Bio


During my doctoral studies, I trained in innate immunity gaining expertise in high throughput genetic engineering, molecular biology, and immunology. My Ph.D. work focused on the macrophage role in the host response to pathogen infection and sterile inflammation. Moving to Stanford, I set myself to work at the forefront of invention and acquire computational skills. Throughout my postdoctoral fellowship, I have worked with surgical pathologists including Drs. Matt van de Rijn, Rob West, Jeanne Shen, and Christian Schürch and leaders in the field of bioinformatics including Drs. Aaron Newman and Andrew Gentes studying macrophages in solid malignancies. In consequence, I effectively transformed from a wet-lab scientist to a computational biologist with expertise in genomics, image analysis, human pathology, and immunology.

Professional Education


  • PhD, Ghent University, Belgium, Innate Imunity (2015)
  • MSc, Intercollegiate Faculty of Biotechnology, University of Gdańsk and Medical University of Gdańsk, Poland, Biotechnology (2012)
  • BSc, Intercollegiate Faculty of Biotechnology, University of Gdańsk and Medical University of Gdańsk, Poland, Biotechnology (2010)

Stanford Advisors


Community and International Work


  • Data Carpentry Instructor and helper, Stanford

    Topic

    programing in R

    Partnering Organization(s)

    Data Carpentry's

    Location

    Bay Area

    Ongoing Project

    Yes

    Opportunities for Student Involvement

    No

Current Research and Scholarly Interests


My research focuses on revealing clinically relevant prognostic markers associated with myeloid cell biology in solid malignancies. I currently. lead two main projects: first, using single-cell RNA Sequencing and bulk tissue genomics to discover tumor-associated macrophage (TAM) diversity and establish their prognostic and predictive markers, second: using multiplex tissue imaging (MIBI) to unravel prognostic markers of spatial heterogeneity in the colon cancer.

All Publications


  • Expression of SARS-CoV-2 entry receptors in the respiratory tract of healthy individuals, smokers and asthmatics. Respiratory research Matusiak, M., Schurch, C. M. 2020; 21 (1): 252

    Abstract

    SARS-CoV-2 is causing a pandemic with currently>29 million confirmed cases and>900,000 deaths worldwide. The locations and mechanisms of virus entry into the human respiratory tract are incompletely characterized. We analyzed publicly available RNA microarray datasets for SARS-CoV-2 entry receptors and cofactors ACE2, TMPRSS2, BSG (CD147) and FURIN. We found that ACE2 and TMPRSS2 are upregulated in the airways of smokers. In asthmatics, ACE2 tended to be downregulated in nasal epithelium, and TMPRSS2 was upregulated in the bronchi. Furthermore, respiratory epithelia were negative for ACE-2 and TMPRSS2 protein expression while positive for BSG and furin, suggesting a possible alternative entry route for SARS-CoV-2.

    View details for DOI 10.1186/s12931-020-01521-x

    View details for PubMedID 32993656