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Article ; Online: Comprehensive analysis of human tissues reveals unique expression and localization patterns of HSF1 and HSF2.

Joutsen, Jenny / Pessa, Jenny C / Jokelainen, Otto / Sironen, Reijo / Hartikainen, Jaana M / Sistonen, Lea

2024 Volume 29, Issue 2, Page(s) 235–271

Abstract: Heat shock factors (HSFs) are the main transcriptional regulators of the evolutionarily conserved heat shock response. Beyond cell stress, several studies have demonstrated that HSFs also contribute to a vast variety of human pathologies, ranging from ... ...

Abstract	Heat shock factors (HSFs) are the main transcriptional regulators of the evolutionarily conserved heat shock response. Beyond cell stress, several studies have demonstrated that HSFs also contribute to a vast variety of human pathologies, ranging from metabolic diseases to cancer and neurodegeneration. Despite their evident role in mitigating cellular perturbations, the functions of HSF1 and HSF2 in physiological proteostasis have remained inconclusive. Here, we analyzed a comprehensive selection of paraffin-embedded human tissue samples with immunohistochemistry. We demonstrate that both HSF1 and HSF2 display distinct expression and subcellular localization patterns in benign tissues. HSF1 localizes to the nucleus in all epithelial cell types, whereas nuclear expression of HSF2 was limited to only a few cell types, especially the spermatogonia and the urothelial umbrella cells. We observed a consistent and robust cytoplasmic expression of HSF2 across all studied smooth muscle and endothelial cells, including the smooth muscle cells surrounding the vasculature and the high endothelial venules in lymph nodes. Outstandingly, HSF2 localized specifically at cell-cell adhesion sites in a broad selection of tissue types, such as the cardiac muscle, liver, and epididymis. To the best of our knowledge, this is the first study to systematically describe the expression and localization patterns of HSF1 and HSF2 in benign human tissues. Thus, our work expands the biological landscape of these factors and creates the foundation for the identification of specific roles of HSF1 and HSF2 in normal physiological processes.
MeSH term(s)	Humans ; Male ; DNA-Binding Proteins/metabolism ; Endothelial Cells/metabolism ; Heat Shock Transcription Factors ; Heat-Shock Proteins/metabolism ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; Heat Shock Transcription Factors ; Heat-Shock Proteins ; HSF2 protein, human (142297-91-4) ; Transcription Factors ; HSF1 protein, human
Language	English
Publishing date	2024-03-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1016/j.cstres.2024.03.001
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Article ; Online: Expression profiles of small non-coding RNAs in breast cancer tumors characterize clinicopathological features and show prognostic and predictive potential.

Kärkkäinen, Emmi / Heikkinen, Sami / Tengström, Maria / Kosma, Veli-Matti / Mannermaa, Arto / Hartikainen, Jaana M

Scientific reports

2022 Volume 12, Issue 1, Page(s) 22614

Abstract: Precision medicine approaches are required for more effective therapies for cancer. As small non-coding RNAs (sncRNAs) have recently been suggested as intriguing candidates for cancer biomarkers and have shown potential also as novel therapeutic targets, ...

Abstract	Precision medicine approaches are required for more effective therapies for cancer. As small non-coding RNAs (sncRNAs) have recently been suggested as intriguing candidates for cancer biomarkers and have shown potential also as novel therapeutic targets, we aimed at profiling the non-miRNA sncRNAs in a large sample set to evaluate their role in invasive breast cancer (BC). We used small RNA sequencing and 195 fresh-frozen invasive BC and 22 benign breast tissue samples to identify significant associations of small nucleolar RNAs, small nuclear RNAs, and miscellaneous RNAs with the clinicopathological features and patient outcome of BC. Ninety-six and five sncRNAs significantly distinguished (Padj < 0.01) invasive local BC from benign breast tissue and metastasized BC from invasive local BC, respectively. Furthermore, 69 sncRNAs significantly associated (Padj < 0.01) with the tumor grade, hormone receptor status, subtype, and/or tumor histology. Additionally, 42 sncRNAs were observed as candidates for prognostic markers and 29 for predictive markers for radiotherapy and/or tamoxifen response (P < 0.05). We discovered the clinical relevance of sncRNAs from each studied RNA type. By introducing new sncRNA biomarker candidates for invasive BC and validating the potential of previously described ones, we have guided the way for further research that is warranted for providing novel insights into BC biology.
MeSH term(s)	Humans ; Animals ; Female ; RNA, Small Untranslated/genetics ; RNA, Small Untranslated/metabolism ; Breast Neoplasms/genetics ; Prognosis ; Sequence Analysis, RNA ; Mammary Neoplasms, Animal
Chemical Substances	RNA, Small Untranslated
Language	English
Publishing date	2022-12-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-26954-w
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Article ; Online: The debatable presence of PIWI-interacting RNAs in invasive breast cancer.

Kärkkäinen, Emmi / Heikkinen, Sami / Tengström, Maria / Kosma, Veli-Matti / Mannermaa, Arto / Hartikainen, Jaana M

Cancer medicine

2021 Volume 10, Issue 11, Page(s) 3593–3603

Abstract: Numerous factors influence breast cancer (BC) prognosis, thus complicating the prediction of outcome. By identifying biomarkers that would distinguish the cases with poorer response to therapy already at the time of diagnosis, the rate of survival could ... ...

Abstract	Numerous factors influence breast cancer (BC) prognosis, thus complicating the prediction of outcome. By identifying biomarkers that would distinguish the cases with poorer response to therapy already at the time of diagnosis, the rate of survival could be improved. Lately, Piwi-interacting RNAs (piRNAs) have been introduced as potential cancer biomarkers, however, due to the recently raised challenges in piRNA annotations, further evaluation of piRNAs' involvement in cancer is required. We performed small RNA sequencing in 227 fresh-frozen breast tissue samples from the Eastern Finnish Kuopio Breast Cancer Project material to study the presence of piRNAs in BC and their associations with the clinicopathological features and outcome of BC patients. We observed the presence of three small RNAs annotated as piRNA database entries (DQ596932, DQ570994, and DQ571955) in our samples. The actual species of these RNAs however remain uncertain. All three small RNAs were upregulated in grade III tumors and DQ596932 additionally in estrogen receptor negative tumors. Furthermore, patients with estrogen receptor positive BC and higher DQ571955 had shorter relapse-free survival and poorer BC-specific survival, thus indicating DQ571955 as a candidate predictive marker for radiotherapy response in estrogen receptor positive BC. DQ596932 showed possible prognostic value in BC, whereas DQ570994 was identified as a candidate predictive marker for tamoxifen and chemotherapy response. These three small RNAs appear as candidate biomarkers for BC, which could after further investigation provide novel approaches for the treatment of therapy resistant BC. Overall, our results indicate that the prevalence of piRNAs in cancer is most likely not as comprehensive as has been previously thought.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/analysis ; Breast/chemistry ; Breast Neoplasms/chemistry ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Disease-Free Survival ; Female ; Humans ; Neoplasm Grading ; Prognosis ; RNA, Small Interfering/analysis ; Radiotherapy ; Receptors, Estrogen/analysis ; Sequence Analysis, RNA ; Tamoxifen/therapeutic use ; Treatment Outcome ; Up-Regulation
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; RNA, Small Interfering ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2021-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.3915
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Article: Circulating Cell-Free DNA Reflects the Clonal Evolution of Breast Cancer Tumors.

Kujala, Jouni / Hartikainen, Jaana M / Tengström, Maria / Sironen, Reijo / Auvinen, Päivi / Kosma, Veli-Matti / Mannermaa, Arto

Cancers

2022 Volume 14, Issue 5

Abstract: Liquid biopsy of cell-free DNA (cfDNA) is proposed as a potential method for the early detection of breast cancer (BC) metastases and following the clonal evolution of BC. Though the use of liquid biopsy is a widely discussed topic in the field, only a ... ...

Abstract	Liquid biopsy of cell-free DNA (cfDNA) is proposed as a potential method for the early detection of breast cancer (BC) metastases and following the clonal evolution of BC. Though the use of liquid biopsy is a widely discussed topic in the field, only a few studies have demonstrated such usage so far. We sequenced the DNA of matched primary tumor and metastatic sites together with the matched cfDNA samples from 18 Eastern Finnish BC patients and investigated how well cfDNA reflected the clonal evolution of BC interpreted from tumor DNA. On average, liquid biopsy detected 56.2 ± 7.2% of the somatic variants that were present either in the matched primary tumor or metastatic sites. Despite the high discordance observed between matched samples, liquid biopsy was found to reflect the clonal evolution of BC and identify novel driver variants and therapeutic targets absent from the tumor DNA. Tumor-specific somatic variants were detected in cfDNA at the time of diagnosis and 8.4 ± 2.4 months prior to detection of locoregional recurrence or distant metastases. Our results demonstrate that the sequencing of cfDNA may be used for the early detection of locoregional and distant BC metastases. Observed discordance between tumor DNA sequencing and liquid biopsy supports the parallel sequencing of cfDNA and tumor DNA to yield the most comprehensive overview for the genetic landscape of BC.
Language	English
Publishing date	2022-03-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14051332
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Article: MCF10CA Breast Cancer Cells Utilize Hyaluronan-Coated EV-Rich Trails for Coordinated Migration.

Aaltonen, Niina / Kyykallio, Heikki / Tollis, Sylvain / Capra, Janne / Hartikainen, Jaana M / Matilainen, Johanna / Oikari, Sanna / Rilla, Kirsi

Frontiers in oncology

2022 Volume 12, Page(s) 869417

Abstract: Invasion of tumor cells through the stroma is coordinated in response to migratory cues provided by the extracellular environment. One of the most abundant molecules in the tumor microenvironment is hyaluronan, a glycosaminoglycan known to promote many ... ...

Abstract	Invasion of tumor cells through the stroma is coordinated in response to migratory cues provided by the extracellular environment. One of the most abundant molecules in the tumor microenvironment is hyaluronan, a glycosaminoglycan known to promote many hallmarks of tumor progression, including the migratory potential of tumor cells. Strikingly, hyaluronan is also often found to coat extracellular vesicles (EVs) that originate from plasma membrane tentacles of tumor cells crucial for migration, such as filopodia, and are abundant in tumor niches. Thus, it is possible that hyaluronan and hyaluronan-coated EVs have a cooperative role in promoting migration. In this work, we compared the hyaluronan synthesis, EV secretion and migratory behavior of normal and aggressive breast cell lines from MCF10 series. Single live cell confocal imaging, electron microscopy and correlative light and electron microscopy experiments revealed that migrating tumor cells form EV-rich and hyaluronan -coated trails. These trails promote the pathfinding behavior of follower cells, which is dependent on hyaluronan. Specifically, we demonstrated that plasma membrane protrusions and EVs left behind by tumor cells during migration are strongly positive for CD9. Single cell tracking demonstrated a leader-follower behavior, which was significantly decreased upon removal of pericellular hyaluronan, indicating that hyaluronan promotes the pathfinding behavior of follower cells. Chick chorioallantoic membrane assays
Language	English
Publishing date	2022-04-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.869417
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Article ; Online: DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2.

Kaarijärvi, Roosa / Kaljunen, Heidi / Nappi, Lucia / Fazli, Ladan / Kung, Sonia H Y / Hartikainen, Jaana M / Paakinaho, Ville / Capra, Janne / Rilla, Kirsi / Malinen, Marjo / Mäkinen, Petri I / Ylä-Herttuala, Seppo / Zoubeidi, Amina / Wang, Yuzhuo / Gleave, Martin E / Hiltunen, Mikko / Ketola, Kirsi

Communications biology

2024 Volume 7, Issue 1, Page(s) 108

Abstract: Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer resistant to androgen receptor (AR) inhibitors. Our study unveils that AR suppresses the neuronal development protein ... ...

Abstract	Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer resistant to androgen receptor (AR) inhibitors. Our study unveils that AR suppresses the neuronal development protein dihydropyrimidinase-related protein 5 (DPYSL5), providing a mechanism for neuroendocrine transformation under androgen deprivation therapy. Our unique CRPC-NEPC cohort, comprising 135 patient tumor samples, including 55 t-NEPC patient samples, exhibits a high expression of DPYSL5 in t-NEPC patient tumors. DPYSL5 correlates with neuroendocrine-related markers and inversely with AR and PSA. DPYSL5 overexpression in prostate cancer cells induces a neuron-like phenotype, enhances invasion, proliferation, and upregulates stemness and neuroendocrine-related markers. Mechanistically, DPYSL5 promotes prostate cancer cell plasticity via EZH2-mediated PRC2 activation. Depletion of DPYSL5 decreases proliferation, induces G1 phase cell cycle arrest, reverses neuroendocrine phenotype, and upregulates luminal genes. In conclusion, DPYSL5 plays a critical role in regulating prostate cancer cell plasticity, and we propose the AR/DPYSL5/EZH2/PRC2 axis as a driver of t-NEPC progression.
MeSH term(s)	Male ; Humans ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Androgen Antagonists ; Prostate/pathology ; Hydrolases ; Microtubule-Associated Proteins ; Enhancer of Zeste Homolog 2 Protein/genetics
Chemical Substances	Androgen Antagonists ; DPYSL5 protein, human (EC 3.-) ; Hydrolases (EC 3.-) ; Microtubule-Associated Proteins ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43)
Language	English
Publishing date	2024-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-05741-x
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Article ; Online: High mutation burden of circulating cell-free DNA in early-stage breast cancer patients is associated with a poor relapse-free survival.

Kujala, Jouni / Hartikainen, Jaana M / Tengström, Maria / Sironen, Reijo / Kosma, Veli-Matti / Mannermaa, Arto

Cancer medicine

2020 Volume 9, Issue 16, Page(s) 5922–5931

Abstract: Background: High tumor mutation burden is shown to be associated with a poor clinical outcome. As the tumor-derived fraction of circulating cell-free DNA (cfDNA) is shown to reflect the genetic spectrum of the tumor, we examined whether the mutation ... ...

Abstract	Background: High tumor mutation burden is shown to be associated with a poor clinical outcome. As the tumor-derived fraction of circulating cell-free DNA (cfDNA) is shown to reflect the genetic spectrum of the tumor, we examined whether the mutation burden of cfDNA could be used to predict the clinical outcomes of early-stage breast cancer (BC) patients. Methods: We selected a set of 79 Finnish early-stage BC cases with a good prognosis based on traditional prognostic parameters but some of which still developed relapsed disease during follow-up. cfDNA was isolated from the serum collected at the time of diagnosis, sequenced, and compared to matched primary tumors, clinical parameters, and survival data. Results: High cfDNA mutation burden was associated with the poor relapse-free survival (RFS) (P = .016, HR = 2.23, 95% Cl 1.16-4.27) when patients were divided into high and low mutation burden according to the median number of somatic variants. A high discordance was observed between the matched tumor and cfDNA samples, thus highlighting the challenges related to the liquid biopsy of early-stage cancer cases. Despite the low number of detected tumor-specific variants, the presence of tumor-specific somatic variants in the cfDNA was associated with the poor RFS (P = .009, HR = 2.31, 95% Cl 1.23-4.31). Conclusions: Our results confirm previously observed challenges about the accuracy of liquid biopsy-based genotyping of early-stage cancers and support the parallel sequencing of tumor and cfDNA while also demonstrating how the presence of tumor-specific somatic variants and the high mutation burden in the cfDNA are both associated with the poor RFS, thus indicating the prognostic potential of liquid biopsy in the context of early-stage cancers.
MeSH term(s)	Adult ; Aged ; Breast Neoplasms/blood ; Breast Neoplasms/genetics ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Cell-Free Nucleic Acids/blood ; Cell-Free Nucleic Acids/genetics ; Circulating Tumor DNA/blood ; Circulating Tumor DNA/genetics ; Disease-Free Survival ; Female ; Finland ; Genotype ; Humans ; Liquid Biopsy ; Middle Aged ; Mutation ; Prognosis ; Sequence Analysis, DNA
Chemical Substances	Cell-Free Nucleic Acids ; Circulating Tumor DNA
Language	English
Publishing date	2020-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2045-7634
ISSN (online)	2045-7634
DOI	10.1002/cam4.3258
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Article ; Online: Predicting breast cancer risk using interacting genetic and demographic factors and machine learning.

Behravan, Hamid / Hartikainen, Jaana M / Tengström, Maria / Kosma, Veli-Matti / Mannermaa, Arto

Scientific reports

2020 Volume 10, Issue 1, Page(s) 11044

Abstract: Breast cancer (BC) is a multifactorial disease and the most common cancer in women worldwide. We describe a machine learning approach to identify a combination of interacting genetic variants (SNPs) and demographic risk factors for BC, especially factors ...

Abstract	Breast cancer (BC) is a multifactorial disease and the most common cancer in women worldwide. We describe a machine learning approach to identify a combination of interacting genetic variants (SNPs) and demographic risk factors for BC, especially factors related to both familial history (Group 1) and oestrogen metabolism (Group 2), for predicting BC risk. This approach identifies the best combinations of interacting genetic and demographic risk factors that yield the highest BC risk prediction accuracy. In tests on the Kuopio Breast Cancer Project (KBCP) dataset, our approach achieves a mean average precision (mAP) of 77.78 in predicting BC risk by using interacting genetic and Group 1 features, which is better than the mAPs of 74.19 and 73.65 achieved using only Group 1 features and interacting SNPs, respectively. Similarly, using interacting genetic and Group 2 features yields a mAP of 78.00, which outperforms the system based on only Group 2 features, which has a mAP of 72.57. Furthermore, the gene interaction maps built from genes associated with SNPs that interact with demographic risk factors indicate important BC-related biological entities, such as angiogenesis, apoptosis and oestrogen-related networks. The results also show that demographic risk factors are individually more important than genetic variants in predicting BC risk.
MeSH term(s)	Algorithms ; Breast Neoplasms/etiology ; Breast Neoplasms/genetics ; Databases, Factual ; Databases, Genetic ; Demography ; Epistasis, Genetic ; Female ; Genetic Predisposition to Disease ; Humans ; Machine Learning ; Polymorphism, Single Nucleotide ; Risk Factors
Language	English
Publishing date	2020-07-06
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/s41598-020-66907-9
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Article ; Online: M1 Macrophages Induce Protumor Inflammation in Melanoma Cells through TNFR-NF-κB Signaling.

Kainulainen, Kirsi / Takabe, Piia / Heikkinen, Sami / Aaltonen, Niina / de la Motte, Carol / Rauhala, Leena / Durst, Franziska C / Oikari, Sanna / Hukkanen, Taija / Rahunen, Eija / Ikonen, Ella / Hartikainen, Jaana M / Ketola, Kirsi / Pasonen-Seppänen, Sanna

The Journal of investigative dermatology

2022 Volume 142, Issue 11, Page(s) 3041–3051.e10

Abstract: The tumor microenvironment, with distinctive cell types and a complex extracellular matrix has a tremendous impact on cancer progression. In this study, we investigated the effects of proinflammatory (M1) and immunosuppressive (M2) macrophages on ... ...

Abstract	The tumor microenvironment, with distinctive cell types and a complex extracellular matrix has a tremendous impact on cancer progression. In this study, we investigated the effects of proinflammatory (M1) and immunosuppressive (M2) macrophages on hyaluronan (HA) matrix formation and inflammatory response in melanoma cells. Proinflammatory factors secreted from M1 macrophages stimulated the formation of a thick pericellular HA matrix in melanoma cells due to upregulation of HA synthase 2 (HAS2). HAS2 silencing reversed the effect of M1 conditioned medium on pericellular HA coat formation, and interestingly, it also partly downregulated the M1 conditioned medium‒induced upregulation of inflammation-related genes (IL1β, IL6), as did the inhibitors for TNFR and IKKγ. Gene set enrichment analysis revealed that genes related to inflammatory responses and TNF-α signaling via NF-κB are enriched in the M1 conditioned medium‒treated melanoma cells. Moreover, the expression of matrix metalloproteinase 9 and three-dimensional cell invasion were induced in these cells, whereas M2 macrophages had no effect on HA synthesis, inflammatory response, or invasion. Our results indicate that the activation of TNFR-NF-κB signaling in M1 conditioned medium‒treated cells leads to HAS2 upregulation, which associates with a protumor inflammatory and invasive phenotype of melanoma cells.
MeSH term(s)	Humans ; NF-kappa B/metabolism ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Hyaluronic Acid/metabolism ; Culture Media, Conditioned/pharmacology ; Culture Media, Conditioned/metabolism ; Interleukin-6/metabolism ; Macrophages/metabolism ; Inflammation/pathology ; Melanoma/pathology ; Tumor Microenvironment
Chemical Substances	NF-kappa B ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Tumor Necrosis Factor-alpha ; Hyaluronic Acid (9004-61-9) ; Culture Media, Conditioned ; Interleukin-6
Language	English
Publishing date	2022-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2022.04.024
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Article ; Online: Application of radiation omics in the development of adverse outcome pathway networks: an example of radiation-induced cardiovascular disease.

Azimzadeh, Omid / Moertl, Simone / Ramadan, Raghda / Baselet, Bjorn / Laiakis, Evagelia C / Sebastian, Soji / Beaton, Danielle / Hartikainen, Jaana M / Kaiser, Jan Christian / Beheshti, Afshin / Salomaa, Sisko / Chauhan, Vinita / Hamada, Nobuyuki

International journal of radiation biology

2022 Volume 98, Issue 12, Page(s) 1722–1751

Abstract: Background: Epidemiological studies have indicated that exposure of the heart to doses of ionizing radiation as low as 0.5 Gy increases the risk of cardiac morbidity and mortality with a latency period of decades. The damaging effects of radiation to ... ...

Abstract	Background: Epidemiological studies have indicated that exposure of the heart to doses of ionizing radiation as low as 0.5 Gy increases the risk of cardiac morbidity and mortality with a latency period of decades. The damaging effects of radiation to myocardial and endothelial structures and functions have been confirmed radiobiologically at high dose, but much less are known at low dose. Integration of radiation biology and epidemiology data is a recommended approach to improve the radiation risk assessment process. The adverse outcome pathway (AOP) framework offers a comprehensive tool to compile and translate mechanistic information into pathological endpoints which may be relevant for risk assessment at the different levels of a biological system. Omics technologies enable the generation of large volumes of biological data at various levels of complexity, from molecular pathways to functional organisms. Given the quality and quantity of available data across levels of biology, omics data can be attractive sources of information for use within the AOP framework. It is anticipated that radiation omics studies could improve our understanding of the molecular mechanisms behind the adverse effects of radiation on the cardiovascular system. In this review, we explored the available omics studies on radiation-induced cardiovascular disease (CVD) and their applicability to the proposed AOP for CVD. Results: The results of 80 omics studies published on radiation-induced CVD over the past 20 years have been discussed in the context of the AOP of CVD proposed by Chauhan et al. Most of the available omics data on radiation-induced CVD are from proteomics, transcriptomics, and metabolomics, whereas few datasets were available from epigenomics and multi-omics. The omics data presented here show great promise in providing information for several key events (KEs) of the proposed AOP of CVD, particularly oxidative stress, alterations of energy metabolism, extracellular matrix (ECM), and vascular remodeling. Conclusions: The omics data presented here shows promise to inform the various levels of the proposed AOP of CVD. However, the data highlight the urgent need of designing omics studies to address the knowledge gap concerning different radiation scenarios, time after exposure, and experimental models. This review presents the evidence to build a qualitative omics-informed AOP and provides views on the potential benefits and challenges in using omics data to assess risk-related outcomes.
MeSH term(s)	Humans ; Adverse Outcome Pathways ; Cardiovascular Diseases/etiology ; Proteomics/methods ; Metabolomics/methods ; Cardiovascular System
Language	English
Publishing date	2022-08-24
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.1080/09553002.2022.2110325
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