Author

Matthew S. DiStefano

Icahn School of Medicine at Mount Sinai

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Systems Biology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:statistical model· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Approach:simulation· 1

Frequent Co-Authors

Marc R. BirtwistleiD· 2 shared Mehdi BouhaddouiD· 2 shared Adriana ScanteianuiD· 1 shared Alan D. SterniD· 1 shared Alex E. Mertz· 1 shared Anne Marie BarretteiD· 1 shared Annie L. Tan· 1 shared DeAnalisa C. JonesiD· 1 shared

Activity by Year

2018-2018 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersSystems Biology

Marc R. BirtwistleORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

An Integrated Mechanistic Model of Pan-Cancer Driver Pathways Predicts Stochastic Proliferation and Death

Mehdi Bouhaddou, Anne Marie Barrette, Rick J. Koch, Matthew S. DiStefano, Eric A. Riesel, Alan D. Stern, LETÍCIA VITÓRIA DA SILVA SANTOS, Annie L. Tan, Alex E. Mertz, Marc R. Birtwistle

The paper constructs a mechanistic model of pan-cancer driver pathways to predict stochastic proliferation and death in cancer cells.

PLoS Computational Biology · Mar 26, 2018Peer-reviewedSystems Biology

Analysis of Copy Number Loss of the ErbB4 Receptor Tyrosine Kinase in Glioblastoma

DeAnalisa C. Jones, Adriana Scanteianu, Matthew S. DiStefano, Mehdi Bouhaddou, Marc R. Birtwistle

The paper investigates copy number loss of the ERBB4 gene in glioblastoma, finding it is not a driver mutation or predisposing factor, despite initial hypotheses from cell line data.

PLoS ONE · Jan 17, 2018Peer-reviewedSystems Biology