Search Results - (Author, Cooperation:M. Warmuth)
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1M. Rasmussen ; S. L. Anzick ; M. R. Waters ; P. Skoglund ; M. DeGiorgio ; T. W. Stafford, Jr. ; S. Rasmussen ; I. Moltke ; A. Albrechtsen ; S. M. Doyle ; G. D. Poznik ; V. Gudmundsdottir ; R. Yadav ; A. S. Malaspinas ; S. S. t. White ; M. E. Allentoft ; O. E. Cornejo ; K. Tambets ; A. Eriksson ; P. D. Heintzman ; M. Karmin ; T. S. Korneliussen ; D. J. Meltzer ; T. L. Pierre ; J. Stenderup ; L. Saag ; V. M. Warmuth ; M. C. Lopes ; R. S. Malhi ; S. Brunak ; T. Sicheritz-Ponten ; I. Barnes ; M. Collins ; L. Orlando ; F. Balloux ; A. Manica ; R. Gupta ; M. Metspalu ; C. D. Bustamante ; M. Jakobsson ; R. Nielsen ; E. Willerslev
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-02-14Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Archaeology ; Asia/ethnology ; Bone and Bones ; Burial ; Chromosomes, Human, Y/genetics ; DNA, Mitochondrial/genetics ; Emigration and Immigration/history ; Europe/ethnology ; Gene Flow/genetics ; Genome, Human/*genetics ; Haplotypes/genetics ; History, Ancient ; Humans ; Indians, North American/*genetics ; Infant ; Male ; Models, Genetic ; Molecular Sequence Data ; Montana ; *Phylogeny ; Population Dynamics ; Radiometric DatingPublished by: -
2J. Barretina ; G. Caponigro ; N. Stransky ; K. Venkatesan ; A. A. Margolin ; S. Kim ; C. J. Wilson ; J. Lehar ; G. V. Kryukov ; D. Sonkin ; A. Reddy ; M. Liu ; L. Murray ; M. F. Berger ; J. E. Monahan ; P. Morais ; J. Meltzer ; A. Korejwa ; J. Jane-Valbuena ; F. A. Mapa ; J. Thibault ; E. Bric-Furlong ; P. Raman ; A. Shipway ; I. H. Engels ; J. Cheng ; G. K. Yu ; J. Yu ; P. Aspesi, Jr. ; M. de Silva ; K. Jagtap ; M. D. Jones ; L. Wang ; C. Hatton ; E. Palescandolo ; S. Gupta ; S. Mahan ; C. Sougnez ; R. C. Onofrio ; T. Liefeld ; L. MacConaill ; W. Winckler ; M. Reich ; N. Li ; J. P. Mesirov ; S. B. Gabriel ; G. Getz ; K. Ardlie ; V. Chan ; V. E. Myer ; B. L. Weber ; J. Porter ; M. Warmuth ; P. Finan ; J. L. Harris ; M. Meyerson ; T. R. Golub ; M. P. Morrissey ; W. R. Sellers ; R. Schlegel ; L. A. Garraway
Nature Publishing Group (NPG)
Published 2012Staff ViewPublication Date: 2012-03-31Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Lineage ; Chromosomes, Human/genetics ; Clinical Trials as Topic/methods ; *Databases, Factual ; Drug Screening Assays, Antitumor/*methods ; *Encyclopedias as Topic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras/genetics ; Genome, Human/genetics ; Genomics ; Humans ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; *Models, Biological ; Neoplasms/*drug therapy/genetics/metabolism/*pathology ; Pharmacogenetics ; Plasma Cells/cytology/drug effects/metabolism ; Precision Medicine/methods ; Receptor, IGF Type 1/antagonists & inhibitors/metabolism ; Receptors, Aryl Hydrocarbon/genetics/metabolism ; Sequence Analysis, DNA ; Topoisomerase Inhibitors/pharmacologyPublished by: -
3Burstein, H. J. ; Ramirez, M. J. ; Petros, W. P. ; Clarke, K. D. ; Warmuth, M. A. ; Marcom, P. K. ; Matulonis, U. A. ; Parker, L. M. ; Harris, L. N. ; Winer, E. P.
Springer
Published 1999Staff ViewISSN: 1569-8041Keywords: Doxil ; metastatic breast cancer ; phase I ; vinorelbineSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Background: Vinorelbine and Doxil (liposomal doxorubicin) are active chemotherapeutic agents in metastatic breast cancer. A phase I study was designed to evaluate combination therapy. Patients and methods: Thirty women with metastatic breast cancer were enrolled. Dose-limiting toxicity was determined through a dose escalation scheme, and defined for the first treatment cycle, only. Pharmacokinetic studies were performed during the first cycle of treatment. Results: In the first cohort of Doxil 30 mg/m2 day 1 and vinorelbine 25 mg/m2 days 1 and 8, patients experienced severe neutropenia. Vinorelbine administration was changed thereafter to days 1 and 15 of each cycle. Dose limiting toxicity was observed at Doxil 50 mg/m2 and vinorelbine 25 mg/m2. Doxil 40 mg/m2 and vinorelbine 30 mg/m2 was defined as the maximally tolerated dose. Few toxicities (principally neutropenia) were seen at this dose level, with the notable absence of significant nausea, vomiting, or alopecia. Though 63% of patients had received prior anthracycline-based chemotherapy, only one patient developed grade 2 cardiac toxicity. Pharmacokinetic studies revealed prolonged exposure to high doxorubicin concentrations for several days following Doxil administration. Conclusions: Combination chemotherapy with Doxil and vinorelbine affords treatment with two active drugs in women with metastatic breast cancer, and appears to have a favorable toxicity profile. A schedule of Doxil 40 mg/m2 day 1 and vinorelbine 30 mg/m2 days 1 and 15 given every 28 days is recommended for phase II studies.Type of Medium: Electronic ResourceURL: -
4Staff View
ISSN: 1432-0584Keywords: Key words Chronic myeloid leukemia ; Signal transduction ; bcr-abl ; Philadelphia translocationSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract With an annual incidence of about ten in 1,000,000 people, chronic myeloid leukemia (CML) accounts for most cases of myeloproliferative disease and for 20% of all leukemias. While novel therapies such as treatment with interferon-α or bone marrow transplantation have successively improved the outcome of CML treatment, hope for future progress in the therapy of CML lies in an almost unique feature of this hematological malignancy. In contrast to many other forms or subforms of leukemias which display a great diversity in chromosomal alterations, most cases (〉95%) of CML seem to be caused by an almost invariably found cytogenetic aberration, the so-called Philadelphia chromosome (Ph), resulting in the bcr-abl fusion gene. Its gene product, p210bcr-abl (Bcr-Abl), is believed to be essential for hematopoietic cell transformation and seems to exert its effects by interfering with cellular signal transduction pathways, normally involved in the control of cell death and proliferation. Several partially interacting pathways have been shown to be induced by Bcr-Abl. The role of most of them is still unclear and, as understanding their biological functions should lead to novel therapeutic strategies on a molecular basis, much effort is spent on identifying their precise roles in CML. This review focuses on our current understanding of Bcr-Abl-induced signal transduction and outlines its importance for the biological effects of Bcr-Abl.Type of Medium: Electronic ResourceURL: