Dr. Aldema Sas-Chen is an assistant professor (senior lecturer) in the Shmunis School of Biomedicine and Cancer Research since 2021. She obtained a B.Sc. in Psychobiology from The Hebrew University of Jerusalem and a M.Sc. and a Ph.D. in Biology from The Weizmann Institute of Science. In her Ph.D. she studied the role of non-coding RNAs in cancer progression and explored the role of long non-coding RNAs in cellular migration and in metastasis formation. In her postdoctoral studies she focused on an emerging layer of gene regulation – the epitranscriptome – which defines the landscape of >100 types of RNA modifications that effect the life cycle of the RNA. She developed high-throughput methods to detect a variety of RNA modifications by combining experimental and computational methodologies. Utilizing these methods she explored the functions of these modifications in human disease and across evolution.
Dr. Aldema Sas-Chen
2006 Bsc in Psychobiology, The Hebrew University of Jerusalem
2016 PhD in Biology, The Weizmann Institute of Science
2016-2019 Postdoctoral Fellow, The Weizmann Institute of Science
2019-2021 Senior Postdoctoral Fellow, The Weizmann Institute of Science
Cells respond to changes in their environment by activating transcriptional networks, which regulation the dynamic expression of coding and non-coding genes. Regulation of gene expression is further modulated by post-transcriptional modifications of RNA molecules, termed ‘the epitranscriptome’, which impact cellular outcomes by affecting the life cycle of the RNA.
Our lab studies RNA-based mechanisms of gene regulation and investigates the impact of RNA modifications on shaping cellular processes in health and disease.
One of our main focuses is studying the role of RNA modifications in the physiology of cancer. Utilizing cancer models at a molecular, cellular and organism level, our lab combines cutting-edge experimental and computational methodologies to explore the interplay between the complex landscape of RNA modifications and cancer etiology. Our aim is to uncover RNA-dependent mechanisms, crucial for tumor development, which could facilitate both diagnosis and treatment of human cancer.
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For the full list.
- Begik O*, Lucas MC*, Pryszcz LP, Ramirez JM, Medina R, Milenkovic I, Cruciani S, Liu H, Santos Vieira HG, Sas-Chen A, Mattick JS, Schwartz S and Novoa EM. (accepted). Quantitative profiling of native RNA modifications and their dynamics using nanopore sequencing. Nature Biotechnology.
- Gamage ST*, Sas-Chen A*, Schwartz S, Meier J (2021). Quantitative nucleotide resolution profiling of RNA cytidine acetylation by ac4C-seq. Nature Protocols. 16(4):2286-2307.
- Sas-Chen A, Nir R, Schwartz S. (2021). mito-Ψ-Seq: A high-throughput method for systematic mapping of pseudouridine within mitochondrial RNA. Methods in Molecular Biology. 2192:103-115.
- Sas-Chen A*, Thomas JM*, Matzov D*, Taoka M, Nance KD, Nir R, Bryson KM, Shachar R, Liman GLS, Burkhart BW, Gamage ST, Nobe Y, Briney CA, Levy MJ, Fuchs RT, Robb GB, Hartmann J, Sharma S, Lin Q, Florens L, Washburn MP, Isobe T, Santangelo TJ, Shalev-Benami M, Meier JL, Schwartz S (2020). Dynamic RNA acetylation revealed by quantitative cross-evolutionary mapping. Nature. 583, 638–643.
- Sas-Chen A, Schwartz S. (2019). Misincorporation signatures for detecting modifications in mRNA: Not as simple as it sounds. Methods. 1;156:53-59. doi: 10.1016/j.ymeth.2018.10.011.
- Thomas JM, Briney CA, Nance KD, Lopez JE, Thorpe AL, Fox SD, Bortolin-Cavaille ML, Sas-Chen A, Arango D, Oberdoerffer S, Cavaille J, Andresson T, Meier JL. (2018). A Chemical Signature for Cytidine Acetylation in RNA. Journal of the American Chemical Society. 140(40):12667-12670. doi: 10.1021/jacs.8b06636.
- Roth L, Srivastava S, Lindzen M, Sas-Chen A, Scheffer M, Lauriola M, Enuka Y, Noronha A, Mancini M, Lavi S, Tarcic G, Pines G, Nevo N, Heyman O, Ziv T, Rueda OM, Gnocchi D, Pikarsky E, Admon A, Caldas C, Yarden Y. (2018). SILAC identifies LAD1 as an oncogenic filamin binder regulating actin dynamics in response to EGF and marking aggressive breast tumors. Science Signaling. 11(515). doi: 10.1126/scisignal.aan0949.
- Safra M, Sas-Chen A, Nir R, Winkler R, Nachshon A, Bar-Yaacov D, Erlacher M, Rossmanith W, Stern-Ginossar N, Schwartz S. (2017). The m1A landscape on cytosolic and mitochondrial mRNA at single-base resolution. Nature. doi:10.1038/nature24456.
- Enuka Y, Feldman ME, Chowdhury A, Srivastava S, Lindzen M, Sas-Chen A, Massart R, Cheishvili D, Suderman MJ, Zaltsman Y, Mazza CA, Shukla K, Körner C, Furth N, Lauriola M, Oren M, Wiemann S, Szyf M, Yarden Y. (2017). Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone. Nucleic Acids Research. doi: 10.1093/nar/gkx865.
- Sas-Chen A, Srivastava S, Yarden Y (2017). The short and the long: Non-coding RNAs and growth factors in cancer progression. Biochemical Society Transactions. 8;45(1):51-64.
- Sas‐Chen A, Aure MR, Leibovich L, Carvalho S, Enuka Y, Körner C, Polycarpou‐Schwarz M, Lavi S, Nevo N, Kuznetsov Y, Yuan J, Azuaje F, Oslo Breast Cancer Research Consortium (OSBREAC), Ulitsky I, Diederichs S, Wiemann S, Yakhini Z, Kristensen VN, Børresen‐Dale AL, Yarden Y. (2016). LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer. EMBO Molecular Medicine. pii: e201606198.
- Enuka Y, Lauriola M, Feldman ME, Sas-Chen A, Ulitsky I, Yarden Y (2016). Circular RNAs are long-lived and display only minimal early alterations in response to a growth factor. Nucleic Acids Research. pii: gkv1367.
- Kedmi M, Sas-Chen A, Yarden Y (2015). MicroRNAs and Growth Factors: An Alliance Propelling Tumor Progression. Journal of Clinical Medicine. 4(8):1578-99.
- Blandino G, Fazi F, Donzelli S, Kedmi M, Sas-Chen A, Muti P, Strano S, Yarden Y. (2014). Tumor suppressor microRNAs: a novel non-coding alliance against cancer. FEBS Letters. 588(16):2639-52.
- Sas-Chen A, Avraham R, Yarden Y. (2012). A crossroad of microRNAs and immediate early genes (IEGs) encoding oncogenic transcription factors in breast cancer. Journal of Mammary Gland Biology and Neoplasia. 17(1):3-14.
- Zwang Y, Sas-Chen A, Drier Y, Shay T, Avraham R, Lauriola M, Shema E, Lidor-Nili E, Jacob-Hirsch J, Amariglio N, Lu Y, Mills GB, Rechavi G, Oren M, Domany E, Yarden Y. (2011). Two phases of mitogenic signaling unveil roles for p53 and EGR1 in elimination of inconsistent growth signals. Molecular Cell. 42(4):524-35.
- Avraham R, Sas-Chen A, Manor O, Steinfeld I, Shalgi R, Tarcic G, Bossel N, Zeisel A, Amit I, Zwang Y, Enerly E, Russnes HG, Biagioni F, Mottolese M, Strano S, Blandino G, Børresen-Dale AL, Pilpel Y, Yakhini Z, Segal E, Yarden Y. (2010). EGF decreases the abundance of microRNAs that restrain oncogenic transcription factors. Science Signaling. , 3(124):ra43.
- Kaushansky N, Zilkha-Falb R, Hemo R, Lassman H, Eisenstein M, Sas A, Ben-Nun A. (2007). Pathogenic T cells in MOBP-induced murine EAE are predominantly focused to recognition of MOBP21F and MOBP27P epitopic residues. European Journal of Immunology. 37(11):3281-92.
- Ben-Ari S, Toiber D, Sas AS, Soreq H & Ben-Shaul Y (2006). Modulated splicing-associated gene expression in P19 cells expressing distinct acetylcholinesterase splice variants. Journal of Neurochemistry, 97 (s1), 24-34.