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New Contributions in Undergraduate Research
PSU McNair Scholars Online Journal Volume 11 Issue 1 Without Borders: Original Contributions Article 6 in Undergraduate Research 2017 Wings Outstretched: New Contributions in Undergraduate Research Follow this and additional works at: https://pdxscholar.library.pdx.edu/mcnair Let us know how access to this document benefits ou.y Recommended Citation (2017) "Wings Outstretched: New Contributions in Undergraduate Research," PSU McNair Scholars Online Journal: Vol. 11: Iss. 1, Article 6. https://doi.org/10.15760/mcnair.2017.01 This open access Full Issue is distributed under the terms of the Creative Commons Attribution-NonCommercial- ShareAlike 4.0 International License (CC BY-NC-SA 4.0). All documents in PDXScholar should meet accessibility standards. If we can make this document more accessible to you, contact our team. Portland State University McNair Research Journal 2017 Without Borders: Original Contributions in Undergraduate Research 2017 Ronald E. McNair Scholars Journal Portland State University 1 About the Program The Portland State University (PSU) Ronald E. McNair Scholars Program at Portland State University works with motivated and talented undergraduates who want to pursue PhDs. It introduces juniors and seniors who are first-generation and low income, and/or members of under-represented groups to academic research and to effective strategies for getting into and graduating from PhD programs. The McNair Scholars Program has academic-year activities and a full-time summer research internship. Scholars take academic and skills-building seminars and workshops during the year, and each scholar works closely with a faculty mentor on original research in the summer. Scholars present their research findings at the McNair Summer Symposium and at other conferences, and are encouraged to publish their papers in the McNair Journal and other scholarly publications. -
Chronic Lymphocytic Leukemia
Amsterdam, the Netherlands, June 14 – 17, 2012 Chronic lymphocytic leukemia - Clinical 1 assumed efficacy especially in high-risk situations (early relapse, unfavourable prognostic markers), was used in 202 patients. The overall survival in the CHOP-collective was significantly shorter than in the comparative group (p<0.0001) although median observation time was not significantly differ - 0144 ent. However, this observation might reflect a bias in the selection of high risk patients for this relapse treatment. No influence on survival was INFLUENCE OF DIFFERENT TREATMENT REGIMENS ON SURVIVAL IN observed in patients receiving a mitoxantrone-containing regimen at any PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA - A META-ANALY - time during the treatment course. Summary and Conclusions. This meta- SIS OF THE GERMAN CLL STUDY GROUP (GCLLSG) analysis shows that the advances in the development of strategies for first- S Isfort 1, P Cramer 2, J Bahlo 2, R Busch 3, K Fischer 2, AM Fink 2, V Goede 2, T line therapies result in prolongation of treatment-free and overall survival Elter 2, M Bergmann 4, M Stauch 5, S Stilgenbauer 4, CM Wendtner 6, M Hallek 2, for patients with CLL and need of treatment. Chemoimmunotherapies pro - B Eichhorst 2 long the survival independently of the time point of chemoimmunotherapy 1Department of Medicine IV, University Hospital Aachen, Aachen, Germany administration (for first-line therapy or relapse). 2Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany 3 Institute for Medical Statistic and Epidemiology, Technical University Munich, 0145 Munich, Germany 4 Department III of Internal Medicine, University Hospital Ulm, Ulm, Germany A SINGLE-ARM MULTI-CENTER TRIAL OF BENDAMUSTINE GIVEN 5 Private practice and day time clinic for Hematology and Oncology, Kronach, WITH OFATUMUMAB (BENDOFA) IN PATIENTS WITH REFRACTORY OR Kronach, Germany RELAPSED CHRONIC LYMPHOCYTIC LEUKEMIA. -
National Cancer Institute Cancer National
DIVISION OF CANCER TREATMENT AND DIAGNOSIS National Cancer Institute Cancer National PROGRAM ACCOMPLISHMENTS 2006 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health TABLE OF CONTENTS Foreword . iii Division of Cancer Treatment and Diagnosis Overview . .1 Major Ongoing Initiatives and Accomplishments . .7 Biometric Research Branch Overview . 11 Partnerships and Collaborations . 12 Scientific Advances . 17 Other Biostatistical Research . 24 Tools, Products, and Resources . 27 Cancer Diagnosis Program Overview . 29 Major Ongoing Initiatives . 30 Current Funding Opportunities . 34 Partnerships and Collaborations . 36 Scientific Advances . 39 Tools, Products, and Resources . 41 Cancer Imaging Program Overview . 45 Major Ongoing Initiatives . 47 Current Funding Opportunities . 54 Partnerships and Collaborations . 57 Scientific Advances . 61 Tools, Products, and Resources . 63 Cancer Therapy Evaluation Program Overview . 65 Major Ongoing Initiatives . 67 Significant Ongoing Clinical Trials . 71 Current Funding Opportunities . 73 Partnerships and Collaborations . 75 Scientific Advances . 79 Tools, Products, and Resources . 92 TABLE OF CONTENTS ■ i Developmental Therapeutics Program Overview . 95 New Initiatives . 97 Major Ongoing Initiatives . .100 Current Funding Opportunities . .104 Tools, Products, and Resources . .105 History-Marking Event . .114 Scientific Advances . .115 Radiation Research Program Overview . .119 Partnerships and Collaborations . .121 Scientific Advances . .127 Tools, Products, and Resources . .129 -
Supporting Information
Supporting Information Pouryahya et al. SI Text Table S1 presents genes with the highest absolute value of Ricci curvature. We expect these genes to have significant contribution to the network’s robustness. Notably, the top two genes are TP53 (tumor protein 53) and YWHAG gene. TP53, also known as p53, it is a well known tumor suppressor gene known as the "guardian of the genome“ given the essential role it plays in genetic stability and prevention of cancer formation (1, 2). Mutations in this gene play a role in all stages of malignant transformation including tumor initiation, promotion, aggressiveness, and metastasis (3). Mutations of this gene are present in more than 50% of human cancers, making it the most common genetic event in human cancer (4, 5). Namely, p53 mutations play roles in leukemia, breast cancer, CNS cancers, and lung cancers, among many others (6–9). The YWHAG gene encodes the 14-3-3 protein gamma, a member of the 14-3-3 family proteins which are involved in many biological processes including signal transduction regulation, cell cycle pro- gression, apoptosis, cell adhesion and migration (10, 11). Notably, increased expression of 14-3-3 family proteins, including protein gamma, have been observed in a number of human cancers including lung and colorectal cancers, among others, suggesting a potential role as tumor oncogenes (12, 13). Furthermore, there is evidence that loss Fig. S1. The histogram of scalar Ricci curvature of 8240 genes. Most of the genes have negative scalar Ricci curvature (75%). TP53 and YWHAG have notably low of p53 function may result in upregulation of 14-3-3γ in lung cancer Ricci curvatures. -
Draft COMP Agenda 16-18 January 2018
12 January 2018 EMA/COMP/818236/2017 Inspections, Human Medicines Pharmacovigilance and Committees Committee for Orphan Medicinal Products (COMP) Draft agenda for the meeting on 16-18 January 2018 Chair: Bruno Sepodes – Vice-Chair: Lesley Greene 16 January 2018, 09:00-19:30, room 2F 17 January 2018, 08:30-19:30, room 2F 18 January 2018, 08:30-18:30, room 2F Health and safety information In accordance with the Agency’s health and safety policy, delegates are to be briefed on health, safety and emergency information and procedures prior to the start of the meeting. Disclaimers Some of the information contained in this agenda is considered commercially confidential or sensitive and therefore not disclosed. With regard to intended therapeutic indications or procedure scopes listed against products, it must be noted that these may not reflect the full wording proposed by applicants and may also vary during the course of the review. Additional details on some of these procedures will be published in the COMP meeting reports once the procedures are finalised. Of note, this agenda is a working document primarily designed for COMP members and the work the Committee undertakes. Note on access to documents Some documents mentioned in the agenda cannot be released at present following a request for access to documents within the framework of Regulation (EC) No 1049/2001 as they are subject to on- going procedures for which a final decision has not yet been adopted. They will become public when adopted or considered public according to the principles stated in the Agency policy on access to documents (EMA/127362/2006). -
Patent Application Publication ( 10 ) Pub . No . : US 2019 / 0192440 A1
US 20190192440A1 (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2019 /0192440 A1 LI (43 ) Pub . Date : Jun . 27 , 2019 ( 54 ) ORAL DRUG DOSAGE FORM COMPRISING Publication Classification DRUG IN THE FORM OF NANOPARTICLES (51 ) Int . CI. A61K 9 / 20 (2006 .01 ) ( 71 ) Applicant: Triastek , Inc. , Nanjing ( CN ) A61K 9 /00 ( 2006 . 01) A61K 31/ 192 ( 2006 .01 ) (72 ) Inventor : Xiaoling LI , Dublin , CA (US ) A61K 9 / 24 ( 2006 .01 ) ( 52 ) U . S . CI. ( 21 ) Appl. No. : 16 /289 ,499 CPC . .. .. A61K 9 /2031 (2013 . 01 ) ; A61K 9 /0065 ( 22 ) Filed : Feb . 28 , 2019 (2013 .01 ) ; A61K 9 / 209 ( 2013 .01 ) ; A61K 9 /2027 ( 2013 .01 ) ; A61K 31/ 192 ( 2013. 01 ) ; Related U . S . Application Data A61K 9 /2072 ( 2013 .01 ) (63 ) Continuation of application No. 16 /028 ,305 , filed on Jul. 5 , 2018 , now Pat . No . 10 , 258 ,575 , which is a (57 ) ABSTRACT continuation of application No . 15 / 173 ,596 , filed on The present disclosure provides a stable solid pharmaceuti Jun . 3 , 2016 . cal dosage form for oral administration . The dosage form (60 ) Provisional application No . 62 /313 ,092 , filed on Mar. includes a substrate that forms at least one compartment and 24 , 2016 , provisional application No . 62 / 296 , 087 , a drug content loaded into the compartment. The dosage filed on Feb . 17 , 2016 , provisional application No . form is so designed that the active pharmaceutical ingredient 62 / 170, 645 , filed on Jun . 3 , 2015 . of the drug content is released in a controlled manner. Patent Application Publication Jun . 27 , 2019 Sheet 1 of 20 US 2019 /0192440 A1 FIG . -
Phenotype-Based Drug Screening Reveals Association Between Venetoclax Response and Differentiation Stage in Acute Myeloid Leukemia
Acute Myeloid Leukemia SUPPLEMENTARY APPENDIX Phenotype-based drug screening reveals association between venetoclax response and differentiation stage in acute myeloid leukemia Heikki Kuusanmäki, 1,2 Aino-Maija Leppä, 1 Petri Pölönen, 3 Mika Kontro, 2 Olli Dufva, 2 Debashish Deb, 1 Bhagwan Yadav, 2 Oscar Brück, 2 Ashwini Kumar, 1 Hele Everaus, 4 Bjørn T. Gjertsen, 5 Merja Heinäniemi, 3 Kimmo Porkka, 2 Satu Mustjoki 2,6 and Caroline A. Heckman 1 1Institute for Molecular Medicine Finland, Helsinki Institute of Life Science, University of Helsinki, Helsinki; 2Hematology Research Unit, Helsinki University Hospital Comprehensive Cancer Center, Helsinki; 3Institute of Biomedicine, School of Medicine, University of Eastern Finland, Kuopio, Finland; 4Department of Hematology and Oncology, University of Tartu, Tartu, Estonia; 5Centre for Cancer Biomarkers, De - partment of Clinical Science, University of Bergen, Bergen, Norway and 6Translational Immunology Research Program and Department of Clinical Chemistry and Hematology, University of Helsinki, Helsinki, Finland ©2020 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2018.214882 Received: December 17, 2018. Accepted: July 8, 2019. Pre-published: July 11, 2019. Correspondence: CAROLINE A. HECKMAN - [email protected] HEIKKI KUUSANMÄKI - [email protected] Supplemental Material Phenotype-based drug screening reveals an association between venetoclax response and differentiation stage in acute myeloid leukemia Authors: Heikki Kuusanmäki1, 2, Aino-Maija -
US10851148.Pdf
US 10,851,148 B2 Page 2 ( 56 ) References Cited Hue et al , “ Potential Role of NKG2D / MHC Class I - Related Chain A Interaction in Intrathymic Maturation of Single - Positive CD8 T Cells , " J Immunol. 171 : 1909-1917 ( 2003 ) . OTHER PUBLICATIONS Hue S , et al . , " A Direct Role for NKG2D / MICA Interaction in Villous Atrophy during Celiac Disease , " Immunity 21 : 367-377 Bahram et al . , “ Nucleotide sequence of the human MHC class I ( 2004 ) . MCA gene, ” Immunogenetics 44 : 80-81 ( 1996 ) . Jimenez - Perez et al . , “ Cervical cancer cell lines expressing Bahram et al . , “ Nucleotide sequence of a human MHC class I MICB NKG2Dligands are able to down -modulate the NKG2D receptor on cDNA , ” Immunogenetics 43 : 230-233 ( 1996 ) . NKL cells with functional implications, ” BMC Immunology 13 : 7 Barlow et al ., “ Continuous and discontinuous antigenic determi ( 2012 ) . nants, ” Nature 322 : 747-748 ( 1986 ) . Jinushi et al . , “ Therapy - induced antibodies to MHC class I chain Bauer et al . , “ Expression and purification , crystallization and crys related protein A antagonize immune suppression and stimulate tallographic characterization of the human MHC class 1 related antitumor cytotoxicity , ” Proc Natl Acad Sci USA . 103 ( 24 ) :9190 protein MICA , ” Acta Cryst D54 : 451-453 ( 1998 ) . 9195 ( 2006 ) . Bauer et al ., “ Activation of NK Cells and T Cells by NKG2D , a Jinushi et al . , “ MHC class I chain - related protein A antibodies and Receptor for Stress - Inducible MICA , " Science 285 ( 5428 ) : 727-9 shedding are associated with the progression of multiple myeloma , " ( 1999 ) . Proc Natl Acad Sci USA . 105 ( 4 ) : 1285-1290 ( 2008 ) . Boissel et al . , “ BCR ABL Oncogene Directly Controls MHC Class Jonjic et al . -
(12) Patent Application Publication (10) Pub. No.: US 2009/0226431 A1 Habib (43) Pub
US 20090226431A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2009/0226431 A1 Habib (43) Pub. Date: Sep. 10, 2009 (54) TREATMENT OF CANCER AND OTHER Publication Classification DISEASES (51) Int. Cl. A 6LX 3/575 (2006.01) (76)76) InventorInventor: Nabilabil Habib,Habib. Beirut (LB(LB) C07J 9/00 (2006.01) Correspondence Address: A 6LX 39/395 (2006.01) 101 FEDERAL STREET A6IP 29/00 (2006.01) A6IP35/00 (2006.01) (21) Appl. No.: 12/085,892 A6IP37/00 (2006.01) 1-1. (52) U.S. Cl. ...................... 424/133.1:552/551; 514/182: (22) PCT Filed: Nov.30, 2006 514/171 (86). PCT No.: PCT/US2O06/045665 (57) ABSTRACT .."St. Mar. 6, 2009 The present invention relates to a novel compound (e.g., 24-ethyl-cholestane-3B.5C,6C.-triol), its production, its use, and to methods of treating neoplasms and other tumors as Related U.S. Application Data well as other diseases including hypercholesterolemia, (60) Provisional application No. 60/741,725, filed on Dec. autoimmune diseases, viral diseases (e.g., hepatitis B, hepa 2, 2005. titis C, or HIV), and diabetes. F2: . - 2 . : F2z "..., . Cz: ".. .. 2. , tie - . 2 2. , "Sphagoshgelin , , re Cls Phosphatidiglethanolamine * - 2 .- . t - r y ... CBs .. A . - . Patent Application Publication Sep. 10, 2009 Sheet 1 of 16 US 2009/0226431 A1 E. e'' . Phosphatidylcholine. " . Ez'.. C.2 . Phosphatidylserias. * . - A. z' C. w E. a...2 .". is 2 - - " - B 2. Sphingoshgelin . Cls Phosphatidglethanglamine Figure 1 Patent Application Publication Sep. 10, 2009 Sheet 2 of 16 US 2009/0226431 A1 Chile Phosphater Glycerol Phosphatidylcholine E. -
Synergistic Inhibition of Erbb Signaling by Combined Treatment
Cancer Therapy: Preclinical Synergistic Inhibition of ErbB Signaling by Combined Treatment with Seliciclib and ErbB-Targeting Agents IanN.Fleming,MoragHogben,SheelaghFrame,StevenJ.McClue,andSimonR.Green Abstract Purpose: The aims of this studywere to investigate whether the cyclin-dependent kinase inhi- bitor seliciclib could synergize with agents that target ErbB receptors and to elucidate the mole- cular mechanism of the observed synergy. Experimental Design: Synergy between seliciclib and ErbB receptor targeted agents was in- vestigated in various cell lines using the Calcusyn median effect model.The molecular mechanism of the observed synergy was studied in cultured cells, and the combination of seliciclib and the epidermal growth factor receptor (EGFR) inhibitor erlotinib was evaluated in an H358 xenograft model. Results: Seliciclib synergized with the anti-HER2 antibody trastuzumab in a breast cancer cell line, which overexpresses the HER2 receptor, and with the erlotinib analogue AG1478 in non ^ small cell lung cancer cell lines. In the H358 non ^ small cell lung cancer cell line, synergy involved decreased signaling from the EGFR, with AG1478 directlyinhibiting kinase activitywhile seliciclib decreased the levels of keycomponents of the receptor signaling pathway,resulting in enhanced loss of phosphorylated extracellular signal-regulated kinase and cyclin D1.The combination of seliciclib and erlotinib was evaluated further in an H358 xenograft and shown to be significantly more active than either agent alone. An enhanced loss of cyclin D1was also seen in vivo. Conclusions: This is the first report that investigates combining seliciclib with an EGFR inhibitor. The combination decreased signaling from the EGFR in vitro and in vivo and was effective in cell lines containing either wild-type or mutant EGFR, suggesting that it may expand the range of tumors that respond to erlotinib, and therefore, such combinations are worth exploring in the clinic. -
New Directions for Emerging Therapies in Acute Myeloid Leukemia: the Next Chapter Naval Daver 1,Andrewh.Wei2, Daniel A
Daver et al. Blood Cancer Journal (2020) 10:107 https://doi.org/10.1038/s41408-020-00376-1 Blood Cancer Journal REVIEW ARTICLE Open Access New directions for emerging therapies in acute myeloid leukemia: the next chapter Naval Daver 1,AndrewH.Wei2, Daniel A. Pollyea3,AmirT.Fathi4,PareshVyas 5 and Courtney D. DiNardo 1 Abstract Conventional therapy for acute myeloid leukemia is composed of remission induction with cytarabine- and anthracycline-containing regimens, followed by consolidation therapy, including allogeneic stem cell transplantation, to prolong remission. In recent years, there has been a significant shift toward the use of novel and effective, target- directed therapies, including inhibitors of mutant FMS-like tyrosine kinase 3 (FLT3) and isocitrate dehydrogenase (IDH), the B-cell lymphoma 2 inhibitor venetoclax, and the hedgehog pathway inhibitor glasdegib. In older patients the combination of a hypomethylating agent or low-dose cytarabine, venetoclax achieved composite response rates that approximate those seen with standard induction regimens in similar populations, but with potentially less toxicity and early mortality. Preclinical data suggest synergy between venetoclax and FLT3- and IDH-targeted therapies, and doublets of venetoclax with inhibitors targeting these mutations have shown promising clinical activity in early stage trials. Triplet regimens involving the hypomethylating agent and venetoclax with FLT3 or IDH1/2 inhibitor, the TP53- modulating agent APR-246 and magrolimab, myeloid cell leukemia-1 inhibitors, or immune therapies such as CD123 antibody-drug conjugates and programmed cell death protein 1 inhibitors are currently being evaluated. It is hoped that such triplets, when applied in appropriate patient subsets, will further enhance remission rates, and more importantly remission durations and survival. -
Quantitative Modeling and Analysis of Drug Screening Data for Personalized Cancer Medicine
UNIVERSITY OF HELSINKI FACULTY OF MEDICINE QUANTITATIVE MODELING AND ANALYSIS OF DRUG SCREENING DATA FOR PERSONALIZED CANCER MEDICINE Lenalidomide Momelotinib Imiquimod Tacedinaline Tofacitinib Temsirolimus Ruxolitinib Roscovitine Tofacitinib Entinostat Gefitinib RoscovitineRuxolitinib Refametinib Pimasertib Sirolimus Selumetinib Tandutinib EverolimusNilotinib PF−04691502 NVP−BEZ235 Trametinib Palbociclib Melphalan Belinostat CUDC−101 AZD8055 Erlotinib Gefitinib Momelotinib Tacedinaline Cediranib SNS−032 Levamisole PF−04691502 Motesanib Panobinostat NVP−AUY922 Palbociclib OSI−027 Erlotinib OSI−027 Axitinib BIIB021 Imatinib Alvespimycin Masitinib TemsirolimusVorinostat Ponatinib Sunitinib Dasatinib Tanespimycin Melphalan Sorafenib Masitinib Pazopanib Sirolimus NVP−SNSAUY922−032 Vatalanib Dasatinib Regorafenib Everolimus Sunitinib MGCD−265 Panobinostat Tivozanib AZD8055 Foretinib NVP−BEZ235 Regorafenib Entinostat Prednisolone Tivozanib Dexamethasone Vincristine Cediranib Belinostat Methylprednisolone Pazopanib CUDC100−101 100 Vinblastine 100 100 Refametinib −40−20 0 20 40 Vatalanib Vorinostat Pimasertib MK1775 Sorafenib MGCD−80265 80 Trametinib ABT−751 80 80 Vandetanib Logistic Selumetinib Axitinib Alvespimycin DSS Triethylenemelamine S−trityl−L−cysteine 60 function3 60 DSS / sDSS 60 AA 60 Canertinib Tanespimycin Mechlorethamine Camptothecin Crizotinib Ponatinib Mitomycin C Paclitaxel Fingolimod 40 IC50 40 Lapatinib Calculation 40 40 Afatinib Imiquimod Patupilone AddictionDrug response score 100 Slope Chlorambucil DSS Tandutinib BIIB021