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Sökning: WFRF:(Schmidt Linnéa)

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2.
  • Abenius, Tobias, 1979, et al. (författare)
  • System-scale network modeling of cancer using EPoC
  • 2012
  • Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer New York. - 0065-2598. - 9781441972095 ; 736:5, s. 617-643
  • Tidskriftsartikel (refereegranskat)abstract
    • One of the central problems of cancer systems biology is to understand the complex molecular changes of cancerous cells and tissues, and use this understanding to support the development of new targeted therapies. EPoC (Endogenous Perturbation analysis of Cancer) is a network modeling technique for tumor molecular profiles. EPoC models are constructed from combined copy number aberration (CNA) and mRNA data and aim to (1) identify genes whose copy number aberrations significantly affect target mRNA expression and (2) generate markers for long- and short-term survival of cancer patients. Models are constructed by a combination of regression and bootstrapping methods. Prognostic scores are obtained from a singular value decomposition of the networks. We have previously analyzed the performance of EPoC using glioblastoma data from The Cancer Genome Atlas (TCGA) consortium, and have shown that resulting network models contain both known and candidate disease-relevant genes as network hubs, as well as uncover predictors of patient survival. Here, we give a practical guide how to perform EPoC modeling in practice using R, and present a set of alternative modeling frameworks.
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  • Castell, Alina, et al. (författare)
  • MYCMI-7 : A Small MYC-Binding Compound that Inhibits MYC: MAX Interaction and Tumor Growth in a MYC-Dependent Manner
  • 2022
  • Ingår i: Cancer Research Communications. - : American Association For Cancer Research (AACR). - 2767-9764. ; 2:3, s. 182-201
  • Tidskriftsartikel (refereegranskat)abstract
    • Deregulated expression of MYC family oncogenes occurs frequently in human cancer and is often associated with aggressive disease and poor prognosis. While MYC is a highly warranted target, it has been considered "undruggable," and no specific anti-MYC drugs are available in the clinic. We recently identified molecules named MYCMIs that inhibit the interaction between MYC and its essential partner MAX. Here we show that one of these molecules, MYCMI-7, efficiently and selectively inhibits MYC:MAX and MYCN:MAX interactions in cells, binds directly to recombinant MYC, and reduces MYC-driven transcription. In addition, MYCMI-7 induces degradation of MYC and MYCN proteins. MYCMI-7 potently induces growth arrest/apoptosis in tumor cells in a MYC/MYCN-dependent manner and downregulates the MYC pathway on a global level as determined by RNA sequencing. Sensitivity to MYCMI-7 correlates with MYC expression in a panel of 60 tumor cell lines and MYCMI-7 shows high efficacy toward a collection of patient-derived primary glioblastoma and acute myeloid leukemia (AML) ex vivo cultures. Importantly, a variety of normal cells be- come G1 arrested without signs of apoptosis upon MYCMI-7 treatment. Finally, in mouse tumor models of MYC-driven AML, breast cancer, and MYCN-amplified neuroblastoma, treatment with MYCMI-7 downregu- lates MYC/MYCN, inhibits tumor growth, and prolongs survival through apoptosis with few side effects. In conclusion, MYCMI-7 is a potent and selective MYC inhibitor that is highly relevant for the development into clinically useful drugs for the treatment of MYC-driven cancer.Significance: Our findings demonstrate that the small-molecule MYCMI-7 binds MYC and inhibits interaction between MYC and MAX, thereby ham- pering MYC-driven tumor cell growth in culture and in vivo while sparing normal cells.
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5.
  • Claesson, Elin, 1989, et al. (författare)
  • The primary structural photoresponse of phytochrome proteins captured by a femtosecond X-ray laser
  • 2020
  • Ingår i: eLife. - 2050-084X. ; 9
  • Tidskriftsartikel (refereegranskat)abstract
    • Phytochrome proteins control the growth, reproduction, and photosynthesis of plants, fungi, and bacteria. Light is detected by a bilin cofactor, but it remains elusive how this leads to activation of the protein through structural changes. We present serial femtosecond X-ray crystallographic data of the chromophore-binding domains of a bacterial phytochrome at delay times of 1 ps and 10 ps after photoexcitation. The data reveal a twist of the D-ring, which leads to partial detachment of the chromophore from the protein. Unexpectedly, the conserved so-called pyrrole water is photodissociated from the chromophore, concomitant with movement of the A-ring and a key signaling aspartate. The changes are wired together by ultrafast backbone and water movements around the chromophore, channeling them into signal transduction towards the output domains. We suggest that the observed collective changes are important for the phytochrome photoresponse, explaining the earliest steps of how plants, fungi and bacteria sense red light.
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6.
  • Gerlee, Philip, 1980, et al. (författare)
  • Searching for Synergies: Matrix Algebraic Approaches for Efficient Pair Screening
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:7
  • Tidskriftsartikel (refereegranskat)abstract
    • Functionally interacting perturbations, such as synergistic drugs pairs or synthetic lethal gene pairs, are of key interest in both pharmacology and functional genomics. However, to find such pairs by traditional screening methods is both time consuming and costly. We present a novel computational-experimental framework for efficient identification of synergistic target pairs, applicable for screening of systems with sizes on the order of current drug, small RNA or SGA (Synthetic Genetic Array) libraries (>1000 targets). This framework exploits the fact that the response of a drug pair in a given system, or a pair of genes' propensity to interact functionally, can be partly predicted by computational means from (i) a small set of experimentally determined target pairs, and (ii) pre-existing data (e.g. gene ontology, PPI) on the similarities between targets. Predictions are obtained by a novel matrix algebraic technique, based on cyclical projections onto convex sets. We demonstrate the efficiency of the proposed method using drug-drug interaction data from seven cancer cell lines and gene-gene interaction data from yeast SGA screens. Our protocol increases the rate of synergism discovery significantly over traditional screening, by up to 7-fold. Our method is easy to implement and could be applied to accelerate pair screening for both animal and microbial systems.
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7.
  • Hansson, Caroline, 1981, et al. (författare)
  • Influence of ghrelin on the central serotonergic signaling system in mice
  • 2014
  • Ingår i: Neuropharmacology. - : Elsevier BV. - 0028-3908. ; 79, s. 498-505
  • Tidskriftsartikel (refereegranskat)abstract
    • The central ghrelin signaling system engages key pathways of importance for feeding control, recently shown to include those engaged in anxiety-like behavior in rodents. Here we sought to determine whether ghrelin impacts on the central serotonin system, which has an important role in anxiety. We focused on two brain areas, the amygdala (of importance for the mediation of fear and anxiety) and the dorsal raphe (i.e. the site of origin of major afferent serotonin pathways, including those that project to the amygdala). In these brain areas, we measured serotonergic turnover (using HPLC) and the mRNA expression of a number of serotonin-related genes (using real-time PCR). We found that acute central administration of ghrelin to mice increased the serotonergic turnover in the amygdala. It also increased the mRNA expression of a number of serotonin receptors, both in the amygdala and in the dorsal raphe. Studies in ghrelin receptor (GHS-R1A) knock-out mice showed a decreased mRNA expression of serotonergic receptors in both the amygdala and the dorsal raphe, relative to their wild-type littermates. We conclude that the central serotonin system is a target for ghrelin, providing a candidate neurochemical substrate of importance for ghrelin's effects on mood. © 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
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  • Johansson, Patrik, et al. (författare)
  • A Patient-Derived Cell Atlas Informs Precision Targeting of Glioblastoma
  • 2020
  • Ingår i: Cell Reports. - : Elsevier BV. - 2211-1247. ; 32:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Glioblastoma (GBM) is a malignant brain tumor with few therapeutic options. The disease presents with a complex spectrum of genomic aberrations, but the pharmacological consequences of these aberrations are partly unknown. Here, we report an integrated pharmacogenomic analysis of 100 patient-derived GBM cell cultures from the human glioma cell culture (HGCC) cohort. Exploring 1,544 drugs, we find that GBM has two main pharmacological subgroups, marked by differential response to proteasome inhibitors and mutually exclusive aberrations in TP53 and CDKN2A/B. We confirm this trend in cell and in xenotransplantation models, and identify both Bcl-2 family inhibitors and p53 activators as potentiators of proteasome inhibitors in GBM cells, We can further predict the responses of individual cell cultures to several existing drug classes, presenting opportunities for drug repurposing and design of stratified trials. Our functionally profiled biobank provides a valuable resource for the discovery of new treatments for GBM.
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  • Johard, Helena, et al. (författare)
  • HCN Channel Activity Balances Quiescence and Proliferation in Neural Stem Cells and Is a Selective Target for Neuroprotection During Cancer Treatment
  • 2020
  • Ingår i: Molecular Cancer Research. - 1541-7786 .- 1557-3125. ; 18:10, s. 1522-1533
  • Tidskriftsartikel (refereegranskat)abstract
    • Children suffering from neurologic cancers undergoing chemotherapy and radiotherapy are at high risk of reduced neurocognitive abilities likely via damage to proliferating neural stem cells (NSC). Therefore, strategies to protect NSCs are needed. We argue that induced cell-cycle arrest/quiescence in NSCs during cancer treatment can represent such a strategy. Here, we show that hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channels are dynamically expressed over the cell cycle in NSCs, depolarize the membrane potential, underlie spontaneous calcium oscillations and are required to maintain NSCs in the actively proliferating pool. Hyperpolarizing pharmacologic inhibition of HCN channels during exposure to ionizing radiation protects NSCs cells in neurogenic brain regions of young mice. In contrast, brain tumor-initiating cells, which also express HCN channels, remain proliferative during HCN inhibition.
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13.
  • Jörnsten, Rebecka, 1971, et al. (författare)
  • Network modeling of the transcriptional effects of copy number aberrations in glioblastoma
  • 2011
  • Ingår i: Molecular Systems Biology. - : EMBO. - 1744-4292. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • DNA copy number aberrations (CNAs) are a hallmark of cancer genomes. However, little is known about how such changes affect global gene expression. We develop a modeling framework, EPoC (Endogenous Perturbation analysis of Cancer), to (1) detect disease-driving CNAs and their effect on target mRNA expression, and to (2) stratify cancer patients into long- and short-term survivors. Our method constructs causal network models of gene expression by combining genome-wide DNA- and RNA-level data. Prognostic scores are obtained from a singular value decomposition of the networks. By applying EPoC to glioblastoma data from The Cancer Genome Atlas consortium, we demonstrate that the resulting network models contain known disease-relevant hub genes, reveal interesting candidate hubs, and uncover predictors of patient survival. Targeted validations in four glioblastoma cell lines support selected predictions, and implicate the p53-interacting protein Necdin in suppressing glioblastoma cell growth. We conclude that large-scale network modeling of the effects of CNAs on gene expression may provide insights into the biology of human cancer. Free software in MATLAB and R is provided.
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14.
  • Karlsson-Lindahl, Linda, 1972, et al. (författare)
  • Heparanase affects food intake and regulates energy balance in mice.
  • 2012
  • Ingår i: PloS one. - San Francisco : Public Library of Science (PLoS). - 1932-6203. ; 7:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Mutation of the melanocortin-receptor 4 (MC4R) is the most frequent cause of severe obesity in humans. Binding of agouti-related peptide (AgRP) to MC4R involves the co-receptor syndecan-3, a heparan sulfate proteoglycan. The proteoglycan can be structurally modified by the enzyme heparanase. Here we tested the hypothesis that heparanase plays a role in food intake behaviour and energy balance regulation by analysing body weight, body composition and food intake in genetically modified mice that either lack or overexpress heparanase. We also assessed food intake and body weight following acute central intracerebroventricular administration of heparanase; such treatment reduced food intake in wildtype mice, an effect that was abolished in mice lacking MC4R. By contrast, heparanase knockout mice on a high-fat diet showed increased food intake and maturity-onset obesity, with up to a 40% increase in body fat. Mice overexpressing heparanase displayed essentially the opposite phenotypes, with a reduced fat mass. These results implicate heparanase in energy balance control via the central melanocortin system. Our data indicate that heparanase acts as a negative modulator of AgRP signaling at MC4R, through cleavage of heparan sulfate chains presumably linked to syndecan-3.
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15.
  • Niklasson, Mia, et al. (författare)
  • Membrane-Depolarizing Channel Blockers Induce Selective Glioma Cell Death by Impairing Nutrient Transport and Unfolded Protein/Amino Acid Responses
  • 2017
  • Ingår i: Cancer Research. - : AMER ASSOC CANCER RESEARCH. - 0008-5472 .- 1538-7445. ; 77:7, s. 1741-1752
  • Tidskriftsartikel (refereegranskat)abstract
    • Glioma-initiating cells (GIC) are considered the underlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and undermining the efficacy of conventional chemotherapy. Here we report the discovery that inhibiting T-type voltage-gated Ca2+ and KCa channels can effectively induce selective cell death of GIC and increase host survival in an orthotopic mouse model of human glioma. At present, the precise cellular pathways affected by the drugs affecting these channels are unknown. However, using cell-based assays and integrated proteomics, phosphoproteomics, and transcriptomics analyses, we identified the downstreamsignaling events these drugs affect. Changes in plasma membrane depolarization and elevated intracellular Na+, which compromised Na+-dependent nutrient transport, were documented. Deficits in nutrient deficit acted in turn to trigger the unfolded protein response and the amino acid response, leading ultimately to nutrient starvation and GIC cell death. Our results suggest new therapeutic targets to attack aggressive gliomas.
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16.
  • Nissling, Linnea, 1991, et al. (författare)
  • Effectiveness of and processes related to internet-delivered acceptance and commitment therapy for adolescents with anxiety disorders : a randomized controlled trial
  • 2023
  • Ingår i: RESEARCH IN PSYCHOTHERAPY-PSYCHOPATHOLOGY PROCESS AND OUTCOME. - : PAGEPress Publications. - 2499-7552 .- 2239-8031. ; 26:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Early access to evidence-based help is crucial for adolescents with anxiety disorders. Internet-delivered acceptance and commitment therapy (iACT) may offer adolescents increased access to care and more flexibility in engaging with treatment when and how they prefer. Process-based therapies, such as ACT, focus on the-oretically derived and empirically tested key mechanisms in treat-ment that enable change. This study aimed to investigate the effectiveness of iACT for adolescents with anxiety disorders. The study also assessed the relationship between psychological flexi-bility and treatment outcomes and the relationship between par-ticipating adolescents' and therapists' perceived alliance and treatment outcomes. This was a randomized controlled trial com-paring a 10-week intervention group with a wait-list control group. The 52 participants, aged 15 to 19, were recruited from all over Sweden. The treatment was effective in increasing quality of life and psychological flexibility, with moderate between-group effect sizes based on observed values. Changes in psychological flexibility was associated with changes in anxiety symptoms. The results further showed a statistically significant between-group difference in post-treatment diagnoses. No significant time per group interaction was found for anxiety symptoms, as both groups improved. Working alliance was rated as high by both participat-ing adolescents and therapists but showed no significant relation-ship with treatment outcomes. Participants found the treatment an acceptable intervention. This study shows promising results for iACT in treating adolescents with anxiety disorders. The results suggest the model of psychological flexibility as an important process of change in treatment outcomes. Future research should validate these findings in larger samples and clinical contexts.
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17.
  • Nissling, Linnea, 1991, et al. (författare)
  • Internet-delivered Acceptance and Commitment Therapy for adolescents with anxiety disorders
  • 2023
  • Ingår i: SweSRII – The 12th Swedish Congress on Internet Interventions..
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Background Anxiety disorders are common causes of mental illness in adolescents. Acceptance and Commitment Therapy delivered through internet (iACT) shows promising results for adults with anxiety disorders, but few studies exist on internet-delivered ACT programs for adolescents. Aims investigate the effectiveness of internet-delivered ACT for adolescents with anxiety disorders assess the relationship between psychological flexibility and treatment outcomes assess the relationship between adolescents and therapists perceived alliance and treatment outcomes. Population 52 adolescents aged 15 to 19 and from all over Sweden were recruited through advertisements on social media, in schools, primary health care centers and outpatient psychiatric clinics and were assessed by the diagnostic interview M.I.N.I Kid as meeting criteria for one or several anxiety diagnosis. Intervention An internet-delivered ACT treatment, “Ångesthjälpen UNG”, was developed (Psykologpartners, 2017). Outcomes The treatment increased the adolescents’ self-rated quality of life and psychological flexibillity (moderate between-group effect sizes, d=.65 and d=.51) Post treatment assessment with M.I.N.I Kid showed diminished anxiety diagnoses No significant group difference was found for anxiety symptoms, as both groups improved Changes in psychological flexibility were associated with changes in anxiety symptoms Working alliance was rated as high by both adolescents and therapists but showed no significant relationship with treatment outcomes Take-home message This study shows promising results for internet-delivered ACT in treating adolescents with anxiety disorders. The results suggest the model of psychological flexibility as an important process of change in treatment outcomes. Future research should validate these findings in larger samples and in clinical contexts.
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18.
  • Schmidt, Linnéa, et al. (författare)
  • Case-specific potentiation of glioblastoma drugs by pterostilbene
  • 2016
  • Ingår i: Oncotarget. - : Impact Journals, LLC. - 1949-2553. ; 7:45, s. 73200-73215
  • Tidskriftsartikel (refereegranskat)abstract
    • Glioblastoma multiforme (GBM, astrocytoma grade IV) is the most common malignant primary brain tumor in adults. Addressing the shortage of effective treatment options for this cancer, we explored repurposing of existing drugs into combinations with potent activity against GBM cells. We report that the phytoalexin pterostilbene is a potentiator of two drugs with previously reported anti-GBM activity, the EGFR inhibitor gefitinib and the antidepressant sertraline. Combinations of either of these two compounds with pterostilbene suppress cell growth, viability, sphere formation and inhibit migration in tumor GBM cell (GC) cultures. The potentiating effect of pterostilbene was observed to a varying degree across a panel of 41 patient-derived GCs, and correlated in a case specific manner with the presence of missense mutation of EGFR and PIK3CA and a focal deletion of the chromosomal region 1p32. We identify pterostilbene-induced cell cycle arrest, synergistic inhibition of MAPK activity and induction of Thioredoxin interacting protein (TXNIP) as possible mechanisms behind pterostilbene's effect. Our results highlight a nontoxic stilbenoid compound as a modulator of anticancer drug response, and indicate that pterostilbene might be used to modulate two anticancer compounds in well-defined sets of GBM patients.
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19.
  • Stjärngrim, Jessica, et al. (författare)
  • Post-endoscopy colorectal cancer after colectomy in inflammatory bowel disease patients : a population-based register study
  • 2023
  • Ingår i: European Journal of Gastroenterology and Hepathology. - : Lippincott Williams & Wilkins. - 0954-691X .- 1473-5687. ; 35:3, s. 288-293
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Long-standing inflammatory bowel disease (IBD) colitis is an indication for endoscopic surveillance. Postcolonoscopy colorectal cancer (PCCRC), cancer detected after a negative colonoscopy, is a quality indicator for colonoscopy. In analogy with PCCRC, we aimed to assess postendoscopy CRC (PECRC) in individuals with IBD who had undergone colectomy.Methods: This register study included Swedish adults with an IBD diagnosis who had undergone colectomy and later were examined by either colonoscopy or sigmoidoscopy during 2001-2012. The final study population had a CRC diagnosis within 36 months of the index examination. Poisson regression was used to assess the relative risks (RR) of PECRC.Results: A total of 33 individuals, 12 with an ileorectal anastomosis and 21 with a rectal remnant, had a CRC diagnosis within 36 months of the index endoscopy. Eleven cancers were detected as CRCs, and 22 (67%) were PECRCs. Compared with individuals aged >70 years, individuals aged <30 years had an RR of 3.1 (P = 0.054) and individuals aged 30-50 years had a RR of 2.6 (P = 0.030). A longer interval between colectomy and index endoscopy (>10 vs. <10 years) was associated with a lower risk of PCCRC (RR = 0.5; P = 0.007). There was no significant difference between the risk for Crohn's disease vs. ulcerative colitis, or between ileorectal anastomosis and rectal remnant risks.Conclusions: Continuous surveillance of IBD patients after colectomy is important. In the postcolectomy context, PECRC may be used as a quality indicator.
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20.
  • Thorén, Matilda Munksgaard, et al. (författare)
  • Integrin α10, a novel therapeutic target in glioblastoma, regulates cell migration, proliferation, and survival
  • 2019
  • Ingår i: Cancers. - : MDPI AG. - 2072-6694. ; 11:4
  • Tidskriftsartikel (refereegranskat)abstract
    • New, effective treatment strategies for glioblastomas (GBMs), the most malignant and invasive brain tumors in adults, are highly needed. In this study, we investigated the potential of integrin α10Β1 as a therapeutic target in GBMs. Expression levels and the role of integrin α10Β1 were studied in patient-derived GBM tissues and cell lines. The effect of an antibody-drug conjugate (ADC), an integrin a10 antibody conjugated to saporin, on GBM cells and in a xenograft mouse model was studied. We found that integrin α10Β1 was strongly expressed in both GBM tissues and cells, whereas morphologically unaffected brain tissues showed only minor expression. Partial or no overlap was seen with integrins α3, α6, and α7, known to be expressed in GBM. Further analysis of a subpopulation of GBM cells selected for high integrin α10 expression demonstrated increased proliferation and sphere formation. Additionally, siRNA-mediated knockdown of integrin α10 in GBM cells led to decreased migration and increased cell death. Furthermore, the ADC reduced viability and sphere formation of GBM cells and induced cell death both in vitro and in vivo. Our results demonstrate that integrin α10Β1 has a functional role in GBM cells and is a novel, potential therapeutic target for the treatment of GBM.
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21.
  • Wee, Shimei, et al. (författare)
  • Selective Calcium Sensitivity in Immature Glioma Cancer Stem Cells
  • 2014
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Tumor-initiating cells are a subpopulation in aggressive cancers that exhibit traits shared with stem cells, including the ability to self-renew and differentiate, commonly referred to as stemness. In addition, such cells are resistant to chemo- and radiation therapy posing a therapeutic challenge. To uncover stemness-associated functions in glioma-initiating cells (GICs), transcriptome profiles were compared to neural stem cells (NSCs) and gene ontology analysis identified an enrichment of Ca2+ signaling genes in NSCs and the more stem-like (NSC-proximal) GICs. Functional analysis in a set of different GIC lines regarding sensitivity to disturbed homeostasis using A23187 and Thapsigargin, revealed that NSC-proximal GICs were more sensitive, corroborating the transcriptome data. Furthermore, Ca2+ drug sensitivity was reduced in GICs after differentiation, with most potent effect in the NSC-proximal GIC, supporting a stemness-associated Ca2+ sensitivity. NSCs and the NSC-proximal GIC line expressed a larger number of ion channels permeable to potassium, sodium and Ca2+. Conversely, a higher number of and higher expression levels of Ca2+ binding genes that may buffer Ca2+, were expressed in NSC-distal GICs. In particular, expression of the AMPA glutamate receptor subunit GRIA1, was found to associate with Ca2+ sensitive NSC-proximal GICs, and decreased as GICs differentiated along with reduced Ca2+ drug sensitivity. The correlation between high expression of Ca2+ channels (such as GRIA1) and sensitivity to Ca2+ drugs was confirmed in an additional nine novel GIC lines. Calcium drug sensitivity also correlated with expression of the NSC markers nestin (NES) and FABP7 (BLBP, brain lipid-binding protein) in this extended analysis. In summary, NSC-associated NES+/FABP7(+)/GRIA1(+) GICs were selectively sensitive to disturbances in Ca2+ homeostasis, providing a potential target mechanism for eradication of an immature population of malignant cells.
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