Hematopoietic growth factors (HGFs) are glycoproteins that control hemopoiesis. They have potential usefulness in a range of clinical conditions including the treatment of patients with myelosuppression induced by chemotherapy. Among HGFs, Stem Cell Factor (SCF) and Interleukin 6 (IL-6) are attracting interest for their capacity to stimulate early hematopoietic progenitors. Furthermore, their use in combination with late-acting growth factors with a more lineage-restricted potential (such as granulocyte colony-stimulating factor, G-CSF) might be expected to offer optimal marrow stimulation and usefulness in clinical oncology. Since non-hematopoietic malignant cells may express receptors for HGFs and respond to these peptides in vitro, we investigated clonal growth 3H-thymidine incorporation and cell cycle analysis by flow cytometry of 5 human solid tumor cell lines under the influence of SCF and IL-6 with or without G-CSF. Our experiments show that these cytokines have no effects on the proliferative capacity of the cell lines tested. Based on our and previously reported data, the use of these HGFs can be considered safe in cancer patients.

Cell Adhesion Molecules↗

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Recombinant human G-CSF: how wide is the field of clinical applicability?

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Bone Marrow Transplantation↗

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Myelodysplastic syndromes: the pediatric point of view.

Myelodysplastic syndromes (MDS) are clonal disorders of the multipotent hematopoietic stem cell characterized by ineffective hematopoiesis and associated with marrow hypercellularity, increased intramedullary cell death and peripheral cytopenias of varying severity. Patients with myelodysplasia have a propensity (20% to 30% of cases) to undergo transformation into acute myeloid leukemia (AML), and a large body of evidence indicates that MDS represent steps in the multiphasic evolution of AML. Progression of the disease is characterized by expansion of the abnormal clone and inhibition of normal hematopoiesis leading to deterioration of the blood cell count and/or development of AML. MDS are relatively unusual in childhood, representing only 3% of pediatric hematological malignancies, although it has been reported that up to 17% of pediatric AML cases may have a previous myelodysplastic phase. The first systematic attempt at morphological classification of MDS was provided by the French-American-British (FAB) group. However, the FAB classification of MDS is only partially applicable in children. Some variants are extremely rare or absent (refractory anemia with ring sideroblasts and chronic myelomonocytic leukemia), and other peculiar pediatric disorders, represented by juvenile chronic myelogenous leukemia (JCML) and the monosomy 7 syndrome, are not included. Moreover, since there is a partial overlap between pediatric MDS and myeloproliferative disorders and the variants occurring in young children have rather specific features, some confusion still surrounds the nosographical definition of childhood MDS, so that none of the proposed classifications are widely accepted and used. Characteristically, some genetic conditions such as Fanconi's anemia, Shwachman's and Down's syndromes predispose to the development of MDS in childhood. The most common variants of childhood MDS are represented by JCML and the monosomy 7 syndrome, both disorders typically occurring in young children. JCML is characterized by a spontaneous growth of granulocyte-macrophage progenitors that show a striking hypersensitivity to granulocyte-macrophage colony-stimulating factor. Clinical presentation resembles that of some myeloproliferative disorders, with massive organomegaly usually not observed in the classically reported variants of MDS. Clinical features of the monosomy 7 syndrome resemble those observed in JCML and a differential diagnosis between these two entities relies upon the higher percentage of fetal hemoglobin, the more pronounced decrease in platelet count and, in some cases, the lack of the peculiar cytogenetic abnormality in the latter. With the number of children being cured of cancer constantly rising, a significant increase in secondary or chemotherapy-related myelodysplasia is being observed, and these disorders represent a formidable challenge for pediatric hematologists due to their poor response to chemotherapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Child↗

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[Diet therapy in preventing the progression of chronic renal insufficiency].

The effect of a low protein diet (LPD) on the progression of chronic renal insufficiency (CRI) was investigated by reviewing the published studies. Only the trials of Rosman, Ihle and Locatelli fulfilled the main methodological criteria of being randomized, prospective and controlled. They involved 811 patients (671 evaluated: 338 on an LPD, 333 as controls) and had a mean follow-up of 29 months (range 18-48) for an estimated total of about 17,335 patient-months. The only trial whose results showed that LPD had a positive effect on the progression of chronic renal failure (CRF) was Ihle's study with the lowest weight (6.7%) and which involved the most severe CRF; effects limited to the patients with more advanced CRF were found in Roman's study, with an intermediate weight (41.8%); and little effect, if any, in Locatelli's trial accounting for 51.5% of patient-months, with less severe CRI. In conclusion, analysis of published randomized, prospective and controlled trials offers little or no evidence for the hypothesis that an LPD has a greater clinically significant effect on early CRI progression than a controlled protein diet, although a very low protein diet seems to postpone the need for dialysis.

Dietary Proteins↗