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Florian  Karreth

Florian Karreth

Florian Karreth
Assistant Professor


Office: SRB 23043
Phone: 813/745-1851


01/2010 Ph.D. (Dr. rer. nat.) in Genetics, University of Vienna, Austria

10/2010-02/2014 Postdoctoral fellow, Beth Israel Deaconess Medical Center, Boston, USA (PI: Pier Paolo Pandolfi)

03/2014-05/2016 Postdoctoral fellow, Weill Cornell Medical College, New York, USA (PI: Lewis C. Cantley, co-supervised by Pier Paolo Pandolfi)


My lab is interested in the molecular determinants that promote progression and drug resistance of cancers driven by the MAP kinase pathway, with an emphasis on melanoma. Research over the last decade has significantly improved our mechanistic understanding of oncogenic transformation by mutant BRAF and other activators of the MAPK pathway. This led to the development of several drugs targeting this pathway, and a plethora of clinical trials in melanoma and other cancers. While these targeted therapies often improve patient survival by a few months, they are far from curative as drug resistance to such therapies quickly emerges. In addition to the initiating, MAPK-activating mutations, cancer cells acquire multiple secondary mutations during tumor evolution that are critical for progression and drug resistance. Targeting these secondary mutations in combination with the MAPK pathway may be a powerful therapeutic approach with long-lasting effects.

Over the next years, we will focus on the aims listed below to identify and characterize secondary drivers of tumor progression, and determine their suitability as therapeutic targets. To this end, we are utilizing a variety of molecular biology, biochemistry, and mouse modeling approaches.

1) Speedy-mouse models of melanoma. We are currently developing an innovative mouse modeling platform that will allow for rapid generation of transgenic mice. This approach is compatible with the newest genetic techniques (for instance inducible shRNA approaches or the CRISPR/Cas9 system), and significantly increases the number of candidate cancer genes that can be tested. Using this approach, we are examining the function of putative drivers of melanoma progression and resistance that we identified in in vivo transposon mutagenesis screens (Karreth et al., Cell 2011; Perna et al., PNAS 2015).

2) miRNA deregulation in melanoma. My lab also studies how deregulation of non-coding RNAs in general, and miRNAs in particular, contributes to cancer development. We are focused on two different mechanisms of miRNA deregulation: transcriptional deregulation by oncogenic signaling and miRNA sequestration by competitive endogenous RNA (Karreth et al., Cell 2011; Karreth et al., Cell 2015). These are underexplored mechanisms of miRNA deregulation, and a better understanding of affected pathways will provide novel opportunities for therapeutic intervention. Ultimately, we will use the speedy-mouse platform to preclinically test new therapies in miRNA-deregulation mouse models.

3) Atypical MAPK activation. The MAPK pathway is often robustly hyperactivated in cancer by a variety of mechanisms. Interestingly, recent evidence suggested that mutational events that result in moderate activation of the pathway could also promote cancer. Using novel mouse models, we are exploring i) the oncogenic potential of such mutations, ii) their cooperation with other oncogenic pathways, iii) their ability to enhance the effect of mutations that robustly activate MAPK, iv) their sensitivity to MAPK inhibition and ability to induce drug resistance. Our analyses will provide insight into oncogenic signaling thresholds and help identify patients that could benefit from MAPK inhibition.

Graduate Students

Ilah "Ella"