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- Bone, B, et al.
(författare)
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Mechanism of contrast enhancement in breast lesions at MR imaging
- 1998
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Ingår i: Acta radiologica (Stockholm, Sweden : 1987). - : SAGE Publications. - 0284-1851 .- 1600-0455. ; 39:5, s. 494-500
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: the aim of the study was to explain why breast lesions are enhanced by contrast medium at MR imaging and to elucidate the histopathological basis for the overlap in the enhancement patterns of benign and malignant breast lesions Material and Methods: Ten invasive breast carcinomas and 10 benign breast lesions were selected for the study. of the 10 carcinomas, 5 showed a strong and early contrast enhancement, and 5 did not. of the 10 benign lesions, 5 showed a strong and early contrast enhancement, and 5 showed no enhancement. the following morphometric variables were evaluated: proliferation cell index of neoplastic parenchymal cells, S-phase fraction, nuclear ploidy analysed by image DNA-cytometry, microvessel density, and the percentage proportion of the interstitial area Results: Contrast enhancement was related to the proliferating activity of the hyperplastic or neoplastic parenchymal cells and was inversely correlated with the interstitial area in carcinomas as well as in benign tumours and non-neo-plastic lesions of the breast Conclusion: Morphometric variables play an important role in the general mechanism of MR contrast enhancement in examinations of the breast and explain the histopathological basis for the overlap in the enhancement patterns of benign and malignant breast lesions
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- Onieva, JL, et al.
(författare)
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High IGKC-Expressing Intratumoral Plasma Cells Predict Response to Immune Checkpoint Blockade
- 2022
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Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 23:16
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Tidskriftsartikel (refereegranskat)abstract
- Resistance to Immune Checkpoint Blockade (ICB) constitutes the current limiting factor for the optimal implementation of this novel therapy, which otherwise demonstrates durable responses with acceptable toxicity scores. This limitation is exacerbated by a lack of robust biomarkers. In this study, we have dissected the basal TME composition at the gene expression and cellular levels that predict response to Nivolumab and prognosis. BCR, TCR and HLA profiling were employed for further characterization of the molecular variables associated with response. The findings were validated using a single-cell RNA-seq data of metastatic melanoma patients treated with ICB, and by multispectral immunofluorescence. Finally, machine learning was employed to construct a prediction algorithm that was validated across eight metastatic melanoma cohorts treated with ICB. Using this strategy, we have unmasked a major role played by basal intratumoral Plasma cells expressing high levels of IGKC in efficacy. IGKC, differentially expressed in good responders, was also identified within the Top response-related BCR clonotypes, together with IGK variants. These results were validated at gene, cellular and protein levels; CD138+ Plasma-like and Plasma cells were more abundant in good responders and correlated with the same RNA-seq-defined fraction. Finally, we generated a 15-gene prediction model that outperformed the current reference score in eight ICB-treated metastatic melanoma cohorts. The evidenced major contribution of basal intratumoral IGKC and Plasma cells in good response and outcome in ICB in metastatic melanoma is a groundbreaking finding in the field beyond the role of T lymphocytes.
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- Parrado-Fernandez, C, et al.
(författare)
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Corrigendum
- 2019
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Ingår i: Journal of cellular and molecular medicine. - : Wiley. - 1582-4934 .- 1582-1838. ; 23:6, s. 4489-4489
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Rodriguez-Rodriguez, P, et al.
(författare)
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Corrigendum
- 2018
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Ingår i: Brain : a journal of neurology. - : Oxford University Press (OUP). - 1460-2156. ; 141:5, s. e43-
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Tidskriftsartikel (refereegranskat)
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- Tajeddinn, W., et al.
(författare)
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5-HT1B and other related serotonergic proteins are altered in APPswe mutation
- 2015
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940 .- 1872-7972. ; 594, s. 137-143
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Tidskriftsartikel (refereegranskat)abstract
- Serotonergic dysfunction is implicated in Alzheimer's disease (AD). In addition, reductions in brain of both monoamine synthesis and release have been reported. Serotonin 1B receptors (5-HT1B), along with serotonin transporter (SERT) are among the regulators of extracellular 5-HT levels. We investigated the effect of the familial AD APP (Amyloid precursor protein) K670N/M671L double mutation, APP Swedish mutation (APPswe), on the expression of 5-HT1B, SERT, MAOA, p11 and 5-HT and its metabolite 5-HIAA in SH-SY5Y human neuroblastoma cell line stably transfected with APPswe mutation. In addition, hippocampal expressions of 5-HT1B and SERT were assessed in wild type and transgenic mice expressing APPswe mutation (Tg2576) at different age groups. We found a reduction of 5-HT1B as well as SERT in both APPswe in vitro and ex vivo. P11 and 5HT were also reduced, whereas 5HT turnover and MAOA were increased. Our results indicate that APPswe induced decreased 5-HT1B expression and 5-HT release, as well as increased MAOA activity and 5-HT breakdown. Further studies to explore the detailed mechanism behind reduced 5-HT1B and SERT in AD and their clinical implications are needed.
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- Tajeddinn, W., et al.
(författare)
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Pharmacological Modulations of the Serotonergic System in a Cell-Model of Familial Alzheimer's Disease
- 2016
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Ingår i: Journal of Alzheimers Disease. - : IOS Press. - 1387-2877 .- 1875-8908. ; 53:1, s. 349-361
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Tidskriftsartikel (refereegranskat)abstract
- Serotonin (5-HT) plays a central role in the integrity of different brain functions. The 5-HT homeostasis is regulated by many factors, including serotonin transporter (SERT), monoamine oxidase enzyme (MAO), and several 5-HT receptors, including the 5-HT1B. There is little knowledge how the dynamics of this system is affected by the amyloid-beta (A beta) burden of Alzheimer's disease (AD) pathology. SH-SY5Y neuroblastoma cells transfected with the amyloid precursor protein (APP) gene containing the Swedish mutations causing familial AD (APPswe), were used as a model to explore the effect of A beta pathology on 5-HT1B and related molecules including the receptor adaptor protein (p11), SERT and MAOA gene expression, and MAOA activity after treatment with selective serotonin reuptake inhibitor (SSRI) (sertraline), and a 5-HT1B receptor antagonist. Sertraline led more than 70 fold increase of 5-HT1B gene expression (p < 0.001), an increased serotonin turnover in both APPswe and control cells and reduced intracellular serotonin levels by 75% in APPswe cells but not in controls (p > 0.05). Treatment with the 5-HT1B receptor antagonist increased SERT gene-expression in control cells but not in the APPswe cells. 5-HT and 5-HT1B antagonist treatment resulted in different p11 expression patterns in APPswe cells compared to controls. Although MAOA gene expression was not changed by APPswe overexpression, adding 5-HT lead to a significant increase in MAOA gene expression in APPswe but not control cells. These findings suggest that the sensitivity of the 5-HT1B receptor and related systems is affected by APPswe overexpression, with potential relevance for pharmacologic intervention in AD. This may at least partly explain the lack of effect of SSRIs in patients with AD and depression.
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