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Article ; Online: A Prospective Study of Lipids in Adult Women With Turner Syndrome.

Sandahl, Kristian Juul / Just, Jesper / Erlandsen, Mogens / Mortensen, Kristian Havmand / Andersen, Niels Holmark / Gravholt, Claus Højbjerg

Journal of the Endocrine Society

2023 Volume 7, Issue 11, Page(s) bvad124

Abstract: Context: Turner syndrome (TS) is a rare genetic syndrome with an increased mortality, mainly attributed to cardiovascular disease.: Objective: This work aimed to investigate and correlate the lipid profile in adult women with TS to clinical ... ...

Abstract	Context: Turner syndrome (TS) is a rare genetic syndrome with an increased mortality, mainly attributed to cardiovascular disease. Objective: This work aimed to investigate and correlate the lipid profile in adult women with TS to clinical characteristics. Methods: A 12-year prospective cohort study, including 4 study visits, was conducted at a specialist hospital. A total of 102 women with TS qualified for inclusion. Excluding missing variables and participants lost to follow-up, 86 women (mean age 38.1 years; range, 18.4-62.1 years) were included in this study. Fifty-three women completed the study. Repeated-measurement analysis was performed, using total cholesterol (Total-C), low-density lipoprotein (LDL), triglycerides (TGs), and high-density lipoprotein (HDL) as outcome variables and age, karyotype, body mass index (BMI), treatment with statins, antidiabetics, and hormone replacement therapy as explanatory variables. Principal component analysis (PCA) and partial least squares (PLS) analysis were performed at the first study visit. Results: Hyperlipidemia was present in 30% of the TS cohort. Total-C increased with age (0.12 mmol/L/y; Conclusion: Hyperlipidemia is more prevalent in adult women with TS across adulthood compared to the background population. Total-C, LDL, TGs, and HDL were significantly associated with BMI characterizing the atherogenic profile in adult women with TS.
Language	English
Publishing date	2023-09-29
Publishing country	United States
Document type	Journal Article
ISSN	2472-1972
ISSN (online)	2472-1972
DOI	10.1210/jendso/bvad124
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Article ; Online: The testicular microvasculature in Klinefelter syndrome is immature with compromised integrity and characterized by excessive inflammatory cross-talk.

Johannsen, Emma B / Skakkebæk, Anne / Kalucka, Joanna M / Fedder, Jens / Gravholt, Claus H / Just, Jesper

Human reproduction (Oxford, England)

2023 Volume 38, Issue 12, Page(s) 2339–2349

Abstract: Study question: Does Klinefelter syndrome (KS) lead to a distinct gene expression pattern at single-cell level in the testes that could provide insight into the reported microvascular dysfunction in the testes?: Summary answer: A distinct gene ... ...

Abstract	Study question: Does Klinefelter syndrome (KS) lead to a distinct gene expression pattern at single-cell level in the testes that could provide insight into the reported microvascular dysfunction in the testes? Summary answer: A distinct gene expression pattern within microvascular-associated cells of males with KS suggests excessive endothelial cell (EC) activation, disorganized vessel formation, and the presence of immature vessels with compromised integrity. What is known already: Recent studies show that males with KS exhibit microvascular dysfunction in their testes, which affects blood flow and is associated with lower circulating levels of testosterone. Study design, size, duration: A comparative cross-sectional study of males with KS (n = 6), non-obstructive azoospermia (NOA) (n = 5), cryptozoospermia (n = 3), and controls (n = 15) was carried out. Participants/materials, setting, methods: We analyzed publicly available single-cell RNA sequencing data of testicular cells from males with KS, males with NOA, males with cryptozoospermia, and controls. The integration of these datasets allowed us to analyze gene expression profiles and communication patterns among the cell types within the testis and to identify capillary ECs to investigate changes at the microvascular level. Main results and the role of chance: Rooted in changes at the single-cell level, our study demonstrates a shift in gene expression forming the foundation for altered cellular communication, microvascular remodeling, and pro-inflammatory responses within the testes of males with KS. We identified genes that were dysregulated in capillary ECs from males with KS (Padj < 0.05). Specifically, the unique microvascular gene expression in males with KS indicated enhanced capillary EC activation and increased inflammatory cross-talk, leading to impaired vessel maturation and increased EC barrier permeability. Limitations, reasons for caution: Our study is constrained by an unbalanced design, with varying sample sizes and number of cells within each group. We acknowledge the restricted access to clinical information. In addition, our findings were deduced from changes in gene expression, which limits us to infer potential biological consequences arising from these alterations. Furthermore, the absence of a pre-pubertal age group limits the generalizability of our findings and warrants further investigation. Wider implications of the findings: This study offers novel insights into the testicular pathophysiology in KS and underscores the potential contribution of microvascular dysfunction to the hypogonadism and infertility observed in males with KS. While this study aims to better understand the microvascular dysfunction in KS, the precise connections to testosterone deficiency and testicular atrophy remain to be fully elucidated. Study funding/competing interest(s): A.S. was supported by the Independent Research Fund Denmark (0134-00130B). C.H.G. was supported by Novo Nordisk Foundation (NNF15OC0016474, NNF20OC0060610), 'Fonden til lægevidenskabens fremme', the Familien Hede Nielsen foundation and the Independent Research Fund Denmark (0134-00406A). E.B.J. was supported by Aarhus University and E.B.J. and C.H.G by the Independent Research Fund Denmark (2096-00165A). J.M.K. was supported by Lundbeckfonden (R307-2018-3667), Carlsberg Fonden (CF19-0687), Novo Nordisk Fonden (0073440) and Steno Diabetes Center Aarhus (SDCA). The authors declare no conflicts of interest. Trial registration number: N/A.
MeSH term(s)	Male ; Humans ; Testis ; Klinefelter Syndrome/genetics ; Klinefelter Syndrome/complications ; Oligospermia ; Cross-Sectional Studies ; Testosterone ; Microvessels
Chemical Substances	Testosterone (3XMK78S47O)
Language	English
Publishing date	2023-11-01
Publishing country	England
Document type	Journal Article
ZDB-ID	632776-x
ISSN	1460-2350 ; 0268-1161 ; 1477-741X
ISSN (online)	1460-2350
ISSN	0268-1161 ; 1477-741X
DOI	10.1093/humrep/dead224
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Article: The multi-omic landscape of sex chromosome abnormalities: current status and future directions.

Tallaksen, Helene Bandsholm Leere / Johannsen, Emma B / Just, Jesper / Viuff, Mette Hansen / Gravholt, Claus H / Skakkebæk, Anne

Endocrine connections

2023 Volume 12, Issue 9

Abstract: Sex chromosome abnormalities (SCAs) are chromosomal disorders with either a complete or partial loss or gain of sex chromosomes. The most frequent SCAs include Turner syndrome (45,X), Klinefelter syndrome (47,XXY), Trisomy X syndrome (47,XXX), and Double ...

Abstract	Sex chromosome abnormalities (SCAs) are chromosomal disorders with either a complete or partial loss or gain of sex chromosomes. The most frequent SCAs include Turner syndrome (45,X), Klinefelter syndrome (47,XXY), Trisomy X syndrome (47,XXX), and Double Y syndrome (47,XYY). The phenotype seen in SCAs is highly variable and may not merely be due to the direct genomic imbalance from altered sex chromosome gene dosage but also due to additive alterations in gene networks and regulatory pathways across the genome as well as individual genetic modifiers. This review summarizes the current insight into the genomics of SCAs. In addition, future directions of research that can contribute to decipher the genomics of SCA are discussed such as single-cell omics, spatial transcriptomics, system biology thinking, human-induced pluripotent stem cells, and animal models, and how these data may be combined to bridge the gap between genomics and the clinical phenotype.
Language	English
Publishing date	2023-08-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2668428-7
ISSN	2049-3614
ISSN	2049-3614
DOI	10.1530/EC-23-0011
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Article ; Online: Testosterone Replacement Therapy in Klinefelter Syndrome-Follow-up Study Associating Hemostasis and RNA Expression.

Chang, Simon / Just, Jesper / Skakkebæk, Anne / Johannsen, Emma B / Fedder, Jens / Gravholt, Claus H / Münster, Anna-Marie B

The Journal of clinical endocrinology and metabolism

2023 Volume 109, Issue 4, Page(s) 978–991

Abstract: Background: Men with Klinefelter syndrome (KS) develop hypergonadotropic hypogonadism, are in need of testosterone replacement therapy (TRT), and present with a more than 4-fold increased risk of thrombosis. TRT in KS has the potential to modify ... ...

Abstract	Background: Men with Klinefelter syndrome (KS) develop hypergonadotropic hypogonadism, are in need of testosterone replacement therapy (TRT), and present with a more than 4-fold increased risk of thrombosis. TRT in KS has the potential to modify thrombotic risk, but data are scarce. Aim: To assess effects of 18 months of TRT on hemostasis in KS and identify genes associated with the prothrombotic phenotype. Methods: Untreated and TRT-treated men with KS were included at baseline and matched to healthy controls. TRT was initiated in untreated KS and all groups were reassessed after 18 months of follow-up. Thrombin generation was evaluated with or without thrombomodulin, and fibrin clot lysis was evaluated by turbidity measurements. RNA expression was assessed in blood, fat, and muscle tissue of patients with TRT-treated KS and controls. Results: Thrombin generation with thrombomodulin was slightly increased in untreated KS, but overall KS was not associated with a hypercoagulable state. KS presented with fibrinolytic impairment associated with higher body fat and higher levels of fibrinogen. Eighteen months of TRT in KS was associated with a reduction in body fat and fibrinogen, attenuating the prothrombotic profile. The expression of ENPP4 was higher in men with KS and served as a key player among a group of genes associated with impaired fibrinolysis. Conclusion: KS is associated with a specific expression profile contributing to fibrinolytic impairment and increased thrombotic risk in the patients. TRT in patients with KS has the potential for alleviating the prothrombotic phenotype, in particular by reducing body fat and fibrinogen.
MeSH term(s)	Male ; Humans ; Klinefelter Syndrome/complications ; Klinefelter Syndrome/drug therapy ; Klinefelter Syndrome/genetics ; Follow-Up Studies ; Thrombomodulin/genetics ; Thrombomodulin/therapeutic use ; Thrombin/metabolism ; Hypogonadism/drug therapy ; Hypogonadism/genetics ; Hypogonadism/complications ; Thrombosis ; Testosterone/therapeutic use ; Hemostasis/genetics ; Fibrinogen ; RNA
Chemical Substances	Thrombomodulin ; Thrombin (EC 3.4.21.5) ; Testosterone (3XMK78S47O) ; Fibrinogen (9001-32-5) ; RNA (63231-63-0)
Language	English
Publishing date	2023-12-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad658
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Article: Extracellular Vesicles in Acute Stroke Diagnostics.

Stenz, Katrine Tang / Just, Jesper / Blauenfeldt, Rolf Ankerlund / Drasbek, Kim Ryun

Biomedicines

2020 Volume 8, Issue 8

Abstract: There is a large unmet need for fast and reliable diagnostics in several diseases. One such disease is stroke, where the efficacy of modern reperfusion therapies is highly time-dependent. Diagnosis of stroke and treatment initiation should be performed ... ...

Abstract	There is a large unmet need for fast and reliable diagnostics in several diseases. One such disease is stroke, where the efficacy of modern reperfusion therapies is highly time-dependent. Diagnosis of stroke and treatment initiation should be performed as soon as possible, and preferably before arrival at the stroke center. In recent years, several potential blood biomarkers for stroke have been evaluated, but without success. In this review, we will go into detail on the possibility of utilizing extracellular vesicles (EVs) released into the blood as novel biomarkers for stroke diagnostics. EVs are known to reflect the immediate state of the secreting cells and to be able to cross the blood-brain barrier, thus making them attractive as diagnostic biomarkers of brain diseases. Indeed, several studies have reported EV markers that enable differentiation between stroke patients and controls and, to a lesser extent, the ability to correctly classify the different stroke types. Most of the studies rely on the use of sophisticated and time-consuming methods to quantify specific subpopulations of the nanosized EVs. As these methods cannot be easily implemented in a rapid point of care (POC) test, technical developments followed by prospective clinical studies are needed.
Language	English
Publishing date	2020-07-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines8080248
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Article ; Online: The Changing Face of Turner Syndrome.

Gravholt, Claus H / Viuff, Mette / Just, Jesper / Sandahl, Kristian / Brun, Sara / van der Velden, Janielle / Andersen, Niels H / Skakkebaek, Anne

Endocrine reviews

2022 Volume 44, Issue 1, Page(s) 33–69

Abstract: Turner syndrome (TS) is a condition in females missing the second sex chromosome (45,X) or parts thereof. It is considered a rare genetic condition and is associated with a wide range of clinical stigmata, such as short stature, ovarian dysgenesis, ... ...

Abstract	Turner syndrome (TS) is a condition in females missing the second sex chromosome (45,X) or parts thereof. It is considered a rare genetic condition and is associated with a wide range of clinical stigmata, such as short stature, ovarian dysgenesis, delayed puberty and infertility, congenital malformations, endocrine disorders, including a range of autoimmune conditions and type 2 diabetes, and neurocognitive deficits. Morbidity and mortality are clearly increased compared with the general population and the average age at diagnosis is quite delayed. During recent years it has become clear that a multidisciplinary approach is necessary toward the patient with TS. A number of clinical advances has been implemented, and these are reviewed. Our understanding of the genomic architecture of TS is advancing rapidly, and these latest developments are reviewed and discussed. Several candidate genes, genomic pathways and mechanisms, including an altered transcriptome and epigenome, are also presented.
MeSH term(s)	Female ; Humans ; Diabetes Mellitus, Type 2/complications ; Endocrine System Diseases ; Infertility ; Turner Syndrome/diagnosis ; Turner Syndrome/genetics ; Turner Syndrome/complications
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/endrev/bnac016
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Article ; Online: Women With Turner Syndrome Are Both Estrogen and Androgen Deficient: The Impact of Hormone Replacement Therapy.

Viuff, Mette Hansen / Just, Jesper / Brun, Sara / Dam, Tine Vrist / Hansen, Mette / Melgaard, Lars / Hougaard, David M / Lappe, Michael / Gravholt, Claus Højbjerg

The Journal of clinical endocrinology and metabolism

2022 Volume 107, Issue 7, Page(s) 1983–1993

Abstract: Context: Women with Turner syndrome (TS) suffer from hypergonadotropic hypogonadism, causing a deficit in gonadal hormone secretion. As a consequence, these women are treated with estrogen from the age of 12 years, and later in combination with ... ...

Abstract	Context: Women with Turner syndrome (TS) suffer from hypergonadotropic hypogonadism, causing a deficit in gonadal hormone secretion. As a consequence, these women are treated with estrogen from the age of 12 years, and later in combination with progesterone. However, androgens have been given less attention. Objective: To assess sex hormone levels in women with TS, both those treated and those nontreated with hormone replacement therapy (HRT), and investigate the impact of HRT on sex hormone levels. Methods: At Aarhus University Hospital, 99 women with TS were followed 3 times from August 2003 to February 2010. Seventeen were lost during follow-up. Control group 1 consisted of 68 healthy age-matched control women seen once during this period. Control group 2 consisted of 28 young, eumenorrheic women sampled 9 times throughout the same menstrual cycle. Serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17β-estradiol, estrone sulfate, DHEAS, testosterone, free androgen index, androstenedione, 17-OH progesterone, and sex hormone-binding globulin (SHBG) were analyzed. Results: All androgens, 17-OH progesterone, and sex hormone-binding globulin (SHBG) were 30% to 50% lower in TS compared with controls (P < 0.01). FSH, LH, and estrone sulfate were more than doubled in women with TS compared with controls (P < 0.02). Using principal component analysis, we describe a positive correlation between women with TS receiving HRT, elevated levels of SHBG, and decreased levels of androgens. Conclusion: The sex hormone profile in TS reveals a picture of androgen deficiency, aggravated further by HRT. Conventional HRT does not normalize estradiol levels in TS.
MeSH term(s)	Androgens/deficiency ; Estradiol ; Estrogens/deficiency ; Female ; Follicle Stimulating Hormone ; Gonadal Steroid Hormones/therapeutic use ; Hormone Replacement Therapy ; Humans ; Luteinizing Hormone ; Progesterone/therapeutic use ; Sex Hormone-Binding Globulin/analysis ; Testosterone ; Turner Syndrome/drug therapy
Chemical Substances	Androgens ; Estrogens ; Gonadal Steroid Hormones ; Sex Hormone-Binding Globulin ; Testosterone (3XMK78S47O) ; Progesterone (4G7DS2Q64Y) ; Estradiol (4TI98Z838E) ; Luteinizing Hormone (9002-67-9) ; Follicle Stimulating Hormone (9002-68-0)
Language	English
Publishing date	2022-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgac167
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Article ; Online: Dosage of the pseudoautosomal gene SLC25A6 is implicated in QTc interval duration.

Skakkebæk, Anne / Kjær-Sørensen, Kasper / Matchkov, Vladimir V / Christensen, Lise-Lotte / Just, Jesper / Cömert, Cagla / Andersen, Niels Holmark / Oxvig, Claus / Gravholt, Claus Højbjerg

Scientific reports

2023 Volume 13, Issue 1, Page(s) 12089

Abstract: The genetic architecture of the QT interval, defined as the period from onset of depolarisation to completion of repolarisation of the ventricular myocardium, is incompletely understood. Only a minor part of the QT interval variation in the general ... ...

Abstract	The genetic architecture of the QT interval, defined as the period from onset of depolarisation to completion of repolarisation of the ventricular myocardium, is incompletely understood. Only a minor part of the QT interval variation in the general population has been linked to autosomal variant loci. Altered X chromosome dosage in humans, as seen in sex chromosome aneuploidies such as Turner syndrome (TS) and Klinefelter syndrome (KS), is associated with altered QTc interval (heart rate corrected QT), indicating that genes, located in the pseudoautosomal region 1 of the X and Y chromosomes may contribute to QT interval variation. We investigate the dosage effect of the pseudoautosomal gene SLC25A6, encoding the membrane ADP/ATP translocase 3 in the inner mitochondrial membrane, on QTc interval duration. To this end we used human participants and in vivo zebrafish models. Analyses in humans, based on 44 patients with KS, 44 patients with TS, 59 male and 22 females, revealed a significant negative correlation between SLC25A6 expression level and QTc interval duration. Similarly, downregulation of slc25a6 in zebrafish increased QTc interval duration with pharmacological inhibition of K
MeSH term(s)	Animals ; Female ; Humans ; Male ; Adenosine Triphosphate ; Electrocardiography ; Klinefelter Syndrome ; Long QT Syndrome/genetics ; Turner Syndrome ; X Chromosome ; Zebrafish/genetics ; Adenine Nucleotide Translocator 3
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; Adenine Nucleotide Translocator 3
Language	English
Publishing date	2023-07-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-38867-3
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Article ; Online: X chromosome dosage and the genetic impact across human tissues.

Viuff, Mette / Skakkebæk, Anne / Johannsen, Emma B / Chang, Simon / Pedersen, Steen Bønlykke / Lauritsen, Katrine Meyer / Pedersen, Mette Glavind Bülow / Trolle, Christian / Just, Jesper / Gravholt, Claus H

Genome medicine

2023 Volume 15, Issue 1, Page(s) 21

Abstract: Background: Sex chromosome aneuploidies (SCAs) give rise to a broad range of phenotypic traits and diseases. Previous studies based on peripheral blood samples have suggested the presence of ripple effects, caused by altered X chromosome number, ... ...

Abstract	Background: Sex chromosome aneuploidies (SCAs) give rise to a broad range of phenotypic traits and diseases. Previous studies based on peripheral blood samples have suggested the presence of ripple effects, caused by altered X chromosome number, affecting the methylome and transcriptome. Whether these alterations can be connected to disease-specific tissues, and thereby having clinical implication for the phenotype, remains to be elucidated. Methods: We performed a comprehensive analysis of X chromosome number on the transcriptome and methylome in blood, fat, and muscle tissue from individuals with 45,X, 46,XX, 46,XY, and 47,XXY. Results: X chromosome number affected the transcriptome and methylome globally across all chromosomes in a tissue-specific manner. Furthermore, 45,X and 47,XXY demonstrated a divergent pattern of gene expression and methylation, with overall gene downregulation and hypomethylation in 45,X and gene upregulation and hypermethylation in 47,XXY. In fat and muscle, a pronounced effect of sex was observed. We identified X chromosomal genes with an expression pattern different from what would be expected based on the number of X and Y chromosomes. Our data also indicate a regulatory function of Y chromosomal genes on X chromosomal genes. Fourteen X chromosomal genes were downregulated in 45,X and upregulated in 47,XXY, respectively, in all three tissues (AKAP17A, CD99, DHRSX, EIF2S3, GTPBP6, JPX, KDM6A, PP2R3B, PUDP, SLC25A6, TSIX, XIST, ZBED1, ZFX). These genes may be central in the epigenetic and genomic regulation of sex chromosome aneuploidies. Conclusion: We highlight a tissue-specific and complex effect of X chromosome number on the transcriptome and methylome, elucidating both shared and non-shared gene-regulatory mechanism between SCAs.
MeSH term(s)	Humans ; X Chromosome ; Sex Chromosome Aberrations ; Y Chromosome ; Phenotype ; Aneuploidy ; GTP-Binding Proteins ; Transcription Factors
Chemical Substances	GTPBP6 protein, human ; GTP-Binding Proteins (EC 3.6.1.-) ; ZBED1 protein, human ; Transcription Factors
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-023-01169-4
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Article ; Online: T-cell derived extracellular vesicles prime macrophages for improved STING based cancer immunotherapy.

Hansen, Aida S / Jensen, Lea S / Gammelgaard, Kristine R / Ryttersgaard, Kristoffer G / Krapp, Christian / Just, Jesper / Jønsson, Kasper L / Jensen, Pia B / Boesen, Thomas / Johansen, Mogens / Etzerodt, Anders / Deleuran, Bent W / Jakobsen, Martin R

Journal of extracellular vesicles

2023 Volume 12, Issue 8, Page(s) e12350

Abstract: A key phenomenon in cancer is the establishment of a highly immunosuppressive tumour microenvironment (TME). Despite advances in immunotherapy, where the purpose is to induce tumour recognition and hence hereof tumour eradication, the majority of ... ...

Abstract	A key phenomenon in cancer is the establishment of a highly immunosuppressive tumour microenvironment (TME). Despite advances in immunotherapy, where the purpose is to induce tumour recognition and hence hereof tumour eradication, the majority of patients applicable for such treatment still fail to respond. It has been suggested that high immunological activity in the tumour is essential for achieving effective response to immunotherapy, which therefore have led to exploration of strategies that triggers inflammatory pathways. Here activation of the stimulator of interferon genes (STING) signalling pathway has been considered an attractive target, as it is a potent trigger of pro-inflammatory cytokines and types I and III interferons. However, immunotherapy combined with targeted STING agonists has not yielded sustained clinical remission in humans. This suggests a need for exploring novel adjuvants to improve the innate immunological efficacy. Here, we demonstrate that extracellular vesicles (EVs), derived from activated CD4
MeSH term(s)	Humans ; T-Lymphocytes ; Extracellular Vesicles/metabolism ; Interferons/genetics ; Interferons/metabolism ; Immunotherapy ; Macrophages/metabolism ; Neoplasms/metabolism ; Tumor Microenvironment
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2023-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2683797-3
ISSN	2001-3078 ; 2001-3078
ISSN (online)	2001-3078
ISSN	2001-3078
DOI	10.1002/jev2.12350
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