitor (TKI) that has clinical activity in HER2-amplified breast cancer. In vitro studies have shown that lapatinib enhances the effects of the monoclonal antibody trastuzumab suggesting partially non-overlapping mechanisms of action. To dissect these mechanisms, we have studied the effects of lapatinib and trastuzumab on receptor expression and receptor signaling and have identified a new potential mechanism for the enhanced antitumor activity of the combination. Lapatinib, given alone or in combination with trastuzumab to HER2-overexpressing breast cancer cells SKBR3 and MCF7-HER2, inhibited HER2 phosphorylation, prevented receptor ubiquitination and resulted in a marked accumulation of inactive receptors at the cell surface. By contrast, trastuzumab alone caused enhanced HER2 phosphorylation, ubiquitination and degradation of the receptor. By immunoprecipitation and computational protein modeling techniques we have shown that the lapatinib-induced HER2 accumulation at the cell surface also results in the stabilization of inactive HER2 homo- (HER2/HER2) and hetero- (HER2/EGFR and HER2/HER3) dimers. Lapatinib-induced accumulation of HER2 and trastuzumab-mediated downregulation of HER2 was also observed in vivo, where the combination of the two agents triggered complete tumor remissions in all cases after 10 days of treatment. Accumulation of HER2 at the cell surface by lapatinib enhanced immune-mediated trastuzumab-dependent cytotoxicity. We propose that this is a novel mechanism of action of the combination that may be clinically relevant and exploitable in the therapy of patients with HER2-positive tumors.
382 citations
••
TL;DR: A review of the literature is provided, with the aim of differentiating the genomic contexts in which these various types of inhibitors may potentially have superior activity.
Abstract: The frequent activation of the PI3K/AKT/mTOR pathway in cancer, and its crucial role in cell growth and survival, has made it a much desired target for pharmacologic intervention. Following the regulatory approval of the rapamycin analogs everolimus and temsirolimus, recent years have seen an explosion in the number of phosphoinositide 3-kinase (PI3K) pathway inhibitors under clinical investigation. These include: ATP-competitive, dual inhibitors of class I PI3K and mTORC1/2; "pan-PI3K" inhibitors, which inhibit all four isoforms of class I PI3K (α, β, δ, γ); isoform-specific inhibitors of the various PI3K isoforms; allosteric and catalytic inhibitors of AKT; and ATP-competitive inhibitors of mTOR only (and thus mTORC1 and mTORC2). With so many agents in development, clinicians are currently faced with a wide array of clinical trials investigating a multitude of inhibitors with different mechanisms of action, being used both as single agents and in combination with other therapies. Here, we provide a review of the literature, with the aim of differentiating the genomic contexts in which these various types of inhibitors may potentially have superior activity.
380 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 |