Melissa Ko earned an S.B. in biology from MIT and a PhD in cancer biology from Stanford University. Her research aims to develop novel computational pipelines to make sense of the deluge of single-cell high-dimensional data collected by biologists. Using visualizations and modeling, Melissa reveals mechanisms of drug resistance in cancer and identifies more effective treatment combinations. During her graduate career, Melissa received support from the National Science Foundation (NSF) Graduate Research Fellowship, Stanford’s Diversifying Academia, Recruiting Excellence (DARE) Fellowship, and the National Cancer Institute F99/K00 Fellowship. Melissa has taught computational and cancer biology workshops at Stanford University as well as general biology at Foothill College. As a Thinking Matters Fellow, Melissa teaches THINK 3: Breaking Codes, Finding Patterns, THINK 61: Living with Viruses, and THINK 23: The Cancer Problem: Causes, Treatments, and Prevention.

In addition, Melissa has been involved with numerous educational outreach programs including the Splash program at MIT, Stanford, and Berkeley. Through these programs and related efforts, she has taught middle school and high school students in a variety of subjects, from cancer biology to personal finance to poetry. Melissa is dedicated to improving the experience of underrepresented students in all STEM disciplines. She served as a mentor and program leader for numerous Stanford Bioscience programs including SSRP and ADVANCE. Through prior work with Stanford’s Vice Provost for Teaching and Learning, Melissa has also developed diversity and inclusion content for instructors of in-person, online, and hybrid format classes.

Outside of work, Melissa enjoys cooking, playing video games, reading poetry, and going on walks in the park.

Academic Appointments

  • Lecturer, Stanford Introductory Studies - Thinking Matters

Honors & Awards

  • Diversifying Academia, Recruiting Excellence (DARE) Fellowship, Stanford University (2016-2018)
  • F99/K00 Predoctoral to Postdoctoral Fellow Transition Award, National Cancer Institute (2016-2018)
  • Graduate Research Fellowship, National Science Foundation (2013-2016)

Professional Education

  • SB, Massachusetts Institute of Technology, Biology (2012)
  • PhD, Stanford University, Cancer Biology (2018)

All Publications

  • CDX2 is an amplified lineage-survival oncogene in colorectal cancer PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Salari, K., Spulak, M. E., Cuff, J., Forster, A. D., Giacomini, C. P., Huang, S., Ko, M. E., Lin, A. Y., van de Rijn, M., Pollack, J. R. 2012; 109 (46): E3196-E3205


    The mutational activation of oncogenes drives cancer development and progression. Classic oncogenes, such as MYC and RAS, are active across many different cancer types. In contrast, "lineage-survival" oncogenes represent a distinct and emerging class typically comprising transcriptional regulators of a specific cell lineage that, when deregulated, support the proliferation and survival of cancers derived from that lineage. Here, in a large collection of colorectal cancer cell lines and tumors, we identify recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor 2 (CDX2), a regulator of normal intestinal lineage development and differentiation, as a target of the amplification. In contrast to its described role as a colorectal tumor suppressor, CDX2 when amplified is required for the proliferation and survival of colorectal cancer cells. Further, transcriptional profiling, binding-site analysis, and functional studies link CDX2 to Wnt/β-catenin signaling, itself a key oncogenic pathway in colorectal cancer. These data characterize CDX2 as a lineage-survival oncogene deregulated in colorectal cancer. Our findings challenge a prevailing view that CDX2 is a tumor suppressor in colorectal cancer and uncover an additional piece in the multistep model of colorectal tumorigenesis.

    View details for DOI 10.1073/pnas.1206004109

    View details for PubMedID 23112155