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No full textMultipotent human stromal cells isolated from cord blood, term placenta and adult bone marrow show distinct differences in gene expression pattern. Electrical stimulation of human mesenchymal stem cells on conductive nanofibers enhances their differentiation toward osteogenic outcomes. Genome-wide microRNA and gene analysis of mesenchymal stem cell chondrogenesis identifies an essential role and multiple targets for miR-140-5p. Adipose-derived mesenchymal stem cells promote cell proliferation and invasion of epithelial ovarian cancer. Human bone marrow- and adipose-mesenchymal stem cells secrete exosomes enriched in distinctive miRNA and tRNA species. Bone marrow-derived mesenchymal stromal cells differ in their attachment to fibronectin-derived peptides from term placenta-derived mesenchymal stromal cells. Mesenchymal stromal cells induce peculiar alternatively activated macrophages capable of dampening both innate and adaptive immune responses. Human mesenchymal stem cells genetically engineered to overexpress brain-derived neurotrophic factor improve outcomes in Huntington's disease mouse models
The mesenchymal stem cell, the mesenchymal stromal cell, and the mesenchymal stromal cell exosome
No full textStem cells have two properties: they must be able to divide and be self-renewing and they must be able to differentiate down a specific lineage or set of lineages to produce functional cells. In the case of hematopoietic stem cells (HSC) this was readily shown first in animal models and subsequently in humans that if the recipient's bone marrow was ablated by high-dose chemotherapy, donor bone marrow cells infused into the recipient after the high dose treatment reconstituted the recipient's bone marrow both short term and long term. Mesenchymal stromal cells (MSC) have been shown to mediate therapeutic benefit in a wide range of animal models of disease and in clinical trials in many diseases apart from musculo-skeletal disorders. The exosome is the best characterized of all the extracellular vesicles (EVs) described to date and can be differentiated from other EVs by its biogenesis
Therapeutic decision making in SCT for amyloidosis
No full textDefinition Amyloidosis results from altered protein folding, leading to the deposit of insoluble amyloid fibrils in possibly every organ or organ system of the body. Untreated, systemic amyloidosis is generally fatal
Therapeutic decision making in BMT/SCT for Hodgkin lymphoma
No full textDisease classification Disease staging Modified Ann Arbor Staging System: Stage I: involvement of a single lymph node region (I) or of a single extralymphatic organ or site (IE). Stage II: involvement of two or more lymph node regions on the same side of the diaphragm (II) or localized involvement of an extralymphatic organ or site and of one or more lymph node regions on the same side of the diaphragm (IIE). Stage III: involvement of lymph node regions on both sides of the diaphragm (III), which may also be accompanied by localized involvement of an extralymphatic organ or site (IIIE). Stage IV: diffuse or disseminated involvement of one or more extralymphatic organs in tissues with or without associated lymph node enlargement
Therapeutic decision making in BMT/SCT for congenital immunodeficiencies
No full textIntroduction Among the early successes of allogeneic BMT were those achieved in the area of congenital immunodeficiencies. In certain diseases and certain donor–recipient combinations, over 90% of patients can be cured by allogeneic transplantation. Worldwide, over 3000 patients with congenital immunodeficiencies have been treated by allogeneic transplantation. The following table gives a list of the current indications. Patients with congenital immunodeficiencies generally manifest as severe infections within the first year of life. In the absence of a hematopoietic SCT or BMT, most severe immunodeficiencies are fatal. The European Society for Immunodeficiencies (ESID) in collaboration with the EBMT provides guidelines for the conditioning regimens in use for primary immunodeficiencies (www.esid.org and www.ebmt.org). For reviews related to BMT and congenital immunodeficiencies, see Buckley, 2003; Buckley et al., 1999; and Steward and Jarisch, 2005. Szabolcs et al. (2010) gave a very detailed overview of the primary immunodeficiencies treated by BMT/SCT. With the advent of genetic mapping, SCID is now increasingly classified on a genetic basis. This gives a more precise characterization of the immunological defects. Thus, it is becoming clear which types have the best cure rate, allowing the stratification of therapy. For example, patients with a mutation in the antigen receptor gene Artemis (resulting in a T-B- NK+ phenotype) were described as having a worse prognosis
Practical aspects and procedures, including conditioning protocols and haploidentical transplantation
No full textAge limits and exclusion criteria for transplantation Commonly used upper age limits for transplantation In special situations, for example, biological functioning of a patient and using special conditioning protocols, these age limits can be extended. (See Klepin & Hurd (2006) for a discussion of these issues in myeloma patients.) Mineishi (2011) discussed the issues related to nonmyeloablative transplants in patients between the ages of 60 and 75 years in an editorial. In this age group, a long-term survival (5+ years) of 35% included most of these patients who survived without disease. (See also p. 5.
Therapeutic decision making in BMT/SCT for chronic myeloid leukemia and other myeloproliferative syndromes
No full textClassification of chronic myeloid leukemia (CML) Clinical variants of CML: Typical CML (Philadelphia chromosome present, BCR/ABL-positive [94%]) Atypical CML (Philadelphia chromosome absent, BCR/ABL-positive [4%]) Atypical BCR/ABL negative CML (Philadelphia chromosome absent, BCR/ABL-negative [2%]) Staging of CML Chronic phase: No significant symptoms None of the features of accelerated phase or blastic phase Sensitive to tyrosine kinase inhibitors (TKIs) (most newly diagnosed cases, see page 64) Resistant to TKIs Accelerated phase (any one or more of the following criteria): WBC count difficult to control with conventional use of TKI or busulfan/hydroxyurea in terms of doses required Rapid doubling of WBC count (≥5 days) ≥10% blasts in blood or marrow ≥20% blasts plus promyelocytes in blood or marrow ≥20% basophils plus eosinophils in blood Anemia or thrombocytopenia unresponsive to TKI Persistent thrombocytosis Additional chromosome changes (evolving new clone) Increasing splenomegaly Development of chloromas or myelofibrosis Patient in a second (or subsequent) chronic phase after blast crisi
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