
Robert Babak Faryabi
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2007–2025
About
Robert Babak Faryabi, Ph.D., is an Associate Professor of Pathology and Laboratory Medicine at the University of Pennsylvania's Perelman School of Medicine. He is also an Associate Investigator at the Abramson Family Cancer Research Institute, a member of the Abramson Cancer Center, and a Senior Fellow at the Institute for Biomedical Informatics. Dr. Faryabi serves as a Core Faculty Member at the Penn Epigenetics Institute and is involved in multiple research initiatives related to cancer genomics and epigenetics. His research focuses on advancing the mechanistic understanding of human cancer genome architecture and regulation. His lab employs multidisciplinary approaches to explore chromatin organization, transcriptional regulation, and gene expression in cancer, with current projects centered on lymphoma and breast cancer. These projects investigate how epigenetic control of gene expression is disrupted, how transcriptional dependencies develop, and how heterogeneity and plasticity in transcriptional regulation contribute to drug resistance. Dr. Faryabi's work aims to elucidate the cause-and-effect relationships between chromatin organization and cancer progression, contributing to the development of targeted therapies and diagnostic tools.
Research topics
- Biology
- Cancer research
- Cell biology
- Computational biology
- Computer science
Selected publications
2025-11-03
articleOpen access<p>The adoptive transfer model mimics pathways that are constitutively activated in human MCL.</p>
2025-11-03
articleOpen access<p>Disease characteristics of the mice that developed lymphoma</p>
2025-11-03
articleOpen access<p>Reagents used for histology and immunohistochemistry </p>
bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-12
preprintOpen accessSenior authorCorrespondingMultiple enhancers, often located across vast genomic distances, regulate key genes. However, how chromatin topology organization at individual alleles enables cell-type-restricted multi-enhancer gene regulation remains unclear. Using acute protein degradation and time-course population-average chromatin conformation capture in lymphoma, we found that the B-cell- lineage-determining transcription factor EBF1 preferentially positions multiple enhancers at loci containing sparsely distributed genes essential for B-cell identity and oncogenesis. Our time-resolved sub-diffraction optical chromatin architecture tracing of >100,000 alleles in individual lymphoma cells further revealed diverse topological conformations facilitating multi-enhancer interactions. Mechanistically, we found that positioning of enhancers at allelic topological centers is required for their interactions with target promoters, with EBF1 serving as a barrier to the loop-extruding cohesin on enhancers. These findings, which we demonstrate their generalizability to the T-cell-lineage-determining transcription factor TCF1 in T-cell leukemia, suggest that lineage-determining transcription factors radially position enhancers and promoters to enable multi-enhancer regulation of key oncogenes.
2025-11-03
articleOpen access<p>ion torrent mouse chip design</p>
2025-11-03
articleOpen access<p>Heterogenous morphology of MCL-like developed by Eµ-SOX11CCND1 animals</p>
bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-23
preprintOpen accessSenior authorCorrespondingSUMMARY Accurate classification of somatic variations from high-throughput sequencing data has become integral to diagnostics and prognostics across various cancers. However, the classification of these variations remains highly manual, inherently variable, and largely inaccessible outside specialized laboratories. Here, we introduce Azurify - a computational tool that integrates machine learning, public resources recommended by professional societies, and clinically annotated data to classify the pathogenicity of variations in precision cancer medicine. Trained on over 15,000 clinically classified variants from 8,202 patients across 138 cancer phenotypes, Azurify achieves 99.1% classification accuracy for concordant pathogenic variants in data from two external clinical laboratories. Additionally, Azurify reliably performs precise molecular profiling in leukemia cases. Azurify’s unified, scalable, and modular framework can be easily deployed within bioinformatics pipelines and retrained as new data emerges. In addition to supporting clinical workflows, Azurify offers a high-throughput screening solution for research, enabling genomic studies to identify meaningful variant-disease associations with greater efficiency and consistency.
2025-11-03
articleOpen access<p>Additional immune profiling of adoptive transfer and transgenic mice.</p>
2025-11-03
articleOpen access<p>Antibodies and markers used for spectral flowcytometry.</p>
Clinical Cancer Research · 2025-08-26
articleOpen accessPURPOSE: Mantle cell lymphoma (MCL) remains incurable despite therapeutic advances, highlighting the need for improved preclinical models. Existing transgenic MCL mouse models have significant limitations, restricting their translational value. EXPERIMENTAL DESIGN: We generated an immunocompetent MCL model by overexpressing the key oncogenic drivers SRY-box transcription factor 11 (SOX11) and Cyclin D1 (CCND1) under the Eµ enhancer in C57BL/6 mice, aiming to replicate human MCL's biological and pathologic features. RESULTS: Eµ-SOX11CCND1 mice developed lymphoma marked by clonal B1a cell expansion in lymphatic and extranodal tissues. Morphologic, immunophenotypic, and transcriptional profiling revealed strong similarity to human MCL, with pathway analysis confirming significant molecular overlap. Importantly, lymphoma cells could be adoptively transferred into wild-type recipients, enabling therapeutic testing within an intact immune system. CONCLUSIONS: The Eµ-SOX11CCND1 mouse represents a robust and biologically relevant model that faithfully recapitulates human MCL. Its immunocompetent nature and adoptive transfer capability make it a valuable model for studying disease mechanisms and evaluating novel therapeutic approaches for patients with MCL.
Recent grants
Human Pancreas Analysis Program for Type 2 Diabetes (HPAP-T2D)
NIH · $25.0M · 2019–2029
NIH · $2.1M · 2022–2027
Notch-driven Epigenetic Program of MYC and CCND1 in Triple-Negative Breast Cancer
NIH · $2.1M · 2019–2026
Frequent coauthors
- 74 shared
Gregory W. Schwartz
University Health Network
- 59 shared
Yeqiao Zhou
California University of Pennsylvania
- 58 shared
Warren S. Pear
- 55 shared
Jelena Petrovic
- 51 shared
Golnaz Vahedi
University of Pennsylvania
- 31 shared
Maria Fasolino
California University of Pennsylvania
- 27 shared
Naomi Goldman
California University of Pennsylvania
- 27 shared
Lanwei Xu
University of Pennsylvania
Labs
Faryabi LabPI
Education
- 2015
Postdoctoral training
National Cancer Institute
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with Robert Babak Faryabi
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup