Agenda

09/02/2021

Heterogeneity, cross-talks and origin of pancreatic cancer: Insights from the transcriptome and methylome of purified cell populations

Virtual, a les 15:30h

Us convidem al proper IMIM Invited external speakers Seminar, que tindrà lloc el dimarts 09/02/2021 a les 15:30 h. El títol serà "Heterogeneity, cross-talks and origin of pancreatic cancer: Insights from the transcriptome and methylome of purified cell populations", a càrrec de la Dra. Elisa Espinet PhD. German Cancer Research Center (DKFZ) and Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM GmbH).

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We invite you to the next IMIM Invited external speakers Seminar, which will take place on Tuesday 09/02/2021 at 15:30 h. The title will be "Heterogeneity, cross-talks and origin of pancreatic cancer: Insights from the transcriptome and methylome of purified cell populations", a càrrec de la Dra. Elisa Espinet PhD. German Cancer Research Center (DKFZ) and Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM GmbH).

Poster

Link to acces

Abstract
Desmoplasia is a hallmark of pancreatic ductal adenocarcinoma (PDAC), still one of the most deadly cancer types. Typically, epithelial tumor cells represent just a minority of the malignant tissue embedded in a massive amount of stroma. This profound desmoplasia highlights the importance of understanding the interactions between tumor and stromal cells to find novel treatment options. At the same time, it represents a technical challenge when aiming to extract the cell-type-specific signals using molecular analyses of bulk tumor samples. To overcome this problem, we have FACS-purified the major cell types present within primary human PDAC tumors (cancer associated fibroblasts (CAFs), immune, endothelial and epithelial cancer cells) and supplemented these with the same cell populations isolated from tumor-free adjacent (normal) pancreas samples. From these we have generated a comprehensive analysis at the transcriptomic and methylome (epithelial cells only) level. We have revised the contribution of the different cell types to pathways involved in PDAC and have used cell-cell interaction network analyses to identify the cross-talks taking place between different cell types. The comparison of PDAC and normal pancreas datasets allowed us to identify a number of genes and pathways deregulated during PDAC tumorigenesis at the cell-type level. As example, our analysis revealed the activation of interferon signalling-related signatures in a subset of patients. This generates a complex interactome between epithelial cancer cells and their environment to which various cell types contribute and which is associated with poor outcome. I will show that the activation of this interferon program associates to a specific DNA methylome profile of the epithelial tumor cells and discuss how this suggests the existence of different cells of origin for distinct PDAC subsets.

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