Disease relevance of TBCC

• Primitive blast colony-forming cells (BI-CFC) from chronic myeloid leukemia (CML) patients are defective in their attachment to bone marrow-derived stromal cells compared with normal BI-CFC [1].
• Gene transfer was significantly higher in the presence of 36SF in mass culture cells, CFC, LTCIC, and NOD/SCID repopulating cells (SRC) [2].
• Twenty-two cases of CFC have been described but there is debate as to whether it is distinct from Noonan syndrome [3].
• This assay supports the growth of lymphoma colonies (ML-CFC) as well as normal granulocytic colonies (CFU-C) and thus a direct comparison between the antineoplastic and myelosuppressive effects of a drug can be determined [4].
• In the present study, an in vitro system for both primary growth and passage of malignant lymphoblastic colony-forming cells (ML-CFC) was established, and for the first time, colony-forming cells from non-Hodgkin's lymphoma patients were cultured, and cell lines were established from individual colonies [5].

High impact information on TBCC

• Using an in vitro culture system which allows investigation of adhesion to stromal layers and subsequent colony formation by blast colony-forming cells (B1-CFC) in normal marrow and Ph+ chronic myeloid leukaemic (CML) blood, we compared the adhesive properties of normal and malignant progenitor cells [6].
• Difficulties with CFC-free salbutamol inhaler [7].
• EGF-CFC genes encode extracellular proteins that play key roles in intercellular signaling pathways during vertebrate embryogenesis [8].
• Megakaryocyte numbers in bone marrow and spleen were elevated, as were bone marrow and spleen megakaryocyte colony-forming cells (MEG-CFC) [9].
• The number of MEG-CFC in the bone marrow of rhIL-11-treated, splenectomized mice was increased twofold compared with controls on both days 3 and 7 of the study [10].

Biological context of TBCC

• Cytokines prevented apoptosis, expanded CD34(+) cell number, and maintained CFC and LTCIC frequencies [2].
• MATERIALS AND METHODS: IL-12-treated lethally or sublethally irradiated animals were examined for the survival/lifespan, the function assays (bone marrow transplantation, CFU-S(12), CFC) of bone marrow cell subsets, and apoptosis assay [11].
• We postulate that the radiation resistance of both hemopoietic CFC and CFU-F in -/- mice is a consequence of the failure of DNA/chromosome damage to trigger apoptosis or permanent cell cycle arrest to the same extent as in the +/+ or +/- mice: hence the lack of correlation between chromosome damage and cell death in the three mouse types [12].
• The aim of our study was to compare the radiation response of hemopoietic colony-forming cells (in vitro CFC) and of fibroblastoid colony-forming cells or units (CFU-F) within the same tissue (marrow) in p53 null mice (-/-), heterozygotes (+/-) and wild-type animals (+/+) [12].
• Comparison of the systemic pharmacodynamic effects and pharmacokinetics of salmeterol delivered by CFC propellant and non-CFC propellant metered dose inhalers in healthy subjects [13].

Anatomical context of TBCC

• Blast colony-forming cells (BI-CFC) and pre-colony-forming unit-granulocyte, monocyte (CFU-GM) in human bone marrow bind to marrow-derived stromal layers grown in the presence of methylprednisolone (MP+), but do not bind to stroma grown without MP (MP-) [14].
• At 50 U/mL we found that: (1) the capacity of stromal cells to bind two types of CML primitive progenitor cells (BI-CFC and long-term culture-initiating cells) was increased; and (2) the amount of sulfated glycosaminoglycans (GAGs) in the stromal layer was increased [1].
• Anti-platelet IgG extensively absorbed with brain, thymus, and peritoneal cells bound selectively to stem cells, megakaryocyte progenitor cells (Mk-CFC), and megakaryocytes in CBA mouse bone marrow and to blood platelets [15].
• The combination of continuous flow centrifugation and filtration leukapheresis (CFC-FL) in nine of the 30 runs resulted in a highly significant increase of the yield to a mean of 59.6 X 1o(9) granulocytes as compared with a mean of 30.8 X 10(9) granulocytes obtained with conventional CFC [16].
• The 5/9 aplastic cases that did not form fat cells spontaneously also bound BI-CFC moderately better than normal stroma [17].

Associations of TBCC with chemical compounds

• HPP-CFC were only depleted to 57% of normal at 2 days after FU treatment, whereas the cells responsive to PMUE alone (low proliferative potential, LPP-CFC) were depleted to 1.2%, indicating a marked difference in cycling status of the respective types of progenitor cells [18].
• Addition of appropriate concentrations of PGE1 to the agar culture assay should improve detection of HPP-CFC by inhibiting the proliferation of LPP-CFC [19].
• Ligands for integrin receptors (e.g., fibronectin) did not participate in BI-CFC binding because the synthetic pentapeptide glycine-arginine-glycine-asparagine-serine did not compete with stroma in binding BI-CFCs [20].
• These findings indicate that heparan sulfate in the bone marrow microenvironment is necessary for BI-CFC binding to ECM and may contribute to localizing hemopoietic stem cells in hemopoietic tissue [20].
• Dominant role of cytochrome P-450 2E1 in human hepatic microsomal oxidation of the CFC-substitute 1,1,1,2-tetrafluoroethane [21].

Analytical, diagnostic and therapeutic context of TBCC

• Little is known about rates and time frames of the CFC release from foams especially after treatment and disposal of foam containing waste products [22].
• The total median CFC count in the bone marrow differed significantly between the patient and the control group [23].
• The gene transfer efficiency of the recombinant virus was evaluated by flow cytometry, in vitro assays for committed (CFC) and primitive (LTC-CFC) progenitors, as well as a clonal assay for B and NK lymphoid progenitors [24].
• The thermal property of CO2 and its trans-critical refrigeration cycle is very different from that of the traditional CFC or HCFC system [25].

References