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  • 1
    Keywords: IN-VIVO ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MEMORY T-CELLS ; TGF-BETA ; MESENCHYMAL STEM-CELLS ; HORMONE-RELATED PROTEIN ; zoledronic acid ; METASTATIC BREAST-CANCER ; TARGETED THERAPY ; DORMANT TUMOR-CELLS
    Abstract: The bone marrow (BM) of cancer patients is considered an essential secondary lymphoid organ with substantial impact on tumor cell dissemination and tumor-immune responses. Recent advances in the understanding of BM/primary tumor crosstalk, homing processes, premetastatic niche formation, tumor cell dormancy, and ultimately, identification of the BM micromilieu cytokines, chemokines, and growth factors may provide the basis for the development of targeted therapeutic strategies potentially rendering primary cancers and cancer bone metastases more susceptible to chemotherapy. The present review aims to dissect the individual components of the BM microenvironment in cancer patients, compare it to the healthy BM, and discuss its impact on interactions between the tumor and the immune system.
    Type of Publication: Journal article published
    PubMed ID: 23081701
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  • 2
  • 3
    Keywords: CANCER ; proliferation ; tumor ; TUMOR-NECROSIS-FACTOR ; DENDRITIC CELLS ; COLON-CANCER ; POLYPOSIS ; TISSUE-SPECIFIC EXPRESSION ; inflammation ; malignant pleural mesothelioma ; REGULATORY T-CELLS ; regulatory T cell ; PROTEINASE-ACTIVATED RECEPTORS ; chymase ; ACUTE SEPTIC PERITONITIS ; ANTIGEN-INDUCED RECRUITMENT ; C-KIT RECEPTOR ; FAVORABLE PROGNOSTIC-FACTOR ; Immune Surviellance ; Mast cell ; Mast cell progenitor ; PRIMARY COLORECTAL-CANCER ; Tryptase
    Abstract: Mast cells (MC) are a bone marrow-derived, long-lived, heterogeneous cellular population that function both as positive and negative regulators of immune responses. They are arguably the most productive chemical factory in the body and influence other cells through both soluble mediators and cell-to-cell interaction. MC are commonly seen in various tumors and have been attributed alternatively with tumor rejection or tumor promotion. Tumor-infiltrating MC are derived both from sentinel and recruited progenitor cells. MC can directly influence tumor cell proliferation and invasion but also help tumors indirectly by organizing its microenvironment and modulating immune responses to tumor cells. Best known for orchestrating inflammation and angiogenesis, the role of MC in shaping adaptive immune responses has become a focus of recent investigations. MC mobilize T cells and antigen-presenting dendritic cells. They function as intermediaries in regulatory T cells (Treg)-induced tolerance but can also modify or reverse Treg-suppressive properties. The central role of MC in the control of innate and adaptive immunity endows them with the ability to tune the nature of host responses to cancer and ultimately influence the outcome of disease and fate of the cancer patient
    Type of Publication: Journal article published
    PubMed ID: 21287360
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  • 4
    Keywords: squamous cell carcinoma ; basal cell carcinoma ; cyclooxygenase ; SKIN INFLAMMATION ; prostaglandin ; non-melanoma skin cancer ; NSAID ; COX ; Tumor model ; UV light-induced cancer ; Multi-stage chemical carcinogenesis ; COXib
    Abstract: Cyclooxygenase (COX)-derived prostaglandins (PGs) exhibit manifold functions in acute and chronic skin inflammation induced by a number of physical (ultraviolet (UV) light, wounding) and chemical (12-O-tetradecanoylphorbol 13-acetate (TPA), arachidonic acid) noxious stimuli. Depending on the challenge and the context, constitutively expressed COX-1 or the transiently induced COX-2 isoform are of relevance. Moreover, squamous cell carcinoma (SCC) of skin is a prominent example of epithelial neoplasia that consistently overexpresses COX-2 in the parenchyme and the mesenchyme of premalignant and malignant lesions, while COX-1 expression remains unaltered. Pharmacological, clinical, and experimental animal studies as well as a few epidemiological studies document the importance of PG signaling in non-melanoma skin cancer including SCC and basal cell carcinoma (BCC) in humans and mice. Increased levels of PGE(2) and PGF(2 alpha) in premalignant and/or malignant epithelial skin cancers are due to the constitutive upregulation of enzymes involved in PG biosynthesis, such as COX-2, and downregulation of the tumor suppressor gene 15-hydroxy-prostaglandin dehydrogenase (15-PGDH), which is involved in the inactivation of PG, thus counteracting the activities of COX. Most remarkably, genetic studies show that mice which are deficient in COX-2 or COX-1 are protected from the development of SCC when applying the multi-stage chemical carcinogenesis protocol. Conversely, the forced overexpression of COX-2 in the proliferative basal compartment of the stratified skin epidermis results in spontaneous hyperplasia and dysplasia in transgenic mice and furthermore a sensitization for cancer development by conferring an auto-promoted skin phenotype. In multi-stage carcinogenesis, it also becomes clear that aberrant COX-2 overexpression and activity are causally involved in tumor promotion and tumor progression rather than initiation. In contrast, using as inducer of carcinogenesis the complete carcinogen UV B light, depletion of COX-2 but not of COX-1 makes mouse skin resistant for SCC, indicating that here, only COX-2 is essential. Depending on the type of challenge, COX-2-dependent signaling contributes to the pre-invasive growth of the skin epidermis by a delayed onset of terminal differentiation, or stimulation of hyperproliferation and survival. With respect to BCC, the genetic ablation of COX-2 but also of COX-1 leads to a strongly reduced tumor burden in the skin of Patched (Ptch)1(+/-) mice, which due to the deletion of a Ptch1 allele, spontaneously develop BCC resembling human familial basal cell nevus syndrome and sporadic BCC. Nonsteroidal anti-inflammatory drugs and the COX-2-selective inhibitors (COXibs) exhibit impressive efficacy inhibiting tumor burden in various mouse models of SCC and BCC. Most importantly, in humans the interruption of COX-2 signaling is an effective strategy to treat and chemo-prevent non-melanoma skin cancer in individuals who are at high risk for the disease. However, any potential beneficial effect of this medicine has to be balanced against the adverse effects that are known to be associated with these drugs in a subset of patients.
    Type of Publication: Journal article published
    PubMed ID: 22038018
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 1 (1982), S. 3-3 
    ISSN: 1573-7233
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 11 (1992), S. 433-433 
    ISSN: 1573-7233
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 12 (1993), S. 1-2 
    ISSN: 1573-7233
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-7233
    Keywords: progression ; prostate cancer ; molecular markers ; metastasis suppressor genes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-7233
    Keywords: anticoagulants ; malignancy ; fibrinolysis ; clinical trials
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Clinical trials of drugs that influence coagulation and fibrinolysis pathways have been undertaken in patients with malignancy because these pathways are capable of influencing malignant progression. The validity of this concept was originally confirmed in experimental animal models of malignancy. Earlier pilot studies in human disease have been succeeded by definitive prospective randomized clinical trials that have revealed heterogeneity of responsiveness to anticoagulant and fibrinolytic agents that may be attributable to differences in mechanisms of interaction of the tumor cells of various types of malignancy with these pathwaysin vivo. In certain tumor types studied thus far, increased tumor response rates and prolongation of survival have been observed that suggest the possibility that substantial benefit may be realized from this treatment approach in patients with malignancy. In addition, the availability of newer and potentially more effective therapeutic agents holds promise for even greater gains in previously tested tumor types. The ability to design treatment regimens that correspond to defined mechanisms that pertain to specific tumor types should permit future studies to be designed rationally. Current data suggest that anticoagulant and fibrinolytic agents might reasonably be tested in tumor types characterized by the existence of a tumor cell-associated coagulation pathway with thrombin generation and conversion of fibrinogen to fibrin (such as small cell carcinoma of the lung). By contrast, protease inhibitors might reasonably be tested in tumor types characterized by expression of tumor cell plasminogen activators. Expansion of current views on the possible role of antithrombic drugs in cancer therapy is justified. For example, antithrombotic drugs classified as nonsteroidal anti-inflammatory agents may inhibit carcinogenesis while polyanionic drugs with anticoagulant properties, such as suramin and heparin, may inhibit growth factor interactions with cells. Intriguing new opportunities clearly exist for interactions between clinical and basic investigators that may provide both novel biologic insights and improved patient care.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-7233
    Keywords: prostate cancer ; invasion ; E-cadherin ; progression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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