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Nasim Barapour

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Articles

A comparison of deep multiomics profiles across ethnicity, geography, and age

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By Nasim Barapour, John Cao, Yue Wu, Shubham Gupta, Michael R. Hoopmann, Rui Qin, Mukul K. Midha, Myriam Mireault, Pablo Juanes-Velasco, Casey Hanson, Sara Ahadi, Emily Higgs, David Baxter Verified, Christian Diener, Orit Dagan-Rosenfeld, Daniel Hornburg, Fredrik Edfors, Stephanie Church Verified, Mohan Babu, Christopher Jin, Shannon Rego, Lettie McGuire, Thomas V. Karathanos, Daniel J. Panyard, Martín Parra, Aubrey Roberts, Ekanath Srihari Rangan, Melanie Ashland, Kevin Castillo, Gavin M. Traber, Matthew Ellenberger, Ryan Kellogg, Wenyu Zhou, Hannes Röst, Martin Kjellberg, Tejaswini Mishra, Charu Kapil, Ulrike Kusebauch, Sushmita Patwardhan, Alicia Landeira-Viñuela, Ángela-Patricia Hernández, Maliha Mashkoor, Tea Dodig-Crnkovic, Annika Bendes, Leo Dahl, Sean Gibbons, P. Venkat Rangan, Allan Stensballe, Jochen Schwenk, Richard Unwin, Manuel Fuentes, Lekha Sleno, Robert L. Moritz, Lara K. Mahal, Michael Snyder, Songjie Che, Durga Thota, Tristan Chou, Monika Avina, Jessi W. Li, Amarnath K. Ranjit, Mikkel Eggert Thomsen, Thanadol Sutantiwanichkul
| Cell Press Verified
Results Following the study design (Figure 1A; Table S1; STAR Methods), we collected samples across multiple continents during annual meetings of HUPO between 2016 and 2019. Sampling occurred at five sites, including a pilot cohort in Massachusetts (n = 31), followed by Taiwan (n = 106), Ireland (n = 113), and Florida (n = 87). An additional collection in California (n = 41) expanded the US cohort (Figures 1A, 1B, and S1A–S1E). Figure 1 Study design and demographics (A) Overview of hPOP study.
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Polyclonal origins of human premalignant colorectal lesions - Nature

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By Debra Van Egeren, Aziz K. Khan, Aaron M Horning, Edward D. Esplin, Winston R. Becker, Casey Hanson, Hayan Lee, Hao Zhang, Zhen He, Ruiqi Jian, Jeanne Shen, Anshul Kundaje, William J. Greenleaf, Zheng Hu, James Ford, Michael Snyder, Nasim Barapour, Bahareh Bahmani
| Nature Verified
Abstract Cancer is generally thought to be caused by expansion of a single mutant cell1. However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations2,3. Detecting polyclonal tumor initiation is challenging in patients, as it requires profiling early-stage lesions before clonal sweeps obscure diversity.
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