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SELECTBIO Conferences Circulating Biomarkers 2014

Nik Sol's Biography

Nik Sol, CSO, VUmc

Thomas Wurdinger obtained his PhD in virology and gene therapy at Utrecht University, Utrecht, The Netherlands. After that he moved to Boston, USA to start his post-doc period as a research fellow at Massachusetts General Hospital and Harvard Medical School under the guidance of Prof. dr. X.O. Breakefield and Prof. dr. R. Weissleder. Currently, he has a permanent tenured position as associate professor at VU University Medical Center and Cancer Center Amsterdam, The Netherlands. Furthermore, he holds a research fellow position at Massachusetts General Hospital and Harvard Medical School. He is co-founder and CSO of thromboDx BV ( thromboDx is a molecular diagnostics company based in Amsterdam, The Netherlands. The intellectual property for the platelet diagnostics technology developed at VU University, Amsterdam is exclusively licensed to thromboDx, formed in 2012, and fully focused on developing blood platelet-powered diagnostics tests. The company is co-founded by the inventors of the blood platelet nucleic acid technology and all IP is exclusively licensed to thromboDx, providing full freedom to operate. Technological needs and multiple clinical partnerships have been established and the company now seeks to rapidly validate and market its first product line for chemotherapy selection for lung cancer patients.

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Blood platelets of NSCLC patients take up EML4-ALK, c-Met, BRAFv600e, KRAS G12D, and EGFR T790M RNA Biomarkers

Tuesday, 25 March 2014 at 11:00

Add to Calendar ▼2014-03-25 11:00:002014-03-25 12:00:00Europe/LondonBlood platelets of NSCLC patients take up EML4-ALK, c-Met, BRAFv600e, KRAS G12D, and EGFR T790M RNA BiomarkersCirculating Biomarkers 2014 in Boston, Massachusetts, USABoston, Massachusetts,

Each year an estimated 1.3 million people are diagnosed with lung cancer, compromising 12.4% of all new cancer cases. Approximately 80% of lung cancer cases are diagnosed as non-small cell lung carcinoma (NSCLC), continuing as the leading cause of cancer-related death in both men and women. Depending on the patient’s medical status and stage of disease, systemic cytotoxic chemotherapy, surgery, and/or targeted therapies are the mainstay for treatment for NSCLC patients. The discovery of various molecular alterations that underlie lung cancer has opened-up a new era in the development of specifically targeted therapies employing specific biomarker-dependent inhibitors. The identification of alterations in oncogenes associated with NSCLC can help to determine which patients are more likely to benefit from targeted therapy. In the vast majority of NSCLC patients genetic alterations occur in EGFR (20-25%), KRAS (25-30%), BRAF (3%), and ALK (3-10%), mostly in a mutual exclusive manner. In addition, c-Met amplification is emerging as a potent stratification marker and therapeutic target. Hence, patient stratification for c-Met, EGFR, KRAS, BRAF, and ALK aberrations is becoming common practice among oncologists, and more potential mutations are being identified. NSCLC patients with activating EGFR mutations are generally responsive to the EGFR-directed inhibitors erlotinib and gefitinib, whereas NSCLC patients with ALK translocations respond significantly to the ALK inhibitor crizotinib. The genetic tumor profile of NSCLC patients is considered dynamic and can change in due course of the disease and in response to therapy. For instance, treatment with EGFR inhibitors can result in the outgrowth of resistant NSCLC clones with amplified c-Met, although point mutations in EGFR, e.g. T790M, can also convey resistance to EGFR inhibitors. Resistance to crizotinib in EML4-ALK positive NSCLC patients is described to be caused by several acquired ALK mutations, including in exons 2

Add to Calendar ▼2014-03-24 00:00:002014-03-25 00:00:00Europe/LondonCirculating Biomarkers 2014Circulating Biomarkers 2014 in Boston, Massachusetts, USABoston, Massachusetts,