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DTSTART:19960101T000000 END:STANDARD BEGIN:STANDARD TZNAME:GMT TZOFFSETFROM:+0100 TZOFFSETTO:+0000 DTSTART:19961027T020000 RRULE:FREQ=YEARLY;BYMONTH=10;BYDAY=-1SU END:STANDARD END:VTIMEZONE BEGIN:VEVENT DTSTAMP:20260614T195908Z DTSTART;VALUE=DATE-TIME:20170426T100000 DTEND;VALUE=DATE-TIME:20170426T110000 SUMMARY:Seminar: How cancer cells respond and become resistant to microtu bule-interacting drugs\, Dr Patrick Meraldi\, Translational Research Cen tre in Oncohematology\, Cell Physiology and Metabolism Department\, Univ ersity of Geneva TZID:Europe/London UID:20170426-8a17841a5b3d6cd7015b8a66ea092b0c@warwick.ac.uk CREATED:20170420T080732Z DESCRIPTION:Abstract: Microtubule-interacting drugs are amongst the most efficient chemotherapeutic agents used in the treatment of breast cancer \, prostate cancer or leukemia. Although it is often assumed that these drugs act in a general\, cytotoxic manner by disrupting mitosis\, the ex act mechanisms by which these agents kill cancer cells remains unclear. Here we compared taxol to two next generation microtubule interfering dr ugs: the halichrondrin B analogue eribulin\, which is approved for breas t cancer treatment since 6 years\, and BAL27682\, which is currently in Phase 1/2A clinical evaluation in advanced cancer patients. While taxol has been extensively studied\, the two other drugs have never been exten sively investigated at the cell biological level. I will present data sh owing that these drugs kill cancer cells via mechanisms that are distinc t from taxol\, and that they elicit separate resistance mechanisms\, ind icating that each drug targets cancer cells via specific pathways. LOCATION:MBU\, A1.51\, ÌÇÐÄTV Medical School CATEGORIES:BiomedicalSciences,BMS_CDB LAST-MODIFIED:20170420T081332Z ORGANIZER;CN=Jas Bains: END:VEVENT END:VCALENDAR