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  1. Article ; Online: Epithelial-mesenchymal plasticity determines estrogen receptor positive breast cancer dormancy and epithelial reconversion drives recurrence

    Patrick Aouad / Yueyun Zhang / Fabio De Martino / Céline Stibolt / Simak Ali / Giovanna Ambrosini / Sendurai A. Mani / Kelly Maggs / Hazel M. Quinn / George Sflomos / Cathrin Brisken

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Volume 17

    Abstract: The study of tumour dormancy is limited by suitable in vivo models. Here the authors show that mammary intraductal breast cancer (BC) xenografts model estrogen receptor α-positive (ER+) BC dormancy and rapid metastatic progression characteristic of ... ...

    Abstract The study of tumour dormancy is limited by suitable in vivo models. Here the authors show that mammary intraductal breast cancer (BC) xenografts model estrogen receptor α-positive (ER+) BC dormancy and rapid metastatic progression characteristic of triple-negative (TN) BC. The dormant disseminated ER+ BC cells display characteristics of epithelial-mesenchymal plasticity and forced expression of E-cadherin allows them to overcome dormancy.
    Keywords Science ; Q
    Language English
    Publishing date 2022-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Author Correction

    Linda Smith / Raed Farzan / Simak Ali / Laki Buluwela / Adrian T. Saurin / David W. Meek

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    The responses of cancer cells to PLK1 inhibitors reveal a novel protective role for p53 in maintaining centrosome separation

    2018  Volume 1

    Abstract: A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper. ...

    Abstract A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2018-03-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: The responses of cancer cells to PLK1 inhibitors reveal a novel protective role for p53 in maintaining centrosome separation

    Linda Smith / Raed Farzan / Simak Ali / Laki Buluwela / Adrian T. Saurin / David W. Meek

    Scientific Reports, Vol 7, Iss 1, Pp 1-

    2017  Volume 12

    Abstract: Abstract Polo-like kinase-1 (PLK1) plays a major role in driving mitotic events, including centrosome disjunction and separation, and is frequently over-expressed in human cancers. PLK1 inhibition is a promising therapeutic strategy and works by ... ...

    Abstract Abstract Polo-like kinase-1 (PLK1) plays a major role in driving mitotic events, including centrosome disjunction and separation, and is frequently over-expressed in human cancers. PLK1 inhibition is a promising therapeutic strategy and works by arresting cells in mitosis due to monopolar spindles. The p53 tumour suppressor protein is a short-lived transcription factor that can inhibit the growth, or stimulate the death, of developing cancer cells. Curiously, although p53 normally acts in an anti-cancer capacity, it can offer significant protection against inhibitors of PLK1, but the events underpinning this effect are not known. Here, we show that functional p53 reduces the sensitivity to PLK1 inhibitors by permitting centrosome separation to occur, allowing cells to traverse mitosis and re-enter cycle with a normal complement of 2N chromosomes. Protection entails the activation of p53 through the DNA damage-response enzymes, ATM and ATR, and requires the phosphorylation of p53 at the key regulatory site, Ser15. These data highlight a previously unrecognised link between p53, PLK1 and centrosome separation that has therapeutic implications for the use of PLK1 inhibitors in the clinic.
    Keywords Medicine ; R ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2017-11-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Author Correction

    R. C. Coombes / Sacha Howell / Simon R. Lord / Laura Kenny / Janine Mansi / Zahi Mitri / Carlo Palmieri / Linnea I. Chap / Paul Richards / William Gradishar / Sagar Sardesai / Jason Melear / Joyce O’Shaughnessy / Patrick Ward / Pavani Chalasani / Tobias Arkenau / Richard D. Baird / Rinath Jeselsohn / Simak Ali /
    Glen Clack / Ashwani Bahl / Stuart McIntosh / Matthew G. Krebs

    Nature Communications, Vol 14, Iss 1, Pp 1-

    Dose escalation and expansion cohorts in patients with advanced breast cancer in a Phase I study of the CDK7-inhibitor samuraciclib

    2023  Volume 1

    Keywords Science ; Q
    Language English
    Publishing date 2023-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Light-triggered enzymatic reactions in nested vesicle reactors

    James W. Hindley / Yuval Elani / Catriona M. McGilvery / Simak Ali / Charlotte L. Bevan / Robert V. Law / Oscar Ces

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 6

    Abstract: Matryoshka doll-like, nested vesicles, each containing a different ingredient to a chemical reaction, can serve as microreactors. Here, the authors developed a system in which mixing of the ingredients can be induced by irradiation with ultraviolet light. ...

    Abstract Matryoshka doll-like, nested vesicles, each containing a different ingredient to a chemical reaction, can serve as microreactors. Here, the authors developed a system in which mixing of the ingredients can be induced by irradiation with ultraviolet light.
    Keywords Science ; Q
    Language English
    Publishing date 2018-03-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Light-triggered enzymatic reactions in nested vesicle reactors

    James W. Hindley / Yuval Elani / Catriona M. McGilvery / Simak Ali / Charlotte L. Bevan / Robert V. Law / Oscar Ces

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 6

    Abstract: Matryoshka doll-like, nested vesicles, each containing a different ingredient to a chemical reaction, can serve as microreactors. Here, the authors developed a system in which mixing of the ingredients can be induced by irradiation with ultraviolet light. ...

    Abstract Matryoshka doll-like, nested vesicles, each containing a different ingredient to a chemical reaction, can serve as microreactors. Here, the authors developed a system in which mixing of the ingredients can be induced by irradiation with ultraviolet light.
    Keywords Science ; Q
    Language English
    Publishing date 2018-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  7. Article ; Online: Genome-wide alterations of uracil distribution patterns in human DNA upon chemotherapeutic treatments

    Hajnalka L Pálinkás / Angéla Békési / Gergely Róna / Lőrinc Pongor / Gábor Papp / Gergely Tihanyi / Eszter Holub / Ádám Póti / Carolina Gemma / Simak Ali / Michael J Morten / Eli Rothenberg / Michele Pagano / Dávid Szűts / Balázs Győrffy / Beáta G Vértessy

    eLife, Vol

    2020  Volume 9

    Abstract: Numerous anti-cancer drugs perturb thymidylate biosynthesis and lead to genomic uracil incorporation contributing to their antiproliferative effect. Still, it is not yet characterized if uracil incorporations have any positional preference. Here, we ... ...

    Abstract Numerous anti-cancer drugs perturb thymidylate biosynthesis and lead to genomic uracil incorporation contributing to their antiproliferative effect. Still, it is not yet characterized if uracil incorporations have any positional preference. Here, we aimed to uncover genome-wide alterations in uracil pattern upon drug treatments in human cancer cell line models derived from HCT116. We developed a straightforward U-DNA sequencing method (U-DNA-Seq) that was combined with in situ super-resolution imaging. Using a novel robust analysis pipeline, we found broad regions with elevated probability of uracil occurrence both in treated and non-treated cells. Correlation with chromatin markers and other genomic features shows that non-treated cells possess uracil in the late replicating constitutive heterochromatic regions, while drug treatment induced a shift of incorporated uracil towards segments that are normally more active/functional. Data were corroborated by colocalization studies via dSTORM microscopy. This approach can be applied to study the dynamic spatio-temporal nature of genomic uracil.
    Keywords uracil-DNA ; genome-wide mapping ; U-DNA-Seq ; super-resolution microscopy ; anti-cancer drug treatment ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: ESR1 mutant breast cancers show elevated basal cytokeratins and immune activation

    Zheqi Li / Olivia McGinn / Yang Wu / Amir Bahreini / Nolan M. Priedigkeit / Kai Ding / Sayali Onkar / Caleb Lampenfeld / Carol A. Sartorius / Lori Miller / Margaret Rosenzweig / Ofir Cohen / Nikhil Wagle / Jennifer K. Richer / William J. Muller / Laki Buluwela / Simak Ali / Tullia C. Bruno / Dario A. A. Vignali /
    Yusi Fang / Li Zhu / George C. Tseng / Jason Gertz / Jennifer M. Atkinson / Adrian V. Lee / Steffi Oesterreich

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Volume 18

    Abstract: Mutations of ESR1, the gene encoding the estrogen receptor alpha, are associated with acquired resistance to therapy in luminalbreast cancer. Here the authors show that ESR1 mutant tumors gain basal-like features with increased expression of basal ... ...

    Abstract Mutations of ESR1, the gene encoding the estrogen receptor alpha, are associated with acquired resistance to therapy in luminalbreast cancer. Here the authors show that ESR1 mutant tumors gain basal-like features with increased expression of basal cytokeratines and immune activation.
    Keywords Science ; Q
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Development of a novel molecular sensor for imaging estrogen receptor-coactivator protein-protein interactions.

    Madryn C Lake / Quang-Dé Nguyen / Simak Ali / Eric O Aboagye

    PLoS ONE, Vol 7, Iss 8, p e

    2012  Volume 44160

    Abstract: Anti-estrogens, in particular tissue selective anti-estrogens, have been the bedrock of adjuvant therapy for patients with estrogen receptor alpha (ERα) positive breast cancer. Though current therapies have greatly enhanced patient prognosis, there ... ...

    Abstract Anti-estrogens, in particular tissue selective anti-estrogens, have been the bedrock of adjuvant therapy for patients with estrogen receptor alpha (ERα) positive breast cancer. Though current therapies have greatly enhanced patient prognosis, there continues to be an impetus for the development of improved anti-estrogens. ERα is a nuclear receptor transcription factor which activates gene expression through the recruitment of transcriptional coactivator proteins. The SRC family of coactivators, which includes AIB1, has been shown to be of particular importance for ERα mediated transcription. ERα-AIB1 interactions are indicative of gene expression and are inhibited by anti-estrogen treatment. We have exploited the interaction between ERα and AIB1 as a novel method for imaging ERα activity using a split luciferase molecular sensor. By producing a range of ERα ligand binding domain (ER-LBD) and AIB1 nuclear receptor interacting domain (AIB-RID) N- and C-terminal firefly luciferase fragment fusion proteins, constructs which exhibited more than a 10-fold increase in luciferase activity with E2 stimulation were identified. The specificity of the E2-stimulated luciferase activity to ERα-AIB1 interaction was validated through Y537S and L539/540A ER-LBD fusion protein mutants. The primed nature of the split luciferase assay allowed changes in ERα activity, with respect to the protein-protein interactions preceding transcription, to be assessed soon after drug treatment. The novel assay split luciferase detailed in this report enabled modulation of ERα activity to be sensitively imaged in vitro and in living subjects and potentially holds much promise for imaging the efficacy of novel ERα specific therapies.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Low Dose Iron Treatments Induce a DNA Damage Response in Human Endothelial Cells within Minutes.

    Inês G Mollet / Dilipkumar Patel / Fatima S Govani / Adam Giess / Koralia Paschalaki / Manikandan Periyasamy / Elaine C Lidington / Justin C Mason / Michael D Jones / Laurence Game / Simak Ali / Claire L Shovlin

    PLoS ONE, Vol 11, Iss 2, p e

    2016  Volume 0147990

    Abstract: Spontaneous reports from patients able to report vascular sequelae in real time, and recognition that serum non transferrin bound iron may reach or exceed 10μmol/L in the blood stream after iron tablets or infusions, led us to hypothesize that ... ...

    Abstract Spontaneous reports from patients able to report vascular sequelae in real time, and recognition that serum non transferrin bound iron may reach or exceed 10μmol/L in the blood stream after iron tablets or infusions, led us to hypothesize that conventional iron treatments may provoke acute vascular injury. This prompted us to examine whether a phenotype could be observed in normal human endothelial cells treated with low dose iron.Confluent primary human endothelial cells (EC) were treated with filter-sterilized iron (II) citrate or fresh media for RNA sequencing and validation studies. RNA transcript profiles were evaluated using directional RNA sequencing with no pre-specification of target sequences. Alignments were counted for exons and junctions of the gene strand only, blinded to treatment types.Rapid changes in RNA transcript profiles were observed in endothelial cells treated with 10μmol/L iron (II) citrate, compared to media-treated cells. Clustering for Gene Ontology (GO) performed on all differentially expressed genes revealed significant differences in biological process terms between iron and media-treated EC, whereas 10 sets of an equivalent number of randomly selected genes from the respective EC gene datasets showed no significant differences in any GO terms. After 1 hour, differentially expressed genes clustered to vesicle mediated transport, protein catabolism, and cell cycle (Benjamini p = 0.0016, 0.0024 and 0.0032 respectively), and by 6 hours, to cellular response to DNA damage stimulus most significantly through DNA repair genes FANCG, BLM, and H2AFX. Comet assays demonstrated that 10μM iron treatment elicited DNA damage within 1 hour. This was accompanied by a brisk DNA damage response pulse, as ascertained by the development of DNA damage response (DDR) foci, and p53 stabilization.These data suggest that low dose iron treatments are sufficient to modify the vascular endothelium, and induce a DNA damage response.
    Keywords Medicine ; R ; Science ; Q
    Subject code 612
    Language English
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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