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  1. Article ; Online: Estimation of COVID-19 burden in Egypt.

    Sahmoud, Tarek

    The Lancet. Infectious diseases

    2020  Volume 20, Issue 8, Page(s) 895–896

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus Infections ; Egypt ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza, Human ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2
    Keywords covid19
    Language English
    Publishing date 2020-04-27
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 2061641-7
    ISSN 1474-4457 ; 1473-3099
    ISSN (online) 1474-4457
    ISSN 1473-3099
    DOI 10.1016/S1473-3099(20)30318-2
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  3. Article ; Online: Estimation of COVID-19 burden in Egypt

    Sahmoud, Tarek

    The Lancet Infectious Diseases

    2020  Volume 20, Issue 8, Page(s) 895–896

    Keywords Infectious Diseases ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2061641-7
    ISSN 1474-4457 ; 1473-3099
    ISSN (online) 1474-4457
    ISSN 1473-3099
    DOI 10.1016/s1473-3099(20)30318-2
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Correction: PIK3CA Genotype and a PIK3CA Mutation-Related Gene Signature and Response to Everolimus and Letrozole in Estrogen Receptor Positive Breast Cancer.

    Loi, Sherene / Michiels, Stefan / Baselga, Jose / Bartlett, John M S / Singhal, Sandeep K / Sabine, Vicky S / Sims, Andrew H / Sahmoud, Tarek / Michael Dixon, J / Piccart, Martine J / Sotiriou, Christos

    PloS one

    2019  Volume 14, Issue 4, Page(s) e0216175

    Abstract: This corrects the article DOI: 10.1371/journal.pone.0053292.]. ...

    Abstract [This corrects the article DOI: 10.1371/journal.pone.0053292.].
    Language English
    Publishing date 2019-04-23
    Publishing country United States
    Document type Published Erratum
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0216175
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  5. Article ; Online: Correction

    Sherene Loi / Stefan Michiels / Jose Baselga / John M S Bartlett / Sandeep K Singhal / Vicky S Sabine / Andrew H Sims / Tarek Sahmoud / J Michael Dixon / Martine J Piccart / Christos Sotiriou

    PLoS ONE, Vol 14, Iss 4, p e

    PIK3CA Genotype and a PIK3CA Mutation-Related Gene Signature and Response to Everolimus and Letrozole in Estrogen Receptor Positive Breast Cancer.

    2019  Volume 0216175

    Abstract: This corrects the article DOI:10.1371/journal.pone.0053292.]. ...

    Abstract [This corrects the article DOI:10.1371/journal.pone.0053292.].
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
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  6. Article: Current and future perspectives on fulvestrant.

    Gradishar, William J / Sahmoud, Tarek

    Clinical breast cancer

    2005  Volume 6 Suppl 1, Page(s) S23–9

    Abstract: Fulvestrant, an estrogen receptor antagonist with no known agonist effects, is effective and well tolerated in the treatment of hormone-sensitive breast cancer after antiestrogen failure in postmenopausal women. Numerous phase II and III clinical trials ... ...

    Abstract Fulvestrant, an estrogen receptor antagonist with no known agonist effects, is effective and well tolerated in the treatment of hormone-sensitive breast cancer after antiestrogen failure in postmenopausal women. Numerous phase II and III clinical trials of fulvestrant that are designed to build on its efficacy in breast cancer and explore its value in other tumors are ongoing or in the final planning stage. Favorable safety, dose-response, and pharmacokinetic data led to the initiation of clinical trials to evaluate loading and higher doses with the aim of building on the well-defined efficacy of fulvestrant. Recently reported results of phase II trials by the North Central Cancer Treatment Group and the Swiss Group for Clinical Cancer Research support the clinical activity of fulvestrant after recurrence or progression on a nonsteroidal aromatase inhibitor, and 2 international phase III trials are ongoing in this setting. As a first-line treatment for metastatic disease, fulvestrant is currently being evaluated in combination with anastrozole versus anastrozole alone in 2 phase III trials, 1 by the Southwest Oncology Group and the other being conducted mainly in Scandinavia. Preclinical data have also led to randomized phase II trials of fulvestrant in combination with the epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib, and the HER2/neu-targeted antibody trastuzumab. Additional phase II and III trials are currently evaluating fulvestrant plus tipifarnib, Theratope vaccine, or the dual kinase inhibitor, GW572016. Although fulvestrant is undergoing robust clinical development as a treatment for breast cancer, investigation of this agent in other types of solid tumors has only just begun.
    MeSH term(s) Anastrozole ; Antineoplastic Agents, Hormonal/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Estradiol/analogs & derivatives ; Estradiol/therapeutic use ; Female ; Fulvestrant ; Humans ; Nitriles/therapeutic use ; Receptors, Estrogen/metabolism ; Triazoles/therapeutic use
    Chemical Substances Antineoplastic Agents, Hormonal ; Nitriles ; Receptors, Estrogen ; Triazoles ; Fulvestrant (22X328QOC4) ; Anastrozole (2Z07MYW1AZ) ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2005-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2106734-X
    ISSN 1938-0666 ; 1526-8209
    ISSN (online) 1938-0666
    ISSN 1526-8209
    DOI 10.3816/cbc.2005.s.011
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  7. Article ; Online: Covalent ERα Antagonist H3B-6545 Demonstrates Encouraging Preclinical Activity in Therapy-Resistant Breast Cancer.

    Furman, Craig / Puyang, Xiaoling / Zhang, Zhaojie / Wu, Zhenhua J / Banka, Deepti / Aithal, Kiran B / Albacker, Lee A / Hao, Ming-Hong / Irwin, Sean / Kim, Amy / Montesion, Meagan / Moriarty, Alyssa D / Murugesan, Karthikeyan / Nguyen, Tuong-Vi / Rimkunas, Victoria / Sahmoud, Tarek / Wick, Michael J / Yao, Shihua / Zhang, Xun /
    Zeng, Hao / Vaillancourt, Frédéric H / Bolduc, David M / Larsen, Nicholas / Zheng, Guo Zhu / Prajapati, Sudeep / Zhu, Ping / Korpal, Manav

    Molecular cancer therapeutics

    2022  Volume 21, Issue 6, Page(s) 890–902

    Abstract: Nearly 30% of patients with relapsed breast cancer present activating mutations in estrogen receptor alpha (ERα) that confer partial resistance to existing endocrine-based therapies. We previously reported the development of H3B-5942, a covalent ERα ... ...

    Abstract Nearly 30% of patients with relapsed breast cancer present activating mutations in estrogen receptor alpha (ERα) that confer partial resistance to existing endocrine-based therapies. We previously reported the development of H3B-5942, a covalent ERα antagonist that engages cysteine-530 (C530) to achieve potency against both wild-type (ERαWT) and mutant ERα (ERαMUT). Anticipating that the emergence of C530 mutations could promote resistance to H3B-5942, we applied structure-based drug design to improve the potency of the core scaffold to further enhance the antagonistic activity in addition to covalent engagement. This effort led to the development of the clinical candidate H3B-6545, a covalent antagonist that is potent against both  ERαWT/MUT, and maintains potency even in the context of ERα C530 mutations. H3B-6545 demonstrates significant activity and superiority over standard-of-care fulvestrant across a panel of ERαWT and ERαMUT palbociclib sensitive and resistant models. In summary, the compelling preclinical activity of H3B-6545 supports its further development for the potential treatment of endocrine therapy-resistant ERα+ breast cancer harboring wild-type or mutant ESR1, as demonstrated by the ongoing clinical trials (NCT03250676, NCT04568902, NCT04288089).
    Summary: H3B-6545 is an ERα covalent antagonist that exhibits encouraging preclinical activity against CDK4/6i naïve and resistant ERαWT and ERαMUT tumors.
    MeSH term(s) Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Clinical Trials as Topic ; Estrogen Receptor alpha/genetics ; Female ; Fulvestrant/therapeutic use ; Humans ; Indazoles ; Neoplasm Recurrence, Local ; Pyridines
    Chemical Substances Estrogen Receptor alpha ; H3B-6545 ; Indazoles ; Pyridines ; Fulvestrant (22X328QOC4)
    Language English
    Publishing date 2022-05-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-21-0378
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  8. Article ; Online: Development of everolimus, a novel oral mTOR inhibitor, across a spectrum of diseases.

    Lebwohl, David / Anak, Ozlem / Sahmoud, Tarek / Klimovsky, Judith / Elmroth, Ingrid / Haas, Tomas / Posluszny, Joseph / Saletan, Stephen / Berg, William

    Annals of the New York Academy of Sciences

    2013  Volume 1291, Page(s) 14–32

    Abstract: Everolimus is a potent, oral inhibitor of the mammalian target of rapamycin (mTOR) that has been investigated in multiple clinical development programs since 1996. A unique collaboration between academic and pharmaceutical experts fostered research that ... ...

    Abstract Everolimus is a potent, oral inhibitor of the mammalian target of rapamycin (mTOR) that has been investigated in multiple clinical development programs since 1996. A unique collaboration between academic and pharmaceutical experts fostered research that progressed rapidly, with simultaneous indication findings across numerous tumor types. Initially developed for the prophylaxis of organ transplant rejection, everolimus has demonstrated efficacy and safety for the treatment of patients with various types of cancer (renal cell carcinoma, neuroendocrine tumors of pancreatic origin, and breast cancer) and for adult and pediatric patients with tuberous sclerosis complex. The FDA approval of everolimus for these diseases has addressed several unmet medical needs and is widely accepted by the medical community where treatment options may be limited. An extensive clinical development program is ongoing to establish the role of everolimus as monotherapy, or in combination with other agents, in the treatment of a broad spectrum of malignancies.
    MeSH term(s) Administration, Oral ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/immunology ; Clinical Trials as Topic/methods ; Everolimus ; Humans ; Immunosuppressive Agents/administration & dosage ; Immunosuppressive Agents/chemistry ; Neoplasms/drug therapy ; Neoplasms/immunology ; Sirolimus/administration & dosage ; Sirolimus/analogs & derivatives ; Sirolimus/immunology ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/immunology ; Tuberous Sclerosis/drug therapy ; Tuberous Sclerosis/immunology
    Chemical Substances Antineoplastic Agents ; Immunosuppressive Agents ; Everolimus (9HW64Q8G6G) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Sirolimus (W36ZG6FT64)
    Language English
    Publishing date 2013-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/nyas.12122
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  9. Article ; Online: GM-CSF inhibition reduces cytokine release syndrome and neuroinflammation but enhances CAR-T cell function in xenografts.

    Sterner, Rosalie M / Sakemura, Reona / Cox, Michelle J / Yang, Nan / Khadka, Roman H / Forsman, Cynthia L / Hansen, Michael J / Jin, Fang / Ayasoufi, Katayoun / Hefazi, Mehrdad / Schick, Kendall J / Walters, Denise K / Ahmed, Omar / Chappell, Dale / Sahmoud, Tarek / Durrant, Cameron / Nevala, Wendy K / Patnaik, Mrinal M / Pease, Larry R /
    Hedin, Karen E / Kay, Neil E / Johnson, Aaron J / Kenderian, Saad S

    Blood

    2018  Volume 133, Issue 7, Page(s) 697–709

    Abstract: Chimeric antigen receptor T (CAR-T) cell therapy is a new pillar in cancer therapeutics; however, its application is limited by the associated toxicities. These include cytokine release syndrome (CRS) and neurotoxicity. Although the IL-6R antagonist ... ...

    Abstract Chimeric antigen receptor T (CAR-T) cell therapy is a new pillar in cancer therapeutics; however, its application is limited by the associated toxicities. These include cytokine release syndrome (CRS) and neurotoxicity. Although the IL-6R antagonist tocilizumab is approved for treatment of CRS, there is no approved treatment of neurotoxicity associated with CD19-targeted CAR-T (CART19) cell therapy. Recent data suggest that monocytes and macrophages contribute to the development of CRS and neurotoxicity after CAR-T cell therapy. Therefore, we investigated neutralizing granulocyte-macrophage colony-stimulating factor (GM-CSF) as a potential strategy to manage CART19 cell-associated toxicities. In this study, we show that GM-CSF neutralization with lenzilumab does not inhibit CART19 cell function in vitro or in vivo. Moreover, CART19 cell proliferation was enhanced and durable control of leukemic disease was maintained better in patient-derived xenografts after GM-CSF neutralization with lenzilumab. In a patient acute lymphoblastic leukemia xenograft model of CRS and neuroinflammation (NI), GM-CSF neutralization resulted in a reduction of myeloid and T cell infiltration in the central nervous system and a significant reduction in NI and prevention of CRS. Finally, we generated GM-CSF-deficient CART19 cells through CRISPR/Cas9 disruption of GM-CSF during CAR-T cell manufacturing. These GM-CSF
    MeSH term(s) Animals ; Antibodies, Neutralizing/pharmacology ; Cell Proliferation ; Cytokines/metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Humans ; Immune System Diseases/immunology ; Immune System Diseases/metabolism ; Immune System Diseases/therapy ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/therapy ; Macrophages/drug effects ; Macrophages/immunology ; Mice ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/immunology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Receptors, Antigen, T-Cell/therapeutic use ; Receptors, Chimeric Antigen/immunology ; Receptors, Chimeric Antigen/metabolism ; Syndrome ; Transplantation, Heterologous ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
    Chemical Substances Antibodies, Neutralizing ; Cytokines ; Receptors, Antigen, T-Cell ; Receptors, Chimeric Antigen ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; tisagenlecleucel (Q6C9WHR03O)
    Language English
    Publishing date 2018-11-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-10-881722
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    Zs.MO 364: Show issues

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  10. Article ; Online: Phase I trial of oral mTOR inhibitor everolimus in combination with trastuzumab and vinorelbine in pre-treated patients with HER2-overexpressing metastatic breast cancer.

    Jerusalem, Guy / Fasolo, Angelica / Dieras, Veronique / Cardoso, Fatima / Bergh, Jonas / Vittori, Luc / Zhang, Yufen / Massacesi, Cristian / Sahmoud, Tarek / Gianni, Luca

    Breast cancer research and treatment

    2011  Volume 125, Issue 2, Page(s) 447–455

    Abstract: To determine the feasible dose and schedule for everolimus, an oral mTOR inhibitor, combined with vinorelbine and trastuzumab for patients with HER2-overexpressing metastatic breast cancer pretreated with trastuzumab. In this phase Ib multicenter, ... ...

    Abstract To determine the feasible dose and schedule for everolimus, an oral mTOR inhibitor, combined with vinorelbine and trastuzumab for patients with HER2-overexpressing metastatic breast cancer pretreated with trastuzumab. In this phase Ib multicenter, Bayesian dose-escalation study, 50 patients received everolimus 5 mg/day, 20 mg/week, or 30 mg/week plus vinorelbine (25 mg/m² on day 1 and 8 every 3 weeks) and trastuzumab (2 mg/kg weekly). Endpoints included end-of-cycle-1 dose-limiting toxicity (DLT) rate (primary endpoint), safety, relative dose intensity, overall response rate (ORR), and pharmacokinetics. Grade 3/4 neutropenia was the most common end-of-cycle-1 DLT and occurred in 10 of 30 and 4 of 14 patients in the 5 mg/day and 30 mg/week cohorts, respectively. Other end-of-cycle-1 DLTs included single cases of febrile neutropenia, grade 3 stomatitis with concomitant fatigue, grade 2 stomatitis, grade 3 anorexia, and grade 2 acneiform dermatitis, all in the 5-mg/day cohort. Based on the recorded DLTs and global safety, everolimus 5 mg/day and 30 mg/week were chosen as the optimal dose levels for the daily and weekly arms. Forty-seven patients were evaluable for efficacy. ORR was 19.1%, with a disease control rate of 83.0% and median progression-free survival of 30.7 weeks. No drug interaction was observed between everolimus and vinorelbine. Everolimus combined with weekly vinorelbine and trastuzumab generally was well tolerated and had encouraging antitumor activity in heavily pretreated patients with HER2-overexpressing metastatic breast cancer that progressed on trastuzumab (NCT00426530).
    MeSH term(s) Adult ; Aged ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Disease-Free Survival ; Drug Administration Schedule ; Everolimus ; Female ; Genes, erbB-2 ; Humans ; Middle Aged ; Neoplasm Metastasis ; Prognosis ; Sirolimus/administration & dosage ; Sirolimus/analogs & derivatives ; Sirolimus/therapeutic use ; Survival Analysis ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; Trastuzumab ; Treatment Outcome ; Vinblastine/administration & dosage ; Vinblastine/analogs & derivatives ; Vinblastine/therapeutic use
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Vinblastine (5V9KLZ54CY) ; Everolimus (9HW64Q8G6G) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Trastuzumab (P188ANX8CK) ; vinorelbine (Q6C979R91Y) ; Sirolimus (W36ZG6FT64)
    Language English
    Publishing date 2011-01
    Publishing country Netherlands
    Document type Clinical Trial, Phase I ; Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 604563-7
    ISSN 1573-7217 ; 0167-6806
    ISSN (online) 1573-7217
    ISSN 0167-6806
    DOI 10.1007/s10549-010-1260-x
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