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Article ; Online: Corrigendum to 'p53 Reactivation by PRIMA-1Met (APR-246) sensitises V600E/KBRAF melanoma to vemurafenib'[Eur J of Cancer 55 (2016) 98-110].

Krayem, Mohammad / Journe, Fabrice / Wiedig, Murielle / Morandini, Renato / Najem, Ahmad / Salès, François / van Kempen, Leon C / Sibille, Catherine / Awada, Ahmad / Marine, Jean-Christophe / Ghanem, Ghanem

European journal of cancer (Oxford, England : 1990)

2022 Volume 175, Page(s) 336–338

Language	English
Publishing date	2022-09-24
Publishing country	England
Document type	Published Erratum
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2022.09.002
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Zs.A 456: 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)
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Article ; Online: Prominent role of cyclic adenosine monophosphate signalling pathway in the sensitivity of (WT)BRAF/(WT)NRAS melanoma cells to vemurafenib.

Krayem, Mohammad / Journe, Fabrice / Wiedig, Murielle / Morandini, Renato / Sales, François / Awada, Ahmad / Ghanem, Ghanem

European journal of cancer (Oxford, England : 1990)

2014 Volume 50, Issue 7, Page(s) 1310–1320

Abstract: Vemurafenib improves survival in patients with melanoma bearing the (V600E)BRAF mutation, but it did not show any benefit in clinical trials focusing on wild type tumours while it may well inhibit (WT)BRAF considering the dosage used and the ... ...

Abstract	Vemurafenib improves survival in patients with melanoma bearing the (V600E)BRAF mutation, but it did not show any benefit in clinical trials focusing on wild type tumours while it may well inhibit (WT)BRAF considering the dosage used and the bioavailability of the drug. As tumours may contain a mixture of mutant and wild type BRAF cells and this has been also put forward as a resistance mechanism, we aimed to evaluate the sensitivity/resistance of six, randomly selected, (WT)BRAF/(WT)NRAS lines to vemurafenib and found four sensitive. The sensitivity to the drug was accompanied by a potent inhibition of both phospho-ERK and phospho-AKT, and a significant induction of apoptosis while absent in lines with intrinsic or acquired resistance. Phospho-CRAF expression was low in all sensitive lines and high in resistant ones, and MEK inhibition can effectively potentiate the drug effect. A possible explanation for CRAF modulation is cyclic adenosine monophosphate (cAMP), a mediator of melanocortin receptor 1 (MC1R) signalling, since it can actually inhibit CRAF. Indeed, we measured cAMP and found that all four sensitive lines contained significantly higher constitutive cAMP levels than the resistant ones. Consequently, vemurafenib and cAMP stimulator combination resulted in a substantial synergistic effect in lines with both intrinsic and acquired resistance but only restricted to those where cAMP was effectively increased. The use of a cAMP agonist overcame such restriction. In conclusion, we report that (WT)BRAF/(WT)NRAS melanoma lines with low phospho-CRAF and high cAMP levels may be sensitive to vemurafenib and that CRAF inhibition through cAMP stimulation may overcome the resistance to the drug.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclic AMP/metabolism ; Cyclic AMP/physiology ; Drug Screening Assays, Antitumor/methods ; GTP Phosphohydrolases/physiology ; Genes, ras ; Humans ; Indoles/pharmacology ; Melanoma/drug therapy ; Melanoma/genetics ; Membrane Proteins/physiology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Signal Transduction/physiology ; Sulfonamides/pharmacology
Chemical Substances	Antineoplastic Agents ; Indoles ; Membrane Proteins ; Protein Kinase Inhibitors ; Sulfonamides ; vemurafenib (207SMY3FQT) ; Cyclic AMP (E0399OZS9N) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
Language	English
Publishing date	2014-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2014.01.021
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Zs.A 456: 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)
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Article ; Online: Sequential use of protein kinase inhibitors potentiates their toxicity to melanoma cells: a rationale to combine targeted drugs based on protein expression inhibition profiles.

Aftimos, Philippe G / Wiedig, Murielle / Langouo Fontsa, Mireille / Awada, Ahmad / Ghanem, Ghanem / Journe, Fabrice

International journal of oncology

2013 Volume 43, Issue 3, Page(s) 919–926

Abstract: Targeted therapy has shown high efficacy in the treatment of metastatic melanoma with impressive response rates. However, resistance appears after a few months, underlining the need for simultaneous multiple signalling pathway inhibition to provide a ... ...

Abstract	Targeted therapy has shown high efficacy in the treatment of metastatic melanoma with impressive response rates. However, resistance appears after a few months, underlining the need for simultaneous multiple signalling pathway inhibition to provide a durable benefit. The aim of our study was to evaluate the possible synergistic effect of various protein kinase inhibitor combinations targeting SRC, MEK, PI3K or JAK on the survival of representative melanoma cell lines with WTNRAS/WTBRAF and harbouring the most frequent mutations (Q61LNRAS/WTBRAF or WTNRAS/V600EBRAF). By comparing IC50s and protein inhibition profiles, cell exposure to a single inhibitor for 3 days (condition 1) showed that both WTBRAF lines were at least 15-fold more sensitive to SRC inhibition while V600EBRAF cells were 30-fold more sensitive to MEK inhibition, confirming that the latter cells are largely dependent on the MAPK pathway for growth. Concomitant treatment for 3 days (condition 2) revealed an antagonistic effect between SRC and JAK inhibitors as compared to treatment by each inhibitor alone in all 3 lines, supporting that both SRC and JAK stimulate the STAT pathway. Finally, sequential cell exposure to inhibitors by pre-treatment with a single effector at non-toxic but effective on target inhibition concentrations for 7 days followed by the addition of each of the other inhibitors for 3 days (condition 3) showed that MEK, PI3K or JAK inhibitor acted in synergy with the SRC inhibitor in both wild-type and Q61LNRAS cells, suggesting that the first inhibitor could activate the SRC/STAT compensatory signalling pathway. In conclusion, a treatment strategy consisting in a sequential use of targeted inhibitors to first render melanoma cells more dependent on alternative compensatory pathways that should subsequently be inhibited, may enhance efficacy. By contrast, concomitant exposure to various combinations of inhibitors at different concentrations failed to produce such effect, further supporting the importance of both the duration of cell exposure to inhibitors and their sequential use.
MeSH term(s)	Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Janus Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Molecular Targeted Therapy ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Protein Kinase Inhibitors/administration & dosage ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transcriptome/drug effects ; src-Family Kinases/antagonists & inhibitors
Chemical Substances	Protein Kinase Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Janus Kinases (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2013-09
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2013.2008
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Article ; Online: p53 Reactivation by PRIMA-1(Met) (APR-246) sensitises (V600E/K)BRAF melanoma to vemurafenib.

European journal of cancer (Oxford, England : 1990)

2016 Volume 55, Page(s) 98–110

Abstract: Intrinsic and acquired resistance of metastatic melanoma to (V600E/K)BRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway, represents a major clinical challenge. Given that p53 is capable of antagonising PI3K/ ... ...

Abstract	Intrinsic and acquired resistance of metastatic melanoma to (V600E/K)BRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway, represents a major clinical challenge. Given that p53 is capable of antagonising PI3K/AKT activation we hypothesised that pharmacological restoration of p53 activity may increase the sensitivity of BRAF-mutant melanoma to MAPK-targeted therapy and eventually delay and/or prevent acquisition of drug resistance. To test this possibility we exposed a panel of vemurafenib-sensitive and resistant (innate and acquired) (V600E/K)BRAF melanomas to a (V600E/K)BRAF inhibitor (vemurafenib) alone or in combination with a direct p53 activator (PRIMA-1(Met)/APR-246). Strikingly, PRIMA-1(Met) synergised with vemurafenib to induce apoptosis and suppress proliferation of (V600E/K)BRAF melanoma cells in vitro and to inhibit tumour growth in vivo. Importantly, this drug combination decreased the viability of both vemurafenib-sensitive and resistant melanoma cells irrespectively of the TP53 status. Notably, p53 reactivation was invariably accompanied by PI3K/AKT pathway inhibition, the activity of which was found as a dominant resistance mechanism to BRAF inhibition in our lines. From all various combinatorial modalities tested, targeting the MAPK and PI3K signalling pathways through p53 reactivation or not, the PRIMA-1(Met)/vemurafenib combination was the most cytotoxic. We conclude that PRIMA-1(Met) through its ability to directly reactivate p53 regardless of the mechanism causing its deactivation, and thereby dampen PI3K signalling, sensitises (V600E/K)BRAF-positive melanoma to BRAF inhibitors.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm ; Drug Synergism ; Genetic Predisposition to Disease ; Humans ; Indoles/pharmacology ; Male ; Melanoma/drug therapy ; Melanoma/enzymology ; Melanoma/genetics ; Melanoma/pathology ; Mice, Nude ; Molecular Targeted Therapy ; Mutation ; Phosphatidylinositol 3-Kinase/metabolism ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Quinuclidines/pharmacology ; Signal Transduction/drug effects ; Skin Neoplasms/drug therapy ; Skin Neoplasms/enzymology ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Sulfonamides/pharmacology ; Time Factors ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Vemurafenib ; Xenograft Model Antitumor Assays
Chemical Substances	Indoles ; Protein Kinase Inhibitors ; Quinuclidines ; Sulfonamides ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Vemurafenib (207SMY3FQT) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; eprenetapopt (Z41TGB4080)
Language	English
Publishing date	2016-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2015.12.002
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Article ; Online: Early expression of the Helicase-Like Transcription Factor (HLTF/SMARCA3) in an experimental model of estrogen-induced renal carcinogenesis

Laurent Guy / Leo Oberdan / Gerbaux Cécile / Wiedig Murielle / Ribaucour Fabrice / Nonclercq Denis / Debauve Gaël / Journé Fabrice / Belayew Alexandra / Toubeau Gérard

Molecular Cancer, Vol 5, Iss 1, p

2006 Volume 23

Abstract: Abstract Background The Helicase-Like Transcription Factor (HLTF/SMARCA3) belongs to the family of SWI/SNF proteins that use the energy of ATP hydrolysis to remodel chromatin in a variety of cellular processes. Several SWI/SNF genes are disrupted in ... ...

Abstract	Abstract Background The Helicase-Like Transcription Factor (HLTF/SMARCA3) belongs to the family of SWI/SNF proteins that use the energy of ATP hydrolysis to remodel chromatin in a variety of cellular processes. Several SWI/SNF genes are disrupted in cancer, suggesting a role of tumor suppressor. Similarly, the HLTF gene was recently found to be inactivated by hypermethylation in a number of advanced colon and gastric tumors. However, other evidences indicated a 20-fold HLTF overexpression in cell lines derived from various neoplasms (ovary, breast, cervix, kidney.). Results In the present study, we investigated HLTF expression by immunohistochemistry in a model of kidney tumors induced by continuous administration of diethylstilbestrol to male Syrian golden hamsters. A strong labeling was already detected in small tumor buds, making HLTF an early cancer marker in this model. Although every cell stained for HLTF at this early stage, the number of HLTF-positive cells decreased to 10% with cancer progression, and these positive cells were dispersed in the tumor mass. HLTF expression was conserved in the HKT-1097 cell line established from kidney tumors, but again only 10% of positive cells were found in xenografts produced by HKT-1097 cells in nude mice. Conclusion In conclusion, our data suggest that HLTF gene activation is linked to initial steps of carcinogenesis in this model and should be investigated in early stages of other neoplasms.
Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	570 ; 616
Language	English
Publishing date	2006-06-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Role of farnesoid X receptor (FXR) in the process of differentiation of bone marrow stromal cells into osteoblasts.

Id Boufker, Hichame / Lagneaux, Laurence / Fayyad-Kazan, Hussein / Badran, Bassam / Najar, Mehdi / Wiedig, Murielle / Ghanem, Ghanem / Laurent, Guy / Body, Jean-Jacques / Journé, Fabrice

Bone

2011 Volume 49, Issue 6, Page(s) 1219–1231

Abstract: Bone tissue contains bile acids which accumulate from serum and which can be released in large amounts in the bone microenvironment during bone resorption. However, the direct effects of bile acids on bone cells remain largely unexplored. Bile acids have ...

Abstract	Bone tissue contains bile acids which accumulate from serum and which can be released in large amounts in the bone microenvironment during bone resorption. However, the direct effects of bile acids on bone cells remain largely unexplored. Bile acids have been identified as physiological ligands of the farnesoid X receptor (FXR, NR1H4). In the present study, we have examined the effects of FXR activation/inhibition on the osteoblastic differentiation of human bone marrow stromal cells (BMSC). We first demonstrated the expression of FXR in BMSC and SaOS2 osteoblast-like cells, and observed that FXR activation by chenodeoxycholic acid (CDCA) or by farnesol (FOH) increases the activity of alkaline phosphatase and the calcification of the extracellular matrix. In addition, we observed that FXR agonists are able to stimulate the expression of osteoblast marker genes [bone sialoprotein (BSP), osteocalcin (OC), osteopontin (OPN) and alkaline phosphatase (ALP)] (FXR involvement validated by shRNA-induced gene silencing), as well as the DNA binding activity of the bone transcription factor RUNX2 (EMSA and ChIP assay). Importantly, we observed that nitrogen-containing bisphosphonates (BPs) inhibit the basal osteoblastic differentiation of BMSC, possibly through suppression of endogenous FOH production, independently of their effects on protein prenylation. Likewise, we found that the FXR antagonist guggulsterone (GGS) inhibits ALP activity, calcium deposition, DNA binding of RUNX2, and bone marker expression, indicating that GGS interferes with osteoblastic differentiation. Furthermore, GGS induced the appearance of lipid vesicles in BMSC and stimulated the expression of adipose tissue markers (peroxisome proliferator activated receptor-gamma (PPARγ), adipoQ, leptin and CCAAT/enhancer-binding protein-alpha (C/EBPα)). In conclusion, our data support a new role for FXR in the modulation of osteoblast/adipocyte balance: its activation stimulates RUNX2-mediated osteoblastic differentiation of BMSC, whereas its inhibition leads to an adipocyte-like phenotype.
MeSH term(s)	Adolescent ; Adult ; Alkaline Phosphatase/metabolism ; Biomarkers/metabolism ; Bone Marrow Cells/cytology ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/enzymology ; Bone Matrix/drug effects ; Bone Matrix/metabolism ; Calcification, Physiologic/drug effects ; Calcification, Physiologic/genetics ; Calcium/metabolism ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Child ; Core Binding Factor Alpha 1 Subunit/metabolism ; DNA/metabolism ; Diphosphonates/pharmacology ; Gene Expression Regulation/drug effects ; Gene Silencing/drug effects ; Humans ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Pregnenediones/pharmacology ; Protein Binding/drug effects ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, Cytoplasmic and Nuclear/agonists ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Stromal Cells/cytology ; Stromal Cells/drug effects ; Stromal Cells/enzymology ; Young Adult
Chemical Substances	Biomarkers ; Core Binding Factor Alpha 1 Subunit ; Diphosphonates ; Pregnenediones ; RNA, Messenger ; RUNX2 protein, human ; Receptors, Cytoplasmic and Nuclear ; farnesoid X-activated receptor ; DNA (9007-49-2) ; pregna-4,17-diene-3,16-dione (A4PW148END) ; Alkaline Phosphatase (EC 3.1.3.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2011.08.013
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Zs.A 1571: 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)
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Article ; Online: Early expression of the Helicase-Like Transcription Factor (HLTF/SMARCA3) in an experimental model of estrogen-induced renal carcinogenesis.

Debauve, Gaël / Nonclercq, Denis / Ribaucour, Fabrice / Wiedig, Murielle / Gerbaux, Cécile / Leo, Oberdan / Laurent, Guy / Journé, Fabrice / Belayew, Alexandra / Toubeau, Gérard

Molecular cancer

2006 Volume 5, Page(s) 23

Abstract: Background: The Helicase-Like Transcription Factor (HLTF/SMARCA3) belongs to the family of SWI/SNF proteins that use the energy of ATP hydrolysis to remodel chromatin in a variety of cellular processes. Several SWI/SNF genes are disrupted in cancer, ... ...

Abstract	Background: The Helicase-Like Transcription Factor (HLTF/SMARCA3) belongs to the family of SWI/SNF proteins that use the energy of ATP hydrolysis to remodel chromatin in a variety of cellular processes. Several SWI/SNF genes are disrupted in cancer, suggesting a role of tumor suppressor. Similarly, the HLTF gene was recently found to be inactivated by hypermethylation in a number of advanced colon and gastric tumors. However, other evidences indicated a 20-fold HLTF overexpression in cell lines derived from various neoplasms (ovary, breast, cervix, kidney...). Results: In the present study, we investigated HLTF expression by immunohistochemistry in a model of kidney tumors induced by continuous administration of diethylstilbestrol to male Syrian golden hamsters. A strong labeling was already detected in small tumor buds, making HLTF an early cancer marker in this model. Although every cell stained for HLTF at this early stage, the number of HLTF-positive cells decreased to 10% with cancer progression, and these positive cells were dispersed in the tumor mass. HLTF expression was conserved in the HKT-1097 cell line established from kidney tumors, but again only 10% of positive cells were found in xenografts produced by HKT-1097 cells in nude mice. Conclusion: In conclusion, our data suggest that HLTF gene activation is linked to initial steps of carcinogenesis in this model and should be investigated in early stages of other neoplasms.
MeSH term(s)	Animals ; Base Sequence ; Cricetinae ; DNA Helicases/metabolism ; DNA-Binding Proteins/analysis ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Diethylstilbestrol/pharmacology ; Disease Progression ; Estrogens/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Immunohistochemistry ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Kidney Neoplasms/chemically induced ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Male ; Mesocricetus ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Sequence Homology, Nucleic Acid ; Transcription Factors/analysis ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptional Activation ; Transplantation, Heterologous ; Tumor Cells, Cultured
Chemical Substances	DNA-Binding Proteins ; Estrogens ; HLTF protein, human ; Transcription Factors ; Diethylstilbestrol (731DCA35BT) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2006-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/1476-4598-5-23
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