Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.1.1.69 (BMT)
2,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is an interim report of the Roferon A/ABMT protocol by ICSG on CML aimed at investigating the feasibility and potential of combining treatment with alpha-IFN with ABMT in Ph+ CML. Of 675 Ph+ CML patients recruited between January 1989 and January 1991 by 44 Italian institutions, 398 were 55 or less years old and eligible for the protocol. Of 132 patients who completed IFN treatment 118 had evaluable karyotype; of these only 48 showed > 25% Ph--metaphases and were eligible for BM harvest. In 24 patients BM was collected and 13 were submitted to ABMT. The major causes of drop out from the protocol were shift to allogeneic BMT, accelerated blastic phase, patient refusal and logistic problems. Data on hematologic reconstitution are presently available in 11 patients: Neutrophils were > 0.5 x 10(9)/l in 23 days (median), (range 16-40 days); platelets reached 50 x 10(9)/l in 28 days (median), (range 25-100 days). One patient had a very delayed BM take and was rescued with autologous peripheral blood stem cells collected at diagnosis.
Leuk Lymphoma 1993
PMID:Karyotypic conversion by interferon as preparative treatment for autologous BMT in Ph positive CML. Italian Cooperative Study Group (ICSG) on Chronic Myeloid Leukemia. 825 9

To evaluate the prognostic features of Ph+ CML patients treated by allogeneic BMT or by IFN, we reviewed the data of 50 consecutive pts who were transplanted between 1984 and 1988 and of 180 consecutive patients who were assigned to continuous IFN treatment between 1986 and 1988. In the BMT group, Sokal's system predicted survival (transplant-associated mortality). In the IFN group, Sokal's system, platelet count, and peripheral blood blast cell percentage predicted karyotypic response. In this group, survival was related more significantly with blast cell than with Sokal's score. The strongest predictor of survival was karyotypic response to IFN, with a 4-year survival of 94% for responders vs. 56% for non-responders.
Leuk Lymphoma 1993
PMID:Prognostic factors in chronic myeloid leukemia. Relationship with interferon and bone marrow transplantation. The Italian Cooperative Study Group on Chronic Myeloid Leukemia. 825 20

Twenty-four patients with a variety of malignant diseases (13 lymphoma, 4 myeloma, 1 ALL, 6 solid tumours) were treated with the alkylating agents busulphan and melphalan as a preparative regimen for autologous BMT. Thirteen males and 11 females, aged 27-53 years (median 39.5 years) received oral busulphan 1 mg/kg q6 h on days -6 to -3, followed by i.v. melphalan 140 mg/m2 on day -2 and infusion of cryopreserved haemopoietic cells on day 0. The major toxicity seen was gastrointestinal with nausea, vomiting and diarrhoea in 17 patients and severe mucositis in 22. There was no evidence of cardiotoxicity, nephrotoxicity, haemorrhagic cystitis or clinical signs of hepatic veno-occlusive disease. Twenty-three patients engrafted with the median duration of neutropenia (< 0.05 x 10(9)/l) 10 days (range 5-63 days) and thrombocytopenia (< 50 x 10(9)/l) 43 days (range 5-350 days). Three patients died of transplant-related complications. Of 15 evaluable patients with active disease at BMT, 9 responded and 6 were refractory. Sixteen evaluable patients were in CR after BMT. Seven relapsed, 1 died in remission and 8 remain in CR 12-46 months (median 29 months) later. Of the group of 13 lymphomas, overall and relapse-free actuarial survival at 36 months was 64% and 58%, respectively, while for the entire group of 24 patients these values were 39% and 34%. Busulphan and melphalan is a safe and inexpensive conditioning regimen for autologous BMT with acceptable toxicity and substantial antitumour activity particularly against lymphomas.
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PMID:Busulphan and melphalan prior to autologous bone marrow transplantation. 827 31

The very rapid development in the last few years of techniques based on use of the polymerase chain reaction (PCR) for characterizing molecular lesions in leukaemia and lymphoma now offers the opportunity for monitoring residual disease at a sensitivity of one malignant cell in 10(5) or 10(6) normal cells. Maximal specificity is presumably achieved when the DNA sequences amplified are truly leukaemia-specific, such as BCR/ABL in chronic myelogenous leukemia, RARA PML/RARA in t(15;17) acute myelogenous leukemia, DEK/CAN in t(6;9) AML, PBX1/E2A in t(1;19) acute lymphoblastic leukemia (ALL), or TAL-1 deletions in other T-ALLs. Comparable sensitivity may be achieved by using immunoglobulin heavy chain (IGH) and T-cell receptor (TCR) gene rearrangements if a clonospecific probe can be generated. However, the presence of similar sequences in IgH genes from normal B lymphocytes may decrease the specificity. For clinical purposes the crucial issues are the following. Can PCR techniques be used for confirmation of diagnosis and evaluation of extent of disease? Can PCR data obtained in remission provide information about the probability of cure or of relapse? Can techniques be developed to quantitate the PCR product and thereby increase its predictive value? These and other issues were addressed at the 4th Workshop of the Molecular Biology/BMT Study Group that took place in Bristol UK on 9-10 May 1992.
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PMID:Molecular evidence of minimal residual disease after treatment for leukaemia and lymphoma: an updated meeting report and review. 835 Jun 33

Although serial detection of bcr-abl positive cells by PCR appears able to identify distinct patient groups with different risks of relapse following BMT, there remain many unanswered questions regarding the clinical utility and biological significance of PCR detectable cells in this disease. Many of the studies summarized have conflicting results and the influence of various clinical parameters which are known to affect the risk of relapse post-BMT has not yet been consistently associated with the ability to detect bcr-abl positive cells by PCR. These clinical parameters include GVHD, T-cell depletion and intensity of immunosuppression following BMT. Prospective studies with larger patient numbers will be necessary to define the impact of these factors in PCR status and relapse. The answers to all these questions will increase our understanding of the biology of chronic myelogenous leukemia and help provide more effective therapies for the future.
Leuk Lymphoma 1993 May
PMID:Clinical significance of bcr-abl gene rearrangement detected by the polymerase chain reaction after allogeneic bone marrow transplantation in chronic myelogenous leukemia. 837 16

Allogeneic bone marrow transplantation has been shown to be a very effective therapy for Chronic Granulocytic Leukemia with long term disease free survivals in excess of 60%. Relapse rates remain low at 15% following histocompatible sibling transplants and lower rates following matched unrelated donor grafts. Relapse rates however, are higher if BMT is carried out in transformation or blast crisis. Leukemic relapse in donor cells following transplantation for CGL is a rare event. The occurrence of donor leukemia however, may be under reported as accurate and sensitive investigation of the origin of relapsed leukemia following BMT requires DNA based technologies. A possible mechanism of donor leukemia in CGL is transfection of donor cells with the chimeric gene which is unique to this disease. It is possible that the malignant cells found in transformed or blast crisis of CGL may have a greater potential to transfect donor haematopoietic material. Careful evaluation of the incidence of donor leukemia using molecular biology methods may elucidate the frequency of this event following BMT for CGL.
Leuk Lymphoma 1993 Aug
PMID:Recurrence of Philadelphia chromosome-positive leukemia in donor cells after bone marrow transplantation for chronic granulocytic leukemia. 840 Nov 78

The results of autologous and allogeneic BMT in 44 patients with Hodgkin's or non-Hodgkin's lymphomas who received preparative therapy consisting of busulfan 16 mg/kg and cyclophosphamide 120 mg/kg are presented. Sixteen patients are surviving free of disease between 8 months and 6 years after transplantation. Thirteen patients either did not attain complete remission or experienced a recurrence of their disease. Fifteen patients died from treatment-related complications. Karnofsky score < or = 70, lactate dehydrogenase greater than twice normal and the development of hepatic veno-occlusive disease were associated with failure to achieve lymphoma-free survival.
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PMID:Preparation for marrow transplantation in Hodgkin's and non-Hodgkin's lymphoma using Bu/CY. 840 59

When allogeneic BMT is used for the treatment of leukemia, depletion of T cells from the donor BM to avoid GVHD may be accompanied by persistence of host cells and post-transplant relapse. In this report, a murine model of MHC-compatible BMT was used to show that delayed infusion of immunocompetent donor cells early after T cell-deficient BMT eliminated residual host cells and provided an antileukemic effect without causing lethal GVHD. AKR (H-2k) recipient mice were pre-conditioned with 9 Gy total body irradiation (LD50) and transplanted with 10(7) BM cells from MHC-matched B10.BR donors. These mice did not develop GVHD and became stable, long-term mixed (donor-host) T cell chimeras. In this model, mixed or incomplete donor T cell chimerism was associated with decreased GVL reactivity. AKR hosts that were transplanted with B10.BR bone marrow admixed with 3 x 10(7) B10.BR spleen cells (as a source of T cells) became complete donor T cell chimeras, but they developed severe and lethal GVHD. However, when the infusion of donor spleen cells was delayed until 21 days after BMT, few mice exhibited any clinical signs of GVHD, and > 95% of the mice became long-term survivors. The infused spleen cells eliminated residual host T cells by 21 days after infusion, and most chimeras were able to resist a supralethal challenge with AKR leukemia/lymphoma cells. Thus, post-transplant adoptive immunotherapy with normal mononuclear cells from the marrow donor may be an effective way to eliminate residual disease or treat leukemia relapse after BMT without causing significant GVHD.
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PMID:Delayed infusion of normal donor cells after MHC-matched bone marrow transplantation provides an antileukemia reaction without graft-versus-host disease. 848 80

Mucormycosis is known to cause rhinocerebral and pulmonary disease in patients with diabetes, leukemia, and lymphoma. However, the characteristics and outcome of these infections have not been well described in the BMT population. In a 17-year consecutive series of BMT patients, 13 of 1500 patients (0.9%) developed mucormycosis. Ten of the transplants were allogeneic and three autologous. Six infections occurred within 90 days of transplant, and six occurred at or within several days of autopsy. Seven patients were neutropenic and another patient had just engrafted at diagnosis of infection. Sites of infection were lung-brain (n = 4), sinonasal region (n = 3), lung (n = 2), disseminated (n = 2), lung-kidney (n = 1), and bone-muscle (n = 1). All patients were treated with prolonged amphotericin B therapy. Surgical debridement was employed in the three sinonasal infections. Death from mucormycosis occurred in ten of 13 (77%) patients. Two patients are alive, including one who had resolution of sinonasal infection. Mucormycosis may occur in both neutropenic and non-neutropenic patients, and may occur long after hospital discharge for BMT. These infections are often fatal, although patients with limited sinonasal disease may have a better prognosis, especially with early diagnosis and aggressive antifungal therapy.
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PMID:Mucormycosis in the BMT population. 850 72

Using strict FAB criteria, 39 cases of monocytic leukemia were identified in 463 consecutive cases of AML. Patients had a median age of 49 with no sex predominance. Extramedullary disease and hyperleukocytosis were common (54% and 36% of patients respectively). Cytogenetic analysis was successful in 38 of 39 patients; 71% had a cytogenetic abnormality and 42% of these involved chromosome 11; 14 of 16 chromosome 11 abnormalities involved the region of 11q23. Non-chromosome 11 abnormalities tended to occur in older patients and to be associated with a lower platelet count; patients with the translocation 9;11 tended to have a lower white count and a higher incidence of therapy-related leukemia. 35 patients were treated with induction therapy including intensive chemotherapy (n = 33) and allogeneic BMT at presentation (n = 2). Patients who entered remission underwent consolidation chemotherapy, autologous BMT, or allogeneic BMT depending on policies at the time of diagnosis. Of 6 patients who underwent further intensive chemotherapy there is 1 long-term disease-free survivor. 3 of 8 patients undergoing autologous BMT and 2 of 3 patients undergoing allogeneic BMT are long-term disease-free survivors. We conclude that this specific subtype of AML, relatively rare when strict criteria are applied, is associated with unique biologic and clinical features and that the high relapse rate associated with conventional therapy makes new treatment approaches involving stem cell transplantation or immunomodulation necessary.
Leuk Lymphoma 1995 Oct
PMID:Acute monocytic leukemia: a single institution experience. 853 17


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