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UID:481@inflames.utu.fi
DTSTART;TZID=Europe/Helsinki:20260507T100000
DTEND;TZID=Europe/Helsinki:20260507T110000
DTSTAMP:20260417T062620Z
URL:https://inflames.utu.fi/events/visiting-professor-scientific-seminar-a
 nna-bigas/
SUMMARY:Visiting professor Scientific seminar by Anna Bigas - The complexit
 y of making blood stem cells: from embryos to cells
DESCRIPTION:Welcome to a Scientific seminar by InFLAMES visiting professor 
 Anna Bigas!\n\nSpeaker: Anna Bigas\; Hospital del Mar Research Institute 
 Barcelona\, Josep Carreras Leukemia Research Institute\, Spanish Cancer Vi
 rtual Center\nTitle: The complexity of making blood stem cells: from embry
 os to cells\nTime: 7 May 2026\, 10-11\nLocation: Osmo Järvi hall\, Medisi
 ina A-C\nHost: Professor Cecilia Sahlgren\, Åbo Akademi University\n\nCo
 ffee and sandwiches will be served at the start of the seminar. 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 scien
 tific career around a fundamental question: how do signaling pathways gove
 rn the balance between stem cell formation\, differentiation\, and maligna
 nt transformation?\n\nTrained as a cell biologist at the University of Bar
 celona and later at the Fred Hutchinson Cancer Research Center in Seattle\
 , Bigas was among the first to demonstrate that Notch signaling actively r
 egulates hematopoietic differentiation. At a time when Notch was largely v
 iewed through a developmental lens\, her work helped position it as a cent
 ral regulator of blood formation.\n\nOver the past two decades\, her labor
 atory has redefined how signaling dosage and context control hematopoietic
  stem cell (HSC) emergence. She demonstrated that Jagged1-mediated Notch s
 ignaling is required for embryonic HSC generation\, that transient Wnt/β-
 catenin activity is essential for definitive hematopoiesis\, and that Notc
 h signal strength\, rather than binary activation\, determines hemogenic e
 ndothelial fate. Her group further identified critical Notch transcription
 al targets in emerging HSCs and uncovered cis-inhibitory mechanisms that s
 ustain embryonic HSC identity. Together\, these discoveries established th
 e principle that stem cell specification depends on tightly calibrated sig
 naling thresholds\, a concept now central to efforts to engineer HSCs in v
 itro.\n\nBigas also revealed how developmental signaling logic becomes hij
 acked in leukemia. In a landmark study\, she demonstrated that Notch susta
 ins constitutive NFκB activation in T-cell acute lymphoblastic leukemia (
 T-ALL) through repression of the tumor suppressor CYLD\, uncovering a dire
 ct mechanistic bridge between two major oncogenic pathways. Her laboratory
  later showed that β-catenin is required for T-ALL initiation\, identifie
 d relapse clones that pre-exist at diagnosis\, and recently defined a β-c
 atenin–dependent RNA biosynthesis program driving therapy resistance.\n\
 nBeyond leukemia\, her work uncovered unexpected chromatin-bound roles of 
 IκBα and IKKα in regulating 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 S
 pain and an elected EMBO member\, Bigas combines fundamental mechanistic d
 iscovery with translational coordination at the national and European leve
 ls\, including contributions to the European Cancer Mission initiative UNC
 AN.eu.\n\nHer work has consistently shown that signaling pathways do not m
 erely switch genes on or off. They operate in gradients\, thresholds and c
 hromatin contexts\, and when those 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 activity of IκBα mediates the exit from naï
 ve pluripotency\, Palma et al.\, 2025\, Elife\, https://doi.org/10.7554/el
 ife.102784\n 	An unbiased genomewide screen uncovers 7 genes that drive he
 matopoietic stem cell fate from mouse embryonic stem cells\, Palma et al.\
 , 2025\, Blood\, https://doi.org/10.1182/blood.2024027742\n 	IκBα contro
 ls dormancy in hematopoietic stem cells via retinoic acid during embryonic
  development\, Thambyrajah et al.\, 2024\, Nat Commun\, https://doi.org/10
 .1038/s41467-024-48854-5\n 	Cis inhibition of NOTCH1 through JAGGED1 susta
 ins embryonic hematopoietic stem cell fate\, Thambyrajah et al.\, 2024\, N
 at Commun\, https://doi.org/10.1038/s41467-024-45716-y\n 	β-Catenin activ
 ity induces an RNA biosynthesis program promoting therapy resistance in T-
 cell acute lymphoblastic leukemia\, García-Hernández  et al.\, 2023\, E
 MBO 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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