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217 results on '"Castoldi, G. L."'

12. Blood, Bone

Author

Kelenyi, Gabriel, Zombai, Elisabeth, Koszewski, Bohdan J., Castoldi, G. L., Merker, H., Wachstein, M., Ortiz, J., Fernandez, C., Goulis, Chr., Kovatsis, A., Ambs, Erhard, Bahr, Gunter F., Zeitler, Elmar, Müller, Hans E., Hübner, K., Schiemer, H. G., Bélanger, Leonard F., Fullmer, Harold M., Link, Clifton, Jr., Schiebler, T. H., editor, Pearse, A. G. E., editor, and Wolff, H. H., editor

Published
1964
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14. Anemia drepanocitica

Author

Cibien, F., Viglione, G. M., Rigolin, Gian Matteo, Cuneo, Antonio, and Castoldi, G. L.

Published
2009

16. Blut, Knochen

Author

Kelenyi, Gabriel, primary, Zombai, Elisabeth, additional, Koszewski, Bohdan J., additional, Castoldi, G. L., additional, Merker, H., additional, Wachstein, M., additional, Ortiz, J., additional, Fernandez, C., additional, Goulis, Chr., additional, Kovatsis, A., additional, Ambs, Erhard, additional, Bahr, Gunter F., additional, Zeitler, Elmar, additional, Müller, Hans E., additional, Hübner, K., additional, Schiemer, H. G., additional, Bélanger, Leonard F., additional, Fullmer, Harold M., additional, and Link, Clifton, additional

Published
1964
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35. Short term treatment with Escheria coli recombinant human granulocyte- macrophage-colony stimulating factor prior to chemotherapy for Hodgkin disease

Author

Aglietta, M., Montemurro, F., Fagioli, F., Volta, C., Botto, B., Cantonetti, M., Racanelli, V., Teofili, L., Amadori, S., Castoldi, G. L., Dammacco, F., Levis, A., and Ferrara, R.

Subjects
procarbazine, Hodgkin disease, bleomycin, Settore MED/06 - Oncologia Medica, Granulocyte- macrophage-colony stimulating factor, Hybrid mechlorethamine, doxorubicin, and dacarbazine, Myeloprotection, Vincristine, vinblastine, and prednisone, Vincristine, procarbazine, and prednisone, doxorubicin, bleomycin, vinblastine, and dacarbazine, Settore MED/15 - Malattie del Sangue
Published
2000

43. Hairy cell leukemia

Author

Federico, Massimo, Frassoldati, A., Artusi, Tullio, Castoldi, G. L., Lauria, F., Pileri, S., Pizzolo, G., Resegotti, L., Semenzato, G., and Damasio, E. E.

Subjects
malattia linfoproliferativa, Hairy Cell Leukemia (HCL)
Published
1995

44. Acute promyelocytic leukemia: morphological aspects

Author

Castoldi, G. L., Liso, V., Giorgina Specchia, and Tomasi, P.

Subjects
Diagnosis, Differential, Cytoplasm, Leukemia, Promyelocytic, Acute, Bone Marrow, Histocytochemistry, Humans, Cytoplasmic Granules, Carboxylic Ester Hydrolases, Basophils, Granulocytes, Peroxidase
Abstract

Among AML with maturation, acute promyelocytic leukemia (APL) represents a distinct subtype which accounts for 5-10% of all the FAB variants. APL may be recognized by different cytological pictures: (i) Hypergranular APL, the most typical form, showing promyelocytes with cytoplasm packed with purple granules. Most of the primary granules may be incorporated into Auer rods, sometimes stacked in bundles of faggots. (ii) Microgranular APL, characterized by fine dust-like granulation in the cytoplasm; some promyelocytes may even appear agranular by light microscopy. Most of the cells show bilobed or folded nuclei, a picture which may simulate that of acute myelomonocytic leukemia. (iii) Hyperbasophilic form, characterized by cells with high N/C ratio, and strongly basophilic cytoplasm with either sparse or no granules. Conspicuous cytoplasmatic budding is usually present, recalling the feature of micromegakaryocytes. Strong positivity for myeloperoxidase, Sudan black B and chloroacetate esterase represents the typical cytochemical pattern of M3; usually a weaker reactivity may be observed in M3v. However, sometimes a degree of cytochemical heterogeneity of APL cells may be observed, as suggested by cases displaying a strong sodium fluoride-sensitive nonspecific esterase reaction. Recently a distinct entity associated with basophilic differentiation has been described. Differential diagnosis of this form with M2-baso subtype and with cases of MDS or AML with basophilia (M2, M4 with t(6;9) translocation) may be obtained by the use of cytochemistry, cytogenetic investigations, and electron microscopy.

Published
1994

45. Abnormal expression of N-CAM (CD56) adhesion molecule on myeloid and progenitor cells from chronic myeloid leukemia

Author

Lanza, F, Sucai, Bi, Castoldi, G. L., and Goldman, Jm

Subjects
N-CAM (CD56) molecules, Antigens, Differentiation, T-Lymphocyte, Myeloproliferative Disorders, Macrophages, Antibodies, Monoclonal, Antigens, CD34, Bone Marrow Cells, Flow Cytometry, Hematopoietic Stem Cells, Immunohistochemistry, CD56 Antigen, NO, Colony-Forming Units Assay, chronic myelogenous leukemia, Antigens, CD, Antigens, Neoplasm, Bone Marrow, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, abnormal expression, Tumor Cells, Cultured, Humans, N-CAM (CD56) molecules, chronic myelogenous leukemia, abnormal expression, Granulocytes
Abstract

Bone marrow and peripheral blood samples from 36 patients with Philadelphia chromosome positive chronic myelogenous leukemia (Ph+ CML) (30 in chronic phase, four in accelerated phase, and two in blastic crisis) were tested with two CD56 monoclonal antibodies (My31 and Eric 1) using the Facscan flow cytometer. Two- and three-color fluorescence experiments indicated that CD13+/CD33+ myeloid cells from 19 out of the 36 patients were positive for CD56 in 12-77% of the cells. In contrast, no CD56 positivity was documented in myeloid cells from bone marrow (BM) of healthy donors. Immunocytochemical staining (APAAP technique) of CML peripheral blood (PB) and BM slides showed that CD56 expression was detectable from the myelocyte stage with the strongest staining in the metamyelocyte stage. Neutrophils were negative both by flow cytometry and APAAP analysis. In individual CML patients, an increasing number of CD56+ cells were recovered with progressively higher density cuts (1.065-1.077 g/ml), supporting the concept that the antigen level tends to increase during myeloid differentiation. Furthermore, 19% of CML patients coexpressed CD56 and CD34 antigens in 10-45% of the CD34+ cells. The myeloid nature of CD56+/CD34+ CML cells has been ascertained by granulocyte-macrophage colony-forming unit (CFU-GM) assays on CD56+ cells sorted on FACS. Furthermore, in six out of eight CML patients in whom we performed a comparative BM and PB analysis, we found that the CD56 expression was brighter and the number of positive cells significantly higher in the peripheral blood myeloid cells as compared to their BM counterpart. In short-term liquid cultures, low doses (50 U/ml) of alpha interferon down-regulated the CD56 expression in CML cells, accompanied by a significant reduction of the Ph positivity. In conclusion, the expression of CD56 on CML myeloid elements seems to represent an aberrant phenomenon which could affect the cell homing mechanisms and, probably, the pattern of tumor cell dissemination. In patients with CD56+ CML, its detection could be further used as a means of monitoring patients undergoing bone marrow transplantation, since its reappearance is associated with early relapse of the disease.

Published
1993

48. RECOMBINANT GAMMA-INTERFERON AS 1ST LINE THERAPY FOR HIGH-RISK MYELODYSPLASTIC SYNDROMES

Author

Maiolo, A. T., Cortelezzi, A., Calori, R., Polli, E. E., Gavosto, F., Piacibello, W., Resegotti, L., Paolino, R., Ascari, E., Cazzola, M., Bernasconi, C., Alessandrino, E. P., Castoldi, G. L., Mandelli, F., Alimena, Giuliana, ALOE SPIRITI, Maria Antonietta, and Cesana, B. M.

Subjects
granulocyte-macrophage, 13-cis retinoic acid, acute myelogenous leukemia, colony-stimulating factor, 13-cis-retinoic acid, acute myeloid-leukemia, dose cytosine-arabinoside, progenitor cells, prognostic factors, scoring system
Published
1990

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