Mesenchymal stromal cells, colony-forming unit fibroblasts, from bone marrow of untreated advanced breast and lung cancer patients suppress fibroblast colony formation from healthy marrow

We have shown that bone marrow (BM) from untreated advanced lung and breast cancer patients (LCP and BCP) have a reduced number of colony-forming unit fibroblasts (CFU-Fs) or mesenchymal stem cells (MSCs). Factors that regulate the proliferation and differentiation of CFU-F are produced by the patie...

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Autor principal: Hofer, E.L
Otros Autores: Labovsky, V., La Russa, V., Vallone, V.F, Honegger, A.E, Belloc, C.G, Wen, H.C, Bordenave, R.H, Bullorsky, E.O, Feldman, L., Chasseing, N.A
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2010
Acceso en línea:Registro en Scopus
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Registro en la Biblioteca Digital
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100 1 |a Hofer, E.L. 
245 1 0 |a Mesenchymal stromal cells, colony-forming unit fibroblasts, from bone marrow of untreated advanced breast and lung cancer patients suppress fibroblast colony formation from healthy marrow 
260 |c 2010 
270 1 0 |m Chasseing, N. A.; Instituto de Biologìa y Medicina Experimental, Vuelta de Obligado 2490, 1428, Buenos Aires, Argentina; email: chaseing@dna.uba.ar 
506 |2 openaire  |e Política editorial 
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504 |a Hofer, E.L., Larussa, V., Honegger, A.E., Bullorsky, E.O., Bordenave, R.H., Chasseing, N.A., Alteration on the expression of IL-1, PDGF, TGF-beta, EGF, and FGF receptors and c-Fos and c-Myc proteins in bone marrow mesenchymal stroma cells from advanced untreated lung and breast cancer patients (2005) Stem Cells Dev, 14, pp. 587-594 
520 3 |a We have shown that bone marrow (BM) from untreated advanced lung and breast cancer patients (LCP and BCP) have a reduced number of colony-forming unit fibroblasts (CFU-Fs) or mesenchymal stem cells (MSCs). Factors that regulate the proliferation and differentiation of CFU-F are produced by the patients' BM microenvironment. We have now examined whether conditioned media (CM) from patients' CFU-F-derived stromal cells also inhibits the colony-forming efficiency (CFE) of CFU-F in primary cultures from healthy volunteers (HV)-BM. Thus the number and proliferation potential of HV-CFU-F were also found to be decreased and similar to colony numbers and colony size of patients' CFU-F. Stromal cells from both of these types of colonies appeared relatively larger and lacked the characteristic spindle morphology typically seen in healthy stromal cells. We developed an arbitrary mesenchymal stromal cell maturational index by taking three measures consisting of stromal cell surface area, longitudinal and horizontal axis. All stromal indices derived from HV-CFU-F grown in patients' CM were similar to those from stromal elements derived from patients' CFU-F. These indices were markedly higher than stromal indices typical of HV-CFU-F cultured in healthy CM or standard medium [-medium plus 20% heat-inactivated fetal bovine serum (FBS)]. Patients' CM had increased concentrations of the CFU-F inhibitor, GM-CSF, and low levels of bFGF and Dkk-1, strong promoters of self-renewal of MSCs, compared to the levels quantified in CM from HV-CFU-F. Moreover, the majority of patients' MSCs were unresponsive in standard medium and healthy CM to give CFU-F, indicating that the majority of mesenchymal stromal cells from patients' CFU-F are locked in maturational arrest. These results show that alterations of GM-CSF, bFGF, and Dkk-1 are associated with deficient cloning and maturation arrest of CFU-F. Defective autocrine and paracrine mechanisms may be involved in the BM microenvironments of LCP and BCP. © Mary Ann Liebert, Inc. 2010.  |l eng 
593 |a Fellow of the Agencia Nacional de Promociòn Cientìfica, Tecnològica y de Innovaciòn Productiva, Buenos Aires, Argentina 
593 |a Instituto de Biologìa y Medicina Experimental, Vuelta de Obligado 2490, 1428, Buenos Aires, Argentina 
593 |a Consejo Nacional de Investigaciones Cientìficas, Técnicas de la Repüblica Argentina (CONICET), New York, United States 
593 |a Cytotherapy Laboratory, Memorial Sloan-Kettering Cancer Center, New York, United States 
593 |a Department of Oncology, I.Iriarte Hospital, Buenos Aires, Argentina 
593 |a Department of Hematology and Bone Marrow Transplantation, Britànico Hospital, Buenos Aires, Argentina 
593 |a Department of Bone Marrow Transplantation, Fundaciòn Favaloro, Buenos Aires, Argentina 
593 |a CONICET, Argentina 
690 1 0 |a DICKKOPF 1 PROTEIN 
690 1 0 |a FIBROBLAST GROWTH FACTOR 
690 1 0 |a GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR 
690 1 0 |a ARTICLE 
690 1 0 |a BREAST CANCER 
690 1 0 |a CANCER PATIENT 
690 1 0 |a CELL MATURATION 
690 1 0 |a CELL PROLIFERATION 
690 1 0 |a CELL RENEWAL 
690 1 0 |a CELL STRUCTURE 
690 1 0 |a CLINICAL ARTICLE 
690 1 0 |a COLONY FORMATION 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a FIBROBLAST 
690 1 0 |a HEMATOPOIETIC STEM CELL 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a IN VITRO STUDY 
690 1 0 |a LUNG CANCER 
690 1 0 |a MESENCHYMAL STEM CELL 
690 1 0 |a MICROENVIRONMENT 
690 1 0 |a MICROMETASTASIS 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a BONE MARROW CELLS 
690 1 0 |a BREAST NEOPLASMS 
690 1 0 |a CELL PROLIFERATION 
690 1 0 |a CELLS, CULTURED 
690 1 0 |a COLONY-FORMING UNITS ASSAY 
690 1 0 |a CULTURE MEDIA, CONDITIONED 
690 1 0 |a FIBROBLAST GROWTH FACTOR 2 
690 1 0 |a FIBROBLASTS 
690 1 0 |a GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR 
690 1 0 |a HUMANS 
690 1 0 |a INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS 
690 1 0 |a LUNG NEOPLASMS 
690 1 0 |a MESENCHYMAL STEM CELLS 
690 1 0 |a STEM CELLS 
690 1 0 |a STROMAL CELLS 
690 1 0 |a TIME FACTORS 
690 1 0 |a BOVINAE 
700 1 |a Labovsky, V. 
700 1 |a La Russa, V. 
700 1 |a Vallone, V.F. 
700 1 |a Honegger, A.E. 
700 1 |a Belloc, C.G. 
700 1 |a Wen, H.C. 
700 1 |a Bordenave, R.H. 
700 1 |a Bullorsky, E.O. 
700 1 |a Feldman, L. 
700 1 |a Chasseing, N.A. 
773 0 |d 2010  |g v. 19  |h pp. 359-369  |k n. 3  |p Stem Cells Dev.  |x 15473287  |t Stem Cells and Development 
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