BEGIN:VCALENDAR VERSION:2.0 PRODID:-//wp-events-plugin.com//7.2.3.1//EN TZID:Europe/Helsinki X-WR-TIMEZONE:Europe/Helsinki BEGIN:VEVENT UID:481@inflames.utu.fi DTSTART;TZID=Europe/Helsinki:20260507T100000 DTEND;TZID=Europe/Helsinki:20260507T110000 DTSTAMP:20260429T071913Z 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). Register for the lunch here: https://link.webr opol.com/s/bigas-lunch.\n\nBiography\n\nAnna Bigas has built her scientifi c career around a fundamental question: how do signaling pathways govern t he balance between stem cell formation\, differentiation\, and malignant t ransformation?\n\nTrained as a cell biologist at the University of Barcelo na and later at the Fred Hutchinson Cancer Research Center in Seattle\, Bi gas was among the first to demonstrate that Notch signaling actively regul ates hematopoietic differentiation. At a time when Notch was largely viewe d through a developmental lens\, her work helped position it as a central regulator of blood formation.\n\nOver the past two decades\, her laborator y has redefined how signaling dosage and context control hematopoietic ste m cell (HSC) emergence. She demonstrated that Jagged1-mediated Notch signa ling is required for embryonic HSC generation\, that transient Wnt/β-cate nin activity is essential for definitive hematopoiesis\, and that Notch si gnal strength\, rather than binary activation\, determines hemogenic endot helial fate. Her group further identified critical Notch transcriptional t argets in emerging HSCs and uncovered cis-inhibitory mechanisms that susta in embryonic HSC identity. Together\, these discoveries established the pr inciple that stem cell specification depends on tightly calibrated signali ng thresholds\, a concept now central to efforts to engineer HSCs in vitro .\n\nBigas also revealed how developmental signaling logic becomes hijacke d in leukemia. In a landmark study\, she demonstrated that Notch sustains constitutive NFκB activation in T-cell acute lymphoblastic leukemia (T-AL L) through repression of the tumor suppressor CYLD\, uncovering a direct m echanistic bridge between two major oncogenic pathways. Her laboratory lat er showed that β-catenin is required for T-ALL initiation\, identified re lapse clones that pre-exist at diagnosis\, and recently defined a β-caten in–dependent RNA biosynthesis program driving therapy resistance.\n\nBey ond leukemia\, her work uncovered unexpected chromatin-bound roles of IκB α and IKKα in regulating stemness\, DNA damage responses and therapy res istance\, and identified fetal-like transcriptional programs that fuel col orectal cancer metastasis.\n\nNow Scientific Director of CIBERONC in Spain and an elected EMBO member\, Bigas combines fundamental mechanistic disco very with translational coordination at the national and European levels\, including contributions to the European Cancer Mission initiative UNCAN.e u.\n\nHer work has consistently shown that signaling pathways do not merel y switch genes on or off. They operate in gradients\, thresholds and chrom atin contexts\, and when those parameters shift\, stem cells emerge or mal ignancies arise. By decoding those rules\, Bigas has reshaped how the fiel d understands stem cell fate and leukemic transformation.\n\nSelected publ ications\n\n Chromatin activity of IκBα mediates the exit from naïve p luripotency\, Palma et al.\, 2025\, Elife\, https://doi.org/10.7554/elife. 102784\n An unbiased genomewide screen uncovers 7 genes that drive hemato poietic stem cell fate from mouse embryonic stem cells\, Palma et al.\, 20 25\, Blood\, https://doi.org/10.1182/blood.2024027742\n IκBα controls d ormancy in hematopoietic stem cells via retinoic acid during embryonic dev elopment\, Thambyrajah et al.\, 2024\, Nat Commun\, https://doi.org/10.103 8/s41467-024-48854-5\n Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic hematopoietic stem cell fate\, Thambyrajah et al.\, 2024\, Nat C ommun\, https://doi.org/10.1038/s41467-024-45716-y\n β-Catenin activity induces an RNA biosynthesis program promoting therapy resistance in T-cell acute lymphoblastic leukemia\, García-Hernández  et al.\, 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 END:VEVENT BEGIN:VTIMEZONE TZID:Europe/Helsinki X-LIC-LOCATION:Europe/Helsinki BEGIN:DAYLIGHT DTSTART:20260329T040000 TZOFFSETFROM:+0200 TZOFFSETTO:+0300 TZNAME:EEST END:DAYLIGHT END:VTIMEZONE END:VCALENDAR