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Biomedical subjects

A Butturini

Publications and source records attributed to A Butturini.

At least 73 records · Page 4Linked to original sources
PubMed1989

Autotransplants in leukaemia.

With bone marrow autotransplants, favourable results are reported in subjects with leukaemia in first and second remission but not in those with advanced disease. Whether autotransplants are equivalent or superior to other therapies such as chemotherapy and allogeneic transplants is uncertain, since prospective trials are not reported and data analysis is confounded by selection of subjects and time-censoring. Major problems of autotransplants include difficulty in eradicating leukaemia in the subject, lack of the graft-versus-leukaemia effect associated with allotransplants, and reinfusion of leukaemia cells.

Adult↗
PubMed1989

Is transplantation in first remission AML more effective than in advanced leukemia?

These data indicate that the increment in the anti-leukemia effect, as expressed as FFR, is comparable for transplants for AML in first remission, advanced leukemia, and in persons never achieving remission. These data are consistent with the notion that the major anti-leukemia effect of HLA-identical bone marrow transplantation in AML results from an immune-mediated graft-versus-leukemia effect rather than from high doses of chemotherapy and radiation. Of course, other factors might explain these results. The superior outcome observed for transplants in first remission versus more advanced disease results not from increased anti-leukemia efficacy of transplants but rather that more persons already cured by chemotherapy receive transplants. Otherwise stated, a substantial portion of the persons cured following transplantation for AML in first remission were cured before receiving a transplant. These data have implications for other aspects of bone marrow transplantation. For example, it is suggested that transplants should be performed earlier in solid tumors when these diseases are more likely to respond to high-dose chemotherapy and radiation. Although this hypothesis may be correct, it need not necessarily be so as evidenced by these data in AML. The data we review show that bone marrow transplants in AML are of comparable anti-leukemia efficacy when performed in first remission, advanced leukemia, and initial resistant disease. Similar conclusions may apply to transplants in CML and ALL. The superior overall outcome observed with transplants in earlier leukemia results from transplanting a greater proportion of subjects already cured by chemotherapy. The increased anti-leukemia efficacy of transplants when compared with chemotherapy is compatible with an anti-leukemia effect other than that of high-dose chemotherapy and radiation. An immune-mediated graft-versus-leukemia effect is a likely explanation. Caution in predicting results of autotransplants in solid tumors is likewise necessary.

Bone Marrow Transplantation↗
PubMed1988

Use of recombinant granulocyte-macrophage colony stimulating factor in the Brazil radiation accident.

8 patients with bone marrow failure after a caesium-137 radiation accident were treated with recombinant human granulocyte-macrophage colony stimulating factor (rHuGM-CSF). The 7 who were evaluable had prompt increases in granulocytes and bone marrow cellularity. 2 patients died of radiation toxicity and haemorrhage and 2 of bacterial sepsis acquired before the start of rHuGM-CSF treatment. 4 patients survive, including 2 who were treated early and never became infected. This therapeutic approach to radiation-induced granulocytopenia may therefore be useful after radiation and nuclear accidents.

Accidents↗
PubMed1988

Oncogenes and human leukemias.

Eukaryotic cells contain a family of genes termed "cellular oncogenes" or "proto-oncogenes," thought to regulate normal cell growth and development. In some circumstances, such as following transduction by retroviruses, activation of these genes causes tumors and leukemias in animals. Possible mechanisms of cellular oncogene activation include: 1) DNA point mutation, deletion or insertion, 2) gene amplification, 3) gene activation by internal rearrangement, chromosomal translocation or promoter insertion, 4) recombinative events resulting in the formation of novel chimeric genes, and others. In this review, we consider data which implicates cellular oncogene activation in the pathogenesis of leukemia in humans. We discuss possible mechanisms by which oncogene activation may induce leukemias, as well as potential diagnostic and therapeutic implications.

Animals↗
PubMed1988

Oncogenes in chronic lymphocytic leukemia.

Oncogenes, in the context of retroviruses, are a common cause of leukemia in animals. Recently, activation of cellular oncogenes has been shown to be associated with leukemia in humans. Relatively few studies of oncogene activation in chronic lymphocytic leukemia (CLL) have been reported. In most instances, rearrangement of oncogenes has not been detected. Exceptions include the bcl-1 oncogene in B-cell prolymphocytic leukemia, the tcl-1 oncogene in T-cell CLL, the Hu-ets-1 and Hu-ets-2 oncogenes in small cell lymphocytic lymphoma and c-myc in a Sezary cell leukemia cell/line. Overall, it appears that oncogene abnormalities are less common in CLL than in other leukemias. The reason for it is uncertain and may relate to the relatively few cases evaluated. Alternatively, novel mechanisms of oncogene involvement or gene other than oncogenes may be important in the etiology or pathogenesis of CLL.

Humans↗
PubMed1988

Oncogenes in human leukemias.

Eukaryotic cells contain a family of genes termed cellular oncogenes or proto-oncogenes thought to regulate normal cell growth and development. In some abnormal circumstances, such as following transduction by retroviruses, activation of these genes causes leukemias in animals. Possible mechanisms of activation of cellular oncogenes include: point mutation, deletion, or insertion; amplification; activation by internal rearrangement, chromosomal translocation, or promoter insertion; recombinatorial events resulting in the formation of novel chimeric genes; among others. In this review, we consider data implicating activation of cellular oncogenes in the pathogenesis of leukemia in humans. We discuss possible mechanisms whereby oncogene activation may induce leukemias, as well as potential diagnostic and therapeutic implications.

DNA↗
PubMed1988

T cell depletion in bone marrow transplantation for leukemia: current results and future directions.

T cell depletion reduces the incidence and severity of graft-versus-host disease (GVHD) following bone marrow transplantation in man. Graft-versus-host disease of more than grade 2 severity is decreased from about 45% to about 10% in recipients of HLA-identical transplants. However, T cell depletion also increases the frequency of graft failure and leukemia relapse. Graft failure increases from about 1 to 10% following HLA-identical transplants. In patients with acute leukemia in first remission or with chronic myelogenous leukemia in chronic phase, leukemia relapse increases from about 20% to about 40%. Thus, although T cell depletion decreases GVHD, it increases graft failure and leukemia relapse such that survival is not convincingly improved. Several approaches to these problems are possible including increased pre- or post-transplant immune suppression, more effective antileukemia therapy or selective T cell depletion. Preliminary results of these approaches are discussed and new directions suggested.

Bone Marrow Transplantation↗
PubMed1987

Which treatment for childhood acute lymphoblastic leukaemia in second remission?

The best therapy for children with acute lymphoblastic leukaemia (ALL) who have an initial bone marrow relapse and subsequently achieve second remission is controversial. Some findings suggest that bone marrow transplantation (BMT) is better than chemotherapy whereas others do not. An analysis of 871 children treated by BMT or chemotherapy showed that outcome was correlated with risk factors at diagnosis and with length of first remission. BMT seemed superior in patients who relapsed within 18 months of first remission while on maintenance chemotherapy. BMT was not demonstrably superior in patients who relapsed more than 18 months after first remission. The choice of treatment in childhood ALL must be based on prognostic variables at diagnosis and on the circumstances of the relapse.

Adolescent↗
PubMed1987

Oncogenes in human leukemias.

Eukaryotic cells contain a family of genes termed cellular oncogenes or proto-oncogenes thought to regulate normal cell growth and development. In some abnormal circumstances, such as following transduction by retroviruses, activation of these genes causes tumors and leukemias in animals. Possible mechanisms of activation of cellular oncogenes include: (1) point mutation, deletion, insertion; (2) amplification; (3) activation by internal rearrangement, chromosomal translocation or promoter insertion, and (4) recombinatorial events resulting in the formation of novel chimeric genes, and others. In this review, we consider data implicating activation of cellular oncogenes in the pathogenesis of leukemia in man. We discuss possible mechanisms whereby oncogene activation may induce leukemias as well as the potential diagnostic and therapeutic implication.

Cell Division↗
PubMed1987

Graft-vs-leukemia following bone marrow transplantation: a model of immunotherapy in man.

Considerable data in animals suggest an antileukemia reaction associated with transplantation of allogeneic bone marrow cells. In some instances, this graft-vs-leukemia (GVL) reaction may be distinct from graft-vs-host-disease (GVHD). Data in humans also support the concept of a GVL effect associated with bone marrow transplantation. These observations include an increased risk of leukemia relapse in identical twin transplants and in recipients of T-cell depleted allogeneic transplants, and a decreased risk of leukemia relapse in individuals who develop acute or chronic GVHD. Although indirect, these findings are among the most convincing evidence that the immune system plays a role against cancer in man. It may be possible to exploit this effect in other settings and with other cancers.

Animals↗
PubMed1987

Graft-versus-leukemia following bone marrow transplantation.

Considerable data in animals suggest an anti-leukemia reaction associated with transplantation of allogeneic bone marrow cells. In some instances, this graft-versus leukemia (GVL) reaction may be distinct from graft-versus-host-disease (GVHD). Data in humans also support the concept of a GVL effect associated with bone marrow transplantation. These observations include an increased risk of leukemia relapse in identical twin transplants and in recipients of T cell-depleted allogeneic transplants, and a decreased risk-of leukemia relapse in individuals who develop acute or chronic GVHD. These findings are among the most convincing evidence that the immune system plays a role against cancer in man.

Animals↗
PubMed1987

The role of T-cells in preventing relapse in chronic myelogenous leukemia.

Bone marrow transplantation is effective in eradicating leukemia in over 90% of patients with chronic myelogenous leukemia (CML). This efficacy relates to some extent to the antileukemia effect of high-dose chemotherapy and radiation. An immune-mediated antileukemia effect of graft-versus-host disease is also important. In CML, a novel T-cell-mediated mechanism of leukemia eradication is also probably active. In this article we describe this novel mechanism, present preliminary data to support the notion and suggest that it might be exploited to treat CML in a context other than bone marrow transplantation.

Bone Marrow Transplantation↗
PubMed1986

Recipient immune-competent T lymphocytes can survive intensive conditioning for bone marrow transplantation.

Bone marrow transplantation is usually preceded by intensive chemotherapy and radiation therapy designed to completely eliminate recipient immune-competent cells that might reject the donor bone marrow. We show that seven of 14 bone marrow transplant recipients who received intensive conditioning retained circulating T lymphocytes that proliferate after incubation with interleukin 2 and phytohemagglutinin and function as effector cells in an in vitro model of graft rejection. These T cells may mediate graft rejection.

Adult↗