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F Caligaris Cappio

Publications and source records attributed to F Caligaris Cappio.

17 recordsLinked to original sources
PubMed2006

MATILDE regimen followed by radiotherapy is an active strategy against primary CNS lymphomas.

The authors assessed MATILDE chemotherapy followed by response-tailored radiation therapy in 41 patients aged 70 years or younger with primary CNS lymphoma in a Phase II trial. With response rates of 76% after MATILDE and 83% after chemotherapy with or without radiation therapy, this was an active strategy, particularly in low- to intermediate-risk patients (International Extranodal Lymphoma Study Group [IELSG] score). Myelosuppression was the dose-limiting toxicity, with 9.5% of lethal complications. After a median follow-up of 49 months, a plateau in the survival curve (5-year overall survival: 41 +/- 7%) was obtained.

Adolescent↗
PubMed1990

Prenatal diagnosis of fetal hemoglobin Lepore-Boston disease on maternal peripheral blood.

Molecular diagnosis of hemoglobin (Hb) Lepore-Boston in the fetus was successfully accomplished using maternal blood as a source for fetal cells in three pregnancies at risk for beta-thalassemia/Hb Lepore disease. Taking advantage of the possibility of amplifying Lepore-specific DNA fragments by polymerase chain reaction and of families in which Hb Lepore was inherited by the paternal side, we demonstrated in two cases and excluded in one case the presence of this hemoglobinopathy in the fetus directly on maternal DNA. The diagnosis was concordant with that obtained by traditional approaches in all three cases. Our results unequivocally show that nucleated fetal cells are present in maternal blood during pregnancy, and demonstrate for the first time that prenatal diagnosis of a genetic disease may be feasible without invasive procedures.

Base Sequence↗
PubMed1988

Recognition by monoclonal antibody CB02 of a surface molecule shared by B lymphocytes and a discrete large granular lymphocyte subset with cytotoxic activity.

Here we present the characterization of a new antigen called CB02 which is present on B cells and on a subset of CD16+ large granular lymphocytes. The pattern of reactivity of this molecule on normal cells, B cell lines, leukemic cells and tissue sections suggests that the CB02 molecule is expressed by B cells before isotype switch and is lost during terminal differentiation. Furthermore, the CB02+ population encompassed natural killer (NK) cells exerting significant cytotoxic activity: in fact, peripheral blood lymphocytes depleted of the CB02+ subset display a marked reduction in NK activity.

Animals↗
PubMed1983

Relevance of monoclonal antibodies in the diagnosis of unusual T-cell acute lymphoblastic leukaemia.

3 cases of adult acute lymphoblastic leukaemia (ALL), the T-cell nature of which was identified only using a panel of monoclonal antibodies (MoAb), are described. All cases were E-rosette negative, surface immunoglobulin (SmIg) negative, common ALL (CALLA) antigen negative, terminal deoxynucleotidyl transferase (TdT) positive, and acid phosphatase positive. The T-cell origin of the blasts was demonstrated by the positivity with RFA-1, a MoAb which detects an antigen of MW 65-69000 present on the membrane of thymocytes and mature T-lymphocytes. In addition, 2 of the 3 cases were positive with OKT6, which recognizes cortical thymocytes. MoAb directed against more mature T lineage cells (OKT3, OKT4, OKT8, OKT11A) were consistently negative (less than or equal to 12%). These findings indicate that the use of a combination of MoAb is important in detecting individual cases of T-ALL, which otherwise might be classified as undifferentiated acute leukaemia or null-ALL. MoAb detecting a T-cell antigenic determinant of MW 65-69000 (e.g. RFA-1, OKT1, Leu1) appear the most specific reagents for T-ALL.

Adolescent↗
PubMed1983

Effect of prostacyclin (PGI2) on immune-complex-induced neutropenia.

This study reports the results of in vitro and in vivo investigations on the effect of prostacyclin (PGI2) on polymorphonuclear neutrophils (PMN) challenged with immune complexes (IC). In vitro, PGI2 does not affect the interaction of IC with PMN membrane receptors, but prevents the ensuing PMN aggregation and secretion of platelet-activating factor, a lipid mediator responsible for immune-induced PMN aggregation. In vivo, the infusion of PGI2 in New Zealand white rabbits injected with IC prevents IC-induced neutropenia and thrombocytopenia as well as the embolization of PMN into the pulmonary peripheral capillary network. These results suggest a physiological role for PGI2 in modulating the interaction between IC and PMN.

Agranulocytosis↗
PubMed1981

Mediators of immune-complex-induced aggregation of polymorphonuclear neutrophils. II. Platelet-activating factor as the effector substance of immune-induced aggregation.

Platelet-activating factor (PAF) is released in vitro during human and rabbit polymorphonuclear neutrophil (PMN) aggregation induced by C5a anaphylatoxin, neutrophil cationic proteins (CP) and their carboxypeptidase-B-derived fragments, C5a des Arg and CP des Arg, as well as phagocytosis of opsonized baker's yeast particles and immune complexes (IC). Purified PAF itself is able to cause in vitro PMN aggregation. By using selective inhibitors, we show that PMN aggregation, induced either by PAF or by other soluble stimuli such as C5a, CP and their des Arg products, follows a similar metabolic pathway, which is both adenosine-diphosphate-(ADP)- and arachidonic acid (AA)- independent. The in vivo injection of purified PAF into rabbits leads both to formation of intravascular PMN aggregates and to development of acute neutropenia, which has the same features as those observed after challenge with IC, C5a and CP. In this respect, electron-microscopic studies of intravascular PMN aggregates in the pulmonary capillary network and glomeruli show identical ultrastructural patterns. Moreover, the intravascular release of PAF is demonstrated after the intravenous injection of IC and temporally correlated with the development of neutropenia. We suggest that PAF is probably the final, common, effector substance of IC-, C5a-, C5a-des-Arg-, CP-, CP-des-Arg-mediated PMN aggregation.

Adenosine Diphosphate↗
PubMed1980

Immune complexes in aplastic anaemia.

Immune complexes (IC) have been detected in nine out of 15 patients presenting with idiopathic aplastic anaemia using the polymorphonuclear neutrophil immunohistochemical technique. Immunosuppressive treatment undertaken in one patient produced a gradual recovery, the bone marrow repopulation being paralleled by the disappearance of IC. The significance of IC in aplastic anaemia and the relationship with possible pathogenesis and therapy of the disease are discussed.

Adult↗
PubMed1980

The role of immune complexes in blood disorders.

The aim of this review is to prevent the role of immune complexes (IC) in blood disorders. Fundamental to this role are the multiple interactions among IC and humoral and cellular receptors which give origin to several biologically active compounds and to profound metabolic, functional, and morphological changes in the involved cells. The end product of all these interactions may be both a phlogistic process and an alteration of blood cells. On this basis, clinical and experimental evidence is provided to demonstrate that IC may be produced as a consequence or a side effect of blood disorders (explaining some peculiar disturbances or proving to be of prognostic importance) or may even be the primary pathogenetic event.

Agranulocytosis↗
PubMedDate not supplied

Oncology in the nineties: from genes to therapy.

Thanks to the impressive development and application of new sophisticated technologies, the last decade has offered remarkable advances in our understanding of the molecular and biological features of human neoplastic cells. DNA analysis in particular has contributed to the unravelling of some of the possible events which give rise to a transformed cell and which enable it to proliferate indiscriminately and to infiltrate. Cloning techniques which have allowed researchers to obtain and utilize purified molecules represent another milestone. This has opened the era of cytokines and growth factors, both in terms of their possible role in the establishment and/or progression of neoplastic conditions (autocrine/paracrine models) and of their use in clinical practice. Thus, growth factors such as granulocyte-macrophage colony stimulating factors (GM-CSF) and interleukin 3 (IL-3) are currently being employed in the management of cancer patients, mainly to support normal hemopoiesis. Conversely, recombinant interleukin 2 (IL-2) through its unique capacity to generate previously unrecognized cytotoxic activity, lymphokine active killer (LAK), has brought about new and more specific immunotherapeutic strategy. Further therapeutic possibilities will arise from the clinical use of monoclonal antibodies. Finally, the development of genetic engineering has opened the way to the early and revolutionary clinical exploitation of gene therapy; the possibility of utilizing in vivo anti-sense oligonucleotides in an attempt to block the action of specific genes is also being contemplated.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Transformation, Neoplastic↗