Tomer Shlomi



Nano Area:
Personal Home Page:

PhD: Computer Science, Tel-Aviv University, 2008

MSc: Computer Science, Tel-Aviv University, 2003

BSc: Computer Science, Tel-Aviv University, 2001


Nano Main Field:

my interest in nanotechnology stems from our work on characterizing and quantifying metabolic aberrations in cancer cells. Towards this end, we apply high-throughput metabolomics and isotope tracing approaches via high resolution mass-spectrometry (detecting molecules whose concentration is in a nano-molar scale).


Research Interests

Achieving a system level understanding of cellular metabolism represents a major challenge from a basic science perspective, considering the complexity of the system, involving the joint activity of hundreds or thousands of biochemical reactions. Our group aims to derive a comprehensive and quantitative view of cellular metabolism by combining experimental and computational tools.  Our major experimental platform is metabolomics via mass-spectrometry (LC/MS), enabling the detection and quantification of hundreds of metabolites per biological sample. To facilitate inference of metabolic flux, we employ isotope-tracing techniques and develop novel analytical approaches and algorithms for interpreting generated data. On the computational front, we further specialize in developing methods for analyzing genome-scale metabolic network models via Constraint-Based Modeling (CBM). 

A special research focus of the lab is on studying cellular metabolic derangements in cancer. We are interested in answering the following questions: How is metabolism altered in specific cancers? Can we comprehensively quantify such metabolic changes? Are metabolic derangements tumorigenic? Or are they simply byproducts of other tumorigenic events? How are these metabolic alterations regulated? Through which signaling pathways? Are they triggered by specific genomic events? Do specific metabolic alterations in cancer cells make them vulnerable to pharmacological intervention? Can we find biomarkers that reflect specific metabolic alterations in cancer cells? How do drug resistance alter metabolism and is there a way around that?