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  • 51.
    Vazquez Rodriguez, Gabriela
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Abrahamsson, Annelie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Jensen, Lasse D
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Pharmacology.
    Dabrosin, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Adipocytes Promote Early Steps of Breast Cancer Cell Dissemination via Interleukin-82018In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 9, p. 1-17, article id 1767Article in journal (Refereed)
    Abstract [en]

    Fat is a major tissue component in human breast cancer (BC). Whether breast adipocytes (BAd) affect early stages of BC metastasis is yet unknown. BC progression is dependent on angiogenesis and inflammation, and interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) are key regulators of these events. Here, we show that BAd increased the dissemination of estrogen receptor positive BC cells (BCC) in vivo in the zebrafish model of metastasis, while dissemination of the more aggressive and metastatic BCC such as estrogen receptor negative was unaffected. While anti-VEGF and anti-IL-8 exhibited equal inhibition of angiogenesis at the primary tumor site, anti-IL-8 reduced BCC dissemination whereas anti-VEGF had minor effects on this early metastatic event. Mechanistically, overexpression of cell-adhesion molecules in BCC and neutrophils via IL-8 increased the dissemination of BCC. Importantly, the extracellular in vivo levels of IL-8 were 40-fold higher than those of VEGF in human BC. Our results suggest that IL-8 is a clinical relevant and promising therapeutic target for human BC.

  • 52.
    Vazquez Rodriguez, Gabriela
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Abrahamsson, Annelie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Jensen, Lasse
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Region Östergötland, Center for Diagnostics, Department of Clinical Pharmacology. Linköping University, Faculty of Medicine and Health Sciences.
    Dabrosin, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Estradiol promotes breast cancer cell migration via recruitment and activation of neutrophils2017In: Cancer Immunology research, ISSN 2326-6066, Vol. 5, no 3, p. 234-247, article id 28159748Article in journal (Refereed)
    Abstract [en]

    Estradiol (E2) plays a key role in breast cancer progression. Most breast cancer recurrences express the estrogen receptor (ER), but nearly 50% of patients are resistant to antiestrogen therapy. Novel therapeutic targets of ER-positive breast cancers are needed. Protumoral neutrophils expressing the lymphocyte function-associated antigen 1 (LFA-1) integrin may mediate cancer metastasis, and TGFβ1 is the major chemoattractant for neutrophils. The role of E2 in neutrophil–ER+ breast cancer cell interactions is unknown. We studied this in vivo using murine breast cancers in immunocompetent mice and human breast cancers in nude mice. Cell dissemination was evaluated in a zebrafish model, and microdialysis of breast cancer patients was performed. In vitro studies were done with mammosphere cultures of breast cancer cells and human neutrophils. We found that E2 increased the number of LFA-1+ neutrophils recruited to the invasive edge of mouse tumors, increased TGFβ1 secretion and promoted neutrophil infiltration in mammospheres, and induced overexpression of LFA-1 in neutrophils. In zebrafish, in the presence of E2, neutrophils increased dissemination of ER+ breast cancer cells via LFA-1 and TGFβ1, thus causing noninvasive cancer cells to be highly metastatic. Time-lapse imaging in zebrafish revealed close interactions of neutrophils with cancer cells, which drove breast cancer metastasis. We also found that extracellular TGFβ1 was overproduced in human breast cancer tissue compared with adjacent normal breast tissue. Thus, E2 can regulate immune/cancer cell interactions in tumor microenvironments. Our results indicate that extracellular TGFβ1 is a relevant target in human breast cancer.

  • 53.
    Vazquez Rodriguez, Gabriela
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Abrahamsson, Annelie
    Linköping University, Department of Clinical and Experimental Medicine.
    Jensen, Lasse
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Pharmacology.
    Dabrosin, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Neutrophils Promote Breast Cancer Progression and Metastasis via LFA-1 Integrin2015Conference paper (Other academic)
    Abstract [en]

    Cancer is considered an inflammatory condition where immune cells play an important role in progression and metastasis. Neutrophils may be pro- or antitumorigenic, depending on their phenotype or the number of infiltrating neutrophils in the tumor microenvironment. Massive infiltration of neutrophils in cancer tissue may elicit a cytotoxic effect, leading to tumor regression, whereas a S139 low-grade neutrophil gradient is tumor progressive. Chemokines, cytokines, and growth factors present in the tumor microenvironment, as well as cell-cell interactions mediated by integrins have shown to be determinant steps for cancer cells to break through the endothelial wall and establish metastatic niches. In this work we evaluated the role of lymphocyte functionassociated antigen 1 (LFA-1) integrin in neutrophils-mediated metastasis of estrogen receptor positive breast cancer cells (MCF-7) cells in a tumor xenograft model in zebrafish and in neutrophil infiltration in MCF-7 mammospheres. The metastatic capability of MCF-7 cells was evaluated in presence or absence of human neutrophils and with/without estradiol treatment. Two days old zebrafish embryos were injected into the perivitelline space with labeled MCF-7 cells and human neutrophils, an anti-human LFA-1 antibody (CD11a) was included. We show that estradiol treatment significantly increased the infiltration of neutrophils into MCF-7 mammospheres and this infiltration was significantly reduced by the presence of an anti-human CD11a antibody. Co-injection of MCF-7 cells with neutrophils significantly increased the migration of MCF-7 cells to distant sites in zebrafish and this effect was inhibited by using an anti-human CD11a antibody. We conclude that neutrophils affect the dissemination of breast cancer cells via LFA-1 integrin. Although estradiol increased the number of infiltrating neutrophils into mammospheres exposure to estradiol seemed to have minor effects on the dissemination in the zebrafish.

  • 54.
    Wang, Zongwei
    et al.
    Department of Urology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
    Dabrosin, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Yin, Xin
    Medicine and Research Services, Veterans Affairs San Diego Healthcare System & University of California, San Diego, San Diego, CA, USA.
    Fuster, Mark M
    Medicine and Research Services, Veterans Affairs San Diego Healthcare System & University of California, San Diego, San Diego, CA, USA.
    Arreola, Alexandra
    Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
    Rathmell, W Kimryn
    Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
    Generali, Daniele
    Molecular Therapy and Pharmacogenomics Unit, AO Isituti Ospitalieri di Cremona, Cremona, Italy.
    Nagaraju, Ganji P
    Department of Hematology and Medical Oncology, Emory University, Atlanta, GA, USA.
    El-Rayes, Bassel
    Department of Hematology and Medical Oncology, Emory University, Atlanta, GA, USA.
    Ribatti, Domenico
    Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy, National Cancer Institute Giovanni Paolo II, Bari, Italy.
    Chen, Yi Charlie
    Department of Biology, Alderson Broaddus University, Philippi, WV, USA.
    Honoki, Kanya
    Department of Orthopedic Surgery, Arthroplasty and Regenerative Medicine, Nara Medical University, Nara, Japan.
    Fujii, Hiromasa
    Department of Orthopedic Surgery, Arthroplasty and Regenerative Medicine, Nara Medical University, Nara, Japan.
    Georgakilas, Alexandros G
    Physics Department, School of Applied Mathematics and Physical Sciences, National Technical University of Athens, Athens, Greece.
    Nowsheen, Somaira
    Mayo Graduate School, Mayo Clinic College of Medicine, Rochester, MN, USA.
    Amedei, Amedeo
    Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
    Niccolai, Elena
    Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
    Amin, Amr
    Department of Biology, College of Science, United Arab Emirate University, United Arab EmiratesFaculty of Science, Cairo University, Cairo, Egypt.
    Ashraf, S Salman
    Department of Chemistry, College of Science, United Arab Emirate University, United Arab Emirates.
    Helferich, Bill
    University of Illinois at Urbana Champaign, Urbana, IL, USA.
    Yang, Xujuan
    University of Illinois at Urbana Champaign, Urbana, IL, USA.
    Guha, Gunjan
    School of Chemical and Bio Technology, SASTRA University, Thanjavur, India.
    Bhakta, Dipita
    School of Chemical and Bio Technology, SASTRA University, Thanjavur, India.
    Ciriolo, Maria Rosa
    Department of Biology, University of Rome “Tor Vergata”, Rome, Italy.
    Aquilano, Katia
    Department of Biology, University of Rome “Tor Vergata”, Rome, Italy.
    Chen, Sophie
    Ovarian and Prostate Cancer Research Trust Laboratory, Guilford, Surrey, UK.
    Halicka, Dorota
    New York Medical College, New York City, NY, USA.
    Mohammed, Sulma I
    Department of Comparative Pathobiology, Purdue University Center for Cancer Research, West Lafayette, IN, USA.
    Azmi, Asfar S
    School of Medicine, Wayne State University, Detroit, MI, USA.
    Bilsland, Alan
    Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
    Keith, W Nicol
    Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
    Jensen, Lasse D
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Broad targeting of angiogenesis for cancer prevention and therapy2015In: Seminars in Cancer Biology, ISSN 1044-579X, E-ISSN 1096-3650, Vol. S1044-579X, no 15, p. 00002-00004Article, review/survey (Refereed)
    Abstract [en]

    Deregulation of angiogenesis - the growth of new blood vessels from an existing vasculature - is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development. Unfortunately the clinically approved anti-angiogenic drugs in use today are only effective in a subset of the patients, and many who initially respond develop resistance over time. Also, some of the anti-angiogenic drugs are toxic and it would be of great importance to identify alternative compounds, which could overcome these drawbacks and limitations of the currently available therapy. Finding "the most important target" may, however, prove a very challenging approach as the tumor environment is highly diverse, consisting of many different cell types, all of which may contribute to tumor angiogenesis. Furthermore, the tumor cells themselves are genetically unstable, leading to a progressive increase in the number of different angiogenic factors produced as the cancer progresses to advanced stages. As an alternative approach to targeted therapy, options to broadly interfere with angiogenic signals by a mixture of non-toxic natural compound with pleiotropic actions were viewed by this team as an opportunity to develop a complementary anti-angiogenesis treatment option. As a part of the "Halifax Project" within the "Getting to know cancer" framework, we have here, based on a thorough review of the literature, identified 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy: (1) endothelial cell migration/tip cell formation, (2) structural abnormalities of tumor vessels, (3) hypoxia, (4) lymphangiogenesis, (5) elevated interstitial fluid pressure, (6) poor perfusion, (7) disrupted circadian rhythms, (8) tumor promoting inflammation, (9) tumor promoting fibroblasts and (10) tumor cell metabolism/acidosis. Following this analysis, we scrutinized the available literature on broadly acting anti-angiogenic natural products, with a focus on finding qualitative information on phytochemicals which could inhibit these targets and came up with 10 prototypical phytochemical compounds: (1) oleic acid, (2) tripterine, (3) silibinin, (4) curcumin, (5) epigallocatechin-gallate, (6) kaempferol, (7) melatonin, (8) enterolactone, (9) withaferin A and (10) resveratrol. We suggest that these plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to cause excessive toxicity. All the targets and phytochemical approaches were further cross-validated against their effects on other essential tumorigenic pathways (based on the "hallmarks" of cancer) in order to discover possible synergies or potentially harmful interactions, and were found to generally also have positive involvement in/effects on these other aspects of tumor biology. The aim is that this discussion could lead to the selection of combinations of such anti-angiogenic compounds which could be used in potent anti-tumor cocktails, for enhanced therapeutic efficacy, reduced toxicity and circumvention of single-agent anti-angiogenic resistance, as well as for possible use in primary or secondary cancer prevention strategies.

  • 55.
    Xue, Yuan
    et al.
    Karolinska Institute.
    Lim, Sharon
    Karolinska Institute.
    Yang, Yunlong
    Karolinska Institute.
    Wang, Zongwei
    Karolinska Institute.
    Dahl Ejby Jensen, Lasse
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences.
    Hedlund, Eva-Maria
    Karolinska Institute.
    Andersson, Patrik
    Karolinska Institute.
    Sasahara, Masakiyo
    Toyama University.
    Larsson, Ola
    Karolinska Institute.
    Galter, Dagmar
    Karolinska Institute.
    Gao, Renhai
    Karolinska Institute.
    Hosaka, Kayoko
    Karolinska Institute.
    Cao, Yihai
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences.
    PDGF-BB modulates hematopoiesis and tumor angiogenesis by inducing erythropoietin production in stromal cells2012In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 18, no 1, p. 100-110Article in journal (Refereed)
    Abstract [en]

    The platelet-derived growth factor (PDGF) signaling system contributes to tumor angiogenesis and vascular remodeling. Here we show in mouse tumor models that PDGF-BB induces erythropoietin (EPO) mRNA and protein expression by targeting stromal and perivascular cells that express PDGF receptor-beta (PDGFR-beta). Tumor-derived PDGF-BB promoted tumor growth, angiogenesis and extramedullary hematopoiesis at least in part through modulation of EPO expression. Moreover, adenoviral delivery of PDGF-BB to tumor-free mice increased both EPO production and erythropoiesis, as well as protecting from irradiation-induced anemia. At the molecular level, we show that the PDGF-BB PDGFR-beta signaling system activates the EPO promoter, acting in part through transcriptional regulation by the transcription factor Atf3, possibly through its association with two additional transcription factors, c-Jun and Sp1. Our findings suggest that PDGF-BB-induced EPO promotes tumor growth through two mechanisms: first, paracrine stimulation of tumor angiogenesis by direct induction of endothelial cell proliferation, migration, sprouting and tube formation, and second, endocrine stimulation of extramedullary hematopoiesis leading to increased oxygen perfusion and protection against tumor-associated anemia.

  • 56.
    Zhang, Fan
    et al.
    NEI, MD USA .
    Li, Yang
    NEI, MD USA .
    Tang, Zhongshu
    NEI, MD USA .
    Kumar, Anil
    NEI, MD USA .
    Lee, Chunsik
    NEI, MD USA .
    Zhang, Liping
    National Institute Dent and Craniofacial Research, MD 20892 USA .
    Zhu, Chaoyong
    NanTong University, Peoples R China .
    Klotzsche-von Ameln, Anne
    University of Dresden, Germany .
    Wang, Bin
    Binzhou Medical University, Peoples R China .
    Gao, Zhiqin
    Weifang Medical University, Peoples R China .
    Zhang, Shizhuang
    Weifang Medical University, Peoples R China .
    Langer, Harald F.
    University of Tubingen, Germany .
    Hou, Xu
    Fourth Mil Medical University, Peoples R China .
    Jensen, Lasse
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences.
    Ma, Wenxin
    NEI, MD 20852 USA .
    Wong, Wai
    NEI, MD 20852 USA .
    Chavakis, Triantafyllos
    University of Dresden, Germany .
    Liu, Yizhi
    Sun Yat Sen University, Peoples R China .
    Cao, Yihai
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences.
    Li, Xuri
    NEI, MD 20852 USA .
    Proliferative and Survival Effects of PUMA Promote Angiogenesis2012In: CELL REPORTS, ISSN 2211-1247, Vol. 2, no 5, p. 1272-1285Article in journal (Refereed)
    Abstract [en]

    The p53 upregulated modulator of apoptosis (PUMA) is known as an essential apoptosis inducer. Here, we report the seemingly paradoxical finding that PUMA is a proangiogenic factor critically required for the proliferation and survival of vascular and microglia cells. Strikingly, Puma deficiency by genetic deletion or small hairpin RNA knockdown inhibited developmental and pathological angiogenesis and reduced microglia numbers in vivo, whereas Puma gene delivery increased angiogenesis and cell survival. Mechanistically, we revealed that PUMA plays a critical role in regulating autophagy by modulating Erk activation and intracellular calcium level. Our findings revealed an unexpected function of PUMA in promoting angiogenesis and warrant more careful investigations into the therapeutic potential of PUMA in treating cancer and degenerative diseases.

12 51 - 56 of 56
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