Publications by authors named "W Quispe-Tintaya"

Article Synopsis
  • Pancreatic ductal adenocarcinoma (PDAC) is difficult to treat due to its ability to evade immune responses, but a new microbiome-based therapy shows promise by introducing a tetanus toxoid protein into tumor cells, reactivating existing T cell responses.
  • In mouse models, this treatment led to the accumulation of the tetanus protein in tumors, recruitment of CD4 T cells, and the production of immune molecules that help kill tumor cells, especially when combined with low doses of gemcitabine (GEM).
  • The combination treatment significantly reduced tumor size (by 80%) and metastases (by 87%), while increasing survival rates in treated mice, suggesting this approach could be a viable alternative for
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Background: The Cancer Genome Atlas identified four molecular subgroups of endometrial cancer with survival differences based on whole genome, transcriptomic, and proteomic characterization. Clinically accessible algorithms that reproduce this data are needed. Our aim was to determine if targeted sequencing alone allowed for molecular classification of endometrial cancer.

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Aneuploidy has been reported to occur at remarkably high levels in normal somatic tissues using Fluorescence In Situ Hybridization (FISH). Recently, these reports were contradicted by single-cell low-coverage whole genome sequencing (scL-WGS) analyses, which showed aneuploidy frequencies at least an order of magnitude lower. To explain these seemingly contradictory findings, we used both techniques to analyze artificially generated mock aneuploid cells and cells with natural random aneuploidy.

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Hepatocyte transplantation is an attractive alternative to liver transplantation. Thus far, however, extensive liver repopulation by adult hepatocytes has required ongoing genetic, physical, or chemical injury to host liver. We hypothesized that providing a regulated proliferative and/or survival advantage to transplanted hepatocytes should enable repopulation in a normal liver microenvironment.

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Many anticancer drugs are genotoxic agents inducing DNA breaks in actively proliferating cancer cells. However, these same drugs also induce mutations, mostly genome structural variations (GSVs). The detection of GSVs in normal cells and tissues is a major challenge due to the very low abundance of these mutations, which are essentially only detectable in clonal outgrowths, such as tumors.

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