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C Rumi

Publications and source records attributed to C Rumi.

At least 55 records · Page 3Linked to original sources
PubMed1997

RhG-CSF-mobilized CD34+ peripheral blood progenitors are myeloperoxidase-negative and noncycling irrespective of CD33 or CD13 coexpression.

Cycling status, myeloperoxidase expression, informative surface markers, and proliferative potential of peripheral blood hemopoietic progenitors (PBHP) were evaluated by flow cytometry in 10 patients affected by resistant lymphoma, and submitted to stem cell mobilization with combination chemotherapy (MiCMA) followed by recombinant human granulocyte colony-stimulating factor (rhG-CSF, 5 micrograms/kg/day). CD34+ PBHP coexpressed myeloid-associated and activation antigens, i.e., CD33 (96%, range 85-99), CD13 (99.5%, range 99.4-99.8), HLA-DR (99%, range 96.5-99.8), and CD38 (98%, range 90-100), lacked intracytoplasmic myeloperoxidase (MPO, < 3%), and resided in the Gzero/G1 phase of the cell cycle (96.5%, range 81-99.5, compared with 70%, range 49-78 bone marrow HP; p = 0.0007), independently of surface membrane phenotype; S-phase percentages of sorted CD34+ CD33(+)/-, CD34+CD38(+)/-, CD34+HLA-DR(+)/-, CD34+CD45RA(+)/-, CD34+CD45RO(+)/-, and CD34+CD41a(+)/- subpopulations were always negligible. In colony assays, 5-week-old long-term cultures seeded with CD34+CD33- cells yielded as many colonies as did CD34+CD33+ cells. In conclusion, rhG-CSF-mobilized CD34+ PBHPs contain noncycling, highly immature progenitors in which the expression of myeloid-associated antigens, i.e., CD33 or CD13, might not be indicative of myeloid commitment.

Antigens, CD↗
PubMed1996

Wiskott-Aldrich syndrome: report of an autosomal dominant variant.

The Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disorder originally described as a clinical triad of thrombocytopenia with small platelets, eczema, and immunodeficiency. Impaired CD43 glycoprotein expression on lymphocytes is a typical hallmark of this disorder. The CD43 gene is located on chromosome 16, and the WAS gene, WASP, was recently isolated from the chromosome X p11.22-p11.23. This gene, mutated in WAS patients, encodes a protein that is likely to play a role in controlling the expression of CD43. However, the molecular mechanism(s) causing WAS are not yet known. Herein, we describe a three-generation family in which clinical and laboratory WAS features were expressed in six of nine subjects available for study. At variance with classic X-linked WAS, this disorder was characterized by the presence of thrombocytopenia with a broad spectrum of platelet size, including giant platelets, and was inherited as an autosomal dominant trait. This last finding led us to hypothesize a mutation of the CD43 gene. However, Southern blot analysis failed to detect structural abnormalities of this gene, and genotype analysis ruled out the possibility that a CD43 allele might be shared by the affected individuals. These findings indicate that an alteration(s) of an autosomal gene distinct from the CD43 gene is responsible for the disease. Thus, results from this family, providing the first observation of an autosomally transmitted WAS variant, indicate that genetic mechanism(s) leading to WAS are more complex than previously recognized.

Adolescent↗
PubMed1996

Hypereosinophilia during 2-chlorodeoxyadenosine treatment for hairy cell leukaemia.

A 43-year-old male with newly diagnosed hairy cell leukaemia underwent a single course of 2-chlorodeoxyadenosine (2-CdA). Skin rash, facial swelling and marked eosinophilia developed 20 d after treatment and were resolved by 7 d of steroid therapy. Eosinophil peak in peripheral of the eosinophil population showed a high expression of the IL-2 receptor alpha-chain (CD25), representing up to 94% of gated cells. HLA-DR and CD4 antigens were constantly negative; eosinophils strongly reacted with the secretory form of the eosinophil cationic protein (ECP), recognized by EG2 monoclonal antibody. IL-5 serum levels were markedly elevated at the onset of eosinophilia, returned to normal levels after its disappearance and positively correlated with eosinophil count (r = 0.94, P = 0.016). Eosinophilia is an uncommon finding after treatment with 2-CdA. It is unclear whether these phenomena represented a true allergic reaction to the drug or the effect of massive tumour cell lysis and haemopoietic pancytopenia with immunosuppression, which induced the release of IL-5 and possibly other cytokines.

Adult↗
PubMed1996

rhG-CSF in healthy donors: mobilization of peripheral hemopoietic progenitors and effect on peripheral blood leukocytes.

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) 16 micrograms/kg/day was given to 9 healthy donors to recruit hemopoietic progenitors (HP) for allogeneic transplantation or donor leukocyte infusion. rhG-CSF was administered s.c. for 5 days. No side effects were encountered except for moderate bone pain and lumbago. Mobilization was effective, reaching a peak median value of 187 x 10(3) CD34+ cells/ml (range 51.2-1127) and 2170 x 10(3) colony-forming units-granulocyte macrophage (CFU-GM)/ml (range 1138-4190). Peak values were obtained at a median of 4 days of rhG-CSF and represented, respectively, a 13-fold and a 37-fold increase from baseline values (p = 0.0007 and p = 0.006). White blood cell (WBC) counts increased 6-fold from baseline values (p < 0.0007) and reached a median peak of 34 x 10(6)/ml (23.5-59). Polymorphonuclear (PMN), and mononuclear (MNC) cells increased 10-fold and 2-fold, respectively (p = 0.0039 and p = 0.0026) and reached a median peak of 32.1 x 10(6)/ml (18.2-52) and 4.42 x 10(6)/ml (3.14-12.42). Absolute lymphocyte and monocyte counts increased at peak day in all donors 1.5-fold and 5.7-fold from baseline values (p = 0.0017 and p = 0.0018). In 7 of 9 donors, lymphocyte subsets were analyzed in detail. CD3+ and CD19+ lymphocytes increased 1.5-fold and 3-fold, respectively (p = 0.032 for both). NK and activated T lymphocytes doubled at a median of 4 days of rhG-CSF (p = 0.032 and p = NS, respectively). Similar changes were observed in lymphocytes collected in leukapheresis product. T helper and T suppressor subsets displayed a similar increase. Thus, besides the anticipated priming effect on HP and PMN, rhG-CSF in healthy donors produced an unexpected and still unexplained modification of lymphocyte subsets in peripheral blood.

Adolescent↗
PubMed1996

Flow cytometric detection of CD44 (H-CAM) in hairy cell leukemia.

Hairy cell leukemia (HCL) is a rare clonal B-cell disorder characterized by a distinctive pattern of infiltration of hairy cells (HCs) in the bone marrow (BM), hepatic sinusoids and splenic red pulp. HCs express a wide spectrum of matrix-binding integrins, which influence their migratory behaviour and subsequent tissue localization. CD44 distribution and staining intensity on HCs from the BM and peripheral blood (PB) were investigated using dual-color flow cytometry. HCs from all cases expressed CD44, but the staining intensity of the positive population was significantly higher than normal residual lymphocytes (p < 0.0005) and medullary HCs in those patients exhibiting additional hairy cell dissemination in the peripheral blood. It is of interest to speculate that the BM microenvironmental may deliver signals which down-regulate CD44 expression on resident HCs compared to HCs recirculating in peripheral blood. CD44 expression on HCs may help clarify their homing mechanisms in the bone marrow and to define phenotypic subsets with different clinical and pathological behaviours.

Adult↗