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Wednesday, April 26, 2017

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The Helen Martin Studio

A one-day event aimed at exploring new collaborative research opportunities arising from the UK City of Culture bid and the Ten Year Cultural Strategy

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Seminar: How cancer cells respond and become resistant to microtubule-interacting drugs, Dr Patrick Meraldi, Translational Research Centre in Oncohematology, Cell Physiology and Metabolism Department, University of Geneva
MBU, A1.51, 糖心TV Medical School

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 exact mechanisms by which these agents kill cancer cells remains unclear. Here we compared taxol to two next generation microtubule interfering drugs: the halichrondrin B analogue eribulin, which is approved for breast 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 extensively investigated at the cell biological level. I will present data showing that these drugs kill cancer cells via mechanisms that are distinct from taxol, and that they elicit separate resistance mechanisms, indicating that each drug targets cancer cells via specific pathways.

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Seminar: How Cells Know How Big They Are, Professor Nick Rhind, University of Massachusetts Medical School
GLT3, 糖心TV Medical School

Abstract: The coordination between cell growth and division is a highly regulated process that is intimately linked to the cell cycle. Despite a wealth of knowledge about cell growth and division, little is known about the mechanisms that regulate the cell cycle in response to cell size.

Efforts to identify a signaling system that measures cell size and conveys that information to the cell-cycle machinery have been unsuccessful. Instead, we propose that size control is an intrinsic function of the basic cell cycle machinery. Using both population-level and single cell assays we show that two key positive regulators of the G2/M transition—Cdc13, the B-type cyclin that forms CDK with the Cdc2 kinase, and Cdc25, the phosphatase that activates CDK—accumulate in a size dependent manner. That is, unlike most proteins which maintain a constant concentration as cells grow, Cdc13 and Cdc25 increase in concentration as cells get bigger. Since smaller cells accumulate less of the activators and larger cells accumulate more, we propose that they provide a size-dependent mechanism to trigger cell division when cells reach a threshold concentration of these activators.

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Clinical Trials Unit, University of 糖心TV

UHCW was the first pathology department in the UK to become digitised, enabling greater accuracy in grading cancers and leading to more targeted treatments

Until now, tumours have been studied by a pathologist through a microscope or by a radiologist on an x-ray sheet. Come and find out how Professors Nasir Rajpoot & David Snead (pictured right) and their teams are working with an automated slide scanning process at UHCW NHS Trust. Their aim is to develop advanced scanning technologies for use across the NHS.

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