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  1. Book: Interstitium, connective tissue and lymphatics

    Reed, Rolf K.

    Glasgow, UK, [1993]

    (Proceedings of the ... congress of the International Union of the Physiological Sciences ; 32 ; Portland Press proceedings ; 9)

    1995  

    Author's details ed. R. K. Reed
    Series title Proceedings of the ... congress of the International Union of the Physiological Sciences ; 32
    Portland Press proceedings ; 9
    Proceedings of the ... congress of the International Union of Physiological Sciences (IUPS)
    Collection Proceedings of the ... congress of the International Union of Physiological Sciences (IUPS)
    Keywords Extracellular Matrix / physiology / congresses ; Connective Tissue / physiology / congresses ; Lymphatic System / physiology / congresses
    Language English
    Size XIV, 341 S. : Ill., graph. Darst.
    Publisher Portland
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT007243462
    ISBN 1-85578-073-9 ; 978-1-85578-073-6
    Database Catalogue ZB MED Medicine, Health

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  2. Book: AUTOREGULATION OF INTERSTITIAL FLUID VOLUME IN RAT SKELETAL MUSCLE

    Reed, Rolf K.

    1982  

    Size GETR. ZAEHLUNG
    Document type Book
    Note BERGEN, UNIV., DISS., 1982
    HBZ-ID HT002724994
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: Stromal integrin α11-deficiency reduces interstitial fluid pressure and perturbs collagen structure in triple-negative breast xenograft tumors.

    Smeland, Hilde Ytre-Hauge / Lu, Ning / Karlsen, Tine V / Salvesen, Gerd / Reed, Rolf K / Stuhr, Linda

    BMC cancer

    2019  Volume 19, Issue 1, Page(s) 234

    Abstract: Background: Cancer progression is influenced by a pro-tumorigenic microenvironment. The aberrant tumor stroma with increased collagen deposition, contractile fibroblasts and dysfunctional vessels has a major impact on the interstitial fluid pressure ( ... ...

    Abstract Background: Cancer progression is influenced by a pro-tumorigenic microenvironment. The aberrant tumor stroma with increased collagen deposition, contractile fibroblasts and dysfunctional vessels has a major impact on the interstitial fluid pressure (PIF) in most solid tumors. An increased tumor PIF is a barrier to the transport of interstitial fluid into and within the tumor. Therefore, understanding the mechanisms that regulate pressure homeostasis can lead to new insight into breast tumor progression, invasion and response to therapy. The collagen binding integrin α11β1 is upregulated during myofibroblast differentiation and expressed on fibroblasts in the tumor stroma. As a collagen organizer and a probable link between contractile fibroblasts and the complex collagen network in tumors, integrin α11β1 could be a potential regulator of tumor PIF.
    Methods: We investigated the effect of stromal integrin α11-deficiency on pressure homeostasis, collagen organization and tumor growth using orthotopic and ectopic triple-negative breast cancer xenografts (MDA-MB-231 and MDA-MB-468) in wild type and integrin α11-deficient mice. PIF was measured by the wick-in-needle technique, collagen by Picrosirius Red staining and electron microscopy, and uptake of radioactively labeled 5FU by microdialysis. Further, PIF in heterospheroids composed of MDA-MB-231 cells and wild type or integrin α11-deficient fibroblasts was measured by micropuncture.
    Results: Stromal integrin α11-deficiency decreased PIF in both the orthotopic breast cancer models. A concomitant perturbed collagen structure was seen, with fewer aligned and thinner fibrils. Integrin α11-deficiency also impeded MDA-MB-231 breast tumor growth, but no effect was observed on drug uptake. No effects were seen in the ectopic model. By investigating the isolated effect of integrin α11-positive fibroblasts on MDA-MB-231 cells in vitro, we provide evidence that PIF regulation was mediated by integrin α11-positive fibroblasts.
    Conclusion: We hereby show the importance of integrin α11β1 in pressure homeostasis in triple-negative breast tumors, indicating a new role for integrin α11β1 in the tumor microenvironment. Our data suggest that integrin α11β1 has a pro-tumorigenic effect on triple-negative breast cancer growth in vivo. The significance of the local microenvironment is shown by the different effects of integrin α11β1 in the orthotopic and ectopic models, underlining the importance of choosing an appropriate preclinical model.
    MeSH term(s) Animals ; Cell Line, Tumor ; Collagen/chemistry ; Cytoprotection ; Extracellular Fluid/metabolism ; Female ; Gene Knockout Techniques ; Humans ; Integrin alpha Chains/genetics ; Integrins/metabolism ; Mice ; Neoplasm Transplantation ; Receptors, Collagen/metabolism ; Stromal Cells ; Triple Negative Breast Neoplasms/chemistry ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Tumor Microenvironment
    Chemical Substances Integrin alpha Chains ; Integrins ; Receptors, Collagen ; integrin alpha11, mouse ; integrin alpha11beta1 ; Collagen (9007-34-5)
    Language English
    Publishing date 2019-03-15
    Publishing country England
    Document type Journal Article
    ISSN 1471-2407
    ISSN (online) 1471-2407
    DOI 10.1186/s12885-019-5449-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Protein expression profiling of plasma and lungs at different stages of metastatic development in a human triple negative breast cancer xenograft model.

    Tveitarås, Maria K / Selheim, Frode / Sortland, Kristina / Reed, Rolf K / Stuhr, Linda

    PloS one

    2019  Volume 14, Issue 5, Page(s) e0215909

    Abstract: The main objective of this study was to identify single proteins or protein networks that might be used as diagnostic biomarkers or for therapeutic purposes by evaluating the protein expression profiling of plasma and lungs at different stages of ... ...

    Abstract The main objective of this study was to identify single proteins or protein networks that might be used as diagnostic biomarkers or for therapeutic purposes by evaluating the protein expression profiling of plasma and lungs at different stages of metastatic development in a human triple negative MDA-MB-231 breast cancer xenograft model. MDA-MB-231 tumour cells were injected into the mammary fat pads on one side of the groin area. The mice were sacrificed day 19 (pre-metastases) and day 54 (metastases). Non-injected mice served as controls. Plasma was collected and lungs harvested for both immunohistochemistry and protein analysis. The most striking observation in plasma was the initial reduction in haptoglobin level at the pre-metastatic stage, to a following significant increase in haptoglobin level at the metastatic stage, with a more than 4000-fold increase from the pre-metastatic to the metastatic phase. A corresponding increase in haptoglobin level was also found in lung tissue after metastasis. Fibrinogen beta chain also had a similar change in expression level in plasma as haptoglobin, however not as prominent. There were also changes in plasma thrombospondin-4 and transferrin receptor protein 1 levels, from an increase at the pre-metastatic stage, to a significant fall when metastases were established. This suggests that especially changes in haptoglobin, but also fibrinogen beta chain, thrombospondin-4 and transferrin receptor protein 1 is indicative of metastasis, at least in this breast cancer model, and should be further evaluated as general breast cancer biomarkers.
    MeSH term(s) Animals ; Biomarkers, Tumor/blood ; Blood Proteins/analysis ; Blood Proteins/metabolism ; Cell Line, Tumor ; Female ; Humans ; Lung/metabolism ; Lung/pathology ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Lung Neoplasms/secondary ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Metastasis ; Neoplasm Staging ; Proteomics/methods ; Transplantation, Heterologous ; Triple Negative Breast Neoplasms/pathology
    Chemical Substances Biomarkers, Tumor ; Blood Proteins
    Language English
    Publishing date 2019-05-01
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0215909
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Epac1 Is Crucial for Maintenance of Endothelial Barrier Function through A Mechanism Partly Independent of Rac1.

    García-Ponce, Alexander / Schuster, Katharina / Døskeland, Stein-Ove / Reed, Rolf K / Curry, Fitz-Roy E / Waschke, Jens / Radeva, Mariya Y

    Cells

    2020  Volume 9, Issue 10

    Abstract: Epac1 (exchange protein activated by cAMP) stabilizes the endothelial barrier, but detailed studies are limited by the side effects of pharmacological Epac1 modulators and transient transfections. Here, we compare the key properties of barriers between ... ...

    Abstract Epac1 (exchange protein activated by cAMP) stabilizes the endothelial barrier, but detailed studies are limited by the side effects of pharmacological Epac1 modulators and transient transfections. Here, we compare the key properties of barriers between endothelial cells derived from wild-type (WT) and Epac1-knockout (KO) mice myocardium. We found that KO cell layers, unlike WT layers, had low and cAMP-insensitive trans-endothelial resistance (TER). They also had fragmented VE-cadherin staining despite having augmented cAMP levels and increased protein expression of Rap1, Rac1, RhoA, and VE-cadherin. The simultaneous direct activation of Rac1 and RhoA by CN04 compensated Epac1 loss, since TER was increased. In KO-cells, inhibition of Rac1 activity had no additional effect on TER, suggesting that other mechanisms compensate the inhibition of the Rac1 function to preserve barrier properties. In summary, Epac1 is crucial for baseline and cAMP-mediated barrier stabilization through mechanisms that are at least partially independent of Rac1.
    MeSH term(s) Animals ; Antigens, CD/genetics ; Cadherins/genetics ; Cell Membrane Permeability/drug effects ; Cyclic AMP/genetics ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Gene Expression Regulation/drug effects ; Guanine Nucleotide Exchange Factors/genetics ; Humans ; Mice ; Mice, Knockout ; Myocardium/metabolism ; Myocardium/pathology ; Neuropeptides/agonists ; Neuropeptides/genetics ; Signal Transduction/genetics ; Transcriptional Activation/drug effects ; rac1 GTP-Binding Protein/agonists ; rac1 GTP-Binding Protein/genetics ; rap1 GTP-Binding Proteins/drug effects ; rhoA GTP-Binding Protein/agonists ; rhoA GTP-Binding Protein/genetics
    Chemical Substances Antigens, CD ; Cadherins ; Epac protein, mouse ; Guanine Nucleotide Exchange Factors ; Neuropeptides ; Rac1 protein, mouse ; cadherin 5 ; Cyclic AMP (E0399OZS9N) ; Rap1 protein, mouse (EC 3.6.5.2) ; RhoA protein, mouse (EC 3.6.5.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; rap1 GTP-Binding Proteins (EC 3.6.5.2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2020-09-25
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells9102170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Hyperbaric oxygen treatment did not significantly affect radiation injury in the mandibular area of rats.

    Sønstevold, Tonje / Johannessen, Anne Christine / Reed, Rolf K / Salvesen, Gerd S / Stuhr, Linda

    Oral surgery, oral medicine, oral pathology and oral radiology

    2018  Volume 125, Issue 2, Page(s) 112–119

    Abstract: Objective: Hyperbaric oxygen therapy (HBOT) has been used to enhance microcirculation and thereby oxygen tension in tissues. The present study aimed to investigate the effect of HBOT on radiation injury in the mandibular area of rats.: Study design: ... ...

    Abstract Objective: Hyperbaric oxygen therapy (HBOT) has been used to enhance microcirculation and thereby oxygen tension in tissues. The present study aimed to investigate the effect of HBOT on radiation injury in the mandibular area of rats.
    Study design: The left mandibles of rats were irradiated by external radiotherapy (15 Gy every other week for a total of 75 Gy). Four HBOT strategies were used: 2 prophylactic groups receiving HBOT either between each radiation treatment or immediately following terminated radiation treatment, and 2 therapeutic groups receiving HBOT after the latent period of 6 weeks after irradiation either every day (standard HBOT protocol) or 3 days a week for 6 weeks. Tissue samples of the irradiated area were taken from skin, the salivary gland, and the mandible. All tissues were stained with hematoxylin and eosin for morphologic examination. Furthermore, skin samples were stained with CD31 for blood vessel analysis.
    Results: There was no change in blood vessel density or morphology between controls and HBOT tissues after radiation. The dentin of 2 of the 5 rats that received HBOT either normalized or was not affected by irradiation.
    Conclusions: HBOT did not affect radiation injury of the mandibular area in rats within 12 weeks after irradiation.
    MeSH term(s) Animals ; Disease Models, Animal ; Hyperbaric Oxygenation/methods ; Male ; Mandible/blood supply ; Mandible/radiation effects ; Microcirculation ; Radiation Dosage ; Radiation Injuries/therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley
    Language English
    Publishing date 2018
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2650843-6
    ISSN 2212-4411 ; 2212-4403
    ISSN (online) 2212-4411
    ISSN 2212-4403
    DOI 10.1016/j.oooo.2017.10.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Integrin α

    Lidén, Åsa / Karlsen, Tine Veronika / Guss, Bengt / Reed, Rolf K / Rubin, Kristofer

    Experimental physiology

    2018  Volume 103, Issue 5, Page(s) 629–634

    Abstract: New findings: What is the central question of this study? Collagen-binding β: Abstract: Accumulated data indicate that cell-mediated contraction of reconstituted collagenous gels in vitro can serve as a model for cell-mediated control of interstitial ...

    Abstract New findings: What is the central question of this study? Collagen-binding β
    Abstract: Accumulated data indicate that cell-mediated contraction of reconstituted collagenous gels in vitro can serve as a model for cell-mediated control of interstitial fluid pressure (P
    MeSH term(s) Animals ; Collagen/metabolism ; Edema/metabolism ; Extracellular Fluid/metabolism ; Extracellular Matrix/metabolism ; Fibronectins/metabolism ; Integrin alphaVbeta3/metabolism ; Integrin beta1/metabolism ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Platelet-Derived Growth Factor/metabolism ; Pressure
    Chemical Substances Fibronectins ; Integrin alphaVbeta3 ; Integrin beta1 ; Platelet-Derived Growth Factor ; Collagen (9007-34-5)
    Language English
    Publishing date 2018-03-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/EP086902
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Transcapillary exchange: role and importance of the interstitial fluid pressure and the extracellular matrix.

    Reed, Rolf K / Rubin, Kristofer

    Cardiovascular research

    2010  Volume 87, Issue 2, Page(s) 211–217

    Abstract: This review will summarize current knowledge on the role of the extracellular matrix (ECM) in general and on the interstitial fluid pressure (P(if)) in particular with regard to their importance in transcapillary exchange. The fluid volume in the ... ...

    Abstract This review will summarize current knowledge on the role of the extracellular matrix (ECM) in general and on the interstitial fluid pressure (P(if)) in particular with regard to their importance in transcapillary exchange. The fluid volume in the interstitial space is normally regulated within narrow limits by automatic re-adjustment of the interstitial hydrostatic and colloid osmotic pressures in response to perturbations in capillary filtration and by the lymphatics. Contrary to this commonly accepted view, P(if) can become an active force and create a fluid flux across the capillaries in several inflammatory reactions and trauma situations rather than limit the changes occurring. The molecular mechanisms involved in the lowering of P(if) include the release of cellular tension exerted on the collagen and microfibril networks in the connective tissue via the collagen-binding beta(1)-integrins, thereby allowing the glycosaminoglycan ground substance, which is normally underhydrated, to expand and take up fluid. Several growth factors and cytokines, including the platelet-derived growth factor BB, are able to reverse a lowering of P(if) and restore the normal compaction of the ECM. The magnitude of the lowering of P(if) varies with the inflammatory response. In several inflammatory reactions, a lowering of P(if) to -5 to -10 mmHg is seen, which will increase capillary filtration by 10-20 times since the normal capillary filtration pressure is usually 0.5-1 mmHg (skin and skeletal muscle). Unless this lowering of P(if) is taken into account, the enhanced solute flux resulting from an inflammatory response will be ascribed to an increased capillary permeability.
    MeSH term(s) Animals ; Body Fluids/metabolism ; Capillaries/immunology ; Capillaries/metabolism ; Capillaries/physiopathology ; Capillary Permeability ; Cytoskeleton/metabolism ; Edema/metabolism ; Edema/physiopathology ; Endothelium, Vascular/immunology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Extracellular Fluid/metabolism ; Extracellular Matrix/metabolism ; Homeostasis ; Humans ; Hydrostatic Pressure ; Inflammation/metabolism ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Integrin alpha2beta1/metabolism ; Integrin beta1/metabolism ; Models, Cardiovascular ; Osmotic Pressure ; Signal Transduction
    Chemical Substances Inflammation Mediators ; Integrin alpha2beta1 ; Integrin beta1
    Language English
    Publishing date 2010-07-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvq143
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Corticotropin-releasing factor reduces tumor volume, halts further growth, and enhances the effect of chemotherapy in 4T1 mammary carcinoma in mice.

    Stuhr, Linda E B / Wei, Eddie T / Reed, Rolf K

    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    2013  Volume 35, Issue 2, Page(s) 1365–1370

    Abstract: The present study examines the effect of the endogenous neuroendocrine factor, corticotropin-releasing factor (CRF), alone or in combination with 5-fluorouracil (5-FU), on 4T1 mammary tumor cells in vitro and in vivo. CRF has been detected in breast ... ...

    Abstract The present study examines the effect of the endogenous neuroendocrine factor, corticotropin-releasing factor (CRF), alone or in combination with 5-fluorouracil (5-FU), on 4T1 mammary tumor cells in vitro and in vivo. CRF has been detected in breast cancer tissues; however, the biological effects reported in the literature are sparse and variable. We found that exogenously administered CRF significantly reduced tumor growth without influencing angiogenesis or cell death. Furthermore, CRF reduced tumor interstitial fluid pressure (Pif) and potentiated the effect of 5-FU. These results show that CRF has antitumor effect on mammary carcinoma in mice.
    MeSH term(s) Animals ; Apoptosis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Corticotropin-Releasing Hormone/administration & dosage ; Female ; Fluorouracil/administration & dosage ; Humans ; Mammary Neoplasms, Animal/drug therapy ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/pathology ; Mice ; Neovascularization, Pathologic
    Chemical Substances Corticotropin-Releasing Hormone (9015-71-8) ; Fluorouracil (U3P01618RT)
    Language English
    Publishing date 2013-09-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605825-5
    ISSN 1423-0380 ; 0289-5447 ; 1010-4283
    ISSN (online) 1423-0380
    ISSN 0289-5447 ; 1010-4283
    DOI 10.1007/s13277-013-1186-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Single factors alone can induce mesenchymal-like morphology, but not promote full EMT in breast cancer cell lines with different hormone statuses.

    Tveitarås, Maria K / Reigstad, Inga / Leiss, Lina / Reed, Rolf K / Stuhr, Linda

    Experimental cell research

    2017  Volume 359, Issue 1, Page(s) 257–265

    Abstract: Background: Epithelial to mesenchymal transition (EMT) is considered to be important for cancer invasion and metastasis. Tumour hypoxia, in addition to Transforming Growth Factor-β (TGF-β) and Notch, amongst others, have been suggested to be involved in ...

    Abstract Background: Epithelial to mesenchymal transition (EMT) is considered to be important for cancer invasion and metastasis. Tumour hypoxia, in addition to Transforming Growth Factor-β (TGF-β) and Notch, amongst others, have been suggested to be involved in EMT. We therefore investigated if hypoxia, TGF-β1 and the Notch ligand Jagged-1 alone induced morphological changes with corresponding EMT signatures in different epithelial breast cancer cell lines in vitro. Furthermore, we also studied whether or not TGF-β1, or Jagged-1 in combination with hypoxia added any effect on EMT.
    Methods: The cells were exposed to normoxia or hypoxia alone or in combination with TGF-β1 or Jagged-1. Morphological responses to treatment were investigated by light microscopy, and changes in markers for EMT and hypoxia were evaluated by western blot analysis and immunofluorescence studies.
    Results: One of the four cell lines (MCF7) became elongated and highly multipolar, indicative of EMT, following hypoxia, TGF-β1 and Jagged-1 treatment per se with the most distinct morphological shift seen with Jagged-1 treatment in combination with hypoxia. Also, when regarding hypoxia, MCF7 cells showed the greatest change in EMT-markers of the four cell lines tested, but these changes were not consistent with a typical EMT pattern. The morphology of BT474 cells was not altered following Jagged-1 treatment, however, Jagged-1 increased E-cadherin levels. Morphology was changed following TGF-β1 treatment of BT474 cells, but it did not affect E-cadherin levels. Neither Jagged-1 nor TGF-β1 altered the levels of Vimentin in the BT474 cell line. The E-cadherin responses to hypoxia varied with end-point in both MCF7 and BT474 cells, and in most cases were not consistent with EMT.
    Conclusion: Our results using four different breast cancer cell lines in vitro do not provide evidence that EMT is induced by hypoxia alone or in combination with TGF-β1 or the Notch ligand Jagged-1. The inconsistency in morphological appearance and EMT-markers, as well as the time dependent variation in E-cadherin responses could not support EMT. Importantly, there was not one single common response pattern to the stimuli used, suggesting that cell lines with different hormone statuses display individual traits that respond differently to the stimuli applied. Thus, based on the present results, common statements that single factors by themselves can induce EMT seem questionable.
    MeSH term(s) Basic Helix-Loop-Helix Transcription Factors/metabolism ; Blotting, Western ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Hypoxia/drug effects ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition/drug effects ; Female ; Hormones/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Ligands ; Mesoderm/drug effects ; Mesoderm/pathology ; Receptors, Notch/metabolism ; Serrate-Jagged Proteins/metabolism ; Transforming Growth Factor beta1/pharmacology
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; HIF1A protein, human ; Hormones ; Hypoxia-Inducible Factor 1, alpha Subunit ; Ligands ; Receptors, Notch ; Serrate-Jagged Proteins ; Transforming Growth Factor beta1 ; endothelial PAS domain-containing protein 1
    Language English
    Publishing date 2017-10-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2017.07.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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