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5 results on '"Eric Mukherjee"'

1. Multiomic single-cell sequencing defines tissue-specific responses in Stevens-Johnson syndrome and toxic epidermal necrolysis

Author

Andrew Gibson, Ramesh Ram, Rama Gangula, Yueran Li, Eric Mukherjee, Amy M. Palubinsky, Chelsea N. Campbell, Michael Thorne, Katherine C. Konvinse, Phuti Choshi, Pooja Deshpande, Sarah Pedretti, Mark W. Fear, Fiona M. Wood, Richard T. O’Neil, Celestine N. Wanjalla, Spyros A. Kalams, Silvana Gaudieri, Rannakoe J. Lehloenya, Samuel S. Bailin, Abha Chopra, Jason A. Trubiano, On behalf of the AUS-SCAR Consortium, Jonny G. Peter, On behalf of the AFRiSCAR Consortium, Simon A. Mallal, and Elizabeth J. Phillips

Subjects
Science
Abstract

Abstract Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) is a rare but life-threatening cutaneous drug reaction mediated by human leukocyte antigen (HLA) class I-restricted CD8+ T cells. For unbiased assessment of cellular immunopathogenesis, here we perform single-cell (sc) transcriptome, surface proteome, and T cell receptor (TCR) sequencing on unaffected skin, affected skin, and blister fluid from 15 SJS/TEN patients. From 109,888 cells, we identify 15 scRNA-defined subsets. Keratinocytes express markers indicating HLA class I-restricted antigen presentation and appear to trigger the proliferation of and killing by cytotoxic CD8+ tissue-resident T cells that express granulysin, granzyme B, perforin, LAG3, CD27, and LINC01871, and signal through the PKM, MIF, TGFβ, and JAK-STAT pathways. In affected tissue, cytotoxic CD8+ T cells express private expanded and unexpanded TCRαβ that are absent or unexpanded in unaffected skin, and mixed populations of macrophages and fibroblasts express pro-inflammatory markers or those favoring repair. This data identifies putative cytotoxic TCRs and therapeutic targets.

Published
2024
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2. Late-Stage Pancreatic Cancer Detected During High-Risk Individual Surveillance: A Systematic Review and Meta-Analysis

Author

Ankit Chhoda, Craig G. Gunderson, Fay Kastrinos, Kapil Wattamwar, James J. Farrell, Alyssa Grimshaw, Anup Sharma, Eric Mukherjee, Ziga Vodusek, and Nita Ahuja

Subjects
Oncology, medicine.medical_specialty, Funnel plot, Time Factors, endocrine system diseases, MEDLINE, Cochrane Library, Endosonography, Risk Factors, Internal medicine, medicine, Humans, Cumulative incidence, Stage (cooking), Watchful Waiting, Neoplasm Staging, Hepatology, business.industry, Incidence, Incidence (epidemiology), Gastroenterology, Publication bias, Magnetic Resonance Imaging, Pancreatic Neoplasms, Meta-analysis, Tomography, X-Ray Computed, business, Carcinoma, Pancreatic Ductal
Abstract

Background and Aims Identification and resection of successful targets, i.e., T1 N0M0 pancreatic ductal adenocarcinoma (PDAC) and high-grade precursors during surveillance of high-risk individuals (HRIs) confers improved survival. Late-stage PDACs refer to T2-4 N0M0 and nodal or distant metastatic PDAC stages diagnosed during the follow-up phase of HRI surveillance. This study aimed to quantify late-stage PDACs during HRI surveillance and identify associated clinicoradiologic factors. Methods A systematic search (PROSPERO:CRD42018117189) from Cochrane Library, Embase, Google Scholar, Medline, PubMed, Scopus, and Web of Science was last performed on April 18, 2021. Only original HRI surveillance manuscripts which specified follow-up strategies were included, while studies with only baseline information were excluded. Cumulative incidences of advanced neoplasia: high-grade precursors and all PDACs, and surveillance-detected/interval late-stage PDACs were calculated through random-effects model. Incidence of late-stage PDACs underwent metaregression to identify association with HRI clinicoradiologic features. Publication bias was assessed through the Funnel plot and Egger’s Regression line. Results Thirteen original surveillance studies included 2169 HRIs followed over 7302.72 patient-years. Cumulative incidence of advanced neoplasia and late-stage PDACs was 3.3 [95% CI:0.6-7.4] and 1.7 [95% CI:0.2-4.0] per 1000 patient-years, respectively. Late-stage PDACs lacked significant association with surveillance imaging, baseline pancreatic morphology, study location, genetic background, gender, or age. Limited information on diagnostic error, symptoms, timing of presentation, lesion site, and surveillance adherence precluded formal meta-analysis. Conclusion A sizable proportion of late-stage PDACs were detected during follow-up. Their incidence lacked association with baseline clinicoradiologic features. Further causal investigation of stage-based outcomes is warranted for overall improvement in HRI surveillance.

Published
2022

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