 Good morning. My name is Neremarotis Otero. I'm an author for the recent Polish paper in Orco-Target. Cancer acetylphabolas confer sheer resistance to circulating tumor cells during prostate cancer metastasis progression. Today I'm going to give a little information about this study and what other findings we had that allow us to go to this kind of research study. To give a little information about myself, I was born and raised in Puerto Rico. I did my bachelor's degree in University of Rico at Mayagüez Campus in industrial biotechnology. After I graduated from my bachelor's degree, I applied to a PhD program at Cornell University in biomedical engineering. My PhD degree is about the analysis and targeting of circulating cells in metastatic cancer patients. Cancer is the second living cause of death worldwide, where metastasis is responsible of about 90% of these cancer-related death. Cancer metastasis is the process where the tumor cells migrate from the primary location to form a secondary tumor in distant organs. During this process, the tumor cells have to detach from the primary tumor, invade the tumor's trauma, and in travasse into the blood vasculature. When the tumor cells are in the blood vasculature, these are known as circulating tumor cells, and these will travel in the bloodstream until these find a permanent environment to grow and form secondary tumor. These circulating tumor cells may travel as single CTCs or CTCs aggregates, which is composed by tumor cells, but also by trauma cells, as for example, cancer-associated fabulas. Cancer-associated fabulas, known as CAF, is one of the main components of the tumor microenvironment. It can compose up to 80% of the solid tumor. This kind of cells can promote cancer migration, can promote cancer progression by several mechanisms. For example, it can promote tumor cells proliferation, it can promote that resistance to cell death, or it can promote cancer invasion and migration. The function of CAFs have been well established by the literature in the primary and in the secondary tumor. However, it still is not clear whether CAF assists in the CTC transit, leading to the worsening clinical outcome in cancer patients. In my PhD degree, I had the chance to analyze, isolate, and analyze circulating tumor cells and cancer-associated fabulas from blood samples collected from metastatic cancer patients. In this project, we found that high level of cancer-associated fabulas correlate with the worsening clinical outcome in this cohort of patients. Suggesting the potential use of this has a cancer prognosis biomarker in blood sample collected from cancer patients. Based on these kind of results, in the strong correlation that we observed between the level of cancer-associated fabulas and the worsening clinical outcome in these metastatic cancer patients, we decided to look a little bit closer about the function of these function of CAFs in the bloodstream. What is the role of these CAFs in the bloodstream in cancer metastases? That's the main reason why we decided to initiate this study that we published, that we recently published in Unco Target. In this study, we demonstrated that when the CAFs are interacting with tumor cells in cell aggregates, it has CTC aggregates that can be released by primary tumors in a patient. These kind of aggregates basically CAFs promote the tumor cells survival when these are experiencing high fluid shear stress. Also, CAFs basically in this aggregated form protect the proliferation capabilities of these tumor cells when these are experiencing high fluid shear stress, which promote cancer proliferation by facilitating the colonization of these sent organs. So here in this paper, we found one of the role of these in the bloodstream, which is facilitating the survival of tumor cells in the bloodstream so these can seed and form secondary tumor in these sent organs. This kind of study explored the function of these CAFs in the bloodstream, but in a specific prostate cancer disease. However, we do not believe that these kind of behavior could happen in another type of carcinoma. Now, looking to future direction, we would like to explore a little bit more about the role of CAFs in the bloodstream in other carcinoma and how we can develop a therapeutic approach to target these CAFs population in the bloodstream. If CAFs are necessary to form metastasis, if CAFs are one of the cells that promote the tumor cell survival in the bloodstream, if we target these kind of population in the bloodstream, we may have a chance to prevent cancer metastasis. So in the future direction, we would like to explore a little bit more about how we can develop this therapeutic approach to target these CAFs population and eliminate these in the bloodstream. Thank you for listening and just going to the end of my talk, I would like to thanks all my funding sources, NSF, Sloan Fellowship that they were a really crucial part to complete my PhD. I also would like to thanks my advisor, Dr. Michael Kinn. He has been an amazing advisor during this whole process to shape in the scientists that I am right now. I also would like to thank all the lab, the Kinn lab members, the people that I work with in the research lab because we really collaborated and vitamin to work with and I think every student was part of my progress and part of my work. And I also would like to thanks to my committee advisor, Dr. David Pondam and Dr. Tracy Astoco because they were also crucial part of my PhD dissertation on my PhD studies. And finally, I would like to thanks to the diversity program at Cornell University that has been an amazing support group for a diverse student at the university and I'm really thankful for all the advice, all the support that I have received from them since day one. Thank you.