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Article ; Online: The hydatidiform mole.

Candelier, Jean-Jacques

Cell adhesion & migration

2016 Volume 10, Issue 1-2, Page(s) 226–235

Abstract: The hydatidiform mole (HM) is a placental pathology of androgenetic origin. Placental villi have an abnormal hyperproliferation event and hydropic degeneration. Three situations can be envisaged at its origin: 1. The destruction/expulsion of the female ... ...

Abstract	The hydatidiform mole (HM) is a placental pathology of androgenetic origin. Placental villi have an abnormal hyperproliferation event and hydropic degeneration. Three situations can be envisaged at its origin: 1. The destruction/expulsion of the female pronucleus at the time of fertilization by 1 or 2 spermatozoa with the former being followed by an endoreplication of the male pronucleus leading to a complete hydatidiform mole (CHM) 2. A triploid zygote (fertilization by 2 spermatozoa) leading to a partial hydatidiform mole (PHM) but can also lead to haploid and diploid clones. The diploid clone may produce a normal fetus while the haploid clone after endoreplication generates a CHM 3. A nutritional defect during the differentiation of the oocytes or the deterioration of the limited oxygen pressure during the first trimester of gestation may lead to the formation of a HM. In countries with poor medical health care system, moles (mainly the CHM) can become invasive or, in rare cases, lead to gestational choriocarcinomas.
MeSH term(s)	Cytogenetics ; Epigenesis, Genetic ; Female ; Humans ; Hydatidiform Mole/epidemiology ; Hydatidiform Mole/genetics ; Hydatidiform Mole/pathology ; Pregnancy
Language	English
Publishing date	2016--03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1933-6926
ISSN (online)	1933-6926
DOI	10.1080/19336918.2015.1093275
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Idiopathic nephrotic syndrome and serum permeability factors: a molecular jigsaw puzzle.

Candelier, Jean-Jacques / Lorenzo, Hans-Kristian

Cell and tissue research

2019 Volume 379, Issue 2, Page(s) 231–243

Abstract: Nephrotic syndrome is traditionally defined using the triad of edema, hypoalbuminemia, and proteinuria, but this syndrome is very heterogeneous and difficult to clarify. Its idiopathic form (INS) is probably the most harmful and essentially comprises two ...

Abstract	Nephrotic syndrome is traditionally defined using the triad of edema, hypoalbuminemia, and proteinuria, but this syndrome is very heterogeneous and difficult to clarify. Its idiopathic form (INS) is probably the most harmful and essentially comprises two entities: minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). We will consider some hypotheses regarding the mechanisms underlying INS: (i) the presence of several glomerular permeability factors in the sera of patients that alter the morphology and function of podocytes leading to proteinuria, (ii) the putative role of immune cells. Thanks to recent data, our understanding of these disorders is evolving towards a more multifactorial origin. In this context, circulating factors may be associated according to sequential kinetic mechanisms or micro-environmental changes that need to be determined. In addition, the resulting proteinuria may trigger more proteinuria enhancing the glomerular destabilization.
MeSH term(s)	Autoantibodies/blood ; Glomerulosclerosis, Focal Segmental/blood ; Humans ; Kidney Glomerulus/pathology ; Nephrotic Syndrome/blood ; Permeability ; Proteinuria/blood
Chemical Substances	Autoantibodies
Language	English
Publishing date	2019-12-17
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-019-03147-y
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Article ; Online: Syndrome néphrotique idiopathique et facteurs circulants - Une Arlésienne ?

Lorenzo, Hans-Kristian / Candelier, Jean-Jacques

Medecine sciences : M/S

2019 Volume 35, Issue 8-9, Page(s) 659–666

Abstract: The renal filtration is ensured by the kidney glomeruli selective for filtering the blood. The main actor of the glomerular filter is the podocyte whose interlaced pedicels bear protein complexes (nephrin, podocin, etc.) creating a molecular sieve (slit ... ...

Title translation	Idiopathic nephrotic syndrome: une Arlésienne?
Abstract	The renal filtration is ensured by the kidney glomeruli selective for filtering the blood. The main actor of the glomerular filter is the podocyte whose interlaced pedicels bear protein complexes (nephrin, podocin, etc.) creating a molecular sieve (slit diaphragm) to achieve the filtration. Alterations of these podocytes lead to massive proteinuria, which characterizes the nephrotic syndrome. The idiopathic form is one of the most malignant and essentially comprises two entities: minimal change disease and focal segmental glomerulosclerosis. Many observations indicated that (1) immune cells are involved and that (2) there are several permeability factors in the blood that affect the morphology and function of podocytes (slit diaphragm with fractional foot processes fusion/effacement). Evidence for a permeability factor was chiefly derived from remission of proteinuria observed after implantation of a kidney with FSGS in healthy recipients or with other kidney diseases. Today, we are moving towards a multifactorial conception of the nephrotic syndrome where all these barely known factors could be associated according to a sequential kinetic mechanism that needs to be determined.
MeSH term(s)	Blood Cells/physiology ; Blood Proteins/adverse effects ; Blood Proteins/physiology ; Glomerulosclerosis, Focal Segmental/blood ; Glomerulosclerosis, Focal Segmental/complications ; Glomerulosclerosis, Focal Segmental/physiopathology ; Humans ; Kidney/pathology ; Kidney/physiology ; Kidney Glomerulus/pathology ; Kidney Glomerulus/physiology ; Nephrotic Syndrome/blood ; Nephrotic Syndrome/etiology ; Nephrotic Syndrome/physiopathology ; Podocytes/pathology ; Podocytes/physiology ; Proteinuria/blood ; Proteinuria/complications ; Proteinuria/physiopathology ; Risk Factors
Chemical Substances	Blood Proteins
Language	French
Publishing date	2019-09-18
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2019128
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Article ; Online: La môle hydatiforme complète.

Candelier, Jean-Jacques

Medecine sciences : M/S

2015 Volume 31, Issue 10, Page(s) 861–868

Abstract: The battle of the sexes begins in the zygote" W. Reik and J. Walter. Complete hydatidiform mole (CHM) is a pathology of the placenta with androgenetic diploid origin (chromosomes only from paternal origin). Placental villi present an abnormal ... ...

Title translation	Complete hydatidiform mole.
Abstract	"The battle of the sexes begins in the zygote" W. Reik and J. Walter. Complete hydatidiform mole (CHM) is a pathology of the placenta with androgenetic diploid origin (chromosomes only from paternal origin). Placental villi present an abnormal hyperproliferation and hydropic degeneration associated with the absence of embryo. Three mechanisms can be envisaged at its origin: (1) destruction/expulsion of the female pronucleus at the time of fertilization by one or two spermatozoa, the former being followed by an endoreplication of the male pronucleus (homozygous mole), (2) a triploid zygote (fertilization by two spermatozoa) leading to a haploid and a diploid clones. The diploid clone may produce a normal fetus while the haploid clone, after endoreplication, generates a complete hydatidiform mole, (3) a nutritional defect during the differentiation of the oocytes of the female embryo that will affect the integrity and maturity of her oocytes during her adult life and lead to hydatidiform mole. In countries with a poor medical health care system, moles can be invasive or, in rare cases, lead to gestational choriocarcinomas.
MeSH term(s)	Adult ; Epigenesis, Genetic ; Female ; Humans ; Hydatidiform Mole/epidemiology ; Hydatidiform Mole/genetics ; Hydatidiform Mole/pathology ; Incidence ; Male ; Placenta/pathology ; Pregnancy ; Uterine Neoplasms/epidemiology ; Uterine Neoplasms/genetics ; Uterine Neoplasms/pathology
Language	French
Publishing date	2015-10
Publishing country	France
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20153110012
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Article ; Online: Roles of tetraspanins during trophoblast development: bioinformatics and new perspectives.

Desterke, Christophe / Dang, Julien / Lorenzo, Hans-Kristian / Candelier, Jean-Jacques

Cell and tissue research

2021 Volume 386, Issue 1, Page(s) 157–171

Abstract: Tetraspanins are a superfamily of membrane proteins found in all eukaryotic organisms. They act as scaffold molecules that regulate the traffic and function of other membrane/signaling proteins, resulting in important downstream cellular consequences. ... ...

Abstract	Tetraspanins are a superfamily of membrane proteins found in all eukaryotic organisms. They act as scaffold molecules that regulate the traffic and function of other membrane/signaling proteins, resulting in important downstream cellular consequences. The aim of this work was to use transcriptomes and bioinformatics analysis to identify the tetraspanins (and their partners) involved in trophoblast differentiation. We built a protein-protein interaction network around tetraspanins which revealed that tetraspanins CD9, CD81, and CD82 show a specific expression during trophoblast differentiation. These proteins appeared to be interconnected and to recruit several membrane partners which include integrins, immune-related molecules, and a variety of receptors. During weeks 8 to 24, a CD9 expression trajectory was identified in extravillous trophoblasts, and a website was developed: ( https://extravillous.shinyapps.io/CD9humanEVT/ ). In conclusion, CD81 may, together with CD9 and CD82, be interconnected in controlling trophoblast invasion in the endometrium. CD9 expression trajectory in extravillous trophoblast between weeks 8 and 24 shows the involvement of CD9 in cell adhesion and migration.
MeSH term(s)	Animals ; Computational Biology/methods ; Female ; Tetraspanins/physiology ; Trophoblasts/physiology
Chemical Substances	Tetraspanins
Language	English
Publishing date	2021-07-19
Publishing country	Germany
Document type	Journal Article
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-021-03502-y
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Article ; Online: A bioinformatics transcriptome meta-analysis highlights the importance of trophoblast differentiation in the pathology of hydatidiform moles.

Desterke, Christophe / Slim, Rima / Candelier, Jean-Jacques

Placenta

2018 Volume 65, Page(s) 29–36

Abstract: Introduction: Hydatidiform mole (HM) is an aberrant human pregnancy with abnormal trophoblastic development, migration/invasion of the extravillous trophoblast in the decidua. These abnormalities are established in a hypoxic environment during the first ...

Abstract	Introduction: Hydatidiform mole (HM) is an aberrant human pregnancy with abnormal trophoblastic development, migration/invasion of the extravillous trophoblast in the decidua. These abnormalities are established in a hypoxic environment during the first trimester of gestation. Methods: Using text mining, we identified 72 unique genes that are linked to HM (HM-linked genes) that we studied by bioinformatic analysis in publicly available transcriptomes of primary chorionic villous cells (cytotrophoblast, syncytiotrophoblast, extravillous trophoblast, and arterial and venous endothelial) isolated from normal placentas or established trophoblastic cell lines cultured under different oxygen concentrations. Results: We show that the majority of HM-linked genes (75%) are involved in normal trophoblastic differentiation, arranged in clusters, and some of them are implicated in chorionic villous invasion or regulated by oxygen concentrations. Discussion: Our analysis integrates the various aspects of the pathophysiology of HM and highlights the importance of trophoblastic differentiation in this pathology.
MeSH term(s)	Cell Differentiation/genetics ; Cell Differentiation/physiology ; Computational Biology ; Female ; Gene Expression Profiling/methods ; Gene Regulatory Networks ; Humans ; Hydatidiform Mole/genetics ; Hydatidiform Mole/pathology ; Microarray Analysis ; Placenta/metabolism ; Placenta/pathology ; Pregnancy ; Transcriptome ; Trophoblasts/pathology ; Trophoblasts/physiology ; Uterine Neoplasms/genetics ; Uterine Neoplasms/pathology ; Validation Studies as Topic
Language	English
Publishing date	2018-04-07
Publishing country	Netherlands
Document type	Journal Article ; Meta-Analysis
ZDB-ID	603951-0
ISSN	1532-3102 ; 0143-4004
ISSN (online)	1532-3102
ISSN	0143-4004
DOI	10.1016/j.placenta.2018.04.002
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Article: Roles of tetraspanins during trophoblast development: bioinformatics and new perspectives

Desterke, Christophe / Dang, Julien / Lorenzo, Hans-Kristian / Candelier, Jean-Jacques

Cell and tissue research. 2021 Oct., v. 386, no. 1

2021

Abstract	Tetraspanins are a superfamily of membrane proteins found in all eukaryotic organisms. They act as scaffold molecules that regulate the traffic and function of other membrane/signaling proteins, resulting in important downstream cellular consequences. The aim of this work was to use transcriptomes and bioinformatics analysis to identify the tetraspanins (and their partners) involved in trophoblast differentiation. We built a protein–protein interaction network around tetraspanins which revealed that tetraspanins CD9, CD81, and CD82 show a specific expression during trophoblast differentiation. These proteins appeared to be interconnected and to recruit several membrane partners which include integrins, immune-related molecules, and a variety of receptors. During weeks 8 to 24, a CD9 expression trajectory was identified in extravillous trophoblasts, and a website was developed: (https://extravillous.shinyapps.io/CD9humanEVT/). In conclusion, CD81 may, together with CD9 and CD82, be interconnected in controlling trophoblast invasion in the endometrium. CD9 expression trajectory in extravillous trophoblast between weeks 8 and 24 shows the involvement of CD9 in cell adhesion and migration.
Keywords	Internet ; bioinformatics ; cell adhesion ; endometrium ; integrins ; protein-protein interactions ; research ; traffic ; transcriptome ; trophoblast
Language	English
Dates of publication	2021-10
Size	p. 157-171.
Publishing place	Springer Berlin Heidelberg
Document type	Article
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-021-03502-y
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis: A New Pathway in Chronic Kidney Disease?

Devocelle, Aurore / Lecru, Lola / Ferlicot, Sophie / Bessede, Thomas / Candelier, Jean-Jacques / Giron-Michel, Julien / François, Hélène

International journal of molecular sciences

2021 Volume 22, Issue 21

Abstract: Chronic kidney disease (CKD), secondary to renal fibrogenesis, is a public health burden. The activation of interstitial myofibroblasts and excessive production of extracellular matrix (ECM) proteins are major events leading to end-stage kidney disease. ... ...

Abstract	Chronic kidney disease (CKD), secondary to renal fibrogenesis, is a public health burden. The activation of interstitial myofibroblasts and excessive production of extracellular matrix (ECM) proteins are major events leading to end-stage kidney disease. Recently, interleukin-15 (IL-15) has been implicated in fibrosis protection in several organs, with little evidence in the kidney. Since endogenous IL-15 expression decreased in nephrectomized human allografts evolving toward fibrosis and kidneys in the unilateral ureteral obstruction (UUO) model, we explored IL-15's renoprotective role by pharmologically delivering IL-15 coupled or not with its soluble receptor IL-15Rα. Despite the lack of effects on myofibroblast accumulation, both IL-15 treatments prevented tubulointerstitial fibrosis (TIF) in UUO as characterized by reduced collagen and fibronectin deposition. Moreover, IL-15 treatments inhibited collagen and fibronectin secretion by transforming growth factor-β (TGF-β)-treated primary myofibroblast cultures, demonstrating that the antifibrotic effect of IL-15 in UUO acts, in part, through a direct inhibition of ECM synthesis by myofibroblasts. In addition, IL-15 treatments resulted in decreased expression of monocyte chemoattractant protein 1 (MCP-1) and subsequent macrophage infiltration in UUO. Taken together, our study highlights a major role of IL-15 on myofibroblasts and macrophages, two main effector cells in renal fibrosis, demonstrating that IL-15 may represent a new therapeutic option for CKD.
MeSH term(s)	Animals ; Chemokine CCL2/metabolism ; Collagen/biosynthesis ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Humans ; Interleukin-15/metabolism ; Interleukin-15/pharmacology ; Interleukin-15/therapeutic use ; Interleukin-15 Receptor alpha Subunit/metabolism ; Interleukin-15 Receptor alpha Subunit/therapeutic use ; Kidney/metabolism ; Kidney/pathology ; Mice, Inbred C57BL ; Myofibroblasts/drug effects ; Myofibroblasts/metabolism ; Nephrosclerosis/prevention & control ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/metabolism ; Ureteral Obstruction ; Mice
Chemical Substances	Chemokine CCL2 ; Interleukin-15 ; Interleukin-15 Receptor alpha Subunit ; Collagen (9007-34-5)
Language	English
Publishing date	2021-10-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222111698
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Article ; Online: IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis

Aurore Devocelle / Lola Lecru / Sophie Ferlicot / Thomas Bessede / Jean-Jacques Candelier / Julien Giron-Michel / Hélène François

International Journal of Molecular Sciences, Vol 22, Iss 11698, p

A New Pathway in Chronic Kidney Disease?

2021 Volume 11698

Abstract	Chronic kidney disease (CKD), secondary to renal fibrogenesis, is a public health burden. The activation of interstitial myofibroblasts and excessive production of extracellular matrix (ECM) proteins are major events leading to end-stage kidney disease. Recently, interleukin-15 (IL-15) has been implicated in fibrosis protection in several organs, with little evidence in the kidney. Since endogenous IL-15 expression decreased in nephrectomized human allografts evolving toward fibrosis and kidneys in the unilateral ureteral obstruction (UUO) model, we explored IL-15’s renoprotective role by pharmologically delivering IL-15 coupled or not with its soluble receptor IL-15Rα. Despite the lack of effects on myofibroblast accumulation, both IL-15 treatments prevented tubulointerstitial fibrosis (TIF) in UUO as characterized by reduced collagen and fibronectin deposition. Moreover, IL-15 treatments inhibited collagen and fibronectin secretion by transforming growth factor-β (TGF-β)-treated primary myofibroblast cultures, demonstrating that the antifibrotic effect of IL-15 in UUO acts, in part, through a direct inhibition of ECM synthesis by myofibroblasts. In addition, IL-15 treatments resulted in decreased expression of monocyte chemoattractant protein 1 (MCP-1) and subsequent macrophage infiltration in UUO. Taken together, our study highlights a major role of IL-15 on myofibroblasts and macrophages, two main effector cells in renal fibrosis, demonstrating that IL-15 may represent a new therapeutic option for CKD.
Keywords	chronic kidney disease ; fibrosis ; unilateral ureteral obstruction ; interleukin-15 ; myofibroblasts ; extracellular matrix ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Altered p16 and Bcl-2 expression reflects pathologic development in hydatidiform moles and choriocarcinoma.

Candelier, Jean-Jacques / Frappart, Lucien / Yadaden, Tarik / Poaty, Henriette / Picard, Jean-Yves / Prévot, Sophie / Coullin, Philippe

Pathology oncology research : POR

2012 Volume 19, Issue 2, Page(s) 217–227

Abstract: Abnormal trophoblast differentiation is the main cause of gestational trophoblast diseases in the case of hydatidiform moles and choriocarcinomas. Here we investigated the expression patterns of two gene products, p16 and Bcl-2, implicated in cell cycle ... ...

Abstract	Abnormal trophoblast differentiation is the main cause of gestational trophoblast diseases in the case of hydatidiform moles and choriocarcinomas. Here we investigated the expression patterns of two gene products, p16 and Bcl-2, implicated in cell cycle regulation and apoptosis, respectively, using immunohistochemistry during normal placenta differentiation, hydatidiform moles (partial, complete and invasive) and post-molar choriocarcinomas. The p16 protein shows a gradual expression in cytotrophoblast of normal villous, from a p16 weak proliferative phenotype to a p16 strong invasive phenotype reaching a maximum around 17 weeks of gestation. The expression pattern in cytotrophoblast was similar in moles in contrast to the villous mesenchyme of invasive moles where p16 was strongly expressed. Bcl-2 expression was syncytiotrophoblast specific in normal placenta and moles and increased gradually during normal differentiation. The results explain the persistence of normal and molar villous fragments during their development and their dramatic invasion in the uterine arteries in case of invasive moles. In choriocarcinomas the weak Bcl-2 expression is associated with weak p16 expression indicating a great apoptotic and proliferative potentials. The results suggest that strong p16 expression in the villous mesenchyme may be responsible in part of the morbidity of the moles, and the key of cancer progression in the choriocarcinomas would be a fast cell-cycle turnover.
MeSH term(s)	Cell Cycle/genetics ; Cell Differentiation/genetics ; Choriocarcinoma/genetics ; Choriocarcinoma/metabolism ; Choriocarcinoma/pathology ; Cyclin-Dependent Kinase Inhibitor p16/biosynthesis ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Disease Progression ; Female ; Gestational Trophoblastic Disease/genetics ; Gestational Trophoblastic Disease/metabolism ; Gestational Trophoblastic Disease/pathology ; Humans ; Hydatidiform Mole/genetics ; Hydatidiform Mole/metabolism ; Hydatidiform Mole/pathology ; Hydatidiform Mole, Invasive/genetics ; Hydatidiform Mole, Invasive/metabolism ; Hydatidiform Mole, Invasive/pathology ; Placenta/pathology ; Pregnancy ; Pregnancy Complications, Neoplastic/genetics ; Pregnancy Complications, Neoplastic/metabolism ; Pregnancy Complications, Neoplastic/pathology ; Proto-Oncogene Proteins c-bcl-2/biosynthesis ; Proto-Oncogene Proteins c-bcl-2/genetics ; Uterine Neoplasms/genetics ; Uterine Neoplasms/metabolism ; Uterine Neoplasms/pathology
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16 ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2012-10-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1375979-6
ISSN	1532-2807 ; 1219-4956
ISSN (online)	1532-2807
ISSN	1219-4956
DOI	10.1007/s12253-012-9572-2
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