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UID:480@inflames.utu.fi
DTSTART;TZID=Europe/Helsinki:20260505T110000
DTEND;TZID=Europe/Helsinki:20260505T120000
DTSTAMP:20260417T062353Z
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).\n
 \nBiography\n\nAnna Bigas has built her scientific career around a fundame
 ntal question: how do signaling pathways govern the balance between stem c
 ell formation\, differentiation\, and malignant transformation?\n\nTrained
  as a cell biologist at the University of Barcelona and later at the Fred 
 Hutchinson Cancer Research Center in Seattle\, Bigas was among the first t
 o demonstrate that Notch signaling actively regulates hematopoietic differ
 entiation. At a time when Notch was largely viewed through a developmental
  lens\, her work helped position it as a central regulator of blood format
 ion.\n\nOver the past two decades\, her laboratory has redefined how signa
 ling dosage and context control hematopoietic stem cell (HSC) emergence. S
 he demonstrated that Jagged1-mediated Notch signaling is required for embr
 yonic HSC generation\, that transient Wnt/β-catenin activity is essential
  for definitive hematopoiesis\, and that Notch signal strength\, rather th
 an binary activation\, determines hemogenic endothelial fate. Her group fu
 rther identified critical Notch transcriptional targets in emerging HSCs a
 nd uncovered cis-inhibitory mechanisms that sustain embryonic HSC identity
 . Together\, these discoveries established the principle that stem cell sp
 ecification 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 landm
 ark study\, she demonstrated that Notch sustains constitutive NFκB activa
 tion 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-exi
 st at diagnosis\, and recently defined a β-catenin–dependent RNA biosyn
 thesis program driving therapy resistance.\n\nBeyond leukemia\, her work u
 ncovered unexpected chromatin-bound roles of IκBα and IKKα in regulatin
 g stemness\, DNA damage responses and therapy resistance\, and identified 
 fetal-like transcriptional programs that fuel colorectal cancer metastasis
 .\n\nNow Scientific Director of CIBERONC in Spain and an elected EMBO memb
 er\, Bigas combines fundamental mechanistic discovery with translational c
 oordination at the national and European levels\, including contributions 
 to the European Cancer Mission initiative UNCAN.eu.\n\nHer work has consis
 tently shown that signaling pathways do not merely switch genes on or off.
  They operate in gradients\, thresholds and chromatin contexts\, and when 
 those parameters shift\, stem cells emerge or malignancies arise. By decod
 ing those rules\, Bigas has reshaped how the field understands stem cell f
 ate and leukemic transformation.\n\nSelected publications\n\n 	Chromatin a
 ctivity of IκBα mediates the exit from naïve pluripotency (2025\, Elife
 ) https://doi.org/10.7554/elife.102784\n 	An unbiased genomewide screen un
 covers 7 genes that drive hematopoietic stem cell fate from mouse embryoni
 c stem cells (2025\, Blood) https://doi.org/10.1182/blood.2024027742\n 	I
 κBα controls dormancy in hematopoietic stem cells via retinoic acid duri
 ng embryonic development (2024\, Nat Commun) https://doi.org/10.1038/s4146
 7-024-48854-5\n 	Cis inhibition of NOTCH1 through JAGGED1 sustains embryon
 ic hematopoietic stem cell fate (2024\, Nat Commun) https://doi.org/10.103
 8/s41467-024-45716-y\n 	β-Catenin activity induces an RNA biosynthesis pr
 ogram 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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