Felicia D. Allard Data-verified
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Associate Professor
faculty
Research Areas
Biography and Research Information
OverviewAI-generated summary
Felicia D. Allard investigates cancer biology and treatment response, with a focus on pancreatic ductal adenocarcinoma. Her recent work has identified Keratin 17 as a prognostic and predictive biomarker for this cancer, exploring its role in predicting chemotherapy response and modulating the tumor's immune environment. Allard also studies liver metabolism, examining the roles of pyruvate and alanine in maintaining antioxidant capacity and the protective effects of exogenous phosphatidic acid against acetaminophen-induced liver injury in mice. Her research extends to medical imaging analysis, including predicting pathologist visual attention when evaluating whole slide images of cancer. She has published 59 papers, accumulating 630 citations, and holds an h-index of 14. Allard collaborates extensively with researchers at the University of Arkansas for Medical Sciences, including Eric U. Yee (13 shared publications) and Mitchell R. McGill (4 shared publications).
Metrics
- h-index: 14
- Publications: 59
- Citations: 639
Selected Publications
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Entrustable professional activities for cytopathology fellowship (2024)
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Keratin 17 modulates the immune topography of pancreatic cancer (2024)
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Keratin 17 is a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma (2024)
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Keratin 17 modulates the immune topography of pancreatic cancer (2024)
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Hepatic pyruvate and alanine metabolism are critical and complementary for maintenance of antioxidant capacity and resistance to oxidative insult (2023)
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Keratin 17 as a Predictor of Chemotherapy Response in Pancreatic Ductal Adenocarcinoma (2023)
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Cytology of Sinonasal Tract Lesions/Tumors (2023)
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Predicting the Visual Attention of Pathologists Evaluating Whole Slide Images of Cancer (2022)
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Hepatic pyruvate and alanine metabolism are critical and complementary for maintenance of antioxidant capacity and resistance to oxidative insult in mice (2022)
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Radiation Effects on Methamphetamine Pharmacokinetics and Pharmacodynamics in Rats (2022)
Collaboration Network
Top Collaborators
- Multi-Class Cell Detection Using Spatial Context Representation
- Hepatic pyruvate and alanine metabolism are critical and complementary for maintenance of antioxidant capacity and resistance to oxidative insult
- Exogenous phosphatidic acid reduces acetaminophen-induced liver injury in mice by activating hepatic interleukin-6 signaling through inter-organ crosstalk
- Predicting the Visual Attention of Pathologists Evaluating Whole Slide Images of Cancer
- Radiation Effects on Methamphetamine Pharmacokinetics and Pharmacodynamics in Rats
Showing 5 of 13 shared publications
- Keratin 17 is a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Keratin 17 modulates the immune topography of pancreatic cancer
- Keratin 17 as a Predictor of Chemotherapy Response in Pancreatic Ductal Adenocarcinoma
- Abstract A042: Keratin 17 is a negative prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Abstract C063: Keratin 17 as a predictor of chemotherapy response in pancreatic ductal adenocarcinoma
Showing 5 of 7 shared publications
- Keratin 17 is a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Keratin 17 modulates the immune topography of pancreatic cancer
- Keratin 17 as a Predictor of Chemotherapy Response in Pancreatic Ductal Adenocarcinoma
- Abstract A042: Keratin 17 is a negative prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Abstract C063: Keratin 17 as a predictor of chemotherapy response in pancreatic ductal adenocarcinoma
Showing 5 of 7 shared publications
- Keratin 17 is a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Keratin 17 modulates the immune topography of pancreatic cancer
- Keratin 17 as a Predictor of Chemotherapy Response in Pancreatic Ductal Adenocarcinoma
- Abstract A042: Keratin 17 is a negative prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Abstract C063: Keratin 17 as a predictor of chemotherapy response in pancreatic ductal adenocarcinoma
Showing 5 of 7 shared publications
- Multi-Class Cell Detection Using Spatial Context Representation
- Predicting the Visual Attention of Pathologists Evaluating Whole Slide Images of Cancer
- Keratin 17 modulates the immune topography of pancreatic cancer
- Multi-Class Cell Detection Using Spatial Context Representation
- Abstract B041: Keratin 17 excludes CD8-positive T cells and recruits CD163-positive macrophages in pancreatic ductal adenocarcinoma
Showing 5 of 6 shared publications
- Keratin 17 is a prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Keratin 17 modulates the immune topography of pancreatic cancer
- Abstract A042: Keratin 17 is a negative prognostic and predictive biomarker in pancreatic ductal adenocarcinoma
- Abstract C063: Keratin 17 as a predictor of chemotherapy response in pancreatic ductal adenocarcinoma
- Abstract B041: Keratin 17 excludes CD8-positive T cells and recruits CD163-positive macrophages in pancreatic ductal adenocarcinoma
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Data from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
- Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism
Showing 5 of 6 shared publications
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