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UID:480@inflames.utu.fi
DTSTART;TZID=Europe/Helsinki:20260505T110000
DTEND;TZID=Europe/Helsinki:20260505T120000
DTSTAMP:20260429T071845Z
URL:https://inflames.utu.fi/events/visiting-professor-career-talk-anna-big
 as/
SUMMARY:Visiting professor Career talk by Anna Bigas - A life in Notch: fro
 m Blood stem cells to leukemia
DESCRIPTION:Welcome to a Career talk by InFLAMES visiting professor Anna Bi
 gas!\n\nSpeaker: Anna Bigas\; Hospital del Mar Research Institute Barcelon
 a\, Josep Carreras Leukemia Research Institute\, Spanish Cancer Virtual Ce
 nter\nTitle: A life in Notch: from Blood stem cells to leukemia\nTime: 5 M
 ay 2026\, 11-12\nLocation: Arje Scheinin hall\, Dentalia\nHost: Professor 
 Cecilia Sahlgren\, Åbo Akademi University\n\nCoffee and sandwiches will b
 e served at the start of the talk. After the presentation professor Bigas 
 will be available for lunch with early career researchers (12:00-13:30). R
 egister for the lunch here: https://link.webropol.com/s/bigas-lunch.\n\nBi
 ography\n\nAnna Bigas has built her scientific career around a fundamental
  question: how do signaling pathways govern the balance between stem cell 
 formation\, differentiation\, and malignant transformation?\n\nTrained as 
 a cell biologist at the University of Barcelona and later at the Fred Hutc
 hinson Cancer Research Center in Seattle\, Bigas was among the first to de
 monstrate that Notch signaling actively regulates hematopoietic differenti
 ation. At a time when Notch was largely viewed through a developmental len
 s\, her work helped position it as a central regulator of blood formation.
 \n\nOver the past two decades\, her laboratory has redefined how signaling
  dosage and context control hematopoietic stem cell (HSC) emergence. She d
 emonstrated that Jagged1-mediated Notch signaling is required for embryoni
 c HSC generation\, that transient Wnt/β-catenin activity is essential for
  definitive hematopoiesis\, and that Notch signal strength\, rather than b
 inary activation\, determines hemogenic endothelial fate. Her group furthe
 r identified critical Notch transcriptional targets in emerging HSCs and u
 ncovered cis-inhibitory mechanisms that sustain embryonic HSC identity. To
 gether\, these discoveries established the principle that stem cell specif
 ication depends on tightly calibrated signaling thresholds\, a concept now
  central to efforts to engineer HSCs in vitro.\n\nBigas also revealed how 
 developmental signaling logic becomes hijacked in leukemia. In a landmark 
 study\, she demonstrated that Notch sustains constitutive NFκB activation
  in T-cell acute lymphoblastic leukemia (T-ALL) through repression of the 
 tumor suppressor CYLD\, uncovering a direct mechanistic bridge between two
  major oncogenic pathways. Her laboratory later showed that β-catenin is 
 required for T-ALL initiation\, identified relapse clones that pre-exist a
 t diagnosis\, and recently defined a β-catenin–dependent RNA biosynthes
 is program driving therapy resistance.\n\nBeyond leukemia\, her work uncov
 ered unexpected chromatin-bound roles of IκBα and IKKα in regulating st
 emness\, DNA damage responses and therapy resistance\, and identified feta
 l-like transcriptional programs that fuel colorectal cancer metastasis.\n\
 nNow Scientific Director of CIBERONC in Spain and an elected EMBO member\,
  Bigas combines fundamental mechanistic discovery with translational coord
 ination at the national and European levels\, including contributions to t
 he European Cancer Mission initiative UNCAN.eu.\n\nHer work has consistent
 ly shown that signaling pathways do not merely switch genes on or off. The
 y operate in gradients\, thresholds and chromatin contexts\, and when thos
 e parameters shift\, stem cells emerge or malignancies arise. By decoding 
 those rules\, Bigas has reshaped how the field understands stem cell fate 
 and leukemic transformation.\n\nSelected publications\n\n 	Chromatin activ
 ity of IκBα mediates the exit from naïve pluripotency (2025\, Elife) ht
 tps://doi.org/10.7554/elife.102784\n 	An unbiased genomewide screen uncove
 rs 7 genes that drive hematopoietic stem cell fate from mouse embryonic st
 em cells (2025\, Blood) https://doi.org/10.1182/blood.2024027742\n 	IκBα
  controls dormancy in hematopoietic stem cells via retinoic acid during em
 bryonic development (2024\, Nat Commun) https://doi.org/10.1038/s41467-024
 -48854-5\n 	Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic he
 matopoietic stem cell fate (2024\, Nat Commun) https://doi.org/10.1038/s41
 467-024-45716-y\n 	β-Catenin activity induces an RNA biosynthesis program
  promoting therapy resistance in T-cell acute lymphoblastic leukemia (2023
 \, EMBO Mol Med) https://doi.org/10.15252/emmm.202216554\n
ATTACH;FMTTYPE=image/jpeg:https://inflames.utu.fi/wp-content/uploads/Anna-
 Bigas-1-2.jpg
CATEGORIES:Events in English,Tapahtumat
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