Sharon prins

sharon prins

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Cisplatin and second-generation alternatives to cisplatin, represent some of the most active and clinically useful agents in the treatment of cancer.

However, their application in the clinic is marred by side-effects and drug resistance. We have identified the binuclear palladacycle, AJ-5, as a lead anticancer compound with potent activity against advanced melanomas and estrogen receptor -positive and -negative breast cancers.

AJ-5 displayed an IC50 of 0. AJ-5 also showed activity against breast cancer stem cells which are associated with drug-resistance and often not targeted by traditional chemotherapeutic agents.

Cytotoxicity assays were performed and sub-micromolar IC50 concentrations were obtained for rhabdomyosarcoma, chondrosarcoma, liposarcoma, synovial sarcoma and osteosarcoma.

Clonogenic assays show that AJ-5 greatly compromises the long-term ability of the sarcoma cells to survive and proliferate.

To determine the underlying molecular mechanisms by which AJ-5 exerts its cytotoxicity, western blot analyses were performed with antibodies to key proteins involved in the DNA damage response in rhabdomyosarcoma cell lines.

AJ-5 treatment also led to autophagy as confirmed by the formation of autophagosomes, increased levels of LC3-II and the presence of LC3 puncta. Finally, pharmacokinetic studies show that AJ-5 has a promising half-life of Thus the PK data correlates well with our observed efficacy of the drug in our mouse model.

Together these findings suggest that AJ-5 may be an effective chemotherapeutic for treating a range of drug-resistant and advanced cancers.

A novel palladacycle complex with anti-cancer activity against breast cancer and melanomas also exhibits potent cytotoxicity in a range of sarcomas [abstract].

Where have we come from and where are we going? Sarcomas are a heterogeneous group of neoplasms of mesenchymal origin.

To date more than sarcoma subtypes have been identified and they vary in molecular characteristics, pathology, clinical presentation and response to treatment.

Surgery in combination with preoperative and postoperative therapies is the primary treatment for localized sarcoma tumours and is the most promising curative possibility.

Metastasized sarcomas, on the other hand, are treated primarily with single-agent or combination chemotherapy, but this rarely leads to a complete and robust response and often becomes a palliative form of treatment.

The heterogeneity of sarcomas results in variable responses to current generalized treatment strategies. In light of this and the lack of curative strategies for metastatic and unresectable sarcomas, there is a need for novel subtype-specific treatment strategies.

With the more recent understanding of the molecular mechanisms underlying the pathogenesis of some of these tumours, the treatment of sarcoma subtypes with targeted therapies is a rapidly evolving field.

This review discusses the current management of sarcomas as well as promising new therapies that are currently underway in clinical trials. Preparation, characterization and evaluation of novel 1,3,5-triazaphosphaadamantane PTA -based palladacycles as anti-cancer agents.

All complexes were fully characterized using IR and NMR spectroscopy, mass spectrometry as well as elemental analysis.

In-vitro evaluation of the complexes as anti-cancer agents against the breast-cancer cell lines MCF7 and MDA-MB as well the melanoma cell line ME shows that four of the five complexes tested are active.

These palladacycles exhibit their cytotoxicity by inducing DNA damage which subsequently triggers apoptosis.

DNA binding studies using electrophoresis and spectroscopic techniques, such as UV-Vis and circular dichroism spectroscopy, confirms that the palladacycle, C2 definitely interacts with DNA.

Results from these DNA binding experiments seem to rule out co-valent and intercalative binding, pointing rather to a non-covalent interaction, with electrostatic binding being the most likely possibility.

It is envisioned that this would probably involve a hydrolysed or solvated derivative of C2. Metformin-induced alterations in nucleotide metabolism cause 5-fluorouracil resistance but gemcitabine susceptibility in oesophageal squamous cell carcinoma: Metformin-induced resistance to 5-FU.

We show that this is due to global alterations in nucleotide metabolism, including elevated expression of thymidylate synthase and thymidine kinase 1 established 5-FU resistance mechanisms , which likely result in an increase in intracellular dTTP pools and a 'dilution' of 5-FU anabolites.

Metformin treatment also increases deoxycytidine kinase dCK expression and, as the chemotherapeutic agent gemcitabine relies on dCK for its efficient activity, we speculated that metformin would enhance the sensitivity of OSCC cells to gemcitabine.

Indeed we show that metformin pre-treatment greatly increases gemcitabine toxicity and DNA fragmentation in comparison to gemcitabine alone.

Taken together, our findings show that metformin alters nucleotide metabolism in OSCC cells and while responsible for inducing resistance to 5-FU, it conversely increases sensitivity to gemcitabine, thereby highlighting metformin and gemcitabine as a potentially novel combination therapy for OSCC.

This article is protected by copyright. The tumour suppressor, miR, inhibits malignant melanoma migration by targetting the TBX3 transcription factor.

The transcription factor, TBX3, is a key driver of malignant melanoma and any drug that impacts its expression is likely to have an impact on the treatment of this highly aggressive and treatment resistant cancer.

Replacement of miRNAs that target oncogenes has gained much attention as a therapy because it is anticipated to be effective with little side-effects since miRNAs are naturally occurring and often target large set of genes in the same oncogenic pathway.

Here we show that miR levels correlate inversely with TBX3 mRNA levels in a panel of melanoma cell lines and in a cohort of patients with primary melanoma.

Low levels of miR and high levels of TBX3 are shown to be associated with poor patient survival. The T-Box transcription factor 3 in development and cancer.

T-box factors comprise an archaic family of evolutionary conserved transcription factors that regulate patterns of gene expression essential for embryonic development.

The T-box transcription factor 3 TBX3 , a member of this family, is expressed in several tissues and plays critical roles in, among other structures, the heart, mammary gland and limbs and haploinsufficiency of the human TBX3 gene is the genetic basis for the autosomal dominant disorder, ulnar-mammary syndrome.

Overexpression of TBX3 on the other hand has been linked to several cancers including melanoma, breast, pancreatic, liver, lung, head and neck, ovarian, bladder carcinomas and a number of sarcoma subtypes.

Furthermore, there is strong evidence that TBX3 promotes oncogenesis by impacting proliferation, tumour formation, metastasis as well as cell survival and drug resistance.

More recently, TBX3 was however shown to also have tumour suppressor activity in fibrosarcomas and thus its functions in oncogenesis appear to be context dependent.

Identification of the upstream regulators of TBX3 and the molecular mechanism s underpinning its oncogenic roles will make valuable contributions to cancer biology.

Synthesis, Structure and Antiproliferative Activity. Research aimed at enhancing the efficacy of organometallic complexes against cancer, has shown that attaching bio-active molecules to metallo drugs often enhances their biological properties.

The antiproliferative activity of the ligands L2 and L3 and complexes C1 to C9 were evaluated in vitro against human promyelocytic leukemia cells HL60 and normal skin fibroblast cells FG0.

The compounds exhibit good activities against HL60 cells and are consistently selective towards cancerous cells over non-tumorous cells. This study demonstrates the potential of such hybrid compounds to target cancer cells specifically.

Jan Encyclopedia of Cancer. Investigating a novel binuclear palladacycle complex for anti-cancer activity in rhabdomyosarcoma cells.

Association of Notch4 with metastasis in human oral squamous cell carcinoma. Despite the development of several therapeutic strategies in the past decades they have failed to improve the survival rate of oral squamous cell carcinoma patients due to the highly metastatic nature of the disease and its high recurrence rate.

However there is accumulating evidence that aberrant Notch4 expression has a critical role in tumorigenesis but its prognostic value and function in OSCC remains uncertain.

This study therefore investigates 1 the expression of Notch4 and its downstream target myelin associated glycoprotein MAG in tissue samples representative of different stages of OSCC with varied clinicopathological features and 2 the possible involvement of Notch4 in the proliferation and migration of OSCC cells.

Further, the metastatic role of Notch4 was analyzed in the HSC-3 cell line by cell proliferation and migration assays. Our study indicates that the aberrant activation of Notch4 promotes OSCC metastasis through perineural spread and ascertains its value as a significant prognostic marker and potential therapeutic target to treat this highly aggressive malignancy.

TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process.

TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes.

The cyclin-dependent kinase inhibitor p21 WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3.

Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21 WAF1 promoter by binding a T-element close to its initiator.

Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21 WAF1 and that pseudo-phosphorylation of a serine proline motif S located within this domain may play an important role in regulating this ability.

Importantly, we demonstrate using knockdown and overexpression experiments that p21 WAF1 repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells.

Results from this study provide a detailed mechanism of how TBX3 transcriptionally represses p21 WAF1 which adds to our understanding of how it may contribute to oncogenesis.

The T-box transcription factor 3 is a promising biomarker and a key regulator of the oncogenic phenotype of a diverse range of sarcoma subtypes.

Sarcomas represent a complex group of malignant neoplasms of mesenchymal origin and their heterogeneity poses a serious diagnostic and therapeutic challenge.

There is therefore a need to elucidate the molecular mechanisms underpinning the pathogenesis of the more than 70 distinguishable sarcoma subtypes.

The transcription factor TBX3, a critical developmental regulator, is overexpressed in several cancers of epithelial origin where it contributes to tumorigenesis by different molecular mechanisms.

However, the status and role of TBX3 in sarcomas have not been reported. Here we show that a diverse subset of soft tissue and bone sarcoma cell lines and patient-derived sarcoma tissues express high levels of TBX3.

We further explore the significance of this overexpression using a small interferring RNA approach and demonstrate that TBX3 promotes the migratory ability of chondrosarcoma, rhabdomyosarcoma and liposarcoma cells but inhibits fibrosarcoma cell migration.

This suggested that TBX3 may play a key role in the development of different sarcoma subtypes by functioning as either an oncoprotein or as a brake to prevent tumour progression.

To further explore this, TBX3 knockdown and overexpression cell culture models were established using chondrosarcoma and fibrosarcoma cells as representatives of each scenario, and the resulting cells were characterized with regard to key features of tumorigenesis.

Results from in vitro and in vivo assays reveal that, while TBX3 promotes substrate-dependent and -independent cell proliferation, migration and tumour formation in chondrosarcoma cells, it discourages fibrosarcoma formation.

Our findings provide novel evidence linking TBX3 to cancers of mesenchymal origin. Furthermore, we show that TBX3 may be a biomarker for the diagnosis of histologically dynamic sarcoma subtypes and that it impacts directly on their oncogenic phenotype.

Indeed, we reveal that TBX3 may exhibit oncogene or tumour suppressor activity in sarcomas, which suggests that its role in cancer progression may rely on cellular context.

Recently palladium Pd complexes have attracted a lot of interest as chemotherapeutic agents because they have been shown to exert a significant cytotoxic effect on cancer cells.

Importantly, Pd complexes have been shown to exert antitumor activity in cisplatin resistant cells and to have less side effects than cisplatin, a widely used platinum-based chemotherapeutic agent.

This led to suggestions that Pd II compounds may have different mechanisms of action from those of cisplatin, but this is still unresolved. It is, however, generally accepted that the cytotoxic effects exerted by most metal-based compounds result from their capacity to trigger DNA double-strand breaks which activate a canonical DNA damage signaling pathway through activating ataxia telangiectasia mutated ATM , the checkpoint kinase 2 CHK2 , and the tumor suppressor protein p These proteins play an important role in deciding cell fate in response to DNA damage through transactivating the cyclin-dependent kinase inhibitor p21 as well as pro-apoptotic proteins.

While most chemotherapeutic agents have been described to induce cell death via apoptosis, there is increasing evidence that they can also function by initiating mitotic catastrophe and autophagy.

Indeed, several studies have confirmed a complex cross-talk between apoptosis and autophagy, but while some studies indicate that autophagy inhibits the process of apoptosis, others suggest a role for autophagy in the induction of cell death.

It would, however, appear that these opposing roles of autophagy depend, in part, on both the cell type and the chemotherapy used. Although extraocular muscles are commonly affected by myasthenia gravis MG at presentation, a treatment-resistant ophthalmoplegic complication of MG OP-MG occurs in younger patients with African-genetic ancestry.

Extending this argument, we hypothesized that OP-MG individuals may harbor African-specific polymorphisms in key genes influencing extraocular muscle remodeling.

We screened the regulatory region of the transforming growth factor beta-1 TGFB1 gene encoding the cytokine pivotal in muscle healing responses.

Journal of Human Genetics advance online publication, 3 December ; doi: Sep Advances in Tendon Research: From Bench to Bedside. The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion.

The palladacycle, AJ-5, exhibits anti-tumour and anti-cancer stem cell activity in breast cancer cells. T-box Transcription Factors in Cancer Biology.

The transcription factor, TBX3, is critical for the formation of, amongst other structures, the heart, limbs and mammary glands and haploinsufficiency of the human TBX3 gene result in ulnar-mammary syndrome which is characterized by hypoplasia of these structures.

On the other hand, the overexpression of TBX3 is a feature of a wide range of cancers and it has been implicated in several aspects of the oncogenic process.

This includes its ability to function as an immortalizing gene and to promote proliferation through actively repressing negative cell cycle regulators.

Together this suggests that TBX3 levels may need to be tightly regulated during the cell cycle. The increased levels of TBX3 in S-phase are shown to occur transcriptionally through activation by c-Myc at E-box motifs located at and bps and posttranslationally by cyclin A-CDK2 phosphorylation.

These results suggest that TBX3 is required for cells to transit through S-phase and that this function may be linked to its role as a pro-proliferative factor.

The AKT3 signalling pathway plays a critical role in melanoma formation and invasion and components of this signalling cascade are therefore attractive targets for the treatment of malignant melanoma.

Recent evidence show that the embryonically important TBX3 transcription factor is upregulated in a subset of melanomas and plays a key role in promoting melanoma formation and invasion, in part by repressing the cell adhesion molecule E-cadherin.

Briefly, using site-directed mutagenesis and in vitro kinase assays, we have identified the AKT3 target site at serine residue in the TBX3 protein and show that this site is phosphorylated in vivo.

Importantly, we show by western blotting, immunofluorescence, reporter, migration and invasion assays that the phosphorylation at S promotes TBX3 protein stability, nuclear localization, transcriptional repression of E-cadherin, and its role in cell migration and invasion.

Our results identify a novel signalling and transcriptional network linking AKT3, TBX3 and E-cadherin during melanoma migration and invasion and reveals TBX3 as a potential target for anti-metastatic therapeutics.

A growing body of work has shown that the highly homologous T-box transcription factors TBX2 and TBX3 play critical but distinct roles in embryonic development and cancer progression.

For example, TBX2 and TBX3 are up-regulated in several cancers and recent evidence suggests that whereas TBX2 functions as a pro-proliferative factor, TBX3 inhibits cell proliferation but promotes cancer cell migration and invasion.

The TBX3 targets responsible for these functions were however not identified. The evolutionarily conserved T-box family of transcription factors have critical and well-established roles in embryonic development.

Of these the best characterised is TBX2, whose expression is upregulated in cancers including breast, pancreatic, ovarian, liver, endometrial adenocarcinoma, glioblastomas, gastric, uterine cervical and melanoma.

Understanding the role and regulation of TBX2, as well as other T-box factors, in contributing directly to tumour progression, and especially in suppression of senescence and control of invasiveness suggests that targeting TBX2 expression or function alone or in combination with currently available chemotherapeutic agents may represent a therapeutic strategy for cancer.

The T-box transcription factor, TBX3, promotes tumourigenesis in soft tissue and bone sarcomas: Genomic instability is a major hallmark of cancer.

To maintain genomic integrity, cells are equipped with dedicated sensors to monitor DNA repair or to force damaged cells into death programs.

The tumor suppressor p53 is central in this process. Here, we report that the ubiquitous transcription factor Upstream Stimulatory factor 1 USF1 coordinates p53 function in making proper cell fate decisions.

USF1 stabilizes the p53 protein and promotes a transient cell cycle arrest, in the presence of DNA damage. Thus, cell proliferation is maintained inappropriately in Usf1 KO mice and in USF1-deficient melanoma cells challenged by genotoxic stress.

In USF1-deficient cells, the level of p53 can be restored by the re-expression of full-length USF1 protein similarly to what is observed using Nutlin-3, a specific inhibitor that prevents pMDM2 interaction.

Consistent with a new function for USF1, a USF1 truncated protein lacking its DNA-binding and transactivation domains can also restore the induction and activity of p These findings establish that p53 function requires the ubiquitous stress sensor USF1 for appropriate cell fate decisions in response to DNA-damage.

They underscore the new role of USF1 and give new clues of how p53 loss of function can occur in any cell type. Finally, these findings are of clinical relevance because they provide new therapeutic prospects in stabilizing and reactivating the p53 pathway.

The emergence of drug resistant tumours that are able to escape cell death pose a major problem in the treatment of cancers.

Combination therapies that induce DNA damage and disrupt the DNA damage repair process may therefore prove to be more effective against such tumours.

The developmentally important transcription factor TBX2 has been suggested as a novel anticancer drug target, as it is overexpressed in several cancers and possesses strong anti-senescence and pro-proliferative functions.

Importantly, we recently showed that when TBX2 is silenced, we are able to reverse several features of transformation in both breast cancer and melanoma cells.

Overexpression of TBX2 has also been linked to drug resistance and we have shown that its ectopic expression results in genetically unstable polyploidy cells with resistance to cisplatin.

Whether the overexpression of endogenous TBX2 levels is associated with cisplatin resistance in TBX2-driven cancers has, however, not been shown.

These results suggest that targeting TBX2 in combination with chemotherapeutic drugs such as cisplatin could improve the efficacy of current anticancer treatments.

The T-box transcription factor, TBX3, is overexpressed in several cancers and has been proposed as a chemotherapeutic target.

Several lines of evidence suggest that TBX3 may be a key contributor to malignant melanoma, a highly aggressive and intractable disease.

Using in vitro and in vivo assays we demonstrate here for the first time that overexpressing TBX3 in non-tumourigenic early stage melanoma cells is sufficient to promote tumour formation and invasion.

Furthermore, we show that TBX3 may play an important role as a reciprocal switch between substrate dependent cell proliferation and tumour invasion.

A novel binuclear palladacycle complex inhibits melanoma growth in vitro and in vivo through apoptosis and autophagy. Malignant melanoma is an aggressive skin cancer and it is reported to be the most treatment-resistant human cancer.

Here we describe the anti-tumour activity of a novel binuclear palladacycle complex AJ-5 in vertical growth phase ME and metastatic WM melanoma cell lines.

We show that compared to normal control cell lines, AJ-5 is more effective in inhibiting the proliferation of ME and WM melanoma cells with IC50 values of 0.

Interestingly, AJ-5 treatment also simultaneously induced the formation of autophagosomes and led to an increase in the autophagy markers LC3II and Beclin1.

Inhibition of autophagy reduced AJ-5 cytotoxicity suggesting that AJ-5 induced autophagy was a cell death and not cell survival mechanism.

Importantly, AJ-5 treatment efficiently reduced tumour growth in melanoma bearing mice and induced high levels of autophagy and apoptosis markers.

Together these findings suggest that AJ-5 may be an effective chemotherapeutic drug in the treatment of melanoma, a highly aggressive and intractable cancer.

The T-box transcription factor, TBX3, plays an important role in embryonic development and haploinsufficiency of TBX3 causes ulnar-mammary syndrome.

The overexpression of TBX3 on the other hand has been associated with several cancers and preliminary evidence suggests that increased levels of TBX3 may inhibit cell proliferation but promote tumor migration and invasion.

While this suggests that deregulated levels of TBX3 are deleterious in development and promotes disease, very little is known about the signaling pathways that regulate TBX3 expression.

Here we show that overexpressing TBX3 inhibits the proliferative ability while promoting the migration of breast epithelial cells. A polymorphism rs within the functional COL5A1 3'-untranslated region UTR has been shown to associate with chronic Achilles tendinopathy and other exercise-related phenotypes.

The aim of this study was to determine whether previously uncharacterized polymorphisms within a functional region of the COL5A1 3'-UTR or the MIR gene are associated with chronic Achilles tendinopathy.

All four genetic markers were independently associated with chronic Achilles tendinopathy. The ulnar-mammary syndrome gene, Tbx3, is a direct target of the retinoic acid signaling pathway, which regulates its expression during mouse limb development.

TBX3, a member of the T-box transcription factor gene family, is a transcriptional repressor that is required for the development of the heart, limbs, and mammary glands.

Mutations in TBX3 that result in reduced functional protein lead to ulnar-mammary syndrome, a developmental disorder characterized by limb, mammary gland, tooth, and genital abnormalities.

Nieuws Nieuws Economie Shownieuws Stel jouw vraag! Facebook Live Dossiers Bij de politierechter Columns. Weerbericht Achtergrond bij het weerbericht Weerfoto Maand- en seizoensoverzicht Video: Dartster Sharon Prins uit Zoetermeer.

De Oranje-dartsters wonnen in Kobe het overall-klassement. En dat was bijzonder, want dat lukte Nederland pas een keer eerder. Ik kijk altijd gewoon per wedstrijd hoe het gaat.

Maar natuurlijk zijn we apetrots op het resultaat. Hier kunnen we echt lang met een goed gevoel op terugkijken. We lieten kansjes liggen en Zweden profiteerde daar goed van.

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Profile von Personen mit dem Namen Sharon Prins anzeigen. So konnte sich Montgomery zurückkämpfen und ausgleichen und ein entscheidendes fünftes Leg erzwingen. Er hatte das entscheidende dritte Set mit 3: Tritt Facebook bei, um dich mit Sharon Prins und anderen Personen, die du kennen könntest, zu. So konnte sich Montgomery zurückkämpfen und ausgleichen und ein entscheidendes fünftes Leg erzwingen. Harm steigerte sich im zweiten Set und holte es sich ohne ein Leg abzugeben. So konnte Waites mit 2: Deine E-Mail-Adresse wird nicht veröffentlicht. Sherrock sicherte sich Spiel entscheidend das dritte Leg des dritten Sets gegen den Wurf, in das sie mit Scores von , und eingestiegen war, und schnappte sich dann auch das folgende Leg zum Sieg, nachdem Hammond zwei Darts auf den Leggewinn verworfen hatte. Aber Montgomery startete schwach ins Leg und Waites stand als Erster auf einem finish und machte 92 Punkte zum Sieg aus. Aber der 47jährige aus Middlesbrough legte seine Nervosität schnell ab, warf im ersten Leg eine und konnte sich die ersten sechs Legs des Spiels ohne Probleme in Folge sichern. So konnte sich Montgomery zurückkämpfen und ausgleichen und ein entscheidendes fünftes Leg erzwingen. Die ersten beiden Sets gingen beide bis in ein Entscheidungsleg, in dem book of ra flash online Male Montgomery einen Dart auf die Doppel 20 zum Setgewinn hatte und beide Male sein Doppel verfehlte. Freebet bwin konnte Waites mit 2: Alle drei Sets gingen bis in ein Entscheidungsleg, das sich dann Telnekes sichern konnte. Hammond konnte nicht mithalten. Das dritte Set gewann der Schwede dann wieder 3: Harris meinte nach dem Spiel, er habe jede Menge Selbstvertrauen und würde planen die Beste Spielothek in Birkacherhof finden zu gewinnen. O'Brien konnte zwar jeweils das erste Leg der beiden Sets gewinnen, hatte aber der Niederländerin sonst nicht viel entgegenzusetzen. Waites konnte Beste Spielothek in Graditschach finden 3: Warren reagierte deutlich frustriert, behielt aber die Fassung und gewann das Leg noch gegen den Wurf und damit auch das erste Set. Sherrock wird in den Viertelfinalen auf Kontodaten überweisung Ashton treffen - eine Wiederholung des Finales vondas Ashton gewinnen konnte. Im dritten Set legte Sherrock zu und traf beständig in die Trippel Beide Spieler holten sich je ein Leg mit einem über er Finish. Sherrock sicherte sich Spiel entscheidend das dritte Leg des dritten Sets gegen den Wurf, Beste Spielothek in Mieders finden das sie mit Scores vonund cash casino görlitz war, und schnappte sich dann auch Beste Spielothek in Vorwerk Monplaisir finden folgende Leg zum Sieg, nachdem Hammond zwei Darts auf den Leggewinn verworfen hatte. Sherrock sicherte sich Spiel entscheidend das dritte Leg des dritten Landespokal brandenburg ergebnisse gegen den Wurf, in das sie mit Scores vonund eingestiegen war, und schnappte sich dann auch das folgende Leg zum Sieg, nachdem Aktien demokonto ohne anmeldung zwei Darts auf den Leggewinn verworfen hatte. Uhr, Ross Montgomery,Scott Waites. Alle drei Sets gingen bis in ein Entscheidungsleg, das sich dann Telnekes sichern konnte. Alle drei Sets gingen bis in ein Entscheidungsleg, das sich dann Telnekes sichern konnte. So konnte Waites mit 2: Sherrock wird in den Viertelfinalen auf Lisa Ashton treffen - eine Wiederholung des Finales vondas Ashton gewinnen konnte. Warren reagierte deutlich frustriert, behielt aber die Fassung und gewann das Leg noch gegen den Wurf und damit auch das erste Set. Danach stieg der 55 Jahre alte Waliser mit einem Darter ins vierte Set ein. Nilssons Durchschnitt lag bei Alle drei Sets gingen bis in ein Http: Nach der Pause hatte der Niederländer durchaus Chancen, das dritte Set zu gewinnen, aber er verwarf drei Darts auf die Doppel und Warren schnappte es sich mit einem nervenstarken er Finish. Am Ende des Spiels hatte er einen Durchschnitt von Vor dem Spiel hatte er noch gemeint, es würde das schwerste Spiel seiner Karriere werden, da Robson so etwas wie ein Angstgegner für ihn sei, Dazu käme noch, dass er sicher unter der Last der Titelverteidigung nervös ins Turnier ginge, während Robson in seinem Vorrundenspiel mehr oder weniger alles getroffen habe. Harris meinte nach dem Spiel, er habe jede Menge Selbstvertrauen und würde planen die Weltmeisterschaft zu gewinnen. So konnte sich Montgomery zurückkämpfen und ausgleichen und ein entscheidendes fünftes Leg erzwingen. Das zweite Set war etwas enger, aber der Schwede konnte es im Entscheidungsleg mit einem 77er Finish gewinnen während Sparidaans schon auf einer Doppel 16 wartete.

TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process.

TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes.

The cyclin-dependent kinase inhibitor p21 WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3.

Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21 WAF1 promoter by binding a T-element close to its initiator.

Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21 WAF1 and that pseudo-phosphorylation of a serine proline motif S located within this domain may play an important role in regulating this ability.

Importantly, we demonstrate using knockdown and overexpression experiments that p21 WAF1 repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells.

Results from this study provide a detailed mechanism of how TBX3 transcriptionally represses p21 WAF1 which adds to our understanding of how it may contribute to oncogenesis.

The T-box transcription factor 3 is a promising biomarker and a key regulator of the oncogenic phenotype of a diverse range of sarcoma subtypes.

Sarcomas represent a complex group of malignant neoplasms of mesenchymal origin and their heterogeneity poses a serious diagnostic and therapeutic challenge.

There is therefore a need to elucidate the molecular mechanisms underpinning the pathogenesis of the more than 70 distinguishable sarcoma subtypes.

The transcription factor TBX3, a critical developmental regulator, is overexpressed in several cancers of epithelial origin where it contributes to tumorigenesis by different molecular mechanisms.

However, the status and role of TBX3 in sarcomas have not been reported. Here we show that a diverse subset of soft tissue and bone sarcoma cell lines and patient-derived sarcoma tissues express high levels of TBX3.

We further explore the significance of this overexpression using a small interferring RNA approach and demonstrate that TBX3 promotes the migratory ability of chondrosarcoma, rhabdomyosarcoma and liposarcoma cells but inhibits fibrosarcoma cell migration.

This suggested that TBX3 may play a key role in the development of different sarcoma subtypes by functioning as either an oncoprotein or as a brake to prevent tumour progression.

To further explore this, TBX3 knockdown and overexpression cell culture models were established using chondrosarcoma and fibrosarcoma cells as representatives of each scenario, and the resulting cells were characterized with regard to key features of tumorigenesis.

Results from in vitro and in vivo assays reveal that, while TBX3 promotes substrate-dependent and -independent cell proliferation, migration and tumour formation in chondrosarcoma cells, it discourages fibrosarcoma formation.

Our findings provide novel evidence linking TBX3 to cancers of mesenchymal origin. Furthermore, we show that TBX3 may be a biomarker for the diagnosis of histologically dynamic sarcoma subtypes and that it impacts directly on their oncogenic phenotype.

Indeed, we reveal that TBX3 may exhibit oncogene or tumour suppressor activity in sarcomas, which suggests that its role in cancer progression may rely on cellular context.

Recently palladium Pd complexes have attracted a lot of interest as chemotherapeutic agents because they have been shown to exert a significant cytotoxic effect on cancer cells.

Importantly, Pd complexes have been shown to exert antitumor activity in cisplatin resistant cells and to have less side effects than cisplatin, a widely used platinum-based chemotherapeutic agent.

This led to suggestions that Pd II compounds may have different mechanisms of action from those of cisplatin, but this is still unresolved.

It is, however, generally accepted that the cytotoxic effects exerted by most metal-based compounds result from their capacity to trigger DNA double-strand breaks which activate a canonical DNA damage signaling pathway through activating ataxia telangiectasia mutated ATM , the checkpoint kinase 2 CHK2 , and the tumor suppressor protein p These proteins play an important role in deciding cell fate in response to DNA damage through transactivating the cyclin-dependent kinase inhibitor p21 as well as pro-apoptotic proteins.

While most chemotherapeutic agents have been described to induce cell death via apoptosis, there is increasing evidence that they can also function by initiating mitotic catastrophe and autophagy.

Indeed, several studies have confirmed a complex cross-talk between apoptosis and autophagy, but while some studies indicate that autophagy inhibits the process of apoptosis, others suggest a role for autophagy in the induction of cell death.

It would, however, appear that these opposing roles of autophagy depend, in part, on both the cell type and the chemotherapy used.

Although extraocular muscles are commonly affected by myasthenia gravis MG at presentation, a treatment-resistant ophthalmoplegic complication of MG OP-MG occurs in younger patients with African-genetic ancestry.

Extending this argument, we hypothesized that OP-MG individuals may harbor African-specific polymorphisms in key genes influencing extraocular muscle remodeling.

We screened the regulatory region of the transforming growth factor beta-1 TGFB1 gene encoding the cytokine pivotal in muscle healing responses.

Journal of Human Genetics advance online publication, 3 December ; doi: Sep Advances in Tendon Research: From Bench to Bedside. The T-box transcription factor, TBX3, is sufficient to promote melanoma formation and invasion.

The palladacycle, AJ-5, exhibits anti-tumour and anti-cancer stem cell activity in breast cancer cells. T-box Transcription Factors in Cancer Biology.

The transcription factor, TBX3, is critical for the formation of, amongst other structures, the heart, limbs and mammary glands and haploinsufficiency of the human TBX3 gene result in ulnar-mammary syndrome which is characterized by hypoplasia of these structures.

On the other hand, the overexpression of TBX3 is a feature of a wide range of cancers and it has been implicated in several aspects of the oncogenic process.

This includes its ability to function as an immortalizing gene and to promote proliferation through actively repressing negative cell cycle regulators.

Together this suggests that TBX3 levels may need to be tightly regulated during the cell cycle. The increased levels of TBX3 in S-phase are shown to occur transcriptionally through activation by c-Myc at E-box motifs located at and bps and posttranslationally by cyclin A-CDK2 phosphorylation.

These results suggest that TBX3 is required for cells to transit through S-phase and that this function may be linked to its role as a pro-proliferative factor.

The AKT3 signalling pathway plays a critical role in melanoma formation and invasion and components of this signalling cascade are therefore attractive targets for the treatment of malignant melanoma.

Recent evidence show that the embryonically important TBX3 transcription factor is upregulated in a subset of melanomas and plays a key role in promoting melanoma formation and invasion, in part by repressing the cell adhesion molecule E-cadherin.

Briefly, using site-directed mutagenesis and in vitro kinase assays, we have identified the AKT3 target site at serine residue in the TBX3 protein and show that this site is phosphorylated in vivo.

Importantly, we show by western blotting, immunofluorescence, reporter, migration and invasion assays that the phosphorylation at S promotes TBX3 protein stability, nuclear localization, transcriptional repression of E-cadherin, and its role in cell migration and invasion.

Our results identify a novel signalling and transcriptional network linking AKT3, TBX3 and E-cadherin during melanoma migration and invasion and reveals TBX3 as a potential target for anti-metastatic therapeutics.

A growing body of work has shown that the highly homologous T-box transcription factors TBX2 and TBX3 play critical but distinct roles in embryonic development and cancer progression.

For example, TBX2 and TBX3 are up-regulated in several cancers and recent evidence suggests that whereas TBX2 functions as a pro-proliferative factor, TBX3 inhibits cell proliferation but promotes cancer cell migration and invasion.

The TBX3 targets responsible for these functions were however not identified. The evolutionarily conserved T-box family of transcription factors have critical and well-established roles in embryonic development.

Of these the best characterised is TBX2, whose expression is upregulated in cancers including breast, pancreatic, ovarian, liver, endometrial adenocarcinoma, glioblastomas, gastric, uterine cervical and melanoma.

Understanding the role and regulation of TBX2, as well as other T-box factors, in contributing directly to tumour progression, and especially in suppression of senescence and control of invasiveness suggests that targeting TBX2 expression or function alone or in combination with currently available chemotherapeutic agents may represent a therapeutic strategy for cancer.

The T-box transcription factor, TBX3, promotes tumourigenesis in soft tissue and bone sarcomas: Genomic instability is a major hallmark of cancer.

To maintain genomic integrity, cells are equipped with dedicated sensors to monitor DNA repair or to force damaged cells into death programs.

The tumor suppressor p53 is central in this process. Here, we report that the ubiquitous transcription factor Upstream Stimulatory factor 1 USF1 coordinates p53 function in making proper cell fate decisions.

USF1 stabilizes the p53 protein and promotes a transient cell cycle arrest, in the presence of DNA damage.

Thus, cell proliferation is maintained inappropriately in Usf1 KO mice and in USF1-deficient melanoma cells challenged by genotoxic stress. In USF1-deficient cells, the level of p53 can be restored by the re-expression of full-length USF1 protein similarly to what is observed using Nutlin-3, a specific inhibitor that prevents pMDM2 interaction.

Consistent with a new function for USF1, a USF1 truncated protein lacking its DNA-binding and transactivation domains can also restore the induction and activity of p These findings establish that p53 function requires the ubiquitous stress sensor USF1 for appropriate cell fate decisions in response to DNA-damage.

They underscore the new role of USF1 and give new clues of how p53 loss of function can occur in any cell type. Finally, these findings are of clinical relevance because they provide new therapeutic prospects in stabilizing and reactivating the p53 pathway.

The emergence of drug resistant tumours that are able to escape cell death pose a major problem in the treatment of cancers. Combination therapies that induce DNA damage and disrupt the DNA damage repair process may therefore prove to be more effective against such tumours.

The developmentally important transcription factor TBX2 has been suggested as a novel anticancer drug target, as it is overexpressed in several cancers and possesses strong anti-senescence and pro-proliferative functions.

Importantly, we recently showed that when TBX2 is silenced, we are able to reverse several features of transformation in both breast cancer and melanoma cells.

Overexpression of TBX2 has also been linked to drug resistance and we have shown that its ectopic expression results in genetically unstable polyploidy cells with resistance to cisplatin.

Whether the overexpression of endogenous TBX2 levels is associated with cisplatin resistance in TBX2-driven cancers has, however, not been shown.

These results suggest that targeting TBX2 in combination with chemotherapeutic drugs such as cisplatin could improve the efficacy of current anticancer treatments.

The T-box transcription factor, TBX3, is overexpressed in several cancers and has been proposed as a chemotherapeutic target. Several lines of evidence suggest that TBX3 may be a key contributor to malignant melanoma, a highly aggressive and intractable disease.

Using in vitro and in vivo assays we demonstrate here for the first time that overexpressing TBX3 in non-tumourigenic early stage melanoma cells is sufficient to promote tumour formation and invasion.

Furthermore, we show that TBX3 may play an important role as a reciprocal switch between substrate dependent cell proliferation and tumour invasion.

A novel binuclear palladacycle complex inhibits melanoma growth in vitro and in vivo through apoptosis and autophagy.

Malignant melanoma is an aggressive skin cancer and it is reported to be the most treatment-resistant human cancer.

Here we describe the anti-tumour activity of a novel binuclear palladacycle complex AJ-5 in vertical growth phase ME and metastatic WM melanoma cell lines.

We show that compared to normal control cell lines, AJ-5 is more effective in inhibiting the proliferation of ME and WM melanoma cells with IC50 values of 0.

Interestingly, AJ-5 treatment also simultaneously induced the formation of autophagosomes and led to an increase in the autophagy markers LC3II and Beclin1.

Inhibition of autophagy reduced AJ-5 cytotoxicity suggesting that AJ-5 induced autophagy was a cell death and not cell survival mechanism.

Importantly, AJ-5 treatment efficiently reduced tumour growth in melanoma bearing mice and induced high levels of autophagy and apoptosis markers.

Together these findings suggest that AJ-5 may be an effective chemotherapeutic drug in the treatment of melanoma, a highly aggressive and intractable cancer.

The T-box transcription factor, TBX3, plays an important role in embryonic development and haploinsufficiency of TBX3 causes ulnar-mammary syndrome.

The overexpression of TBX3 on the other hand has been associated with several cancers and preliminary evidence suggests that increased levels of TBX3 may inhibit cell proliferation but promote tumor migration and invasion.

While this suggests that deregulated levels of TBX3 are deleterious in development and promotes disease, very little is known about the signaling pathways that regulate TBX3 expression.

Here we show that overexpressing TBX3 inhibits the proliferative ability while promoting the migration of breast epithelial cells. A polymorphism rs within the functional COL5A1 3'-untranslated region UTR has been shown to associate with chronic Achilles tendinopathy and other exercise-related phenotypes.

The aim of this study was to determine whether previously uncharacterized polymorphisms within a functional region of the COL5A1 3'-UTR or the MIR gene are associated with chronic Achilles tendinopathy.

All four genetic markers were independently associated with chronic Achilles tendinopathy. The ulnar-mammary syndrome gene, Tbx3, is a direct target of the retinoic acid signaling pathway, which regulates its expression during mouse limb development.

TBX3, a member of the T-box transcription factor gene family, is a transcriptional repressor that is required for the development of the heart, limbs, and mammary glands.

Mutations in TBX3 that result in reduced functional protein lead to ulnar-mammary syndrome, a developmental disorder characterized by limb, mammary gland, tooth, and genital abnormalities.

Increased levels of TBX3 have been shown to contribute to the oncogenic process, and TBX3 is overexpressed in several cancers, including breast cancer, liver cancer, and melanoma.

Despite its important role in development and postnatal life, little is known about the signaling pathways that modulate TBX3 expression. Here we show, using in vitro and in vivo assays, that retinoic acid RA activates endogenous TBX3 expression, which is mediated by an RA-receptor complex directly binding and activating the TBX3 promoter, and we provide evidence that this regulation may be functionally relevant in mouse embryonic limb development.

Our data identify TBX3 as a direct target of the RA signaling pathway and extend our understanding of the role and regulation of TBX3 in limb development.

An important function of all organisms is to ensure that their genetic material remains intact and unaltered through generations. This is an extremely challenging task since the cell's DNA is constantly under assault by endogenous and environmental agents.

To protect against this, cells have evolved effective mechanisms to recognize DNA damage, signal its presence, and mediate its repair.

While these responses are expected to be highly regulated because they are critical to avoid human diseases, very little is known about the regulation of the expression of genes involved in mediating their effects.

Importantly, we show that this occurs through a p53 independent mechanism and that it is coordinated by the stress-responsive transcription factor USF Furthermore, using a mouse model we show that the loss of USF-1 compromises DNA repair, which suggests that USF-1 plays an important role in maintaining genomic stability.

DAPI staining was used to visualize cell nuclei. For all results errors bars indicate s. Basal transcription of the human TBX3 gene, a key developmental regulator which is overexpressed in several cancers, requires functional NF-Y and Sp1 sites.

TBX3 is a member of the T-box family of genes that encode developmentally important transcription factors. To understand the mechanisms regulating TBX3 expression we have previously cloned the 5'-flanking region of the human TBX3 gene and here we describe cis-elements required for its basal transcription.

Our results are consistent with reports that these sites are necessary for efficient basal transcription in genes which lack TATA boxes or an Initiator which we show to be the case for TBX3.

Implications for musculoskeletal soft tissue injuries. To this end we have used a reporter assay in which the COL5A1 3'-UTR from AT patients and controls were cloned downstream of the firefly luciferase gene and luciferase activity measured as an indication of mRNA stability.

The luciferase activity of the C-alleles was significantly lower than that of the T-alleles These results have important implications for our understanding of the molecular basis of musculoskeletal soft tissue injuries and other exercise-related phenotypes.

Sequence variants within the 3'-UTR of the col5a1 gene alters mrna stability: Objective To provide functional evidence for these genetic associations, the aim of this study was to identify common variants of the COL5A1 3'-UTR from patients with chronic AT and asymptomatic controls.

Functional differences between the different variants were tested using reporter gene constructs. The constructs were transiently co-transfected with an internal control HT cells.

The normalised results were expressed as relative luciferase activity. Results Inter-individual variation was demonstrated with a 2.

In addition, an overall significantly higher activity One form WT-allele was predominantly identified in the controls, while the second form TEN-allele was predominately identified in AT subjects.

These results demonstrate that the COL5A1 3'-UTR may play an important regulatory role which could results is susceptibility to musculoskeletal soft tissue injures and other phenotypes.

Retinitis pigmentosa is a highly heterogeneous form of inherited blindness which affects more than 1.

While CAIV is expressed in the choriocapillaries of the eye and renal epithelium, the R14W mutation results in an exclusively ocular phenotype in affected individuals.

In order to investigate the mechanism of disease in RP17 and the lack of kidney phenotype, we compared the subcellular localization and post-translational processing of wild-type WT - and mutant-CAIV in three cell types.

Western blot analyses further reveal that whereas the WT CAIV is processed to its mature form in both these cell lines, significant levels of the R14W mutant protein remain in its immature form.

Interestingly, when the above experiments were repeated in the human embryonic kidney cell line, HEK, strikingly different results were obtained.

This study has important implications for our understanding of the RP17 phenotype. Investigation of novel gene-based therapies for retinitis pigmentosa The T-box transcription factor TBX3 provides an important link between embryonic development and cancer.

TBX3 mediates limb, mammary gland and heart development and, in humans, mutations resulting in haplo-insufficiency of TBX3 lead to ulnar-mammary syndrome.

Importantly, the de-regulation of TBX3 gene expression has been linked to several cancers, where it acts to suppress senescence and promotes proliferation and tumour invasion.

Despite the negative impact of de-regulated TBX3 expression as seen by developmental defects and cancer, surprisingly little is known about the regulation of the TBX3 gene.

Our present results reveal a previously unidentified pathway that up-regulates TBX3 expression and provides additional evidence that increased levels of TBX3 contribute to metastasis.

Although these studies suggest that they may both contribute to the oncogenic process by repressing common targets, whether they have redundant or distinct roles in cancers where they are both overexpressed remains to be elucidated.

Importantly, when Tbx2 function is inhibited in melanoma cells lacking Tbx3, the cells senesce, but whether this is possible in melanoma cells overexpressing both proteins is not known.

An understanding of this issue may have important implications for the design of an effective pro-senescence therapy. In this study, the authors used a sh-RNA approach to knock down TBX2 and TBX3 individually in 2 human melanoma cell lines that overexpress both these factors and then examined their specific involvement in the oncogenic process.

They demonstrate, using in vitro and in vivo cell proliferation, as well as colony- and tumor-forming ability and cell motility assays, that TBX2 and TBX3 have distinct roles in melanoma progression.

In the tested lines, although TBX2 could promote proliferation and transformation and was required by primary melanoma cells for immortality, TBX3 was required for tumor formation and cell migration.

These findings were reproducible in a human breast cancer cell line, which confirms that TBX2 and TBX3, although highly homologous, do not have redundant roles in the transformation process of cancers where they are both overexpressed.

These results have important implications for the development of new cancer treatments and in particular for melanoma, which is a highly aggressive and intractable cancer.

Tbx2 is a member of the T-box family of transcription factors that are crucial in embryonic development. Recent studies suggest that T-box factors may also play a role in controlling cell cycle progression and in the genesis of cancer.

Tbx2 has been implicated in several developmental processes such as coordinating cell fate, patterning and morphogenesis of a wide range of tissues and organs including limbs, kidneys, lungs, mammary glands, heart, and craniofacial structures.

Importantly, Tbx2 is overexpressed in several cancers including melanoma, small cell lung carcinoma, breast, pancreatic, liver, and bladder cancers and can suppress senescence, a cellular process, which serves as a barrier to cancer development.

This review presents a state of the art overview of the role and regulation of Tbx2 in early embryonic development and in cancer.

A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis.

Complement activation in myasthenia gravis MG may damage muscle endplate and complement regulatory proteins such as decay-accelerating factor DAF or CD55 may be protective.

We hypothesize that the increased prevalence of severe extraocular muscle EOM dysfunction among African MG subjects reported earlier may result from altered DAF expression.

To test this hypothesis, we screened the DAF gene sequences relevant to the classical complement pathway and found an association between myasthenics with EOM paresis and the DAF regulatory region c.

This single nucleotide polymorphism SNP results in a twofold activation of a DAF 5'-flanking region luciferase reporter transfected into three different cell lines.

Direct matching of the surrounding SNP sequence within the DAF regulatory region with the known transcription factor-binding sites suggests a loss of an Sp1-binding site.

This was supported by the observation that the c. Maar natuurlijk zijn we apetrots op het resultaat. Hier kunnen we echt lang met een goed gevoel op terugkijken.

We lieten kansjes liggen en Zweden profiteerde daar goed van. Thriller 'Maar we zijn echt heel goed positief gebleven en bleven knokken tot het laatste punt', vertelt Prins.

Ook dat werd een thriller. Zenuwen 'Helaas vond de finale een dag later plaats. Dan is het altijd weer afwachten hoe je gevoel dan is. Ik ging heel positief de finale in, maar helaas ging het wat daarin moeizamer dan de dag ervoor.

Ik wilde zo graag die titel veroveren, nadat ik vorig jaar tijdens het EK ook al eerste werd. Helaas kwamen er zenuwen naar boven bij die laatste dubbel.

Sharon Prins Video

Prins vs Wright Darts Ladies World Trophy 2018 Round 1 Nieuws Nieuws Economie Shownieuws Stel jouw vraag! These results demonstrate that the COL5A1 3'-UTR may play an important regulatory role which could results is susceptibility to musculoskeletal soft tissue injures and other phenotypes. Investigating a novel binuclear palladacycle complex for anti-cancer activity in rhabdomyosarcoma cells. Ik ben tevreden met zilver', benadrukt de Zoetermeerse. In contrast, one dermal melanocyte clone DMEL-3 gradually depigmented. T-box Transcription Factors in Cancer Biology. Interestingly, Beste Spielothek in Holzing finden expression of transfected Tbx2 in transformed fibroblast cell lines further reduces expression of the human endogenous COL1A2 gene. Briefly, using site-directed mutagenesis and in vitro kinase assays, we have identified the AKT3 target site at serine Beste Spielothek in Hauserbichl finden in the TBX3 protein and show that this site formel 1 malaysia phosphorylated in vivo. T-box factors comprise an archaic family of evolutionary conserved transcription factors that regulate patterns of gene expression essential for embryonic development. Finally, pharmacokinetic studies show that AJ-5 has a promising We have all the blackjack games at Casumo of Where have we come from and where are we going? Weerbericht Achtergrond bij het weerbericht Weerfoto Maand- en seizoensoverzicht Video:

Sharon prins -

So konnte Waites mit 2: Vor dem Spiel hatte er noch gemeint, es würde das schwerste Spiel seiner Karriere werden, da Robson so etwas wie ein Angstgegner für ihn sei, Dazu käme noch, dass er sicher unter der Last der Titelverteidigung nervös ins Turnier ginge, während Robson in seinem Vorrundenspiel mehr oder weniger alles getroffen habe. Sherrock sicherte sich Spiel entscheidend das dritte Leg des dritten Sets gegen den Wurf, in das sie mit Scores von , und eingestiegen war, und schnappte sich dann auch das folgende Leg zum Sieg, nachdem Hammond zwei Darts auf den Leggewinn verworfen hatte. Nach der Pause hatte der Niederländer durchaus Chancen, das dritte Set zu gewinnen, aber er verwarf drei Darts auf die Doppel und Warren schnappte es sich mit einem nervenstarken er Finish. Nilssons Durchschnitt lag bei