
Yibin Kang
VerifiedPrinceton University · Molecular Biology
Active 1997–2026
About
Yibin Kang is a Warner-Lambert/Parke-Davis Professor of Molecular Biology at Princeton University. His research focuses on the molecular mechanisms of breast cancer metastasis, employing a multidisciplinary and integrative approach that combines molecular biology, genomics, animal models, and advanced in vivo imaging technologies. His laboratory aims to identify metastasis genes and understand their roles in tumor-stromal interactions during metastasis formation in various organs. Key areas of investigation include the identification of clinically relevant metastasis genes through comprehensive profiling technologies, the molecular characterization of tumor stromal interactions, and the study of early oncogenic events and cellular origins that influence tumor progression and metastasis. Additionally, his work explores the regulatory roles of miRNAs and ncRNAs in tumor progression, particularly their involvement in epithelial-mesenchymal transition and metastasis. Dr. Kang's contributions have led to the discovery of new genes promoting recurrence, metastasis, and chemoresistance in breast cancer, as well as insights into tumor-stromal interactions essential for metastatic growth. His research has significant implications for developing novel therapeutics for metastatic cancer.
Research topics
- Biology
- Bioinformatics
- Cancer research
- Computer Science
- Genetics
- Sociology
- Biochemistry
- Cell biology
- Medicine
- Internal medicine
- Chemistry
- Computational biology
- Molecular biology
- Data science
Selected publications
Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer
bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-21
articleOpen accessSummary Cell growth requires elevated protein synthesis, which depends on the production of ribosomes. Ribosome biogenesis is a complex, multi-step pathway in which newly transcribed precursor ribosomal RNA (rRNA) undergoes coordinated processing and assembly in the nucleolus to produce the small and large ribosomal subunits (SSU and LSU). 1–3 Oncogene activation stimulates rRNA transcription and processing, giving rise to enlarged nucleoli that produce thousands of ribosomes every minute. 4,5 However, efficient ribosome production requires tight coordination across numerous maturation steps, and it remains unclear if elevated rDNA transcription is proportionally converted into mature ribosomes, or whether imperfect coordination constrains the output yield. Here, we quantify pre-rRNA transcription (input) and compare it with newly-assembled cytoplasmic ribosomes (output), revealing that oncogene activation reduces the efficiency of ribosome production. Using a quantitative pulse-chase sequencing approach with mathematical modeling to resolve rRNA maturation kinetics, we found that oncogene activation creates late-stage processing bottlenecks, characterized by delayed precursor maturation and increased degradation. Perturbation of late-stage ribosome biogenesis factors preferentially impaired oncogene-driven cell growth, and limited tumor growth in mouse models, suggesting that these bottlenecks represent selective vulnerabilities in cancer, created by imbalanced biosynthetic flux. Together, these findings reveal that oncogene-driven ribosome production is imperfectly coordinated across maturation steps, and suggest that capacity limits in multi-step assembly pathways may be therapeutically exploitable in cancer and other diseases.
2025-09-25
articleOpen access<p>Gut microbiome taxonomic classification data</p>
2025-09-25
articleOpen access<p>Tumor immune profiling in the PyMT model by flow cytometry</p>
2025-09-25
articleOpen access<p>Serum metabolite peak areas from the YUMM1.1-9 model</p>
2025-09-25
articleOpen access<p>Flow cytometry gating strategy</p>
2025-09-25
articleOpen access<p>Extended serum and fecal metabolomic analyses in the different tumor models</p>
2025-09-25
articleOpen access<p>Fecal metabolite peak areas from the B16-OVA model</p>
2025-09-25
articleOpen access<p>Fecal metabolite peak areas from the YUMM1.1-9 model</p>
2025-09-25
articleOpen access<p>Extended data for the MC-38 tumor model</p>
iScience · 2025-10-04 · 2 citations
articleOpen accessSenior authorand high-throughput screening approach followed by medicinal optimization to identify first-in-class, oral and safe antagonists of ALDH1A3 with potent anti-tumor immunotherapeutic activity and an optimized drug development profile.
Recent grants
Jagged1-dependent tumor-stromal interactions in bone metastasis
NIH · $1.8M · 2017–2021
The Role of miRNAs in Epithelial-Mesenchymal Transition and Metastasis
NIH · $1.6M · 2010–2017
NIH · $1.6M · 2013
Frequent coauthors
- 99 shared
Bryan R. Cullen
Duke Medical Center
- 80 shared
Yong Wei
- 52 shared
Minhong Shen
Princeton University
- 48 shared
Joan Massagué
Memorial Sloan Kettering Cancer Center
- 45 shared
Tianhua Zhou
- 43 shared
Hal P. Bogerd
Duke University Hospital
- 41 shared
Glen A. Coburn
Progenics Pharmaceuticals (United States)
- 40 shared
Min Yuan
Beth Israel Deaconess Medical Center
Education
- 2000
Ph.D., Genetics
Duke University
Awards & honors
- 2016 Komen Scholar Award, Susan G. Komen Foundation
- Innovation Award, Department of Molecular Biology, Princeton…
- Duke Graduate School Few-Glasson Alumni Society, Duke Univer…
- 2014 AACR Outstanding Investigator Award, American Associati…
- 2012 AACR Award for Outstanding Achievement in Cancer Resear…
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