SCAN-B Sweden Cancerome Analysis Network - Bröst (SCAN-B), är ett forskningsprojekt som startade 2010 i den södra sjukvårdsregionen med Lund som centrum. Syftet med projektet är att analysera bröstcancertumörers arvsmassa för att minska dödligheten i bröstcancer genom mer individualiserad behandling. Han utvecklar diagnostiken Intervju med professor Åke Borg, initiativtagare till SCAN-B Ny analysm

https://www.scan-b.lu.se/scan-b - 2025-08-09

SCAN-B initiativet har en stark translationell inriktning med det långsiktiga målet att förbättra vården för framtidens bröstcancerpatienter. Projektet avser att utveckla och införa nya metoder för nyanserad diagnostik, prognostik och mer precis behandling. Vi har skapat ett nätverk mellan cancersjukvård och forskning för fortlöpande inkludering av ”alla” nya patienter med primär bröstcancer och f

https://www.scan-b.lu.se/prov-och-information-samlas-cancerforskning - 2025-08-09

2025Immune Response in Triple-Negative Breast Cancer-Machine Learning-based Insights from Histology and-Omics, Suze Roostee - 25 feb 20252024Selenoproteins as predictors of prognosis after breast cancer diagnosis, Kamil Demircan - 29 nov 2024Regulation of estrogen receptor alpha by promoter methylation, alternative splicing and microRNA, Juliane Albrecht - 23 okt 2024Metabolic and angiogenic bioma

https://www.scan-b.lu.se/scan-bs-provinsamling/avhandlingar - 2025-08-09

SCAN-B är unikt i sitt populationsbaserade koncept och i grunden oselekterade patientunderlag, som speglar nutidens bröstcancersjukdom i form av sjukdomsstadium med till stor andel screening-upptäckta tumörer, liksom en modern behandling.   Scan-B-laboratoriet på avdelningen för Onkologi, IKVL på Medicon Village i Lund. Fotograf: Kennet Ruona. Projektet är också unikt i sin kohort-storlek och det

https://www.scan-b.lu.se/scan-bs-provinsamling - 2025-08-09

Siebzehnrübl FA, Raber KA, Urbach YK, Schulze-Krebs A, Canneva F, Moceri S, Habermeyer J, Achoui D, Gupta B, Steindler DA, Stephan M, Nguyen HP, Bonin M, Riess O, Bauer A, Aigner L, Couillard-Despres S, Paucar MA, Svenningsson P, Osmand A, Andreew A, Zabel C, Weiss A, Kuhn R, Moussaoui S, Blockx I, Van der Linden A, Cheong RY, Roybon L, Petersén Å and von Hörsten S.PNAS 115 (37) E8765-E8774 (2018)

https://www.huntington-research.lu.se/early-postnatal-behavioral-cellular-and-molecular-changes-models-huntington-disease-are-reversible - 2025-08-09

Gisselsson D, Jonson T, Petersén Å, Strombeck B, Dal Cin P, Hoglund M, Mitelman F, Mertens F and Mandahl N.Proceedings of the National Academy of Sciences USA 98: 12683-12688 (2001)AbstractAlthough mechanisms for chromosomal instability in tumors have been described in animal and in vitro models, little is known about these processes in man. To explore cytogenetic evolution in human tumors, chromo

https://www.huntington-research.lu.se/telomere-dysfunction-triggers-extensive-dna-fragmentation-and-evolution-complex-chromosome - 2025-08-09

Petersén Å, Hansson O and Brundin P.In Swedish. Läkartidningen 50: 5756-5761 (2001)AbstractHuntingtons sjukdom är en av flera kända neurologiska sjukdomar som beror på en expanderad CAG-repetition. Symtomen karakteriseras av motoriska, psykiska och kognitiva störningar. Muterat huntingtin uttrycks i hela kroppen, och neurodegeneration och aggregering av det muterade proteinet huntingtin sker i bas

https://www.huntington-research.lu.se/huntingtons-sjukdom-annu-ett-galet-protein - 2025-08-09

Petersén Å, Castilho RF, Hansson O, Wieloch T and Brundin P.Brain Research 857: 20-29 (2000)AbstractDisruption of intracellular calcium homeostasis is thought to play a role in neurodegenerative disorders such as Huntington's disease (HD). To study different aspects of putative pathogenic mechanisms in HD, we aimed to establish an in vitro model of calcium-induced toxicity in striatal neurons. The

https://www.huntington-research.lu.se/oxidative-stress-mitochondrial-permeability-transition-and-activation-caspases-calcium-ionophore - 2025-08-09

Mundt-Petersén U, Petersén Å, Emgård M, Dunnett SB and Brundin P.Experimental Neurology 164:112-120 (2000)AbstractIn transplants of embryonic striatal cells placed into the excitotoxically lesioned rat striatum (a model of Huntington's disease), as many as 60 to 90% of the grafted cells are believed to die. Caspase activation is part of a cascade of events that can lead to apoptosis. We investigat

https://www.huntington-research.lu.se/caspase-inhibition-increases-embryonic-striatal-graft-survival - 2025-08-09

Petersén Å, Hansson O, Emgård M and Brundin P.Cell Transplantation 9: 577-584 (2000)AbstractTransplantation of embryonic ventral mesencephalon is a potential therapy for patients with Parkinson's disease. As only around 5-10% of embryonic dopaminergic neurons survive grafting into the adult striatum, it is considered necessary to use multiple donor embryos. To increase the survival of the grafted

https://www.huntington-research.lu.se/grafting-nigral-tissue-hibernated-tirilazad-mesylate-and-glial-cell-line-derived-neurotrophic-factor - 2025-08-09

Brundin P, Karlsson J, Emgård M, Kaminski Schierle GS, Hansson O, Petersén Å and Castilho RF.Cell Transplantation 9: 179-195 (2000)AbstractNeural transplantation is developing into a therapeutic alternative in Parkinson's disease. A major limiting factor is that only 3-20% of grafted dopamine neurons survive the procedure. Recent advances regarding how and when the neurons die indicate that events

https://www.huntington-research.lu.se/improving-survival-grafted-dopaminergic-neurons-review-over-current-approaches - 2025-08-09

Hansson O, Petersén Å, Leist M, Nicotera P, Castilho RF and Brundin P.Proceedings of the National Academy of Sciences USA 96: 8727-8732 (1999)AbstractHuntington's disease (HD) is a hereditary neurodegenerative disorder presenting with chorea, dementia, and extensive striatal neuronal death. The mechanism through which the widely expressed mutant HD gene mediates a slowly progressing striatal neuro

https://www.huntington-research.lu.se/transgenic-mice-expressing-huntingtons-disease-mutation-are-resistant-quinolinic-acid-induced - 2025-08-09

Petersén Å, Emgård M and Brundin P.Brain Research Bulletin 50: 275-281 (1999)AbstractThe survival of grafted embryonic striatal tissue, dissected from the lateral ganglionic eminence, depends on the status of the host striatum. We found significantly larger volumes of surviving graft tissue and of striatal-like tissue (P-zone) within the graft, when the host striatum had been subjected to an excit

https://www.huntington-research.lu.se/impact-preceding-excitotoxic-lesion-and-treatment-ciliary-neurotrophic-factor-striatal-graft - 2025-08-09

Petersén Å and Brundin P.Experimental Neurology 160: 402-412 (1999)AbstractCiliary neurotrophic factor (CNTF) has a protective effect on the striatum in animal models of Huntington's disease. However, the mechanism through which it exerts its effect is not clear. In this study, we show that there is a concentration-dependent direct protective effect of CNTF against N-methyl-D-aspartate-mediated ex

https://www.huntington-research.lu.se/effect-cntf-and-calcium-ionophore-a23187-induced-death-cultured-embryonic-stratal-neurons - 2025-08-09

Petersén Å, Mani K and Brundin P.Experimental Neurology 157: 1-18 (1999)AbstractWe review recent advances regarding the pathogenesis of Huntington's disease (HD). This genetic neurodegenerative disorder is caused by an expanded CAG repeat in a gene coding for a protein, with unknown function, called huntingtin. There is selective death of striatal and cortical neurons. Both in patients and a trans

https://www.huntington-research.lu.se/recent-advances-pathogenesis-huntingtons-disease - 2025-08-09

Baldo B, Gabery S, Soylu-Kucharz R, Cheong RY, Henningsen JB, Englund E, McLean C, Kirik D, Halliday G and Petersén Å.Neuropathology and Applied Neurobiology 45 (4): 361-379 (2019)AbstractAIMS:Metabolic dysfunction is involved in modulating the disease process in Huntington disease (HD) but the underlying mechanisms are not known. The aim of this study was to investigate if the metabolic regulator

https://www.huntington-research.lu.se/sirt1-increased-affected-brain-regions-and-hypothalamic-metabolic-pathways-are-altered-huntington - 2025-08-09

Brundin P, Petersén Å and Hansson O.Journal of Neurosurgery 90: 804-806 (1999)No abstract available; this is a letter to the editor.The letter 

https://www.huntington-research.lu.se/graft-survival - 2025-08-09

Pircs K, Petri R, Madsen S, Brattås PL, Vuono R, Ottosson DR, St-Amour I, Hersbach BA, Matusiak-Brückner M, Lundh SH, Petersén Å, Déglon N, Hébert SS, Parmar M, Barker RA and Jakobsson J.Cell Reports 24(6): 1397-1406 (2018)AbstractMany neurodegenerative diseases are characterized by the presence of intracellular protein aggregates, resulting in alterations in autophagy. However, the consequences o

https://www.huntington-research.lu.se/huntingtin-aggregation-impairs-autophagy-leading-argonaute-2-accumulation-and-global-microrna - 2025-08-09

Fjalldal S, Follin C, Svärd D, Rylander L, Gabery S, Petersen Å, Van Westen D, Sundgren P, Bjorkman-Burtscher I, Lätt J, Ekman B, Johanson A and Erfurth EM.European Journal of Endocrinology 178 (6): 577-587 (2018)AbstractCONTEXT:Patients with craniopharyngioma (CP) and hypothalamic lesions (HL) have cognitive deficits. Which neural pathways are affected is unknown.OBJECTIVE:To determine whether th

https://www.huntington-research.lu.se/microstructural-white-matter-alterations-and-hippocampal-volumes-are-associated-cognitive-deficits - 2025-08-09

Gawlik KI1, Harandi VM2, Cheong RY3, Petersén Å3, Durbeej M2.1Muscle Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.2Muscle Biology Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.3Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.Matrix Biology 70: 36-79 (20

https://www.huntington-research.lu.se/laminin-a1-reduces-muscular-dystrophy-dy2j-mice - 2025-08-09