CCBIO Special Seminar: "Tumor plasticity and drug resistance”
CCBIO is proud to present a CCBIO Special Seminar April 8th with speakers Rik Thompson of Australia and John Haley of New York.
Main content
Title: "Tumor plasticity and drug resistance”
Time and place: 08.04.2015, 14-16.00, Auditorium 4 BBB
Speakers are :
Rik Thompson, Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
See more introduction here to Rik Thompson.
John D. Haley, Stony Brook School of Medicine New York, SBU Cancer Center and SBU Proteomics Center.
Host: James Lorens, CCBIO
Apart from the interesting talks, the CCBIO seminars are a good way to meet CCBIO members and associates. Please feel free to circulate the invitation as all are welcome!
Abstracts
Rik Thompson: 'Epithelial Mesenchymal Plasticity and Neoadjuvant Chemotherapy in Locally Advanced Breast Cancer '
In addition to initial escape from oncogene-induced senescence and cellular escape from the primary tumour through enhanced migration and invasion, Epithelial Mesenchymal Transition (EMT) has been implicated in increasing resistance to anoikis, enhancing survival in the circulation and reducing proliferative rate, all of which may allow mesenchymally-shifted cells to become resistant to chemotherapies. EMT induction in breast cancer patients by chemotherapy has been described in several studies and supports a role for EMT in chemoresistance.
Our data from a cohort of locally advanced breast cancers treated with neo-adjuvant chemotherapy will be discussed in the context of other published data and in relation to new avenues for therapy.
John D. Haley: 'Epithelial-Mesenchymal Transition in Cancer Progression and Treatment'
It is clear that metastatic cancers are increasingly heterogeneous, that is many different cell types and states are present within cancer tissues, and importantly metastatic cancers show increased resistance to radiation, chemotherapies and targeted therapies. Cellular plasticity plays a major role in the progression of cancer and the acquisition of mesenchymal cancer stem cell-like phenotypes has been correlated with poor prognosis.
Several forms of plasticity have been documented, including epithelial mesenchymal transition (EMT), endothelial-mesenchymal transition and epithelial-neuroendocrine transition. We have shown that EMT is an important cellular change which allows for metastasic behavior and resistance to chemo and targeted therapies in cancer patients. New therapeutics are needed to target the new spectrum of tumor survival signals now present within EMT-derived cells and within related cancer-stem cells.
Through the generation and molecular characterization of EMT models, through RNAi-based target validation studies and follow-on pharmacology studies, we have identified new targets and pathways which promote the death of mesenchymal-like metastatic cells.