LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 17

Search options

  1. Article ; Online: Targeting senescent cells in translational medicine.

    Paez-Ribes, Marta / González-Gualda, Estela / Doherty, Gary J / Muñoz-Espín, Daniel

    EMBO molecular medicine

    2019  Volume 11, Issue 12, Page(s) e10234

    Abstract: Organismal ageing is a complex process driving progressive impairment of functionality and regenerative potential of tissues. Cellular senescence is a state of stable cell cycle arrest occurring in response to damage and stress and is considered a ... ...

    Abstract Organismal ageing is a complex process driving progressive impairment of functionality and regenerative potential of tissues. Cellular senescence is a state of stable cell cycle arrest occurring in response to damage and stress and is considered a hallmark of ageing. Senescent cells accumulate in multiple organs during ageing, contribute to tissue dysfunction and give rise to pathological manifestations. Senescence is therefore a defining feature of a variety of human age-related disorders, including cancer, and targeted elimination of these cells has recently emerged as a promising therapeutic approach to ameliorate tissue damage and promote repair and regeneration. In addition, in vivo identification of senescent cells has significant potential for early diagnosis of multiple pathologies. Here, we review existing senolytics, small molecules and drug delivery tools used in preclinical therapeutic strategies involving cellular senescence, as well as probes to trace senescent cells. We also review the clinical research landscape in senescence and discuss how identifying and targeting cellular senescence might positively affect pathological and ageing processes.
    MeSH term(s) Aging/physiology ; Animals ; Cellular Senescence/physiology ; Humans ; Translational Research, Biomedical/methods
    Language English
    Publishing date 2019-11-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.201810234
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6784: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

  2. Article ; Online: Development of Patient Derived Xenograft Models of Overt Spontaneous Breast Cancer Metastasis: A Cautionary Note.

    Paez-Ribes, Marta / Man, Shan / Xu, Ping / Kerbel, Robert S

    PloS one

    2016  Volume 11, Issue 6, Page(s) e0158034

    Abstract: Several approaches are being evaluated to improve the historically limited value of studying transplanted primary tumors derived by injection of cells from established cell lines for predicting subsequent cancer therapy outcomes in patients and clinical ... ...

    Abstract Several approaches are being evaluated to improve the historically limited value of studying transplanted primary tumors derived by injection of cells from established cell lines for predicting subsequent cancer therapy outcomes in patients and clinical trials. These approaches include use of genetically engineered mouse models (GEMMs) of spontaneous tumors, or patient tumor tissue derived xenografts (PDXs). Almost all such therapy studies utilizing such models involve treatment of established primary tumors. An alternative approach we have developed involves transplanted human tumor xenografts derived from established cell lines to treat mice with overt visceral metastases after primary tumor resection. The rationale is to mimic the more challenging circumstance of treating patients with late stage metastatic disease. These metastatic models entail prior in vivo selection of heritable, phenotypically stable variants with increased aggressiveness for spontaneous metastasis; they were derived by orthotopic injection of tumor cells followed by primary tumor resection and serial selection of distant spontaneous metastases, from which variant cell lines having a more aggressive heritable metastatic phenotype were established. We attempted to adopt this strategy for breast cancer PDXs. We studied five breast cancer PDXs, with the emphasis on two, called HCI-001 and HCI-002, both derived from triple negative breast cancer patients. However significant technical obstacles were encountered. These include the inherent slow growth rates of PDXs, the rarity of overt spontaneous metastases (detected in only 3 of 144 mice), very high rates of tumor regrowths at the primary tumor resection site, the failure of the few human PDX metastases isolated to manifest a more aggressive metastatic phenotype upon re-transplantation into new hosts, and the formation of metastases which were derived from de novo mouse thymomas arising in aged SCID mice that we used for the experiments. We discuss several possible strategies that may be employed to overcome these limitations. Uncovering the basis of the failure to detect a high rate of overt spontaneous distant metastases having a heritable phenotype in PDX models may reveal new insights into the biology and treatment of advanced metastatic disease.
    MeSH term(s) Animals ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Heterografts ; Humans ; Mice ; Mice, SCID ; Neoplasm Metastasis ; Neoplasm Transplantation ; Phenotype ; Triple Negative Breast Neoplasms/pathology
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0158034
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    Order via subito

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

    Inter-library loan at ZB MED

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

  3. Article ; Online: A Two-Photon Probe Based on Naphthalimide-Styrene Fluorophore for the

    Lozano-Torres, Beatriz / Blandez, Juan F / Galiana, Irene / Lopez-Dominguez, José A / Rovira, Miguel / Paez-Ribes, Marta / González-Gualda, Estela / Muñoz-Espín, Daniel / Serrano, Manuel / Sancenón, Félix / Martínez-Máñez, Ramón

    Analytical chemistry

    2021  Volume 93, Issue 5, Page(s) 3052–3060

    Abstract: Cellular senescence is a state of stable cell cycle arrest that can negatively affect the regenerative capacities of tissues and can contribute to inflammation and the progression of various aging-related diseases. Advances in ... ...

    Abstract Cellular senescence is a state of stable cell cycle arrest that can negatively affect the regenerative capacities of tissues and can contribute to inflammation and the progression of various aging-related diseases. Advances in the
    MeSH term(s) Animals ; Cellular Senescence ; Fibroblasts ; Mice ; Naphthalimides ; Photons ; Styrene
    Chemical Substances Naphthalimides ; Styrene (44LJ2U959V)
    Language English
    Publishing date 2021-01-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1508-8
    ISSN 1520-6882 ; 0003-2700
    ISSN (online) 1520-6882
    ISSN 0003-2700
    DOI 10.1021/acs.analchem.0c05447
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 4033: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

  4. Article ; Online: Potential Proinvasive or Metastatic Effects of Preclinical Antiangiogenic Therapy Are Prevented by Concurrent Chemotherapy.

    Paez-Ribes, Marta / Man, Shan / Xu, Ping / Kerbel, Robert S

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2015  Volume 21, Issue 24, Page(s) 5488–5498

    Abstract: Purpose: To resolve a controversy involving the therapeutic impact of antiangiogenic drugs and particularly antibodies targeting the VEGF pathway, namely, a body of preclinical mouse therapy studies showing such drugs can promote invasion and/or distant ...

    Abstract Purpose: To resolve a controversy involving the therapeutic impact of antiangiogenic drugs and particularly antibodies targeting the VEGF pathway, namely, a body of preclinical mouse therapy studies showing such drugs can promote invasion and/or distant metastasis when used as monotherapies. In contrast, clinical studies have not shown such promalignancy effects. However, most such clinical studies have involved patients also treated with concurrent chemotherapy highlighting the possibility that chemotherapy may prevent any potential promalignancy effect caused by an antiangiogenic drug treatment.
    Experimental design: The impact of antiangiogenic therapy using DC101, an antibody targeting mouse VEGFR-2 with or without concurrent chemotherapy was assessed in multiple human breast cancer xenograft models, where impact on orthotopic primary tumors was evaluated. Metastasis was also assessed during adjuvant and neoadjuvant plus adjuvant therapy, after surgical resection of primary tumors, with the same combination therapies.
    Results: Antiangiogenic therapy, while blunting tumor volume growth, was found to increase local invasion in multiple primary tumor models, including a patient-derived xenograft, but this effect was blocked by concurrent chemotherapy. Similarly, the combination of paclitaxel with DC101 caused a marked reduction of micro- or macrometastatic disease in contrast to DC101 monotherapy, which was associated with small increases in metastatic disease.
    Conclusions: Conventional wisdom is that targeted biologic antiangiogenic agents such as bevacizumab when used with chemotherapy increase the efficacy of the chemotherapy treatment. Our results suggest the reverse may be true as well-chemotherapy may improve the impact of antiangiogenic drug treatment and, as a result, overall efficacy. Clin Cancer Res; 21(24); 5488-98. ©2015 AACR.
    MeSH term(s) Angiogenesis Inhibitors/administration & dosage ; Angiogenesis Inhibitors/pharmacology ; Animals ; Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Biomarkers ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Female ; Humans ; Mice ; Neoadjuvant Therapy ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/mortality ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism ; Neovascularization, Pathologic/drug therapy ; Tumor Burden/drug effects ; Vascular Endothelial Growth Factor Receptor-2/antagonists & inhibitors ; Xenograft Model Antitumor Assays
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal ; Antineoplastic Agents ; Biomarkers ; DC101 monoclonal antibody ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
    Language English
    Publishing date 2015-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-15-0915
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 4223: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

  5. Article ; Online: The NALCN channel regulates metastasis and nonmalignant cell dissemination.

    Rahrmann, Eric P / Shorthouse, David / Jassim, Amir / Hu, Linda P / Ortiz, Mariaestela / Mahler-Araujo, Betania / Vogel, Peter / Paez-Ribes, Marta / Fatemi, Atefeh / Hannon, Gregory J / Iyer, Radhika / Blundon, Jay A / Lourenço, Filipe C / Kay, Jonathan / Nazarian, Rosalynn M / Hall, Benjamin A / Zakharenko, Stanislav S / Winton, Douglas J / Zhu, Liqin /
    Gilbertson, Richard J

    Nature genetics

    2022  Volume 54, Issue 12, Page(s) 1827–1838

    Abstract: We identify the sodium leak channel non-selective protein (NALCN) as a key regulator of cancer metastasis and nonmalignant cell dissemination. Among 10,022 human cancers, NALCN loss-of-function mutations were enriched in gastric and colorectal cancers. ... ...

    Abstract We identify the sodium leak channel non-selective protein (NALCN) as a key regulator of cancer metastasis and nonmalignant cell dissemination. Among 10,022 human cancers, NALCN loss-of-function mutations were enriched in gastric and colorectal cancers. Deletion of Nalcn from gastric, intestinal or pancreatic adenocarcinomas in mice did not alter tumor incidence, but markedly increased the number of circulating tumor cells (CTCs) and metastases. Treatment of these mice with gadolinium-a NALCN channel blocker-similarly increased CTCs and metastases. Deletion of Nalcn from mice that lacked oncogenic mutations and never developed cancer caused shedding of epithelial cells into the blood at levels equivalent to those seen in tumor-bearing animals. These cells trafficked to distant organs to form normal structures including lung epithelium, and kidney glomeruli and tubules. Thus, NALCN regulates cell shedding from solid tissues independent of cancer, divorcing this process from tumorigenesis and unmasking a potential new target for antimetastatic therapies.
    MeSH term(s) Humans ; Mice ; Animals ; Neoplasms ; Ion Channels/genetics ; Membrane Proteins/genetics
    Chemical Substances NALCN protein, human ; Ion Channels ; Membrane Proteins ; NALCN protein, mouse
    Language English
    Publishing date 2022-09-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-022-01182-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3613: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 46: Show issues

    Order via subito

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

  6. Article ; Online: Imaging and Molecular Annotation of Xenographs and Tumours (IMAXT): High throughput data and analysis infrastructure.

    González-Solares, Eduardo A / Dariush, Ali / González-Fernández, Carlos / Küpcü Yoldaş, Aybüke / Molaeinezhad, Alireza / Al Sa'd, Mohammad / Smith, Leigh / Whitmarsh, Tristan / Millar, Neil / Chornay, Nicholas / Falciatori, Ilaria / Fatemi, Atefeh / Goodwin, Daniel / Kuett, Laura / Mulvey, Claire M / Páez Ribes, Marta / Qosaj, Fatime / Roth, Andrew / Vázquez-García, Ignacio /
    Watson, Spencer S / Windhager, Jonas / Aparicio, Samuel / Bodenmiller, Bernd / Boyden, Ed / Caldas, Carlos / Harris, Owen / Shah, Sohrab P / Tavaré, Simon / Bressan, Dario / Hannon, Gregory J / Walton, Nicholas A

    Biological imaging

    2023  Volume 3, Page(s) e11

    Abstract: With the aim of producing a 3D representation of tumors, imaging and molecular annotation of xenografts and tumors (IMAXT) uses a large variety of modalities in order to acquire tumor samples and produce a map of every cell in the tumor and its host ... ...

    Abstract With the aim of producing a 3D representation of tumors, imaging and molecular annotation of xenografts and tumors (IMAXT) uses a large variety of modalities in order to acquire tumor samples and produce a map of every cell in the tumor and its host environment. With the large volume and variety of data produced in the project, we developed automatic data workflows and analysis pipelines. We introduce a research methodology where scientists connect to a cloud environment to perform analysis close to where data are located, instead of bringing data to their local computers. Here, we present the data and analysis infrastructure, discuss the unique computational challenges and describe the analysis chains developed and deployed to generate molecularly annotated tumor models. Registration is achieved by use of a novel technique involving spherical fiducial marks that are visible in all imaging modalities used within IMAXT. The automatic pipelines are highly optimized and allow to obtain processed datasets several times quicker than current solutions narrowing the gap between data acquisition and scientific exploitation.
    Language English
    Publishing date 2023-04-14
    Publishing country England
    Document type Journal Article
    ISSN 2633-903X
    ISSN (online) 2633-903X
    DOI 10.1017/S2633903X23000090
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

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

    Inter-library loan at ZB MED

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

  7. Article ; Online: Antitumor Effects of Anti-Semaphorin 4D Antibody Unravel a Novel Proinvasive Mechanism of Vascular-Targeting Agents.

    Zuazo-Gaztelu, Iratxe / Pàez-Ribes, Marta / Carrasco, Patricia / Martín, Laura / Soler, Adriana / Martínez-Lozano, Mar / Pons, Roser / Llena, Judith / Palomero, Luis / Graupera, Mariona / Casanovas, Oriol

    Cancer research

    2019  Volume 79, Issue 20, Page(s) 5328–5341

    Abstract: One of the main consequences of inhibition of neovessel growth and vessel pruning produced by angiogenesis inhibitors is increased intratumor hypoxia. Growing evidence indicates that tumor cells escape from this hypoxic environment to better nourished ... ...

    Abstract One of the main consequences of inhibition of neovessel growth and vessel pruning produced by angiogenesis inhibitors is increased intratumor hypoxia. Growing evidence indicates that tumor cells escape from this hypoxic environment to better nourished locations, presenting hypoxia as a positive stimulus for invasion. In particular, anti-VEGF/R therapies produce hypoxia-induced invasion and metastasis in a spontaneous mouse model of pancreatic neuroendocrine cancer (PanNET), RIP1-Tag2. Here, a novel vascular-targeting agent targeting semaphorin 4D (Sema4D) demonstrated impaired tumor growth and extended survival in the RIP1-Tag2 model. Surprisingly, although there was no induction of intratumor hypoxia by anti-Sema4D therapy, the increase in local invasion and distant metastases was comparable with the one produced by VEGFR inhibition. Mechanistically, the antitumor effect was due to an alteration in vascular function by modification of pericyte coverage involving platelet-derived growth factor B. On the other hand, the aggressive phenotype involved a macrophage-derived Sema4D signaling engagement, which induced their recruitment to the tumor invasive fronts and secretion of stromal cell-derived factor 1 (SDF1) that triggered tumor cell invasive behavior via CXCR4. A comprehensive clinical validation of the targets in different stages of PanNETs demonstrated the implication of both Sema4D and CXCR4 in tumor progression. Taken together, we demonstrate beneficial antitumor and prosurvival effects of anti-Sema4D antibody but also unravel a novel mechanism of tumor aggressivity. This mechanism implicates recruitment of Sema4D-positive macrophages to invasive fronts and their secretion of proinvasive molecules that ultimately induce local tumor invasion and distant metastasis in PanNETs. SIGNIFICANCE: An anti-semaphorin-4D vascular targeting agent demonstrates antitumor and prosurvival effects but also unravels a novel promalignant effect involving macrophage-derived SDF1 that promotes tumor invasion and metastasis, both in animal models and patients.
    MeSH term(s) Animals ; Antigens, CD ; Humans ; Mice ; Neoplasms ; Semaphorins ; Signal Transduction
    Chemical Substances Antigens, CD ; CD100 antigen ; Semaphorins
    Language English
    Publishing date 2019-06-25
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-18-3436
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

  8. Article ; Online: Aflibercept and Ang1 supplementation improve neoadjuvant or adjuvant chemotherapy in a preclinical model of resectable breast cancer.

    Wu, Florence T H / Paez-Ribes, Marta / Xu, Ping / Man, Shan / Bogdanovic, Elena / Thurston, Gavin / Kerbel, Robert S

    Scientific reports

    2016  Volume 6, Page(s) 36694

    Abstract: Phase III clinical trials evaluating bevacizumab (an antibody to the angiogenic ligand, VEGF-A) in breast cancer have found improved responses in the presurgical neoadjuvant setting but no benefits in the postsurgical adjuvant setting. The objective of ... ...

    Abstract Phase III clinical trials evaluating bevacizumab (an antibody to the angiogenic ligand, VEGF-A) in breast cancer have found improved responses in the presurgical neoadjuvant setting but no benefits in the postsurgical adjuvant setting. The objective of this study was to evaluate alternative antiangiogenic therapies, which target multiple VEGF family members or differentially modulate the Angiopoietin/Tie2 pathway, in a mouse model of resectable triple-negative breast cancer (TNBC). Neoadjuvant therapy experiments involved treating established orthotopic xenografts of an aggressive metastatic variant of the MDA-MB-231 human TNBC cell line, LM2-4. Adjuvant therapies were given after primary tumor resections to treat postsurgical regrowths and distant metastases. Aflibercept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) showed greater efficacy than nesvacumab (an anti-Ang2 antibody) as an add-on to neoadjuvant/adjuvant chemotherapy. Concurrent inhibition of Ang1 and Ang2 signaling (through an antagonistic anti-Tie2 antibody) was not more efficacious than selective Ang2 inhibition. In contrast, short-term perioperative BowAng1 (a recombinant Ang1 variant) improved the efficacy of adjuvant chemotherapy. In conclusion, concurrent VEGF pathway inhibition is more likely than Ang/Tie2 pathway inhibition (e.g., anti-Ang2, anti-Ang2/Ang1, anti-Tie2) to improve neoadjuvant/adjuvant chemotherapies for TNBC. Short-term perioperative Ang1 supplementation may also have therapeutic potential in conjunction with adjuvant chemotherapy for TNBC.
    MeSH term(s) Angiopoietin-1/pharmacology ; Animals ; Female ; Humans ; Mice ; Neoadjuvant Therapy ; Neoplasms, Experimental/drug therapy ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Receptors, Vascular Endothelial Growth Factor ; Recombinant Fusion Proteins/pharmacology ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Xenograft Model Antitumor Assays
    Chemical Substances ANGPT1 protein, human ; Angiopoietin-1 ; Recombinant Fusion Proteins ; aflibercept (15C2VL427D) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2016-11-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep36694
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

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

  9. Article ; Online: Pre- and post-operative anti-PD-L1 plus anti-angiogenic therapies in mouse breast or renal cancer models of micro- or macro-metastatic disease.

    Wu, Florence T H / Xu, Ping / Chow, Annabelle / Man, Shan / Krüger, Janna / Khan, Kabir A / Paez-Ribes, Marta / Pham, Elizabeth / Kerbel, Robert S

    British journal of cancer

    2018  Volume 120, Issue 2, Page(s) 196–206

    Abstract: Background: There are phase 3 clinical trials underway evaluating anti-PD-L1 antibodies as adjuvant (postoperative) monotherapies for resectable renal cell carcinoma (RCC) and triple-negative breast cancer (TNBC); in combination with antiangiogenic VEGF/ ...

    Abstract Background: There are phase 3 clinical trials underway evaluating anti-PD-L1 antibodies as adjuvant (postoperative) monotherapies for resectable renal cell carcinoma (RCC) and triple-negative breast cancer (TNBC); in combination with antiangiogenic VEGF/VEGFR2 inhibitors (e.g., bevacizumab and sunitinib) for metastatic RCC; and in combination with chemotherapeutics as neoadjuvant (preoperative) therapies for resectable TNBC.
    Methods: This study investigated these and similar clinically relevant drug combinations in highly translational preclinical models of micro- and macro-metastatic disease that spontaneously develop after surgical resection of primary kidney or breast tumours derived from orthotopic implantation of murine cancer cell lines (RENCA
    Results: In the RENCA
    Conclusions: Our preclinical data suggest that anti-PD-L1 plus sunitinib may warrant further investigation as an adjuvant therapy for RCC, while anti-PD-L1 may be improved by combining with chemotherapy in the neoadjuvant but not the adjuvant setting of treating breast cancer.
    MeSH term(s) Animals ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; Bevacizumab/administration & dosage ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Immunotherapy/methods ; Kidney Neoplasms/immunology ; Kidney Neoplasms/pathology ; Kidney Neoplasms/surgery ; Kidney Neoplasms/therapy ; Mammary Neoplasms, Animal/immunology ; Mammary Neoplasms, Animal/pathology ; Mammary Neoplasms, Animal/surgery ; Mammary Neoplasms, Animal/therapy ; Mice ; Neoadjuvant Therapy/methods ; Neovascularization, Pathologic/immunology ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/therapy ; Paclitaxel/administration & dosage ; Sunitinib/administration & dosage
    Chemical Substances B7-H1 Antigen ; Cd274 protein, mouse ; Bevacizumab (2S9ZZM9Q9V) ; Paclitaxel (P88XT4IS4D) ; Sunitinib (V99T50803M)
    Language English
    Publishing date 2018-11-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/s41416-018-0297-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.142: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

  10. Article ; Online: Anti-oncostatin M antibody inhibits the pro-malignant effects of oncostatin M receptor overexpression in squamous cell carcinoma.

    Kucia-Tran, Justyna A / Tulkki, Valtteri / Scarpini, Cinzia G / Smith, Stephen / Wallberg, Maja / Paez-Ribes, Marta / Araujo, Angela M / Botthoff, Jan / Feeney, Maria / Hughes, Katherine / Caffarel, Maria M / Coleman, Nicholas

    The Journal of pathology

    2018  Volume 244, Issue 3, Page(s) 283–295

    Abstract: The oncostatin M (OSM) receptor (OSMR) shows frequent gene copy number gains and overexpression in cervical squamous cell carcinomas (SCCs), associated with adverse clinical outcomes. In SCC cells that overexpress OSMR, the major ligand OSM induces ... ...

    Abstract The oncostatin M (OSM) receptor (OSMR) shows frequent gene copy number gains and overexpression in cervical squamous cell carcinomas (SCCs), associated with adverse clinical outcomes. In SCC cells that overexpress OSMR, the major ligand OSM induces multiple pro-malignant effects, including invasion, secretion of angiogenic factors, and metastasis. Here, we demonstrate, for the first time, that OSMR overexpression in SCC cells activates cell-autonomous feed-forward signalling, via further expression of OSMR and OSM and sustained STAT3 activation, despite expression of the negative regulator suppressor of cytokine signalling 3 (SOCS3). The pro-malignant effects associated with OSMR overexpression are critically mediated by JAK-STAT3 activation, which is induced by exogenous OSM and also by autocrine OSM-OSMR interactions. Importantly, specific inhibition of OSM-OSMR interactions by neutralizing antibodies significantly inhibits STAT3 activation and feed-forward signalling, leading to reduced invasion, angiogenesis, and metastasis. Our findings are supported by data from 1254 clinical SCC samples, in which OSMR levels correlated with multiple cognate genes, including OSM, STAT3, and downstream targets. These data strongly support the development of OSM-OSMR-blocking antibodies as biologically targeted therapies against SCCs of the cervix and other anatomical sites. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    MeSH term(s) Animals ; Antineoplastic Agents, Immunological/pharmacology ; Autocrine Communication ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/immunology ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/pathology ; Humans ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/immunology ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice, Inbred NOD ; Mice, SCID ; Oncostatin M/genetics ; Oncostatin M/metabolism ; Oncostatin M Receptor beta Subunit/antagonists & inhibitors ; Oncostatin M Receptor beta Subunit/genetics ; Oncostatin M Receptor beta Subunit/immunology ; Oncostatin M Receptor beta Subunit/metabolism ; Phosphorylation ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck/drug therapy ; Squamous Cell Carcinoma of Head and Neck/immunology ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Squamous Cell Carcinoma of Head and Neck/pathology ; Suppressor of Cytokine Signaling 3 Protein/genetics ; Suppressor of Cytokine Signaling 3 Protein/metabolism ; Up-Regulation ; Uterine Cervical Neoplasms/drug therapy ; Uterine Cervical Neoplasms/immunology ; Uterine Cervical Neoplasms/metabolism ; Uterine Cervical Neoplasms/pathology ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents, Immunological ; OSM protein, human ; OSMR protein, human ; Oncostatin M Receptor beta Subunit ; SOCS3 protein, human ; STAT3 Transcription Factor ; STAT3 protein, human ; Suppressor of Cytokine Signaling 3 Protein ; Oncostatin M (106956-32-5) ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
    Language English
    Publishing date 2018-01-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.5010
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.12: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

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

To top