LIVIVO - Search results -

Search results

Result 1 - 10 of total 72

Search options

Article: Translation into Clinical Practice of the G1-G7 Molecular Subgroup Classification of Glioblastoma: Comprehensive Demographic and Molecular Pathway Profiling.

Georgescu, Maria-Magdalena

2024 Volume 16, Issue 2

Abstract: Glioblastoma is the most frequent and malignant primary neoplasm of the central nervous system. In a recent breakthrough study on a prospective Discovery cohort, I proposed the first all-inclusive molecular classification of glioblastoma into seven ... ...

Abstract	Glioblastoma is the most frequent and malignant primary neoplasm of the central nervous system. In a recent breakthrough study on a prospective Discovery cohort, I proposed the first all-inclusive molecular classification of glioblastoma into seven subgroups, G1-G7, based on MAPK pathway activation. New data from a WHO-grade-4 diffuse glioma prospective Validation cohort offers, in this study, an integrated demographic-molecular analysis of a 213-patient Combined cohort. Despite cohort differences in the median age and molecular subgroup distribution, all the prospectively-acquired cases from the Validation cohort mapped into one of the G1-G7 subgroups defined in the Discovery cohort. A younger age of onset, higher tumor mutation burden and expanded G1/EGFR-mutant and G3/NF1 glioblastoma subgroups characterized the glioblastomas from African American/Black relative to Caucasian/White patients. The three largest molecular subgroups were G1/EGFR, G3/NF1 and G7/Other. The fourth largest subgroup, G6/Multi-RTK, was detailed by describing a novel gene fusion
Language	English
Publishing date	2024-01-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers16020361
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article: Multi-Platform Classification of IDH-Wild-Type Glioblastoma Based on ERK/MAPK Pathway: Diagnostic, Prognostic and Therapeutic Implications.

Georgescu, Maria-Magdalena

Cancers

2021 Volume 13, Issue 18

Abstract: Glioblastoma is the most aggressive and frequent glioma in the adult population. Because current therapy regimens confer only minimal survival benefit, molecular subgrouping to stratify patient prognosis and therapy design is warranted. This study ... ...

Abstract	Glioblastoma is the most aggressive and frequent glioma in the adult population. Because current therapy regimens confer only minimal survival benefit, molecular subgrouping to stratify patient prognosis and therapy design is warranted. This study presents a multi-platform classification of glioblastoma by analyzing a large, ethnicity-inclusive 101-adult-patient cohort. It defines seven non-redundant IDH-wild-type glioblastoma molecular subgroups, G1-G7, corresponding to the upstream receptor tyrosine kinase (RTK) and RAS-RAF segment of the ERK/MAPK signal transduction pathway. These glioblastoma molecular subgroups are classified as G1/EGFR, G2/FGFR3, G3/NF1, G4/RAF, G5/PDGFRA, G6/Multi-RTK, and G7/Other. The comprehensive genomic analysis was refined by expression landscaping of all RTK genes, as well as of the major associated growth pathway mediators, and used to hierarchically cluster the subgroups. Parallel demographic, clinical, and histologic pattern analyses were merged with the molecular subgrouping to yield the first inclusive multi-platform classification for IDH-wild-type glioblastoma. This straightforward classification with diagnostic and prognostic significance may be readily used in neuro-oncological practice and lays the foundation for personalized targeted therapy approaches.
Language	English
Publishing date	2021-09-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13184532
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Novel neoplasms associated with syndromic pediatric medulloblastoma: integrated pathway delineation for personalized therapy.

Georgescu, Maria-Magdalena / Whipple, Stephen G / Notarianni, Christina M

Cell communication and signaling : CCS

2022 Volume 20, Issue 1, Page(s) 123

Abstract: Medulloblastoma is the most common pediatric embryonal brain tumor, and may occur in cancer predisposition syndromes. We describe novel associations of medulloblastoma with atypical prolactinoma and dural high-grade sarcoma in Li-Fraumeni syndrome (LFS), ...

Abstract	Medulloblastoma is the most common pediatric embryonal brain tumor, and may occur in cancer predisposition syndromes. We describe novel associations of medulloblastoma with atypical prolactinoma and dural high-grade sarcoma in Li-Fraumeni syndrome (LFS), and epidural desmoid fibromatosis in familial adenomatous polyposis (FAP)/Turcot syndrome. Genomic analysis showing XRCC3 alterations suggested radiotherapy as contributing factor to the progression of LFS-associated medulloblastoma, and demonstrated different mechanisms of APC inactivation in the FAP-associated tumors. The integrated genomic-transcriptomic analysis uncovered the growth pathways driving tumorigenesis, including the prolactin-prolactin receptor (PRLR) autocrine loop and Shh pathway in the LFS-associated prolactinoma and medulloblastoma, respectively, the Wnt pathway in both FAP-associated neoplasms, and the TGFβ and Hippo pathways in the soft tissue tumors, regardless of germline predisposition. In addition, the comparative analysis of paired syndromic neoplasms revealed several growth pathways susceptible to therapeutic intervention by PARP, PRLR, and selective receptor tyrosine kinase (RTK) inhibitors. These could target the defective DNA damage repair in the LFS-associated medulloblastoma, the prolactin autocrine loop in the atypical prolactinoma, the EPHA3/7 and ALK overexpression in the FAP-associated medulloblastoma, and the multi-RTK upregulation in the soft tissue neoplasms. This study presents the spatiotemporal evolution of novel neoplastic associations in syndromic medulloblastoma, and discusses the post-radiotherapy risk for secondary malignancies in syndromic pediatric patients, with important implications for the biology, diagnosis, and therapy of these tumors. Video Abstract.
MeSH term(s)	Adenomatous Polyposis Coli/genetics ; Adenomatous Polyposis Coli/pathology ; Cerebellar Neoplasms/genetics ; Child ; Humans ; Medulloblastoma/genetics ; Medulloblastoma/pathology ; Pituitary Neoplasms ; Prolactin ; Prolactinoma
Chemical Substances	Prolactin (9002-62-4)
Language	English
Publishing date	2022-08-17
Publishing country	England
Document type	Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-022-00930-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Genetic and histologic spatiotemporal evolution of recurrent, multifocal, multicentric and metastatic glioblastoma.

Georgescu, Maria-Magdalena / Olar, Adriana

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 10

Abstract: Glioblastoma is the most frequent and aggressive primary brain tumor, characterized by extensive brain invasion and rarely, systemic metastases. The pathogenesis of metastatic glioblastoma is largely unknown. We present the first integrated clinical/ ... ...

Abstract	Glioblastoma is the most frequent and aggressive primary brain tumor, characterized by extensive brain invasion and rarely, systemic metastases. The pathogenesis of metastatic glioblastoma is largely unknown. We present the first integrated clinical/histologic/genetic analysis of 5 distinct brain and lung foci from a unique case of recurrent, multifocal, multicentric and metastatic glioblastoma. The initial right frontotemporal gliosarcoma received standard surgical/chemoradiation therapy and recurred 1.5 years later, co-occurring with three additional masses localized to the ipsilateral temporal lobe, cerebellum and lung. Synchronous metastatic lung carcinoma was suspected in this long-term smoker patient with family history of cancer. However, glioblastoma was confirmed in all tumors, although with different morphologic patterns, including ependymomatous and epithelioid. Genomic profiling revealed a germline FANCD2 variant of unknown significance, and a 4-gene somatic mutation signature shared by all tumors, consisting of TERT promoter and PTEN, RB1 and TP53 tumor suppressor mutations. Additional GRIN2A and ATM heterozygous mutations were selected in the cerebellar and lung foci, but were variably present in the supratentorial foci, indicating reduced post-therapeutic genetic evolution in brain foci despite morphologic variability. Significant genetic drift characterized the lung metastasis, likely explaining the known resistance of circulating glioblastoma cells to systemic seeding. MET overexpression was detected in the initial gliosarcoma and lung metastasis, possibly contributing to invasiveness. This comprehensive analysis sheds light on the temporospatial evolution of glioblastoma and underscores the importance of genetic testing for diagnosis and personalized therapy.
MeSH term(s)	Brain/pathology ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Female ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Lung/pathology ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Lung Neoplasms/secondary ; Middle Aged ; Mutation ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology
Language	English
Publishing date	2020-02-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-0889-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Multiple Occipital Bone Lytic Lesions Containing Ectopic Cerebellar Parenchyma Mimicking Neoplasia.

Wild, Elizabeth / Sun, Hai / Georgescu, Maria-Magdalena

World neurosurgery

2020 Volume 138, Page(s) 115–119

Abstract: Background: Nonlethal neural tube defects are developmental malformations with complex pathogenesis usually manifested at birth or in childhood.: Case description: We report the case of a 61-year-old woman without significant previous clinical ... ...

Abstract	Background: Nonlethal neural tube defects are developmental malformations with complex pathogenesis usually manifested at birth or in childhood. Case description: We report the case of a 61-year-old woman without significant previous clinical history presenting for neck pain and stiffness. An extensive workup detected multiple lytic lesions within the occipital bone and cervical vertebrae, suspicious for multiple myeloma or metastatic disease. Surgical resection of the occipital bone lesions revealed ectopic cerebellar tissue, some containing folia with mature cortical lamination, and no evidence of malignancy. Conclusions: To our knowledge, this study describes the oldest individual presenting with ectopic cerebellar tissue and the only instance in which oncologic workup for malignancy was carried out prior to resection. It also proposes surgical resection as a diagnostic and curative approach for this complex basicranium and neural developmental defect, and discusses retinoic acid toxicity as a possible cause of its occurrence.
MeSH term(s)	Cerebellar Neoplasms/pathology ; Cerebellar Neoplasms/surgery ; Cerebellum/pathology ; Cerebellum/surgery ; Choristoma/diagnosis ; Choristoma/pathology ; Choristoma/surgery ; Diagnosis, Differential ; Female ; Humans ; Middle Aged ; Neck Pain/etiology ; Neurosurgical Procedures/methods ; Occipital Bone/pathology ; Occipital Bone/surgery ; Skull Neoplasms/diagnosis ; Skull Neoplasms/pathology ; Skull Neoplasms/surgery
Language	English
Publishing date	2020-03-06
Publishing country	United States
Document type	Case Reports
ZDB-ID	2534351-8
ISSN	1878-8769 ; 1878-8750
ISSN (online)	1878-8769
ISSN	1878-8750
DOI	10.1016/j.wneu.2020.02.164
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1159: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: PTEN Tumor Suppressor Network in PI3K-Akt Pathway Control.

Georgescu, Maria-Magdalena

Genes & cancer

2011 Volume 1, Issue 12, Page(s) 1170–1177

Abstract: The PI3K-Akt pathway is a major survival pathway activated in cancer. Efforts to develop targeted therapies have not been fully successful, mainly because of extensive internal intrapathway or external interpathway negative feedback loops or because of ... ...

Abstract	The PI3K-Akt pathway is a major survival pathway activated in cancer. Efforts to develop targeted therapies have not been fully successful, mainly because of extensive internal intrapathway or external interpathway negative feedback loops or because of networking between pathway suppressors. The PTEN tumor suppressor is the major brake of the pathway and a common target for inactivation in somatic cancers. This review will highlight the networking of PTEN with other inhibitors of the pathway, relevant to cancer progression. PTEN constitutes the main node of the inhibitory network, and a series of convergences at different levels in the PI3K-Akt pathway, starting from those with growth factor receptors, will be described. As PTEN exerts enzymatic activity as a phosphatidylinositol-3,4,5-trisphosphate (PIP(3)) phosphatase, thus opposing the activity of PI3K, the concerted actions to increase the availability of PIP(3) in cancer cells, relying either on other phosphoinositide enzymes or on the intrinsic regulation of PTEN activity by other molecules, will be discussed. In particular, the synergy between PTEN and the circle of its direct interacting proteins will be brought forth in an attempt to understand both the activation of the PI3K-Akt pathway and the connections with other parallel oncogenic pathways. The understanding of the interplay between the modulators of the PI3K-Akt pathway in cancer should eventually lead to the design of therapeutic approaches with increased efficacy in the clinic.
Language	English
Publishing date	2011-07-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2538519-7
ISSN	1947-6027 ; 1947-6019
ISSN (online)	1947-6027
ISSN	1947-6019
DOI	10.1177/1947601911407325
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs.

Georgescu, Maria-Magdalena / Islam, Mohammad Zahidul / Li, Yan / Traylor, James / Nanda, Anil

Acta neuropathologica communications

2021 Volume 9, Issue 1, Page(s) 69

Abstract: Prognostic molecular subgrouping of glioblastoma is an ongoing effort and the current classification includes IDH-wild-type and IDH-mutant entities, the latter showing significantly better prognosis. We performed a comparative integrated analysis of the ... ...

Abstract	Prognostic molecular subgrouping of glioblastoma is an ongoing effort and the current classification includes IDH-wild-type and IDH-mutant entities, the latter showing significantly better prognosis. We performed a comparative integrated analysis of the FGFR glioblastoma subgroup consisting of 5 cases from a prospective 101-patient-cohort. FGFR alterations included FGFR2-TACC2 and FGFR2 amplifications arising in a multifocal IDH-mutant glioblastoma with unexpected 2.5-month patient survival, novel FGFR3 carboxy-terminal duplication and FGFR3-TLN1 fusion, and two previously described FGFR3-TACC3 fusions. The FGFR2 tumors showed additional mutations in SERPINE1/PAI-1 and MMP16, as part of extensive extracellular matrix remodeling programs. Whole transcriptomic analysis revealed common proliferation but distinct morphogenetic gene expression programs that correlated with tumor histology. The kinase program revealed EPHA3, LTK and ALK receptor tyrosine kinase overexpression in individual FGFR tumors. Paradoxically, all FGFR-fused glioblastomas shared strong PI3K and MAPK pathway suppression effected by SPRY, DUSP and AKAP12 inhibitors, whereas the FGFR2-TACC2 tumor elicited also EGFR suppression by ERRFI1 upregulation. This integrated analysis outlined the proliferation and morphogenetic expression programs in FGFR glioblastoma, and identified four novel, clinically targetable FGFR2 and FGFR3 alterations that confer aggressive phenotype and trigger canonical pathway feedback inhibition, with important therapeutic implications.
MeSH term(s)	Aged ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Female ; Gene Amplification ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Male ; Middle Aged ; Oncogene Proteins, Fusion ; Phenotype ; Prognosis ; Prospective Studies ; Receptor, Fibroblast Growth Factor, Type 2/genetics ; Receptor, Fibroblast Growth Factor, Type 3/genetics ; Transcriptome
Chemical Substances	Oncogene Proteins, Fusion ; FGFR2 protein, human (EC 2.7.10.1) ; FGFR3 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1)
Language	English
Publishing date	2021-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-021-01170-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: NHERF1: molecular brake on the PI3K pathway in breast cancer.

Georgescu, Maria-Magdalena

Breast cancer research : BCR

2008 Volume 10, Issue 2, Page(s) 106

Abstract: The adaptor protein NHERF1/EBP50 (Na/H exchanger regulatory factor 1/ezrin-radixin-moesin-binding phosphoprotein 50) emerged recently as an important player in breast cancer progression. Consisting of two tandem PDZ domains linked to a carboxyl-terminal ... ...

Abstract	The adaptor protein NHERF1/EBP50 (Na/H exchanger regulatory factor 1/ezrin-radixin-moesin-binding phosphoprotein 50) emerged recently as an important player in breast cancer progression. Consisting of two tandem PDZ domains linked to a carboxyl-terminal ezrin-binding region, NHERF1 assembles macromolecular complexes at the apical membrane of epithelial cells in many epithelial tissues, including the mammary gland. Involved initially in trafficking and regulation of transmembrane ion transporters and G protein-coupled receptors, NHERF1 also couples molecules involved in cell growth, such as the platelet-derived growth factor receptor (PDGFR) and PTEN (phosphatase and tensin homolog deleted on chromosome 10). In the previous issue of Breast Cancer Research, Pan and colleagues show an inhibitory action of NHERF1 on the phosphoinositide-3 kinase (PI3K)/Akt pathway in breast cancer cells via interaction of NHERF1 with PTEN, the physiological antagonist of the PI3K. Additionally, they show that NHERF1 expression confers susceptibility to PDGFR pharmacological inhibition depending on the presence of PTEN tumor suppressor.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/enzymology ; Breast Neoplasms/metabolism ; Female ; Humans ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/metabolism ; Receptors, Platelet-Derived Growth Factor/metabolism ; Signal Transduction ; Sodium-Hydrogen Exchangers/metabolism
Chemical Substances	Biomarkers, Tumor ; Phosphoproteins ; Sodium-Hydrogen Exchangers ; sodium-hydrogen exchanger regulatory factor ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1) ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2008-04-18
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/bcr1992
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5494: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: NHERF1/EBP50 Suppresses Wnt-β-Catenin Pathway–Driven Intestinal Neoplasia

Maria-Magdalena Georgescu / Mihai Gagea / Gilbert Cote

Neoplasia: An International Journal for Oncology Research, Vol 18, Iss 8, Pp 512-

2016 Volume 523

Abstract: NHERF1/EBP50, an adaptor molecule that interacts with β-catenin, YAP, and PTEN, has been recently implicated in the progression of various human malignancies, including colorectal cancer. We report here that NHERF1 acts as a tumor suppressor in vivo for ... ...

Abstract	NHERF1/EBP50, an adaptor molecule that interacts with β-catenin, YAP, and PTEN, has been recently implicated in the progression of various human malignancies, including colorectal cancer. We report here that NHERF1 acts as a tumor suppressor in vivo for intestinal adenoma development. NHERF1 is highly expressed at the apical membrane of mucosa intestinal epithelial cells (IECs) and serosa mesothelial cells. NHERF1-deficient mice show overall longer small intestine and colon that most likely could be attributed to a combination of defects, including altered apical brush border of absorbtive IECs and increased number of secretory IECs. NHERF1 deficiency in ApcMin/+ mice resulted in significantly shorter animal survival due to markedly increased tumor burden. This resulted from a moderate increase of the overall tumor density, more pronounced in females than males, and a massive increase in the number of large adenomas in both genders. The analysis of possible pathways controlling tumor size showed upregulation of Wnt-β-catenin pathway, higher expression of unphosphorylated YAP, and prominent nuclear expression of cyclin D1 in NHERF1-deficient tumors. Similar YAP changes, with relative decrease of phosphorylated YAP and increase of nuclear YAP expression, were observed as early as the adenoma stages in the progression of human colorectal cancer. This study discusses a complex role of NHERF1 for intestinal morphology and presents indisputable evidence for its in vivo tumor suppressor function upstream of Wnt-β-catenin and Hippo-YAP pathways.
Keywords	Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Subject code	570
Language	English
Publishing date	2016-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: NHERF1/EBP50 Suppresses Wnt-β-Catenin Pathway-Driven Intestinal Neoplasia.

Georgescu, Maria-Magdalena / Gagea, Mihai / Cote, Gilbert

Neoplasia (New York, N.Y.)

2016 Volume 18, Issue 8, Page(s) 512–523

Abstract	NHERF1/EBP50, an adaptor molecule that interacts with β-catenin, YAP, and PTEN, has been recently implicated in the progression of various human malignancies, including colorectal cancer. We report here that NHERF1 acts as a tumor suppressor in vivo for intestinal adenoma development. NHERF1 is highly expressed at the apical membrane of mucosa intestinal epithelial cells (IECs) and serosa mesothelial cells. NHERF1-deficient mice show overall longer small intestine and colon that most likely could be attributed to a combination of defects, including altered apical brush border of absorbtive IECs and increased number of secretory IECs. NHERF1 deficiency in Apc(Min/+) mice resulted in significantly shorter animal survival due to markedly increased tumor burden. This resulted from a moderate increase of the overall tumor density, more pronounced in females than males, and a massive increase in the number of large adenomas in both genders. The analysis of possible pathways controlling tumor size showed upregulation of Wnt-β-catenin pathway, higher expression of unphosphorylated YAP, and prominent nuclear expression of cyclin D1 in NHERF1-deficient tumors. Similar YAP changes, with relative decrease of phosphorylated YAP and increase of nuclear YAP expression, were observed as early as the adenoma stages in the progression of human colorectal cancer. This study discusses a complex role of NHERF1 for intestinal morphology and presents indisputable evidence for its in vivo tumor suppressor function upstream of Wnt-β-catenin and Hippo-YAP pathways.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Adenoma/genetics ; Adenoma/metabolism ; Adenoma/pathology ; Animals ; Carcinoma/genetics ; Carcinoma/metabolism ; Carcinoma/pathology ; Cell Cycle Proteins ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Cyclin D1/metabolism ; Genes, APC ; Humans ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Mice ; Mice, Knockout ; Mutation ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Sodium-Hydrogen Exchangers/genetics ; Sodium-Hydrogen Exchangers/metabolism ; Tumor Burden ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Phosphoproteins ; Sodium-Hydrogen Exchangers ; Wnt Proteins ; Yap1 protein, mouse ; beta Catenin ; sodium-hydrogen exchanger regulatory factor ; Cyclin D1 (136601-57-5)
Language	English
Publishing date	2016-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2016.07.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5203: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito