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1.

001-es BibID:BIBFORM069060
Első szerző:Hortobágyi Tibor (patológus)
Cím:Pathophysiology of meningioma growth in pregnancy / Hortobágyi Tibor, Bencze János, Murnyák Balázs, Kouhsari Mahan C., Bognár László, Marko-Varga György
Dátum:2017
ISSN:2391-5463
Megjegyzések:Meningioma is among the most frequent brain tumours predominantly affecting elderly women. Epidemiological studies have shown that at the age of fertility the incidence is relatively low. The biological behaviour of meningioma in pregnancy is different from other meningiomas. The possible explanation is rooted in the complex physiological changes and hormonal differences during pregnancy. The increased meningioma growth observed in pregnancy is presumably the result of endocrine mechanisms. These include increase in progesterone, human placental lactogen (hPL) and prolactin (PRL) serum levels. In contrast, levels of pituitary hormones such as follicle stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG) produced by the placenta are decreasing in the mother prior to childbirth. Besides, vascular factors also play a crucial role. Peritumoral brain edema (PTBE), with well-known causative association with vascular endothelial growth factor (VEGF), can often be seen both with imaging and in the surgical specimens. Our aim is to assess published research on this topic including diagnostic and therapeutic guidelines, and to provide a clinically useful overview on the pathophysiology and biological behaviour of this rare complication of pregnancy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
meningioma
pregnancy
pathophysiology
endocrinology
hemodynamics
Megjelenés:Open Medicine 12 (2017), p. 195-200. -
További szerzők:Bencze János (1991-) (orvos) Murnyák Balázs (1986-) (molekuláris biológus, genetikus) Kouhsari, Mahan C. Bognár László (1958-) (idegsebész, gyermekidegsebész) Marko-Varga György
Pályázati támogatás:KTIA 13 NAP-A-II/7
MTA
GINOP-2.3.2-15-2016-00043
GINOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM071427
035-os BibID:(scopus)85022337933 (wos)000405898900001
Első szerző:Katona Frida
Cím:A melanoma és az agyi áttétképződés molekuláris háttere / Frida Katona, Balázs Murnyák, György Marko-Varga, Tibor Hortobágyi
Dátum:2017
ISSN:0030-6002 1788-6120
Tárgyszavak:Orvostudományok Klinikai orvostudományok magyar nyelvű folyóiratközlemény hazai lapban
folyóiratcikk
Megjelenés:ORVOSI HETILAP. - 158 : 28 (2017), p. 1083-1091. -
További szerzők:Murnyák Balázs (1986-) (molekuláris biológus, genetikus) Marko-Varga György Hortobágyi Tibor (1965-) (patológus)
Pályázati támogatás:KTIA_13_NAP-A-II/7
Egyéb
KTIA_13_ NAP-A-V/3
Egyéb
GINOP-2.3.2-15-2016-00043
GINOP
ÚNKP-16-3
ÚNKP
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM082384
035-os BibID:(cikkazonosító)104509 (WoS)000481565000014 (Scopus)85067554418
Első szerző:Mendonça, Clarissa Ferolla
Cím:Proteomic signatures of brain regions affected by tau pathology in early and late stages of Alzheimer's disease / Clarissa Ferolla Mendonça, Magdalena Kuras, Fábio César Sousa Nogueira, Indira Plá, Tibor Hortobágyi, László Csiba, Miklós Palkovits, Éva Renner, Péter Döme, György Marko-Varga, Gilberto B. Domont, Melinda Rezeli
Dátum:2019
ISSN:0969-9961
Megjegyzések:Background Alzheimer's disease (AD) is the most common neurodegenerative disorder. Depositions of amyloid β peptide (Aβ) and tau protein are among the major pathological hallmarks of AD. Aβ and tau burden follows predictable spatial patterns during the progression of AD. Nevertheless, it remains obscure why certain brain regions are more vulnerable than others; to investigate this and dysregulated pathways during AD progression, a mass spectrometry-based proteomics study was performed. Methods In total 103 tissue samples from regions early (entorhinal and parahippocampal cortices - medial temporal lobe (MTL)) and late affected (temporal and frontal cortices - neocortex) by tau pathology were subjected to label-free quantitative proteomics analysis. Results Considering dysregulated proteins during AD progression, the majority (625 out of 737 proteins) was region specific, while some proteins were shared between regions (101 proteins altered in two areas and 11 proteins altered in three areas). Analogously, many dysregulated pathways during disease progression were exclusive to certain regions, but a few pathways altered in two or more areas. Changes in protein expression indicate that synapse loss occurred in all analyzed regions, while translation dysregulation was preponderant in entorhinal, parahippocampal and frontal cortices. Oxidative phosphorylation impairment was prominent in MTL. Differential proteomic analysis of brain areas in health state (controls) showed higher metabolism and increased expression of AD-related proteins in the MTL compared to the neocortex. In addition, several proteins that differentiate brain regions in control tissue were dysregulated in AD. Conclusions This work provides the comparison of proteomic changes in brain regions affected by tau pathology at different stages of AD. Although we identified commonly regulated proteins and pathways during disease advancement, we found that the dysregulated processes are predominantly region specific. In addition, a distinct proteomic signature was found between MTL and neocortex in healthy subjects that might be related to AD vulnerability. These findings highlight the need for investigating AD's cascade of events throughout the whole brain and studies spanning more brain areas are required to better understand AD etiology and region vulnerability to disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Neurobiology of Disease. - 130 (2019), p. 1-19. -
További szerzők:Kuras, Magdalena Nogueira, Fábio César Sousa Plá, Indira Hortobágyi Tibor (1965-) (patológus) Csiba László (1952-) (neurológus, pszichiáter) Palkovits Miklós Renner Éva Döme Péter Marko-Varga György Domont, Gilberto B. Rezeli, Melinda
Pályázati támogatás:2017-1.2.1-NKP-2017-00002
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM068928
Első szerző:Murnyák Balázs (molekuláris biológus, genetikus)
Cím:PARP1 expression and its correlation with survival is tumour molecular subtype dependent in glioblastoma / Balázs Murnyák, Mahan C. Kouhsari, Rotem Hershkovitch, Bernadette Kálmán, György Marko-Varga, Álmos Klekner, Tibor Hortobágyi
Dátum:2017
ISSN:1949-2553
Megjegyzések:Overexpression of PARP1 exists in various cancers, including glioblastoma (GBM). Although PARP1 inhibition is a promising therapeutic target, no comprehensive study has addressed PARP1's expression characteristics and prognostic role regarding molecular heterogeneity in astrocytomas including GBM. Our aim was to evaluate PARP1's associations with survival, WHO grade, lineage specific markers, and GBM transcriptomic subtypes. We collected genomic and clinical data from the latest glioma datasets of The Cancer Genome Atlas and performed PARP1, ATRX, IDH1, and p53 immunohistochemistry on GBM tissue samples. We demonstrated that PARP1 gain and increased mRNA expression are characteristics of high-grade astrocytomas, particularly of Proneural and Classical GBM subtypes. Additionally, higher PARP1 levels exhibited an inverse correlation with patient survival (p<0.005) in the Classical subgroup. ATRX (p=0.006), and TP53 (p=0.015) mutations were associated with increased PARP1 expression and PARP1 protein level correlated with ATRX loss and p53 overexpression. Furthermore, higher PARP1 expression together with wildtype TP53 indicated shorter survival (p=0.039). Therefore, due to subtype specificity, PARP1 expression level and TP53 mutation status are reliable marker candidates to distinguish Proneural and Classical subtypes, with prognostic and therapeutic implications in GBM.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
glioma
glioblastoma
p53
PARP1
Megjelenés:Oncotarget. - 8 : 28 (2017), p. 46348-46362. -
További szerzők:Kouhsari, Mahan C. Hershkovitch, Rotem Kálmán Bernadette Marko-Varga György Klekner Álmos (1970-) (idegsebész) Hortobágyi Tibor (1965-) (patológus)
Pályázati támogatás:ÚNKP-16-3
Egyéb
KTIA_13_NAP-A-II/7
Egyéb
KTIA_13_NAP-A-V/3
Egyéb
AGR_PIAC_13-1-2013-0008
Egyéb
GINOP-2.3.2-15-2016-00043
GINOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

5.

001-es BibID:BIBFORM099463
035-os BibID:(cikkazonosító)750665 (WoS)000713446000001 (Scopus)85118795095
Első szerző:Velásquez, Erika
Cím:Topological Dissection of Proteomic Changes Linked to the Limbic Stage of Alzheimer's Disease / Erika Velásquez, Beáta Szeitz, Jeovanis Gil, Jimmy Rodriguez, Miklós Palkovits, Éva Renner, Tibor Hortobágyi, Péter Döme, Fábio CS. Nogueira, György Marko-Varga, Gilberto B. Domont, Melinda Rezeli
Dátum:2021
ISSN:1664-3224
Megjegyzések:Alzheimer's disease (AD) is a neurodegenerative disorder and the most common cause of dementia worldwide. In AD, neurodegeneration spreads throughout different areas of the central nervous system (CNS) in a gradual and predictable pattern, causing progressive memory decline and cognitive impairment. Deposition of neurofibrillary tangles (NFTs) in specific CNS regions correlates with the severity of AD and constitutes the basis for disease classification into different Braak stages (I-VI). Early clinical symptoms are typically associated with stages III-IV (i.e., limbic stages) when the involvement of the hippocampus begins. Histopathological changes in AD have been linked to brain proteome alterations, including aberrant posttranslational modifications (PTMs) such as the hyperphosphorylation of Tau. Most proteomic studies to date have focused on AD progression across different stages of the disease, by targeting one specific brain area at a time. However, in AD vulnerable regions, stage-specific proteomic alterations, including changes in PTM status occur in parallel and remain poorly characterized. Here, we conducted proteomic, phosphoproteomic, and acetylomic analyses of human postmortem tissue samples from AD (Braak stage III-IV, n=11) and control brains (n=12), covering all anatomical areas affected during the limbic stage of the disease (total hippocampus, CA1, entorhinal and perirhinal cortices). Overall, ~6000 proteins, ~9000 unique phosphopeptides and 221 acetylated peptides were accurately quantified across all tissues. Our results reveal significant proteome changes in AD brains compared to controls. Among others, we have observed the dysregulation of pathways related to the adaptive and innate immune responses, including several altered antimicrobial peptides (AMPs). Notably, some of these changes were restricted to specific anatomical areas, while others altered according to disease progression across the regions studied. Our data highlights the molecular heterogeneity of AD and the relevance of neuroinflammation as a major player in AD pathology. Data are available via ProteomeXchange with identifier PXD027173.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 12 (2021), p. 1-17. -
További szerzők:Szeitz Beáta Gil, Jeovanis Rodriguez, Jimmy Palkovits Miklós Renner Éva Hortobágyi Tibor (1965-) (patológus) Döme Péter Nogueira, Fábio César Sousa Marko-Varga György Domont, Gilberto B. Rezeli, Melinda
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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