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  • 1
    Language: English
    In: Nature, April 3, 2008, Vol.452(7187), p.xiii(1)
    ISSN: 0028-0836
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  • 2
    Language: English
    In: Cell, 08 February 2018, Vol.172(4), pp.643-644
    Description: While functional heterogeneity of fibroblastic cells populating the tumor microenvironment is increasingly recognized, lack of definitive markers complicates elucidation of roles among ostensibly distinctive fibroblastic states. In this issue of , Su et al. characterize a new pro-tumorigenic cancer-associated fibroblast subset mediating chemoresistance defined and driven by a novel signaling pathway. While functional heterogeneity of fibroblastic cells populating the tumor microenvironment is increasingly recognized, lack of definitive markers complicates elucidation of roles among ostensibly distinctive fibroblastic states. In this issue of , Su et al. characterize a new pro-tumorigenic cancer-associated fibroblast subset mediating chemoresistance defined and driven by a novel signaling pathway.
    Keywords: Biology
    ISSN: 0092-8674
    E-ISSN: 1097-4172
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  • 3
    In: Nature, 2011, Vol.481(7379), p.85
    Description: Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps. Although dissemination of tumour cells seems to be an early and frequent event, the successful initiation of metastatic growth, a process termed 'metastatic colonization', is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites. Prevalent target sites are characteristic of many tumour entities, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease. [PUBLICATION ]
    Keywords: Animals–Pathology ; Breast Neoplasms–Genetics ; Cell Adhesion Molecules–Metabolism ; Cell Adhesion Molecules–Secondary ; Female–Pathology ; Lung Neoplasms–Metabolism ; Mice–Pathology ; Mice, Inbred C57bl–Physiology ; Neoplasm Metastasis–Metabolism ; Neoplastic Stem Cells–Metabolism ; Neoplastic Stem Cells–Metabolism ; Stem Cell Niche–Metabolism ; Stromal Cells–Metabolism ; Wnt Signaling Pathway–Metabolism ; Breast Cancer ; Stem Cells ; Experiments ; Cell Adhesion Molecules ; Postn Protein, Mouse;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 25 May 2010, Vol.107(21), pp.9777-82
    Description: Immune protection from intracellular pathogens depends on the generation of terminally differentiated effector and of multipotent memory precursor CD8 T cells, which rapidly regenerate effector and memory cells during recurrent infection. The identification of factors and pathways involved in CD8 T cell differentiation is of obvious importance to improve vaccination strategies. Here, we show that mice lacking T cell factor 1 (Tcf-1), a nuclear effector of the canonical Wingless/Integration 1 (Wnt) signaling pathway, mount normal effector and effector memory CD8 T cell responses to infection with lymphocytic choriomeningitis virus (LCMV). However, Tcf-1-deficient CD8 T cells are selectively impaired in their ability to expand upon secondary challenge and to protect from recurrent virus infection. Tcf-1-deficient mice essentially lack CD8 memory precursor T cells, which is evident already at the peak of the primary response, suggesting that Tcf-1 programs CD8 memory cell fate. The function of Tcf-1 to establish CD8 T cell memory is dependent on the catenin-binding domain in Tcf-1 and requires the Tcf-1 coactivators and Wnt signaling intermediates beta-catenin and gamma-catenin. These findings demonstrate that the canonical Wnt signaling pathway plays an essential role for CD8 central memory T cell differentiation under physiological conditions in vivo. They raise the possibility that modulation of Wnt signaling may be exploited to improve the generation of CD8 memory T cells during vaccination or for therapies designed to promote sustained cytotoxic CD8 T cell responses against tumors.
    Keywords: Immunologic Memory ; Signal Transduction ; Cd8-Positive T-Lymphocytes -- Immunology ; T Cell Transcription Factor 1 -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: The European journal of neuroscience, April 2011, Vol.33(8), pp.1366-75
    Description: Neurons and glia in the central nervous system originate from neural stem and progenitor cells that reside in the ventricular zones. Here we examine the role of β-catenin in neural stem cell (NSC) regulation in mouse embryos lacking β-catenin specifically in the brain germinal zone. An in vitro clonal neurosphere assay was performed in order to ascertain the status of the NSC population. Intact neurospheres did not form from β-catenin-null cells due to a loss of cell adhesion and the number of expanded cells was reduced. Rescue of β-catenin expression restored adhesion and revealed that the number of NSCs increased in the knockout population. Using a clonal colony-forming assay, which confines precursor cells within a solid collagen matrix, we show that the number of NSCs in the hippocampus is unchanged although the β-catenin knockout striatum actually contains a larger proportion of NSCs. However, these colonies were smaller than those of control cells, due to increased apoptosis in the progenitor population. Furthermore, β-catenin knockout NSCs also retained multipotentiality as shown by their ability to clonally differentiate into neurons and glia. The effects on neural precursor cells were not due to loss of downstream T-cell factor signaling, as this pathway is not active in vivo in regions of the embryonic brain where NSCs and progenitor cells reside, nor is it active in vitro in NSC colonies. These data reveal that β-catenin is not required for the maintenance or differentiation of NSCs, but is required for the adhesion and survival of neural progenitor cells.
    Keywords: Cell Death -- Physiology ; Neural Stem Cells -- Physiology ; Stem Cells -- Physiology ; Beta Catenin -- Metabolism
    ISSN: 0953816X
    E-ISSN: 1460-9568
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  • 6
    In: EMBO Journal, 02 May 2012, Vol.31(9), pp.2064-2066
    Description: Work from Kim Jensen's lab recently published in NCB establishes the crucial role of Lrig1 in the control of intestinal homeostasis.
    Keywords: Animals–Cytology ; Epithelial Cells–Metabolism ; Glycoproteins–Cytology ; Humans–Metabolism ; Intestine, Small–Metabolism ; Intestine, Small–Metabolism ; Membrane Glycoproteins–Cytology ; Mice–Cytology ; Oncogene Proteins V-Erbb–Cytology ; Stem Cells–Cytology ; Homeostasis ; Signal Transduction ; Stem Cells ; Small Intestine ; Glycoproteins ; Lrg1 Protein, Mouse ; Lrig1 Protein, Human ; Membrane Glycoproteins ; Oncogene Proteins V-Erbb;
    ISSN: 0261-4189
    E-ISSN: 1460-2075
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  • 7
    Language: English
    In: Cancer Research, 04/15/2012, Vol.72(8 Supplement), pp.SY28-02-SY28-02
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 8
    Language: English
    In: Experimental Cell Research, 01 July 2013, Vol.319(11), pp.1604-1610
    Description: The appearance of clinically detectable metastases is the end-point of a complex set of biological processes only few cancer cells are capable to complete. Metastatic colonization comprises the most inefficient metastatic steps as it requires a fine-tuned crosstalk between the disseminated cancer (stem) cells and their host microenvironment. The origin of the cancer cell and its intrinsic properties are factors that together with the organ microenvironment and circulation patterns determine the site of metastatic spread, the dormancy period and the extent of metastasis formation. Recent advances provide novel insights into the molecular components required for organ-specific infiltration, the composition of growth-supportive metastatic niches in different tissues and the cancer cell-niche crosstalk.
    Keywords: Metastasis ; Niche ; Cancer Stem Cell ; Extravasation ; Colonization ; Biology
    ISSN: 0014-4827
    E-ISSN: 1090-2422
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  • 9
    Language: English
    In: Gut, 14 September 2012, Vol.61(9), p.1306
    Description: Cyclooxygenase-2 (COX-2) overexpression in colorectal cancer increases levels of its pro-tumorigenic product prostaglandin E2 (PGE). The recently identified colorectal tumour suppressor 15-prostaglandin dehydrogenase (15-PGDH) catalyses prostaglandin turnover and is downregulated at a very early stage in colorectal tumorigenesis; however, the mechanism responsible remains unclear. As Wnt/β-catenin signalling is also deregulated early in colorectal neoplasia, a study was undertaken to determine whether β-catenin represses 15-PGDH expression.
    Keywords: 15-Pgdh ; Β-Catenin ; Pge ; Cyclooxygenase ; Colorectal Cancer Prevention ; Colorectal Neoplasia ; Prostaglandins ; Cell Biology ; Colon Carcinogenesis ; Intestinal Epithelium ; Gastrointestinal Peptides ; Inflammatory Bowel Disease ; Cancer Genetics ; Colorectal Cancer ; Colorectal Cancer Genes ; Colorectal Carcinoma ; Colorectal Neoplasm ; Gene Regulation ; Cell Biology ; Cell Death ; Cancer Prevention ; Chemoprevention ; Cyclooxygenase-2 ; Dietary Fibre ; Butyrate
    ISSN: 0017-5749
    ISSN: 00175749
    E-ISSN: 1468-3288
    E-ISSN: 14683288
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  • 10
    Language: English
    In: PLoS ONE, 2010, Vol.5(1), p.e8960
    Description: Squamous cell carcinoma (SCC) of the lung is a frequent and aggressive cancer type. Gene amplifications, a known activating mechanism of oncogenes, target the 3q26-qter region as one of the most frequently gained/amplified genomic sites in SCC of various types. Here, we used array comparative genomic hybridization to delineate the consensus region of 3q26.3 amplifications in lung SCC. Recurrent amplifications occur in 20% of lung SCC (136 tumors in total) and map to a core region of 2 Mb (Megabases) that encompasses SOX2 , a transcription factor gene. Intense SOX2 immunostaining is frequent in nuclei of lung SCC, indicating potential active transcriptional regulation by SOX2. Analyses of the transcriptome of lung SCC, SOX2-overexpressing lung epithelial cells and embryonic stem cells (ESCs) reveal that SOX2 contributes to activate ESC-like phenotypes and provide clues pertaining to the deregulated genes involved in the malignant phenotype. In cell culture experiments, overexpression of SOX2 stimulates cellular migration and anchorage-independent growth while SOX2 knockdown impairs cell growth. Finally, SOX2 over-expression in non-tumorigenic human lung bronchial epithelial cells is tumorigenic in immunocompromised mice. These results indicate that the SOX2 transcription factor, a major regulator of stem cell function, is also an oncogene and a driver gene for the recurrent 3q26.33 amplifications in lung SCC.
    Keywords: Research Article ; Developmental Biology -- Stem Cells ; Genetics And Genomics -- Bioinformatics ; Genetics And Genomics -- Cancer Genetics ; Genetics And Genomics -- Disease Models ; Genetics And Genomics -- Functional Genomics ; Genetics And Genomics -- Gene Discovery ; Genetics And Genomics -- Gene Expression ; Genetics And Genomics -- Genomics ; Oncology -- Genitourinary Cancers ; Oncology -- Lung Cancer ; Pathology -- Molecular Pathology
    E-ISSN: 1932-6203
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