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239 results on '"Yip-Schneider, Michele T."'

4. Contributions of the Microbiome-Derived Metabolome for Risk Assessment and Prognostication of Pancreatic Cancer

Author

León-Letelier, Ricardo A, primary, Dou, Rongzhang, additional, Vykoukal, Jody, additional, Yip-Schneider, Michele T, additional, Maitra, Anirban, additional, Irajizad, Ehsan, additional, Wu, Ranran, additional, Dennison, Jennifer B, additional, Do, Kim-An, additional, Zhang, Jianjun, additional, Schmidt, C Max, additional, Hanash, Samir, additional, and Fahrmann, Johannes F, additional

Published
2024
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6. Lead-Time Trajectory of CA19-9 as an Anchor Marker for Pancreatic Cancer Early Detection

Author

Fahrmann, Johannes F., Schmidt, C. Max, Mao, Xiangying, Irajizad, Ehsan, Loftus, Maureen, Zhang, Jinming, Patel, Nikul, Vykoukal, Jody, Dennison, Jennifer B., Long, James P., Do, Kim-Anh, Zhang, Jianjun, Chabot, John A., Kluger, Michael D., Kastrinos, Fay, Brais, Lauren, Babic, Ana, Jajoo, Kunal, Lee, Linda S., Clancy, Thomas E., Ng, Kimmie, Bullock, Andrea, Genkinger, Jeanine, Yip-Schneider, Michele T., Maitra, Anirban, Wolpin, Brian M., and Hanash, Samir

Published
2021
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7. Global Protease Activity Profiling Provides Differential Diagnosis of Pancreatic Cysts

Author

Ivry, Sam L, Sharib, Jeremy M, Dominguez, Dana A, Roy, Nilotpal, Hatcher, Stacy E, Yip-Schneider, Michele T, Schmidt, C Max, Brand, Randall E, Park, Walter G, Hebrok, Matthias, Kim, Grace E, O'Donoghue, Anthony J, Kirkwood, Kimberly S, and Craik, Charles S

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Digestive Diseases, Pancreatic Cancer, Rare Diseases, Animals, Biomarkers, Tumor, Carcinoembryonic Antigen, Cathepsin E, Cyst Fluid, Diagnosis, Differential, Fluorescent Dyes, Humans, Mice, Knockout, Mice, Transgenic, Neoplasms, Cystic, Mucinous, and Serous, Pancreatic Cyst, Pancreatic Neoplasms, Pancreatic Pseudocyst, Pepsin A, Peptide Hydrolases, Retrospective Studies, Sensitivity and Specificity, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

Purpose: Pancreatic cysts are estimated to be present in 2%-3% of the adult population. Unfortunately, current diagnostics do not accurately distinguish benign cysts from those that can progress into invasive cancer. Misregulated pericellular proteolysis is a hallmark of malignancy, and therefore, we used a global approach to discover protease activities that differentiate benign nonmucinous cysts from premalignant mucinous cysts.Experimental Design: We employed an unbiased and global protease profiling approach to discover protease activities in 23 cyst fluid samples. The distinguishing activities of select proteases was confirmed in 110 samples using specific fluorogenic substrates and required less than 5 μL of cyst fluid.Results: We determined that the activities of the aspartyl proteases gastricsin and cathepsin E are highly increased in fluid from mucinous cysts. IHC analysis revealed that gastricsin expression was associated with regions of low-grade dysplasia, whereas cathepsin E expression was independent of dysplasia grade. Gastricsin activity differentiated mucinous from nonmucinous cysts with a specificity of 100% and a sensitivity of 93%, whereas cathepsin E activity was 92% specific and 70% sensitive. Gastricsin significantly outperformed the most widely used molecular biomarker, carcinoembryonic antigen (CEA), which demonstrated 94% specificity and 65% sensitivity. Combined analysis of gastricsin and CEA resulted in a near perfect classifier with 100% specificity and 98% sensitivity.Conclusions: Quantitation of gastricsin and cathepsin E activities accurately distinguished mucinous from nonmucinous pancreatic cysts and has the potential to replace current diagnostics for analysis of these highly prevalent lesions. Clin Cancer Res; 23(16); 4865-74. ©2017 AACR.

Published
2017

11. Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers

Author

Cohen, Joshua D., Javed, Ammar A., Thoburn, Christopher, Wong, Fay, Tie, Jeanne, Gibbs, Peter, Schmidt, C. Max, Yip-Schneider, Michele T., Allen, Peter J., Schattner, Mark, Brand, Randall E., Singhi, Aatur D., Petersen, Gloria M., Hong, Seung-Mo, Kim, Song Cheol, Falconi, Massimo, Doglioni, Claudio, Weiss, Matthew J., Ahuja, Nita, He, Jin, Makary, Martin A., Maitra, Anirban, Hanash, Samir M., Molin, Marco Dal, Wang, Yuxuan, Li, Lu, Ptak, Janine, Dobbyn, Lisa, Schaefer, Joy, Silliman, Natalie, Popoli, Maria, Goggins, Michael G., Hruban, Ralph H., Wolfgang, Christopher L., Klein, Alison P., Tomasetti, Cristian, Papadopoulos, Nickolas, Kinzler, Kenneth W., Vogelstein, Bert, and Lennon, Anne Marie

Published
2017

15. Accurate Identification of Mucinous Pancreatic Cystic Lesions Using Small-Volume Analytes

Author

Caiazza, Francesco, primary, Conroy, Patricia C., additional, Ivry, Sam L., additional, York, Tyler, additional, Lin, Joseph, additional, Hernandez, Sophia, additional, Hoffmann, Thomas J., additional, Francis, Stephen S., additional, Park, Walter G., additional, Yip-Schneider, Michele T., additional, Schmidt, C. Max, additional, Brand, Randall, additional, Craik, Charles S., additional, and Kirkwood, Kimberly, additional

Published
2023
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16. Supplementary Figure S1-S9. from Global Protease Activity Profiling Provides Differential Diagnosis of Pancreatic Cysts

Author

Ivry, Sam L., primary, Sharib, Jeremy M., primary, Dominguez, Dana A., primary, Roy, Nilotpal, primary, Hatcher, Stacy E., primary, Yip-Schneider, Michele T., primary, Schmidt, C. Max, primary, Brand, Randall E., primary, Park, Walter G., primary, Hebrok, Matthias, primary, Kim, Grace E., primary, O'Donoghue, Anthony J., primary, Kirkwood, Kimberly S., primary, and Craik, Charles S., primary

Published
2023
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17. Supplementary Table S5 from Global Protease Activity Profiling Provides Differential Diagnosis of Pancreatic Cysts

Author

Ivry, Sam L., primary, Sharib, Jeremy M., primary, Dominguez, Dana A., primary, Roy, Nilotpal, primary, Hatcher, Stacy E., primary, Yip-Schneider, Michele T., primary, Schmidt, C. Max, primary, Brand, Randall E., primary, Park, Walter G., primary, Hebrok, Matthias, primary, Kim, Grace E., primary, O'Donoghue, Anthony J., primary, Kirkwood, Kimberly S., primary, and Craik, Charles S., primary

Published
2023
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21. Amplification-Free, High-Throughput Nanoplasmonic Quantification of Circulating MicroRNAs in Unprocessed Plasma Microsamples for Earlier Pancreatic Cancer Detection

Author

Masterson, Adrianna N., primary, Chowdhury, Nayela N., additional, Fang, Yue, additional, Yip-Schneider, Michele T., additional, Hati, Sumon, additional, Gupta, Prashant, additional, Cao, Sha, additional, Wu, Huangbing, additional, Schmidt, C. Max, additional, Fishel, Melissa L., additional, and Sardar, Rajesh, additional

Published
2023
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22. Intraductal Papillary Mucinous Neoplasia Originating From the Accessory (Santorini) Duct: A Rare Entity.

Author

Soufi, Mazhar, Yip-Schneider, Michele T., Carr, Rose, Roch, Alex, Akisik, Fatih, and Schmidt, C. Max

Abstract

The article focuses on the rare occurrence of intraductal papillary mucinous neoplasia (IPMN) originating from the accessory duct in the pancreas, which requires separate consideration from IPMN originating from the main duct or branch duct. Topics covered include the anatomical variations of the pancreatic duct system, the malignant potential of IPMN, and the need for surgical resection in cases of IPMN involving the accessory duct.

Published
2023
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23. Novel Preoperative Patient-centered Surgical Wellness Program Impacts Length of Stay Following Pancreatectomy

Author

SOUFI, MAZHAR, primary, DEPERALTA, DANIELLE K., additional, SIMPSON, RACHEL, additional, FLICK, KATELYN, additional, YIP-SCHNEIDER, MICHELE T., additional, SCHMIDT, CHRISTIAN M., additional, KILBANE, MOLLY, additional, COLGATE, CAMERON, additional, KELLEY, KRISTEN E., additional, WOODEN, WILLIAM, additional, CEPPA, EUGENE P., additional, HOUSE, MICHAEL, additional, ZYROMSKI, NICHOLAS, additional, NAKEEB, ATILLA, additional, and SCHMIDT, C. MAX, additional

Published
2021
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32. Multiregion whole-exome sequencing of intraductal papillary mucinous neoplasms reveals frequent somatic KLF4 mutations predominantly in low-grade regions

Author

Fujikura, Kohei, primary, Hosoda, Waki, additional, Felsenstein, Matthäus, additional, Song, Qianqian, additional, Reiter, Johannes G, additional, Zheng, Lily, additional, Beleva Guthrie, Violeta, additional, Rincon, Natalia, additional, Dal Molin, Marco, additional, Dudley, Jonathan, additional, Cohen, Joshua D, additional, Wang, Pei, additional, Fischer, Catherine G, additional, Braxton, Alicia M, additional, Noë, Michaël, additional, Jongepier, Martine, additional, Fernández-del Castillo, Carlos, additional, Mino-Kenudson, Mari, additional, Schmidt, C Max, additional, Yip-Schneider, Michele T, additional, Lawlor, Rita T, additional, Salvia, Roberto, additional, Roberts, Nicholas J, additional, Thompson, Elizabeth D, additional, Karchin, Rachel, additional, Lennon, Anne Marie, additional, Jiao, Yuchen, additional, and Wood, Laura D, additional

Published
2020
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39. Multiregion whole-exome sequencing of intraductal papillary mucinous neoplasms reveals frequent somatic KLF4 mutations predominantly in low-grade regions.

Author

Fujikura, Kohei, Hosoda, Waki, Felsenstein, Matthäus, Qianqian Song, Reiter, Johannes G., Zheng, Lily, Guthrie, Violeta Beleva, Rincon, Natalia, Dal Molin, Marco, Dudley, Jonathan, Cohen, Joshua D., Pei Wang, Fischer, Catherine G., Braxton, Alicia M., Noë, Michaël, Jongepier, Martine, Fernández-del Castillo, Carlos, Mino-Kenudson, Mari, Schmidt, C. Max, and Yip-Schneider, Michele T.

Subjects
PANCREATIC cysts, PANCREATIC intraepithelial neoplasia, SOMATIC mutation, MEDICAL sciences, CANCER genetics, TUMORS, TUMOR suppressor genes
Published
2021
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43. Abstract 3121: Characterization of immune profiling of pancreatic intraductal papillary mucinous neoplasm using multiplex immunofluorescence and image analysis approaches

Author

Solis, Luisa M., primary, Uraoka, Naohiro, additional, Parra, Edwin Roger, additional, Shen, Yu, additional, Wei, Wei, additional, Jiang, Mei, additional, Mino, Barbara, additional, Affolter, Kajsa, additional, Scaife, Courtney L., additional, Yip-Schneider, Michele T., additional, Schmidt, C. Max, additional, Firpo, Matthew, additional, Mulvihill, Sean, additional, Koay, Eugene J., additional, Wang, Huamin, additional, Wistuba, Ignacio I., additional, Maitra, Anirban, additional, and Sen, Subrata, additional

Published
2018
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44. Multiregion whole-exome sequencing of intraductal papillary mucinous neoplasms reveals frequent somatic KLF4mutations predominantly in low-grade regions

Author

Fujikura, Kohei, Hosoda, Waki, Felsenstein, Mattha¨us, Song, Qianqian, Reiter, Johannes G, Zheng, Lily, Beleva Guthrie, Violeta, Rincon, Natalia, Dal Molin, Marco, Dudley, Jonathan, Cohen, Joshua D, Wang, Pei, Fischer, Catherine G, Braxton, Alicia M, Noe¨, Michae¨l, Jongepier, Martine, Fernández-del Castillo, Carlos, Mino-Kenudson, Mari, Schmidt, C Max, Yip-Schneider, Michele T, Lawlor, Rita T, Salvia, Roberto, Roberts, Nicholas J, Thompson, Elizabeth D, Karchin, Rachel, Lennon, Anne Marie, Jiao, Yuchen, and Wood, Laura D

Abstract

ObjectiveIntraductal papillary mucinous neoplasms (IPMNs) are non-invasive precursor lesions that can progress to invasive pancreatic cancer and are classified as low-grade or high-grade based on the morphology of the neoplastic epithelium. We aimed to compare genetic alterations in low-grade and high-grade regions of the same IPMN in order to identify molecular alterations underlying neoplastic progression.DesignWe performed multiregion whole exome sequencing on tissue samples from 17 IPMNs with both low-grade and high-grade dysplasia (76 IPMN regions, including 49 from low-grade dysplasia and 27 from high-grade dysplasia). We reconstructed the phylogeny for each case, and we assessed mutations in a novel driver gene in an independent cohort of 63 IPMN cyst fluid samples.ResultsOur multiregion whole exome sequencing identified KLF4, a previously unreported genetic driver of IPMN tumorigenesis, with hotspot mutations in one of two codons identified in >50% of the analyzed IPMNs. Mutations in KLF4were significantly more prevalent in low-grade regions in our sequenced cases. Phylogenetic analyses of whole exome sequencing data demonstrated diverse patterns of IPMN initiation and progression. Hotspot mutations in KLF4were also identified in an independent cohort of IPMN cyst fluid samples, again with a significantly higher prevalence in low-grade IPMNs.ConclusionHotspot mutations in KLF4occur at high prevalence in IPMNs. Unique among pancreatic driver genes, KLF4mutations are enriched in low-grade IPMNs. These data highlight distinct molecular features of low-grade and high-grade dysplasia and suggest diverse pathways to high-grade dysplasia via the IPMN pathway.

Published
2021
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47. Prostaglandin E2: A Pancreatic Fluid Biomarker of Intraductal Papillary Mucinous Neoplasm Dysplasia.

Author

Yip-Schneider, Michele T., Carr, Rosalie A., Wu, Huangbing, and Schmidt, C. Max

Subjects
*PANCREATIC cysts, *DINOPROSTONE, *MUCINOUS adenocarcinoma, *DYSPLASIA, *TUMOR markers, *EXUDATES & transudates, *LONGITUDINAL method, *PANCREATIC tumors, *TUMORS, *DUCTAL carcinoma
Abstract

Background: With the increased frequency of diagnostic imaging, pancreatic cysts are now detected in >3% of American adults. Most of these are intraductal papillary mucinous neoplasms (IPMNs) with well-established but variable malignant potential. A biomarker that predicts malignant potential or dysplastic grade would help determine which IPMNs require removal and which can be observed safely. We previously reported that pancreatic fluid prostaglandin E2 (PGE2) levels might have promise as a predictor of IPMN dysplasia and we seek to validate those results in the current study.Study Design: Pancreatic cyst/duct fluid was prospectively collected from 100 patients with IPMN undergoing pancreatic resection. Surgical pathology revealed 47 low-/moderate-grade, 34 high-grade, and 20 invasive IPMNs. The PGE2 levels were assessed by ELISA and correlated with IPMN dysplasia grade, demographics, clinical radiologic/pathologic variables, acute/chronic pancreatitis, and NSAID use.Results: Mean pancreatic cyst fluid PGE2 levels in high-grade and invasive IPMNs were significantly higher than low-/moderate-grade IPMNs (3.5 and 4.4 pg/μL, respectively, vs 1.2 pg/μL; p < 0.0016). At a threshold of 1.1 pg/μL, PGE2 was 63% sensitive, 79% specific, and 71% accurate for detection of high-grade/invasive IPMNs. When tested in the subset of IPMN patients with preoperative pancreatic cyst fluid CEA >192 ng/mL, PGE2 at a threshold of 0.5 pg/μL demonstrated 78% sensitivity, 100% specificity, and 86% accuracy for detection of high-grade/invasive IPMN.Conclusions: Our results validate pancreatic cyst fluid PGE2 as an indicator of IPMN dysplasia, especially in select patients with preoperative pancreatic cyst fluid CEA >192 ng/mL. The inclusion of PGE2/CEA in a diagnostic biomarker panel can facilitate more optimal treatment stratification of IPMN patients. [ABSTRACT FROM AUTHOR]

Published
2017
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48. Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers.

Author

Fay Wong, Yuxuan Wang, Ptak, Janine, Dobbyn, Lisa, Schaefer, Joy, Silliman, Natalie, Popoli, Maria, Vogelstein, Bert, Cohen, Joshua D., Papadopoulos, Nickolas, Kinzler, Kenneth W., Yip-Schneider, Michele T., Schmidt, C. Max, Allen, Peter J., Schattner, Mark, Brand, Randall E., Singhi, Aatur D., Petersen, Gloria M., Seung-Mo Hong, and Song Cheol Kim

Subjects
PANCREATIC cancer, PANCREATIC cancer diagnosis, CANCER patients, PANCREATIC cancer treatment, BIOPSY, DNA
Abstract

The earlier diagnosis of cancer is one of the keys to reducing cancer deaths in the future. Here we describe our efforts to develop a noninvasive blood test for the detection of pancreatic ductal adenocarcinoma. We combined blood tests for KRAS gene mutations with carefully thresholded protein biomarkers to determine whether the combination of these markers was superior to any single marker. The cohort tested included 221 patients with resectable pancreatic ductal adenocarcinomas and 182 control patients without known cancer. KRAS mutations were detected in the plasma of 66 patients (30%), and every mutation found in the plasma was identical to that subsequently found in the patient's primary tumor (100% concordance). The use of KRAS in conjunction with four thresholded protein biomarkers increased the sensitivity to 64%. Only one of the 182 plasma samples from the control cohort was positive for any of the DNA or protein biomarkers (99.5% specificity). This combinatorial approach may prove useful for the earlier detection of many cancer types. [ABSTRACT FROM AUTHOR]

Published
2017
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49. Cyclooxygenase-2 Expression in Hamster and Human Pancreatic Neoplasia1

Author

Crowell, Pamela L, Schmidt, C Max, Yip-Schneider, Michele T, Savage, Jesse J, Hertzler, Dean A, and Cummings, William O

Subjects
Male, Mesocricetus, Anti-Inflammatory Agents, Non-Steroidal, Antineoplastic Agents, Cell Differentiation, Immunohistochemistry, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Pancreatic Neoplasms, Sulindac, Cyclooxygenase 2, Cell Line, Tumor, Cricetinae, Animals, Humans, Neoplasm Transplantation, Research Article
Abstract

Cyclooxygenase-2 (COX-2) has been implicated in the development of gastrointestinal malignancies. The aim of the present study was to determine COX-2 expression/activity throughout stages of experimental and human pancreatic neoplasia. COX-2 immunohistochemistry was performed in pancreata of hamsters subjected to the carcinogen N-nitrosobis-(2-oxopropyl)amine (BOP) and in human pancreatic tumors. COX-2 activity was determined by prostaglandin E2 assay in tumor versus matched normal pancreatic tissues. The activity of the COX inhibitor sulindac was tested in the PC-1 hamster pancreatic cancer model. COX-2 expression was elevated in all pancreatic intraepithelial neoplasias (PanINs) and adenocarcinomas. In BOP-treated hamsters, there were significant progressive elevations in COX-2 expression throughout pancreatic tumorigenesis. In human samples, peak COX-2 expression occurred in PanIN2 lesions and remained moderately elevated in PanIN3 and adenocarcinoma tissues. COX-2 activity was significantly elevated in hamster and human pancreatic cancers compared to pair-matched normal pancreas. Furthermore, hamster pancreatic tumor engraftment/formation in the PC-1 hamster pancreatic cancer model was reduced 4.9-fold by oral administration of sulindac. Increased COX-2 expression is an early event in pancreatic carcinogeneses. The BOP-induced hamster carcinogenesis model is a representative model used to study the role of COX-2 in well-differentiated pancreatic tumorigenesis. COX inhibitors may have a role in preventing tumor engraftment/formation.

Published
2006

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