
Jenny Z. Xiang
· Professor of Research in Microbiology and ImmunologyVerifiedCornell University · Microbiology and Immunology
Active 2006–2025
About
Jenny Zhaoying Xiang, M.D., is a Professor of Research in Microbiology and Immunology at Weill Cornell Medicine. She directs the Genomics Resources Core Facility (GRCF), a shared resource established in 2000 that provides genomics technologies to the basic, translational, and clinical research communities at Weill Cornell Medicine, NewYork-Presbyterian Hospital, the Hospital for Special Surgery, and external collaborators. Her work involves offering a comprehensive range of high-quality genomics services, including experimental design, sample processing, data analysis, and validation, utilizing a wide array of advanced genomics instruments and sequencing platforms. Her research focus is on supporting biomedical research through state-of-the-art genomics technologies, which have been instrumental in facilitating numerous publications and securing external grants for investigators over more than two decades.
Research topics
- Biology
- Genetics
- Cell biology
- Virology
- Immunology
- Neuroscience
- Internal medicine
- Bioinformatics
- Medicine
- Pharmacology
Selected publications
Blood Advances · 2025-11-25
articleOpen accessABSTRACT: This phase 2 study evaluated the efficacy and safety of combining acalabrutinib and lenalidomide with either rituximab (ALR) or obinutuzumab (ALO), with longitudinal minimal residual disease (MRD) monitoring in frontline MCL treatment. The primary objective was molecular complete response (CR) after 12 cycles of induction, defined by Lugano criteria, and undetectable MRD of <10-6 (uMRD6) by clonoSEQ. Secondary objectives included safety, responses, and survival. Exploratory objectives included tumor mutation profiles and cell-free DNA (cfDNA) by cancer personalized profiling by deep sequencing. Patients in uMRD6 molecular CR were eligible for discontinuation of acalabrutinib plus lenalidomide after 24 cycles; all patients received a minimum of 36 cycles of anti-CD20 antibody treatment. In the ALR cohort, grade 3/4 hematologic toxicities included neutropenia (38%), thrombocytopenia (4%), and anemia (4%). Nonhematologic toxicities included rash (42%), fatigue (4%), nausea (4%), and vomiting (4%). The overall response rate (ORR) was 100%, CR rate was 83%, and molecular CR rate was 67% after 12 cycles of induction, with best molecular CR at 83%. At a median follow-up of 53 months (range, 46-60), the 4-year overall survival (OS) and progression-free survival (PFS) for ALR were 91% and 76%, respectively. TP53 mutations were adversely associated with PFS (P = .026). For ALO, ORR, CR, and molecular CR were 90% after induction, and 2-year OS and PFS were both at 100%. Longitudinal cfDNA analysis in ALR revealed clonal evolution during response and progression. This safe and active regimen is feasible as a time-limited initial therapy for patients with MCL and warrants further evaluation in response-adapted strategy. This trial was registered at www.ClinicalTrials.gov as NCT03863184.
2025-11-27
articleOpen access<p>Supplementary Table 1. Gene expression changes in 8505C after vemurafenib treatment.Supplementary Table 2. Gene expression changes in WRO after vemurafenib treatment.Supplementary Table 3. Gene expression changes in 8505C -Vem-Res 1 relative to parental 8505C.Supplementary Table 4. Gene expression changes in WRO -Vem-Res 6 relative to parental WRO.Supplementary Table 5. Clinical features of thyroid tumors used in Fig. 5.</p>
Nature Medicine · 2025-04-15
erratumOpen accessUsing hESCs to Probe the Interaction of the Diabetes-Associated Genes CDKAL1 and MT1E
Cell Reports · 2025-06-01
erratumOpen accessAs this was article initially published, there are several instances of duplication of immunostaining images presented in Figures 1C,S2A, and S4F.These errors occurred during the final preparation of the figures, when representative images were selected to illustrate the results.To ensure that these errors did not affect the paper's conclusions, the authors verified all raw data used to quantify the results.The results presented in Figure S4F do not affect the quantification results, but the quantification results in Figures 1C andS2A were affected.This quantification was performed again, and the results supported the original conclusions of the paper.The conclusions of this experiment remain unchanged.The corrected versions of the three affected figures appear below.The authors regret the error.
LILRB3 genetic variation is associated with kidney transplant failure in African American recipients
Nature Medicine · 2025-03-10 · 7 citations
articleAdvanced Science · 2025-07-25 · 2 citations
articleOpen accessWhile COVID-19 affects multiple organ systems, the human respiratory system is the primary viral target and main site for disease progression. In this study, spatial transcriptional assays (NanoString CosMx) are utilized to analyze both explant and autopsy samples from non-COVID and COVID-19 lungs, identifying the activation of proinflammatory macrophages in COVID-19 explants. It is further developed immuno-lung organoids comprising hPSC-derived alveolar and airway organoids co-cultured with macrophages to investigate the impact and underlying mechanisms of macrophage-mediated lung damage following SARS-CoV-2 infection. The findings demonstrate that proinflammatory macrophages induce lung cell senescence through the THBS1-(ITGA3+ITGB1) signaling axis, a mechanism further validated using spatial transcriptomics. This study not only establishes physiologically relevant immuno-lung organoid models for modeling macrophage-mediated tissue damage, but also identifies a previous unrecognized role of the THBS1-(ITGA3+ITGB1) pathway in driving lung cell senescence during infectious disease.
2025-11-24
articleOpen access<p>Supplementary Tables S1-S20</p>
2025-11-27
articleOpen access<p>S1. BRAFV600E mutation identified in thyroid cancer cell lines analyzed by RNA-seq.S2. STR analysis in thyroid cancer cell lines used in this study.S3. Gene expression of thyroid-specific genes in thyroid cancer cell lines analyzed by RNA-seq.S4. Dose-dependent toxicity of vemurafenib in BRAFV600E thyroidcancer cells.S5. Vemurafenib dose-dependent curves of vemurafenib-resistantBRAFV600E thyroid cancer cells.S6. Vemurafenib induces apoptosis in 8505C cells.S7. Predicted activators and inhibitors in Vem-resistant BRAF mutant thyroid cancer cells.</p>
Cell stem cell · 2025-06-24 · 5 citations
article2025-11-24
articleOpen access<p>All supplementary figures S1-S17</p>
Recent grants
Frequent coauthors
- 226 shared
Olivier Elemento
Weill Cornell Medicine
- 195 shared
Tuo Zhang
Cornell University
- 190 shared
Andrea Sboner
Weill Cornell Medicine
- 156 shared
Himisha Beltran
- 120 shared
Juan Miguel Mosquera
Weill Cornell Medicine
- 108 shared
Francesca Demichelis
University of Trento
- 98 shared
Robert E. Schwartz
Cornell University
- 93 shared
Shuibing Chen
University of Pennsylvania
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