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477 results for “pancreatic ductal adenocarcinoma”
Datasets: Natural killer cells associate with malignant epithelial cells in the pancreatic ductal adenocarcinoma tumor microenvironment
<p>The following are necessary data files for the manuscript "Natural killer cells associate with malignant epithelial cells in the pancreatic ductal adenocarcinoma tumor microenvironment":</p> <ul> <li>.zip files for TMA_1, TMA_2, TMA_3, and TMA_4 are .mcd files acquired from imaging mass cytometry (IMC) for each slide of the pancreas TMA slide series</li> <li>pancreas_TMA_sample_info.xlxs includes info on all samples of the TMA slide series that were imaged by IMC</li> <li>custom_gates_0.zip includes histoCAT-derived single cell data files from all IMC samples in the pancreas TMA to be used for single cell analyses in R</li> <li>PDAC_IMC.RDS is a Seurat object of the IMC-derived PDAC single cell data to use for single cell and spatial analyses</li> <li>PDAC_sce is a SingleCellExperiment object of IMC-derived PDAC single cell data to use for spatial analyses</li> <li>mat.RDS is a distance matrix of PDAC cell types to use in R to generate network graph (Figure 2)</li> </ul> <p> </p> <p> </p>
CyTOF data of PBMC samples of patients with metastatic pancreatic ductal adenocarcinoma
<p>These two CyTOF datasets are a part of the manuscript by M. Baretti "E<span>ntinostat in combination with nivolumab in metastatic pancreatic ductal adenocarcinoma: a phase 2 clinical trial" accepted in Nature Communications. The datasets contain FCS files of PBMCs samples of patients with metastatic pancreatic ductal adenocarcinoma treated with entinostat and nivolumab. PBMC samples were run with myeloid- and lymphoid-oriented panels.<br></span></p>
Survival-associated cellular response maintained in pancreatic ductal adenocarcinoma (PDAC) switched between soft and stiff 3D microgel culture
<div> <div> <div> <div> <p>Pancreatic ductal adenocarcinoma (PDAC) accounts for about 90% of all pancreatic cancer cases. Five-year survival rates have remained below 12% since the 1970s, in part due to the difficulty in detection before metastasis (migration and invasion into neighboring organs and glands). Mechanical memory is a concept that has emerged over the past decade that may provide a path towards understanding how invading PDAC cells "remember" the mechanical properties of their diseased ("stiff," elastic modulus, E ≈ 10 kPa) microenvironment even whilst invading a healthy ("soft," E ≈ 1 kPa) microenvironment. Here, we investigated the role of mechanical priming by culturing a dilute suspension of PDAC (FG) cells within a 3D, rheologically tunable microgel platform from hydrogels with tunable mechanical properties. We conducted a suite of acute (short-term) priming studies where we cultured PDAC cells in either a soft (E ≈ 1 kPa) or stiff (E ≈ 10 kPa) environment for 6 h, then removed and placed them into a new soft or stiff 3D environment for another 18 h. Following these steps, we conducted RNA-seq analyses to quantify gene expression. Initial priming in 3D culture showed persistent gene expression for the duration of the study, regardless of the subsequent environments (stiff or soft). Stiff 3D culture was associated with the down-regulation of tumor suppressors (LATS1, BCAR3, CDKN2C ), as well as the up-regulation of cancer-associated genes (RAC3). Immunofluorescence staining (BCAR3, RAC3) further supported the persistence of this cellular response, with BCAR3 upregulated in soft culture, and RAC3 upregulated in stiff-primed culture. Stiff-primed genes were stratified against patient data found in The Cancer Genome Atlas (TCGA). Upregulated genes in stiff-primed 3D culture were associated with decreased survival in patient data, suggesting a link between patient survival and mechanical priming.</p> </div> </div> </div> </div>
VISION Invited lecture - Future approaches of pancreatic ductal adenocarcinoma
<p>Recording and presentation of the invited lecture that took place online on 14 October 2020 - <strong>Prof Alfredo Carrato - Future approaches of pancreatic ductal adenocarcinoma.</strong></p> <p>Although pancreatic ductal adenocarcinoma (PDAC) is not so frequent, it is the third leading cause of cancer death. As it shows non-specific symptoms it is diagnosed late and only 20% of patients are surgery candidates. Tumor recurrs locally or distantly after surgery in two thirds of them. Only 5% of PDAC patients survive 10 years. Targeted therapies have not yet proven their efficacy and treatment prescribed consists of chemotherapy combinations.</p> <p>PDAC has a dense stroma that reaches an 80% of the tumor, helping PDAC epithelial tumor cells to evade the immune system and growth, invade and metastasize through a crosstalk among PDAC cells and fibroblasts, macrophages, pericytes, stroma, etc. Targeting the stromal constituents may result in a step forward a better treatment efficacy.</p> <p>PDAC microbiome is unique and has been identified into the cancer cells and the local immune cells. Wisely management of the different resident microbial species could also result in prevention and another alternative for treatment.</p> <p>The identification of the PDAC high-risk population and the development of a convenient screening program is an objective to be reached for an earlier diagnosis and a potential advantage as more patients will be candidates for surgery, but to know in depth and detail the biology of the tumor and its interaction with the host will lead to a better treatment design and a real benefit of our patients.</p>
Study of Efficacy and Safety of NIS793 (With and Without Spartalizumab) in Combination With SOC Chemotherapy in First-line Metastatic Pancreatic Ductal Adenocarcinoma (mPDAC)
ClinicalTrials.gov study NCT04390763. IPD Sharing: YES. Countries: 14. Publications: 0.
Survival-associated cellular response maintained in pancreatic ductal adenocarcinoma (PDAC) switched between soft and stiff 3D microgel culture
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Cadherin-11 deficiency-induced changes in pancreatic ductal adenocarcinoma
<p class="MsoNormal"><span>Pancreatic ductal adenocarcinoma (PDAC) is one of the top five deadliest forms of cancer with very few treatment options. The 5-year survival rate for PDAC is 10% following diagnosis. Cadherin 11 (Cdh11), a cell-to-cell adhesion molecule, has been suggested to promote tumor growth and immunosuppression in PDAC, and Cdh11 inhibition significantly extended survival in mice with PDAC. However, the mechanisms by which Cdh11 deficiency influences PDAC progression and anti-tumor immune responses have yet to be fully elucidated. To investigate <em>Cdh11</em>-deficiency induced changes in PDAC tumor microenvironment (TME), we crossed <em>p48-Cre; LSL-Kras<sup>G12D/+</sup>; LSL-Trp53<sup>R172H/+</sup></em> (KPC) mice with <em>Cdh11<sup>+/-</sup></em> mice and performed single-cell RNA sequencing (scRNA-seq) of the non-immune (CD45<sup>-</sup>) and immune (CD45<sup>+</sup>) compartment of KPC tumor-bearing <em>Cdh11</em> proficient (<em>KPC-Cdh11<sup>+/+</sup></em>) and <em>Cdh11</em> deficient (<em>KPC-Cdh11<sup>+/-</sup></em>) mice. Our analysis showed that <em>Cdh11</em> is expressed primarily in cancer-associated fibroblasts (CAFs) and at low levels in epithelial cells undergoing epithelial-to-mesenchymal transition (EMT). <em>Cdh11</em> deficiency altered the molecular profile of CAFs, leading to a decrease in the expression of myofibroblast markers such as <em>Acta2</em> and <em>Tagln</em> and cytokines such as <em>Il6</em>, <em>Il33</em> and Midkine<em> (Mdk)</em>. We also observed a significant decrease in the presence of monocytes/macrophages and neutrophils in <em>KPC-Cdh11<sup>+/-</sup></em> tumors while the proportion of T cells was increased. Additionally, myeloid lineage cells from <em>Cdh11</em>-deficient tumors had reduced expression of inflammatory cytokines that have previously been shown to play a role in immune suppression. In summary, our data suggests that <em>Cdh11</em> deficiency significantly alters</span> the fibroblast and immune microenvironments and contributes to the downregulation of inflammatory cytokines, leading to an increase in anti-tumor immunity and enhanced survival.</p>
Single-Cell Mapping Reveals Several Immune Subsets Associated with Liver Metastasis of Pancreatic Ductal Adenocarcinoma
<p>Identifying a metastasis-correlated immune cell composition within the tumor microenvironment (TME) of pancreatic ductal adenocarcinoma (PDAC) will help to develop promising and innovative therapeutic strategies. Twenty-six samples from 11 patients (including 11 primary tumor tissues, 10 blood, and 5 lymph nodes) with different stages were used to develop a multiscale immune profile. High-dimensional single-cell analysis with mass cytometry was performed to search for metastasis-correlated immune changes in the microenvironment.</p> <p>The details about the files uploaded are as follows:</p> <p>1. panelA_Blood.zip includes 10 .fcs files from blood samples in Panel A;</p> <p>2. panelA_LN.zip includes 5 .fcs files from lymph node samples in Panel A;</p> <p>3. panelA_Tumor.zip includes 11 .fcs files from tumor tissue samples in Panel A;</p> <p>4. panelB_Tumor.zip includes 11 .fcs files from tumor tissue samples in Panel B;</p> <p>5. panel_metadata.xlsx describes marker used in Panel A and B;</p> <p>6. sample_metadata.xlsx describes detailed sample information.</p>
Gemcitabine and Paclitaxel vs Gemcitabine Alone After FOLFIRINOX Failure in Metastatic Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT03943667. IPD Sharing: Not stated. Countries: 1. Publications: 2.
A Study of Abemaciclib (LY2835219) Alone or in Combination With Other Agents in Participants With Previously Treated Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT02981342. IPD Sharing: YES. Countries: 8. Publications: 1.
Autologous Tumor Infiltrating Lymphocytes MDA-TIL in Treating Patients With Recurrent or Refractory Ovarian Cancer, Colorectal Cancer, or Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT03610490. IPD Sharing: Not stated. Countries: 1. Publications: 2.
A Study of Pembrolizumab and Olaparib for People With Metastatic Pancreatic Ductal Adenocarcinoma and Homologous Recombination Deficiency or Exceptional Treatment Response to Platinum-Based Therapy
ClinicalTrials.gov study NCT04666740. IPD Sharing: YES. Countries: 1. Publications: 1.
Mesothelin-Targeted Immunotoxin LMB-100 Alone or in Combination With Nab-Paclitaxel in People With Previously Treated Metastatic and/or Locally Advanced Pancreatic Ductal Adenocarcinoma and Mesothelin
ClinicalTrials.gov study NCT02810418. IPD Sharing: NO. Countries: 1. Publications: 1.
FAPi PET in Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT07342231. IPD Sharing: NO. Countries: 1. Publications: 1.
Study of Pembrolizumab With or Without Defactinib Following Chemotherapy as a Neoadjuvant and Adjuvant Treatment for Resectable Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT03727880. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Study of Single Agent Idelalisib Followed by Idelalisib in Combination With Chemotherapy in Adults With Metastatic Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT02468557. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study of Multiple Immunotherapy-Based Treatment Combinations in Participants With Metastatic Pancreatic Ductal Adenocarcinoma (Morpheus-Pancreatic Cancer)
ClinicalTrials.gov study NCT03193190. IPD Sharing: Not stated. Countries: 5. Publications: 1.
A Study of ELI-002 in Subjects With KRAS Mutated Pancreatic Ductal Adenocarcinoma (PDAC) and Other Solid Tumors
ClinicalTrials.gov study NCT04853017. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Hyperpolarized 13C Pyruvate MRI for Treatment Response Assessment in Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT04565327. IPD Sharing: NO. Countries: 1. Publications: 1.
Cadherin-11 deficiency-induced changes in pancreatic ductal adenocarcinoma
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Allen Brain Atlas
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