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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Kempf, S. J.; Janik, Dirk; Barjaktarovic, Zarko; Braga-Tanaka III, I.; +5 Authors

    Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer's. The aim of this study was to elucidate the effect on hippocampus of chronic low-dose-rate radiation exposure (1 mGy/day or 20 mGy/day) given over 300 days with cumulative doses of 0.3 Gy and 6.0 Gy, respectively. ApoE deficient mutant C57Bl/6 mouse was used as an Alzheimer's model. Using mass spectrometry, a marked alteration in the phosphoproteome was found at both dose rates. The radiation-induced changes in the phosphoproteome were associated with the control of synaptic plasticity, calcium-dependent signalling and brain metabolism. An inhibition of CREB signalling was found at both dose rates whereas Rac1-Cofilin signalling was found activated only at the lower dose rate. Similarly, the reduction in the number of activated microglia in the molecular layer of hippocampus that paralleled with reduced levels of TNFα expression and lipid peroxidation was significant only at the lower dose rate. Adult neurogenesis, investigated by Ki67, GFAP and NeuN staining, and cell death (activated caspase-3) were not influenced at any dose or dose rate. This study shows that several molecular targets induced by chronic low-dose-rate radiation overlap with those of Alzheimer's pathology. It may suggest that ionising radiation functions as a contributing risk factor to this neurodegenerative disease.

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    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Oncotarget
    Article
    License: CC BY
    Data sources: UnpayWall
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    ENEA Open Archive
    Article . 2016
    Data sources: ENEA Open Archive
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    Oncotarget; ENEA Open Archive
    Article . Other ORP type . 2016 . Peer-reviewed
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    ENEA Open Archive
    Article . 2016
    Data sources: ENEA Open Archive
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      ENEA Open Archive
      Article . 2016
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      Oncotarget; ENEA Open Archive
      Article . Other ORP type . 2016 . Peer-reviewed
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      ENEA Open Archive
      Article . 2016
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Heyn Sørensen, Martin;

    Patienter med type 2-diabetes har en øget risiko for at udvikle hjertesvigt uafhængigt af andre risikofaktorer, såsom arteriosklerose og hypertension. Denne øgede forekomst af hjertesvigt hos patienter med type 2-diabetes har ført til hypotesen om, at der findes en specifik diabetisk kardiomyopati, kendetegnet ved koncentrisk myokardiehypertrofi og diastolisk dysfunktion. Ændringer i hjertets mikrocirkulation og mikrovaskulær dysfunktion i hjertets små kar spiller muligvis en rolle i udviklingen af diabetisk kardiomyopati og hjertesvigt hos patienter med type 2-diabetes, men den nøjagtige mekanisme for, hvordan type 2-diabetes kan forårsage hjertesvigt uafhængigt af andre kardiovaskulære risikofaktorer er fortsat ukendt.I denne ph.d.-afhandling undersøgte vi, hvordan forskelle i den diabetiske fænotype (diabetiske komplikationer, risikofaktorer, anti-diabetesbehandling osv.) påvirker perfusion i myokardiet, som et mål for kardiel mikrovaskulær sygdom, og om ændringer i hjertestruktur og funktion hos patienter med type 2-diabetes er relateret til kardiel mikrovaskulær sygdom, som en mulig mekanisme bag udviklingen af diabetisk kardiomyopati.For at undersøge dette blev 273 patienter med type 2-diabetes og 25 kontrolpersoner uden type 2-diabetes inkluderet i en tværsnitsundersøgelse. Alle deltagere gennemgik klinisk undersøgelse, blodog urinprøveudtagning, ekkokardiografi og avanceret magnetisk resonans scanning af hjertet, inklusive sekvenser for vævskarakterisering og fuld kvantitativ myokardie perfusion i hvile og under farmakologisk stress (adenosin 140 ug/kg/min). Blod- og urinprøver fra alle patienter med type 2-diabetes blev opsamlet og transporteret til Region Sjællands biobank for langtidsopbevaring.Vi fandt, at patienter med type 2-diabetes havde lavere myokardie perfusions reserve sammenlignet med kontrolpersoner, og at denne reduktion i myokardie perfusions reserve var forårsaget af både en Martin Heyn Sørensen, 2020 5 stigning i myokardie perfusion i hvile og reduceret maksimal myokardie perfusion under farmakologisk stress. Patienter med type 2-diabetes kompliceret med albuminuri eller retinopati havde lavere myokardie perfusions reserve og lavere maksimal myokardie perfusion under farmakologisk stress, sammenlignet med patienter med ukompliceret type 2-diabetes. Derudover havde patienter med type 2-diabetes kompliceret med albuminuri eller retinopati højere venstre ventrikel masse og højere E/e* (et ekkokardiografisk mål for diastolisk funktion af venstre ventrikel) end patienter med ukompliceret type 2-diabetes. Vi fandt en signifikant sammenhæng mellem reduceret myokardie perfusions reserve og nedsat diastolisk funktion af venstre ventrikel. Endelig fandt vi, at øgede niveauer af biomarkøren fibroblast vækstfaktor-23, som tidligere er blevet forbundet med øget risiko for hjerte-kar sygdom og hjerte-kar dødelighed hos patienter både med og uden type 2-diabetes, var forbundet med et fald i myokardie perfusions reserve og reduceret maksimal myokardie perfusion under farmakologisk stress samt øget E/e*.Dette ph.d.-studie giver indsigt i, hvordan myokardie perfusionen ændres hos patienter med type 2-diabetes, og hvordan disse ændringer er relateret til de klassiske risikofaktorer og komplikationer ved type 2-diabetes. Derudover viser vores resultater en tilsyneladende sammenhæng mellem kardiel mikrovaskulær sygdom og udvikling af venstre ventrikel diastolisk dysfunktion, et nøglekarakteristikum for diabetisk kardiomyopati. Vores resultater afslører et behov for veldesignede prospektive kliniske forsøg for yderligere at undersøge, hvordan ændringer i den kardielle mikrocirkulation over tid påvirker hjertefunktionen, og risikoen for at udvikle diabetisk kardiomyopati hos patienter med type 2-diabetes. Patients with type 2 diabetes have an increased risk of developing heart failure independent of other risk factors, such as coronary artery disease and hypertension. This increased prevalence of heart failure in type 2 diabetes has led to the hypothesis, that a specific diabetic cardiomyopathy, characterized by concentric myocardial hypertrophy and diastolic dysfunction, exists. Alterations in the myocardial microcirculation and microvascular dysfunction has been suggested to play a role in the development of diabetic cardiomyopathy and heart failure in patients with type 2 diabetes, however, the exact mechanism of how type 2 diabetes can cause heart failure independent of other cardiovascular risk factors still remains partly unknown.In this PhD thesis we investigated how differences in the diabetic phenotype (diabetic complications, risk factors, anti-diabetes therapy, etc.) affects myocardial perfusion, as a measure of coronary microvascular disease, and if changes in cardiac structure and function in patients with type 2 diabetes is related to coronary microvascular disease, as a possible mechanistic pathway for the development of diabetic cardiomyopathy.To investigate this, 273 patients with type 2 diabetes and 25 control subjects without type 2 diabetes were included in a cross-sectional survey. All participants underwent clinical examination, blood and urinary sampling, echocardiography and advanced cardiac magnetic resonance imaging including mapping sequences for tissue characterization and full quantitative myocardial perfusion during both rest and pharmacological stress (adenosine 140 µg/kg/min). Blood- and urinary samples from all patients with type 2 diabetes were collected and transported to Region Zealand’s biobank for long time storage.We found that patients with type 2 diabetes had lower myocardial perfusion reserve when compared to control subjects, and that this reduction in myocardial perfusion reserve was caused by both an increase in myocardial blood flow during rest and reduced maximal myocardial blood flow during vasodilator stress. Patients with type 2 diabetes complicated with albuminuria or retinopathy had lower myocardial perfusion reserve and maximal myocardial blood flow during stress, compared to patients with uncomplicated type 2 diabetes. In addition, patients with type 2 diabetes complicated with albuminuria or retinopathy had higher left ventricular mass and E/e* (an echocardiographic measure of left ventricular diastolic function), than did patients with uncomplicated type 2 diabetes. We found a significant association between reduced myocardial perfusion reserve and impaired left ventricular diastolic function. Finally, we found that increased levels of the biomarker fibroblast growth factor-23, Martin Heyn Sørensen, 2020 4 which has previously been associated with cardiovascular morbidity and mortality in both patients with and without type 2 diabetes, were associated with a decrease in myocardial perfusion reserve and reduced maximal myocardial blood flow during stress as well as increased E/e*.In conclusion, this PhD study provides insight into how myocardial perfusion is altered in patients with type 2 diabetes and how these changes are related to the classic risk factors and complications in type 2 diabetes. Additionally, our data suggests an apparent link between coronary microvascular disease and cardiac diastolic dysfunction, a key characteristic in diabetic cardiomyopathy. Our findings reveal a need for well-designed longitudinal clinical trials, to further investigate how changes in the myocardial microcirculation over time, affects cardiac function and the risk of developing diabetic cardiomyopathy in patients with type 2 diabetes.

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    Authors: Haastrup, Anette Fly;
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    Authors: Johnsen, Anna Thit; Rottmann, Nina;

    En kræftsygdom kan være en stor psykisk belastning. Det er naturligt at reagere. Men hvordan reagerer man typisk? Og hvornår kan man have gavn af støtte eller psykologhjælp?

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    Authors: Boyd, Kenneth;
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    Authors: Holstein, Bjørn Evald;
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    Authors: Ekdahl, David;

    Organiseret computerspil på konkurrenceplan, eller ’esport’, har de sidste ti år gennemgået en enorm vækst og er siden 2020 blevet en milliardindustri. Som følge af denne udvikling, er esportsudøvelse i stigende grad blevet et bredt forskningsområde. Der findes dog i dag kun en meget begrænset mængde af forskning der har undersøgt de former for kropsbevidsthed og kropslighed som esporten kan fordre for udøverne selv. Denne afhandling er et fænomenologisk interviewstudie af esportsudøvelse som et muligt kropsbevidst fænomen. Afhandlingen undersøger og analyserer forskellige former for kropsbevidsthed der karakteriserer præsterende esportsudøveres erfaring – hovedsageligt indenfor spillene League of Legends og Counter Strike: Global Offensive. Resultaterne i denne afhandling baserer sig på fire artikler der enten fremhæver nødvendigheden af fænomenologisk analyse af esportsudøvelse eller gennemfører sådanne analyser. Afhandlingen består af fem overordnede dele. Efter en generel introduktion i første del, begynder afhandlingens anden del med at danne et overblik over esporten samt af den esportsforskning der i dag findes. Dernæst præsenteres diskussionen om esportens forhold til sporten. Med udgangspunkt i de uklarheder og misforståelser der har karakteriseret denne diskussion, argumenterer jeg for nødvendigheden af en klarere forståelse af esporten som et kropsbevidst fænomen. Baseret på dette, præsenterer afhandlingen sine epistemologiske rødder i form af et sæt af fænomenologiske grundantagelser, inklusive begrænsningerne ved dette fænomenologiske greb. Disse fænomenologiske grundantagelser fremlægges som noget der kan facilitere en mere direkte tilgang til esportsudøveres erfaringer og kropsbevidsthed. Dernæst, i tredje del, diskuterer jeg kritisk de metodologiske muligheder for fænomenologisk at undersøge andres erfaringer samt hvordan de interviewede informanters beskrivelser kan bruges til at udvide og udfordre vores nuværende forståelse af både esport samt virtuel kropsbevidsthed. Metodologisk er disse fænomenologiske analyser udført baseret på data generet igennem semistrukturerede, kvalitative interviews med tolv erfarne, danske esportsudøvere. I denne forbindelse følger en punktvis gennemgang af afhandlingens fulgte metode. Efterfølgende, i fjerde del, fremstilles de to esportsspil hvorefter de fænomenologiske analyser af esportsudøvernes beskrivelser præsenteres og diskuteres. Resultaterne af disse analyser fremhæver tre centrale dimensioner af kropsbevidsthed der karakteriserer esportsudøvernes erfaring når de præsterer. Disse er, et, basal kropsbevidsthed: Udøverne erfarer deres virtuelle verdener på grundlæggende kropslige og praksisorienterede måder. To, inkorporering: Med øvelse integrerer de præsterende esportsudøvere både tilgængelige fysiske samt virtuelle redskaber og evner som en del af deres kropslighed. Tre, interkropslighed: Med øvelse erfarer udøverne deres egen samt andres avatarer i kraft af en gensidig kropslig intentionalitet mens de præsterer. I femte og sidste del af afhandlingen vurderes de endelige resultater kritisk før de slutteligt drages ind i en større perspektivering. Organized competitive video gaming or ‘esports’ has undergone immense growth over the past ten years, into a billion-dollar industry as of 2020. Following this trend, a broad scope of research has increasingly been directed at the phenomenon as a set of novel and unique competitive, spectator platforms. Yet, little research on what kind of embodied involvement esports practice can afford has so far been conducted with actual esports practitioners. This thesis is a phenomenological interview study of esports practice, exploring and analyzing the different forms of embodied involvement esports practitioners experience during performance – primarily in the games League of Legends and Counter Strike: Global Offensive. The findings of the thesis are based on four articles that either emphasize the need for phenomenological analysis of esports practice or provide such analyses. The thesis proceeds in five parts. Outside of the overall introduction which makes up Part I, the thesis begins in Part II by providing an overview of esports practice and state-of-the-art research on esports, before engaging directly with the contemporary debate on esports’ relationship to the world of sports. Based on confusions and ambiguities in this debate, I emphasize the need for a clearer understanding of esports practice as embodied. The thesis then introduces a set of phenomenological assumptions as its epistemological roots. These phenomenological assumptions are introduced as elements that can facilitate a more direct engagement with the embodied experiences of esports practitioners. Following this, in Part III, the thesis engages in a critical methodological discussion on how to phenomenologically study the experiences of other subjects and how the interviewed informants’ descriptions can be used to expand and challenge our understanding of esports and virtual embodiment. Methodologically, these phenomenological analyses are conducted based on data generated through semi-structured, qualitative interviews with twelve talented, Danish esports practitioners. In this context, I provide a point-by-point introduction to the method. Then, in Part IV, the two esports games are introduced, before the phenomenological analyses of esports practice are presented and discussed. The results of these analyses show the central importance of three distinct dimensions of embodiment for the esports practitioners. These are, first, basic embodiment: The practitioners experience their virtual worlds in fundamentally embodied and practical ways. Second, incorporation: The practitioners come to integrate both the physical and the virtual tools and abilities available to them during performance into their body. Third, intercorporeality: The practitioners come to experience their own avatars and other players’ avatars reciprocally in terms of bodily intentionality. These final results are then, in Part V, critically assessed before being brought into broader perspectival considerations.

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    Authors: Zinckernagel, Line; Bo, Anne;

    Ugens tal for folkesundhed, 18, 2015

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    Authors: Kavan, Stephanie;

    Brystkræft er den mest udbredte invasive cancerlidelse og den største årsag til cancer relateret død blandt kvinder. En af de største udfordringer i behandlingen af brystkræftpatienter er den ekstensive inter- og intratumorale heterogenitet som er et resultat af naturlig og terapeutisk selektion. Data indhentet fra en bred række af genomiske studier på primære tumorer og metastaser, viser forskellige modeller af evolutionære mønstre, der adskiller sig ved timing af metastaseudløste genetiske forandringer og graden af genetisk konkordans. Karakterisering af det evolutionære landskab i brystkræfttumorer kan bidrage med biologisk forståelse af tumorprogression fra primærcancer til dissemination og kan blive et vigtigt redskab til vejledning af effektiv behandling. Aktuelt er vævsbiopsier betragtet som guldstandard til diagnostik og behandling af cancer, om end der er risiko for, at disse ikke repræsenterer hele det genetiske landskab af tumoren. Disse begrænsninger har ledt til forslag om ”liquid biopsies” som et attraktivt supplement til vævsbiopsier. ”Liquid biopsy” i form af cirkulerende tumor DNA (ctDNA) kan have potentiale til at fange den inter- og intratumorale heterogenitet i metastaserende brystkræft gennem serielle blodprøver, som sporer klonal evolution i cancergenomet.Studie I er en gennemgang af publicerede studier med fokus på intratumoral og temporal genetisk heterogenitet i brystkræft, med vægt på studier, der sporer klonal evolution ved global analyse i multiple progressionstrin fra samme patient. Derudover diskuterer vi potentialet for plasma ctDNA i forhold til vævsbiopsier fra primærtumorer og metastaser, for at opnå et mere komplet overblik over det molekylære landskab i tumorer. Taget i betragtning af de få studier der er udgivet inden for området af globale analyser har vi også inkluderet studier der bruger panelsekvensering. Endelig har vi sammenlignet studier med fokus på relevansen af genetisk heterogenitet og klonal evolution i klinikken. Her argumenterer vi for plasma ctDNA som en kraftfuld tilgang til monitorering af det klonale landskab af cancer under behandling og tilbagefald.Brystkræft er en spatial og temporal dynamisk sygdom, hvor forskelligt udviklede kloner er ansvarlige for progression og klinisk outcome, men betydningen af systemisk behandling for klonal evolution og tumor heterogenitet er fortsat uklar. I Studie II definerer vi de genetiske forandringer i systemisk ubehandlet brystkræft patienter med metastaserende sygdom. Vi analyserede data fra helexomsekvensering af parrede primærtumorer og metastaser fra tre brystkræft patienter, der endnu ikke havde modtaget systemisk behandling. Punktmutationer, copy number forandringer, potentielle driver gener og mutational cancer cell fraktioner blev identificeret ved brug af state-of-the-art metoder i bioinformatik. Genetiske forskelle blev bemærket mellem primærtumor og metastaser, der alle viste høj grad af genetisk divergens. Alle tre patienter fulgte en parallel progressionsmodel med tidlig monoclonal dissemination fra primærtumor efterfulgt af separat klonal evolution. Metastasespecifikke mutationer involverede generne EP300, APOBEC3B, KDM5C, ASXL1 og EPCAM. Alle associeret til cancer migration og progression. Disse resultater blev støttet af pathway analyser, der viste cancer driving pathways hovedsageligt er signifikant i stem mutationer med tilstedeværelse i både primærtumor og metastaser. Det er bemærkelsesværdigt , at påvirkede pathways reflekterede patientens molekylære subtype og metastaselokation. Metastasespecifikke forandringer påvirkede driver gener involveret i kollagen udvikling, muskelkontration, kernemembran depolymerisation. Disseforandringer medvirker til metastiske mekanismer såsom migration, invasion og genomisk instabilitet. De beskrevne mønstre af evolution og den polyklonale natur af brystkræft har potentielt kliniske konsekvenser og bør tages i betragtning i forhold til diagnostik og valg af behandling. Nye studier fokuserer på relevansen af clonal evolution i de kliniske rammer og belyser ”liquid biopsies” som en non-invasiv biomarkør til monitorering af klonal progression og respons til behandling. I klinisk sammenhæng, kan ctDNA sandsynligvis bidrage med en ideel støtte sammen med vævsbiopsier til karakterisering af det genetiske landskab i metastaserende sygdom. Desuden kan ctDNA potentielt forbedre longitudinel monitorering af sygdomsdynamikker og behandlingseffektivitet for derfor bedre, at kunne opspore residual tumorvæv efter resektion, tilbagefald af sygdom eller metastaser.I studie III foretog vi copy-number profiling og detektion af somatiske mutationer på baggrund af helexomsekvensering i primærtumorer, fjernmetastaser og plasma ctDNA fra otte patienter med metastaserende brystkræft. Vores data viste forskellige mønstre af tumor evolution. Selvom lineær udvikling med sen spredning af metastatiske celler blev påvist i nogle tilfælde, observerede vi for det meste parallel udvikling med tidlig spredning fra primære tumorer til fjernmetastaser. Ved sammenligning af vævsprøver med plasmaprøver fandt vi varianter der repræsenterer primærtumor og/eller metastaser. Dette er afhængig af tiden mellem progressionstrin. De gamle mutationer fra den tidlige tumorklon dominerer i plasma, efterfulgt af metastasespecifikke mutationer. Dog blev forskellige mønstre observeret. De genomiske forskelle mellem de forskellige stadier af tumor evolution understreger vigtigheden af molekylær profilering af metastatiske vævsprøver og mulighederne for ”liquid biopsies” og real-time sporing af tumor dynamikker.  Breast cancer is the most common invasive malignancy and the leading cause of cancer-related deaths among women. One of the biggest challenges in handling breast cancer is the extensive inter-and intra-tumoral heterogeneity resulting from a natural or therapeutic selection. Data obtained from various genomic profiling studies on primary tumors and matched metastases suggested different models of evolutionary patterns that differ in timing of metastasis-enabling genomic alterations and the degree of genomic concordance between progression states. Characterizing the evolutionary landscape of breast tumors can provide a biological understanding of tumor progression from primary cancers to dissemination and may be necessary for directing effective treatments. Currently, tissue biopsy is considered the gold standard for diagnosis and treatment guidance in breast cancer, although it may insufficiently represent the entire genomic landscape of a tumor. Multiple limitations of this technique have led to the proposal of liquid biopsies as an attractive complementary tool to tissue biopsies. In the form of circulating tumor DNA (ctDNA), liquid biopsy could potentially capture the inter-and intra-tumoral heterogeneity present in metastatic breast cancer and, through serial blood draws, track the clonal evolution of the cancer genome.Study I is a literature review focused on intratumor and temporal genetic heterogeneity in breast cancer, emphasizing studies tracking clonal evolution by global analysis in multiple progression steps from the same patient. Additionally, we discussed the potential of plasma ctDNA compared to tissue biopsies from primary tumors and metastases for a complete overview of the molecular tumor landscape. Considering the low number of papers published in this part using global analysis, we also included studies using targeted sequencing approaches. Finally, we compared studies focusing on the relevance of genetic heterogeneity and clonal evolution in the clinical setting and discussed plasma circulating tumor DNA as a powerful real-time approach for monitoring the clonal landscape of cancer during treatment and recurrence. Breast Cancer is a spatial and temporal dynamic disease where differently evolving genetic clones are responsible for progression and clinical outcome. Still, the impact of systemic treatment on clonal evolution and tumor heterogeneity is poorly understood. In Study II, we ought to map the repertoire of genetic alterations in systemically untreated breast cancer patients with de novo metastatic disease. We analyzed wholeexome sequencing data from the paired primary tumor and metastatic samples from three breast cancer patients who had not received systemic therapy yet. Point mutations, copy number alterations, potential driver genes, and mutational cancer cell fractions were identified using state-of-the-art bioinformatics methods. Genomic differences were observed between primary tumor and metastatic lesion, showing a high level of genetic divergence. All three patients followed the parallel progression model, with early monoclonal dissemination from the primary tumor followed by separate clonal evolution. Interestingly, metastasis-specific mutations involved genes EP300, APOBEC3B, KDM5C, ASXL1, and EPCAM, all associated with cancer migration and progression. These results were supported by pathway analysis, showing cancer-driving pathways are mainly significant in stem mutations present in both primary tumor and metastasis. Notably, affected pathways reflected the patient’s molecular subtype and metastasis location. Lastly, alterations specific to the metastasis affected driver genes involved in collagen formation, muscle contraction, and nuclear envelope depolymerizations supporting metastatic tumor cell migration, invasion, and genomic instability. The described patterns of evolution and the polyclonal nature of breast cancer have clinical consequences and should be considered during patient diagnosis and treatment selection. Current studies focusing on the relevance of clonal evolution in the clinical setting elucidate the role of liquid biopsy as a noninvasive biomarker for monitoring clonal progression and response to treatment. In the clinical setting, circulating tumor DNA may constitute ideal support for tumor biopsies to characterize the genetic landscape of metastatic disease. This might improve longitudinal monitoring of disease dynamics and treatment effectiveness to detect any residual tumor after resection, relapse, or metastasis within a particular patient.In Study III, we performed copy number profiling and somatic mutation detection based on whole-exome sequencing of primary tumors, distant metastasis, and plasma circulating tumor DNA from eight metastatic breast cancer patients. Our data showed diverse patterns of tumor evolution. Although linear evolution with late dissemination of metastatic cells was detected in some cases, we mainly observed parallel evolution with early dissemination from primary tumors to distant sites. Comparing tissue biopsies with plasma samples, we detected variants mirroring primary tumor and/or metastasis, depending on the period between the progression steps. The old mutations from the early tumor clone dominate in plasma, followed by metastasis-specific mutations. However, different patterns were observed. The genomic discordance between the various stages of tumor evolution emphasizes the importance of molecular profiling of metastatic tissue and the possibilities of liquid biopsies for real-time tracking of tumor dynamics.

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    Authors: Hafner, Sasha; Rennuit, Charlotte;

    Functions for working with biogas data. Both low- and high-level functions are included for carrying out common tasks for analysis of biogas and related data. Molar mass and calculated oxygen demand (COD') can be determined from a chemical formula. Measured gas volume can be corrected for water vapor and to (possibly user-defined) standard temperature and pressure. Gas composition, cumulative production, or other variables can be interpolated to a specified time. Cumulative biogas and methane production (and rates) can be calculated using volumetric, manometric, or gravimetric methods for any number of reactors. With cumulative methane production data and data on reactor contents, biochemical methane potential (BMP) can be calculated and summarized, including subtraction of the inoculum contribution and normalization by substrate mass. Cumulative production and production rates can be summarized in several different ways (e.g., omitting normalization) using the same function. Lastly, biogas and methane production can be predicted from substrate composition and additional, optional data.

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    Authors: Kempf, S. J.; Janik, Dirk; Barjaktarovic, Zarko; Braga-Tanaka III, I.; +5 Authors

    Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer's. The aim of this study was to elucidate the effect on hippocampus of chronic low-dose-rate radiation exposure (1 mGy/day or 20 mGy/day) given over 300 days with cumulative doses of 0.3 Gy and 6.0 Gy, respectively. ApoE deficient mutant C57Bl/6 mouse was used as an Alzheimer's model. Using mass spectrometry, a marked alteration in the phosphoproteome was found at both dose rates. The radiation-induced changes in the phosphoproteome were associated with the control of synaptic plasticity, calcium-dependent signalling and brain metabolism. An inhibition of CREB signalling was found at both dose rates whereas Rac1-Cofilin signalling was found activated only at the lower dose rate. Similarly, the reduction in the number of activated microglia in the molecular layer of hippocampus that paralleled with reduced levels of TNFα expression and lipid peroxidation was significant only at the lower dose rate. Adult neurogenesis, investigated by Ki67, GFAP and NeuN staining, and cell death (activated caspase-3) were not influenced at any dose or dose rate. This study shows that several molecular targets induced by chronic low-dose-rate radiation overlap with those of Alzheimer's pathology. It may suggest that ionising radiation functions as a contributing risk factor to this neurodegenerative disease.

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    Oncotarget
    Article
    License: CC BY
    Data sources: UnpayWall
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    ENEA Open Archive
    Article . 2016
    Data sources: ENEA Open Archive
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    Article . Other ORP type . 2016 . Peer-reviewed
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    Authors: Heyn Sørensen, Martin;

    Patienter med type 2-diabetes har en øget risiko for at udvikle hjertesvigt uafhængigt af andre risikofaktorer, såsom arteriosklerose og hypertension. Denne øgede forekomst af hjertesvigt hos patienter med type 2-diabetes har ført til hypotesen om, at der findes en specifik diabetisk kardiomyopati, kendetegnet ved koncentrisk myokardiehypertrofi og diastolisk dysfunktion. Ændringer i hjertets mikrocirkulation og mikrovaskulær dysfunktion i hjertets små kar spiller muligvis en rolle i udviklingen af diabetisk kardiomyopati og hjertesvigt hos patienter med type 2-diabetes, men den nøjagtige mekanisme for, hvordan type 2-diabetes kan forårsage hjertesvigt uafhængigt af andre kardiovaskulære risikofaktorer er fortsat ukendt.I denne ph.d.-afhandling undersøgte vi, hvordan forskelle i den diabetiske fænotype (diabetiske komplikationer, risikofaktorer, anti-diabetesbehandling osv.) påvirker perfusion i myokardiet, som et mål for kardiel mikrovaskulær sygdom, og om ændringer i hjertestruktur og funktion hos patienter med type 2-diabetes er relateret til kardiel mikrovaskulær sygdom, som en mulig mekanisme bag udviklingen af diabetisk kardiomyopati.For at undersøge dette blev 273 patienter med type 2-diabetes og 25 kontrolpersoner uden type 2-diabetes inkluderet i en tværsnitsundersøgelse. Alle deltagere gennemgik klinisk undersøgelse, blodog urinprøveudtagning, ekkokardiografi og avanceret magnetisk resonans scanning af hjertet, inklusive sekvenser for vævskarakterisering og fuld kvantitativ myokardie perfusion i hvile og under farmakologisk stress (adenosin 140 ug/kg/min). Blod- og urinprøver fra alle patienter med type 2-diabetes blev opsamlet og transporteret til Region Sjællands biobank for langtidsopbevaring.Vi fandt, at patienter med type 2-diabetes havde lavere myokardie perfusions reserve sammenlignet med kontrolpersoner, og at denne reduktion i myokardie perfusions reserve var forårsaget af både en Martin Heyn Sørensen, 2020 5 stigning i myokardie perfusion i hvile og reduceret maksimal myokardie perfusion under farmakologisk stress. Patienter med type 2-diabetes kompliceret med albuminuri eller retinopati havde lavere myokardie perfusions reserve og lavere maksimal myokardie perfusion under farmakologisk stress, sammenlignet med patienter med ukompliceret type 2-diabetes. Derudover havde patienter med type 2-diabetes kompliceret med albuminuri eller retinopati højere venstre ventrikel masse og højere E/e* (et ekkokardiografisk mål for diastolisk funktion af venstre ventrikel) end patienter med ukompliceret type 2-diabetes. Vi fandt en signifikant sammenhæng mellem reduceret myokardie perfusions reserve og nedsat diastolisk funktion af venstre ventrikel. Endelig fandt vi, at øgede niveauer af biomarkøren fibroblast vækstfaktor-23, som tidligere er blevet forbundet med øget risiko for hjerte-kar sygdom og hjerte-kar dødelighed hos patienter både med og uden type 2-diabetes, var forbundet med et fald i myokardie perfusions reserve og reduceret maksimal myokardie perfusion under farmakologisk stress samt øget E/e*.Dette ph.d.-studie giver indsigt i, hvordan myokardie perfusionen ændres hos patienter med type 2-diabetes, og hvordan disse ændringer er relateret til de klassiske risikofaktorer og komplikationer ved type 2-diabetes. Derudover viser vores resultater en tilsyneladende sammenhæng mellem kardiel mikrovaskulær sygdom og udvikling af venstre ventrikel diastolisk dysfunktion, et nøglekarakteristikum for diabetisk kardiomyopati. Vores resultater afslører et behov for veldesignede prospektive kliniske forsøg for yderligere at undersøge, hvordan ændringer i den kardielle mikrocirkulation over tid påvirker hjertefunktionen, og risikoen for at udvikle diabetisk kardiomyopati hos patienter med type 2-diabetes. Patients with type 2 diabetes have an increased risk of developing heart failure independent of other risk factors, such as coronary artery disease and hypertension. This increased prevalence of heart failure in type 2 diabetes has led to the hypothesis, that a specific diabetic cardiomyopathy, characterized by concentric myocardial hypertrophy and diastolic dysfunction, exists. Alterations in the myocardial microcirculation and microvascular dysfunction has been suggested to play a role in the development of diabetic cardiomyopathy and heart failure in patients with type 2 diabetes, however, the exact mechanism of how type 2 diabetes can cause heart failure independent of other cardiovascular risk factors still remains partly unknown.In this PhD thesis we investigated how differences in the diabetic phenotype (diabetic complications, risk factors, anti-diabetes therapy, etc.) affects myocardial perfusion, as a measure of coronary microvascular disease, and if changes in cardiac structure and function in patients with type 2 diabetes is related to coronary microvascular disease, as a possible mechanistic pathway for the development of diabetic cardiomyopathy.To investigate this, 273 patients with type 2 diabetes and 25 control subjects without type 2 diabetes were included in a cross-sectional survey. All participants underwent clinical examination, blood and urinary sampling, echocardiography and advanced cardiac magnetic resonance imaging including mapping sequences for tissue characterization and full quantitative myocardial perfusion during both rest and pharmacological stress (adenosine 140 µg/kg/min). Blood- and urinary samples from all patients with type 2 diabetes were collected and transported to Region Zealand’s biobank for long time storage.We found that patients with type 2 diabetes had lower myocardial perfusion reserve when compared to control subjects, and that this reduction in myocardial perfusion reserve was caused by both an increase in myocardial blood flow during rest and reduced maximal myocardial blood flow during vasodilator stress. Patients with type 2 diabetes complicated with albuminuria or retinopathy had lower myocardial perfusion reserve and maximal myocardial blood flow during stress, compared to patients with uncomplicated type 2 diabetes. In addition, patients with type 2 diabetes complicated with albuminuria or retinopathy had higher left ventricular mass and E/e* (an echocardiographic measure of left ventricular diastolic function), than did patients with uncomplicated type 2 diabetes. We found a significant association between reduced myocardial perfusion reserve and impaired left ventricular diastolic function. Finally, we found that increased levels of the biomarker fibroblast growth factor-23, Martin Heyn Sørensen, 2020 4 which has previously been associated with cardiovascular morbidity and mortality in both patients with and without type 2 diabetes, were associated with a decrease in myocardial perfusion reserve and reduced maximal myocardial blood flow during stress as well as increased E/e*.In conclusion, this PhD study provides insight into how myocardial perfusion is altered in patients with type 2 diabetes and how these changes are related to the classic risk factors and complications in type 2 diabetes. Additionally, our data suggests an apparent link between coronary microvascular disease and cardiac diastolic dysfunction, a key characteristic in diabetic cardiomyopathy. Our findings reveal a need for well-designed longitudinal clinical trials, to further investigate how changes in the myocardial microcirculation over time, affects cardiac function and the risk of developing diabetic cardiomyopathy in patients with type 2 diabetes.

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    Authors: Haastrup, Anette Fly;
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    Authors: Johnsen, Anna Thit; Rottmann, Nina;

    En kræftsygdom kan være en stor psykisk belastning. Det er naturligt at reagere. Men hvordan reagerer man typisk? Og hvornår kan man have gavn af støtte eller psykologhjælp?

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    Authors: Boyd, Kenneth;
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    Authors: Holstein, Bjørn Evald;
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    Authors: Ekdahl, David;

    Organiseret computerspil på konkurrenceplan, eller ’esport’, har de sidste ti år gennemgået en enorm vækst og er siden 2020 blevet en milliardindustri. Som følge af denne udvikling, er esportsudøvelse i stigende grad blevet et bredt forskningsområde. Der findes dog i dag kun en meget begrænset mængde af forskning der har undersøgt de former for kropsbevidsthed og kropslighed som esporten kan fordre for udøverne selv. Denne afhandling er et fænomenologisk interviewstudie af esportsudøvelse som et muligt kropsbevidst fænomen. Afhandlingen undersøger og analyserer forskellige former for kropsbevidsthed der karakteriserer præsterende esportsudøveres erfaring – hovedsageligt indenfor spillene League of Legends og Counter Strike: Global Offensive. Resultaterne i denne afhandling baserer sig på fire artikler der enten fremhæver nødvendigheden af fænomenologisk analyse af esportsudøvelse eller gennemfører sådanne analyser. Afhandlingen består af fem overordnede dele. Efter en generel introduktion i første del, begynder afhandlingens anden del med at danne et overblik over esporten samt af den esportsforskning der i dag findes. Dernæst præsenteres diskussionen om esportens forhold til sporten. Med udgangspunkt i de uklarheder og misforståelser der har karakteriseret denne diskussion, argumenterer jeg for nødvendigheden af en klarere forståelse af esporten som et kropsbevidst fænomen. Baseret på dette, præsenterer afhandlingen sine epistemologiske rødder i form af et sæt af fænomenologiske grundantagelser, inklusive begrænsningerne ved dette fænomenologiske greb. Disse fænomenologiske grundantagelser fremlægges som noget der kan facilitere en mere direkte tilgang til esportsudøveres erfaringer og kropsbevidsthed. Dernæst, i tredje del, diskuterer jeg kritisk de metodologiske muligheder for fænomenologisk at undersøge andres erfaringer samt hvordan de interviewede informanters beskrivelser kan bruges til at udvide og udfordre vores nuværende forståelse af både esport samt virtuel kropsbevidsthed. Metodologisk er disse fænomenologiske analyser udført baseret på data generet igennem semistrukturerede, kvalitative interviews med tolv erfarne, danske esportsudøvere. I denne forbindelse følger en punktvis gennemgang af afhandlingens fulgte metode. Efterfølgende, i fjerde del, fremstilles de to esportsspil hvorefter de fænomenologiske analyser af esportsudøvernes beskrivelser præsenteres og diskuteres. Resultaterne af disse analyser fremhæver tre centrale dimensioner af kropsbevidsthed der karakteriserer esportsudøvernes erfaring når de præsterer. Disse er, et, basal kropsbevidsthed: Udøverne erfarer deres virtuelle verdener på grundlæggende kropslige og praksisorienterede måder. To, inkorporering: Med øvelse integrerer de præsterende esportsudøvere både tilgængelige fysiske samt virtuelle redskaber og evner som en del af deres kropslighed. Tre, interkropslighed: Med øvelse erfarer udøverne deres egen samt andres avatarer i kraft af en gensidig kropslig intentionalitet mens de præsterer. I femte og sidste del af afhandlingen vurderes de endelige resultater kritisk før de slutteligt drages ind i en større perspektivering. Organized competitive video gaming or ‘esports’ has undergone immense growth over the past ten years, into a billion-dollar industry as of 2020. Following this trend, a broad scope of research has increasingly been directed at the phenomenon as a set of novel and unique competitive, spectator platforms. Yet, little research on what kind of embodied involvement esports practice can afford has so far been conducted with actual esports practitioners. This thesis is a phenomenological interview study of esports practice, exploring and analyzing the different forms of embodied involvement esports practitioners experience during performance – primarily in the games League of Legends and Counter Strike: Global Offensive. The findings of the thesis are based on four articles that either emphasize the need for phenomenological analysis of esports practice or provide such analyses. The thesis proceeds in five parts. Outside of the overall introduction which makes up Part I, the thesis begins in Part II by providing an overview of esports practice and state-of-the-art research on esports, before engaging directly with the contemporary debate on esports’ relationship to the world of sports. Based on confusions and ambiguities in this debate, I emphasize the need for a clearer understanding of esports practice as embodied. The thesis then introduces a set of phenomenological assumptions as its epistemological roots. These phenomenological assumptions are introduced as elements that can facilitate a more direct engagement with the embodied experiences of esports practitioners. Following this, in Part III, the thesis engages in a critical methodological discussion on how to phenomenologically study the experiences of other subjects and how the interviewed informants’ descriptions can be used to expand and challenge our understanding of esports and virtual embodiment. Methodologically, these phenomenological analyses are conducted based on data generated through semi-structured, qualitative interviews with twelve talented, Danish esports practitioners. In this context, I provide a point-by-point introduction to the method. Then, in Part IV, the two esports games are introduced, before the phenomenological analyses of esports practice are presented and discussed. The results of these analyses show the central importance of three distinct dimensions of embodiment for the esports practitioners. These are, first, basic embodiment: The practitioners experience their virtual worlds in fundamentally embodied and practical ways. Second, incorporation: The practitioners come to integrate both the physical and the virtual tools and abilities available to them during performance into their body. Third, intercorporeality: The practitioners come to experience their own avatars and other players’ avatars reciprocally in terms of bodily intentionality. These final results are then, in Part V, critically assessed before being brought into broader perspectival considerations.

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    Authors: Zinckernagel, Line; Bo, Anne;

    Ugens tal for folkesundhed, 18, 2015

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    Authors: Kavan, Stephanie;

    Brystkræft er den mest udbredte invasive cancerlidelse og den største årsag til cancer relateret død blandt kvinder. En af de største udfordringer i behandlingen af brystkræftpatienter er den ekstensive inter- og intratumorale heterogenitet som er et resultat af naturlig og terapeutisk selektion. Data indhentet fra en bred række af genomiske studier på primære tumorer og metastaser, viser forskellige modeller af evolutionære mønstre, der adskiller sig ved timing af metastaseudløste genetiske forandringer og graden af genetisk konkordans. Karakterisering af det evolutionære landskab i brystkræfttumorer kan bidrage med biologisk forståelse af tumorprogression fra primærcancer til dissemination og kan blive et vigtigt redskab til vejledning af effektiv behandling. Aktuelt er vævsbiopsier betragtet som guldstandard til diagnostik og behandling af cancer, om end der er risiko for, at disse ikke repræsenterer hele det genetiske landskab af tumoren. Disse begrænsninger har ledt til forslag om ”liquid biopsies” som et attraktivt supplement til vævsbiopsier. ”Liquid biopsy” i form af cirkulerende tumor DNA (ctDNA) kan have potentiale til at fange den inter- og intratumorale heterogenitet i metastaserende brystkræft gennem serielle blodprøver, som sporer klonal evolution i cancergenomet.Studie I er en gennemgang af publicerede studier med fokus på intratumoral og temporal genetisk heterogenitet i brystkræft, med vægt på studier, der sporer klonal evolution ved global analyse i multiple progressionstrin fra samme patient. Derudover diskuterer vi potentialet for plasma ctDNA i forhold til vævsbiopsier fra primærtumorer og metastaser, for at opnå et mere komplet overblik over det molekylære landskab i tumorer. Taget i betragtning af de få studier der er udgivet inden for området af globale analyser har vi også inkluderet studier der bruger panelsekvensering. Endelig har vi sammenlignet studier med fokus på relevansen af genetisk heterogenitet og klonal evolution i klinikken. Her argumenterer vi for plasma ctDNA som en kraftfuld tilgang til monitorering af det klonale landskab af cancer under behandling og tilbagefald.Brystkræft er en spatial og temporal dynamisk sygdom, hvor forskelligt udviklede kloner er ansvarlige for progression og klinisk outcome, men betydningen af systemisk behandling for klonal evolution og tumor heterogenitet er fortsat uklar. I Studie II definerer vi de genetiske forandringer i systemisk ubehandlet brystkræft patienter med metastaserende sygdom. Vi analyserede data fra helexomsekvensering af parrede primærtumorer og metastaser fra tre brystkræft patienter, der endnu ikke havde modtaget systemisk behandling. Punktmutationer, copy number forandringer, potentielle driver gener og mutational cancer cell fraktioner blev identificeret ved brug af state-of-the-art metoder i bioinformatik. Genetiske forskelle blev bemærket mellem primærtumor og metastaser, der alle viste høj grad af genetisk divergens. Alle tre patienter fulgte en parallel progressionsmodel med tidlig monoclonal dissemination fra primærtumor efterfulgt af separat klonal evolution. Metastasespecifikke mutationer involverede generne EP300, APOBEC3B, KDM5C, ASXL1 og EPCAM. Alle associeret til cancer migration og progression. Disse resultater blev støttet af pathway analyser, der viste cancer driving pathways hovedsageligt er signifikant i stem mutationer med tilstedeværelse i både primærtumor og metastaser. Det er bemærkelsesværdigt , at påvirkede pathways reflekterede patientens molekylære subtype og metastaselokation. Metastasespecifikke forandringer påvirkede driver gener involveret i kollagen udvikling, muskelkontration, kernemembran depolymerisation. Disseforandringer medvirker til metastiske mekanismer såsom migration, invasion og genomisk instabilitet. De beskrevne mønstre af evolution og den polyklonale natur af brystkræft har potentielt kliniske konsekvenser og bør tages i betragtning i forhold til diagnostik og valg af behandling. Nye studier fokuserer på relevansen af clonal evolution i de kliniske rammer og belyser ”liquid biopsies” som en non-invasiv biomarkør til monitorering af klonal progression og respons til behandling. I klinisk sammenhæng, kan ctDNA sandsynligvis bidrage med en ideel støtte sammen med vævsbiopsier til karakterisering af det genetiske landskab i metastaserende sygdom. Desuden kan ctDNA potentielt forbedre longitudinel monitorering af sygdomsdynamikker og behandlingseffektivitet for derfor bedre, at kunne opspore residual tumorvæv efter resektion, tilbagefald af sygdom eller metastaser.I studie III foretog vi copy-number profiling og detektion af somatiske mutationer på baggrund af helexomsekvensering i primærtumorer, fjernmetastaser og plasma ctDNA fra otte patienter med metastaserende brystkræft. Vores data viste forskellige mønstre af tumor evolution. Selvom lineær udvikli