Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-seven patients with relapsed or refractory acute leukemia and three with acute blastic chronic myeloid leukemia (CML) were treated in an open Phase II study using mitoxantrone 12 mg/m2 intravenously daily X 5 days. Complete remission (CR) was achieved in 32 of 80 (40%), including 23/45 (52%) with relapsed acute nonlymmphocytic leukemia (ANLL), four of 12 (33%) with relapsed acute lymphocytic leukemia ALL, four of 17 (24%) with ANLL refractory to daunorubicin + cytosine arabinoside, and one of three (33%) with refractory ALL. None of the patients with acute blastic CML achieved CR. Median survival time for all patients was 121 days. Median duration of complete response was 303 days with ten of 32 patients in continuing CR for periods varying from 44+ to 1210+ days. Apart from moderately prolonged hematologic suppression toxicity was mild and subjective side effects were tolerable. Mitoxantrone is an active agent in the treatment of acute leukemia and demonstrates incomplete cross resistance with duanorubicin. Mitoxantrone should be considered for first-line therapy in ANLL.
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PMID:Mitoxantrone for refractory and relapsed acute leukemia. 219 40

DNA aneuploidy (DA) was examined in adult leukemia using flow cytometry, and the method and the clinical implication of DA as a tumor marker were evaluated. The method was simple, rapid, objective, quantitative and further did not need any mitotic cells, so was proved to be very useful for screening of DA. While, DA was detected in 50 (27%) out of 185 adult cases with various types of leukemia. The frequencies of DA in the subtypes of leukemia were 55% in ATL, 26% in ALL, 17% in ANLL, 26% in CML-BC and 6% in CLL, respectively. When compared with other subtypes, the frequency in ATL was significantly higher (p less than 0.01), which suggested a special entity of this disease. In general, however, the frequency of DA in leukemia was rather low, which indicated the difficulty in application of DA by itself in diagnosis of leukemia. While, in cases with DA, DA was very useful as a tumor marker in monitoring the clinical course, for example, in the detection of early relapse or recruitment of leukemic cells. Furthermore, DA was found to be a good prognostic factor which indicates a poor prognosis in cases with ANLL and CML-BC.
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PMID:[Analysis of DNA aneuploidy as a tumor marker]. 221 64

We studied the activity of serum adenosine deaminase (ADA) and its isozyme in 36 leukemic patients (16 ANLL, 11 ALL, and 9 CML) and 8 MDS. Isozyme was measured by erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) inhibitory assay. This assay was simple and reliable. The appearance rate of abnormally high ADA value were 81.24% for ANLL, 100% for ALL, 77.8% for CML and 37.5% for MDS. The ADA level became high when MDS turned into overt leukemia. In isozyme pattern, there was a clear difference between ANLL and ALL. The isozyme I/II ratio was significantly higher (p less than 0.001) in ALL than ANLL. Lymphoblastic crisis of CML also had a high isozyme I/II ratio. There was a correlation between isozyme I and absolute number of peripheral blasts in ALL (r = 0.768). When observed time sequentially, ADA and isozyme changed correlatively with the number of blasts counts. Serum ADA and its isozyme are useful parameters both for leukemic diagnosis and treatment.
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PMID:[Serum adenosine deaminase and its isozyme activity in leukemia and MDS]. 223 54

Since 1976 in Genoa, 291 TBI treatments were performed. Before allogeneic BMT, 1000 cGy/1 fx were prescribed in the first 22 patients, and then 990 cGy/3 fx/3 d in AML and CML, and the same or 1200 cGy/6 fx/3 d in ALL. Survival (S) and probability of remaining in remission (PRR) were 54% and 69% at 80 months in 80 AML; in 62 CML 45% and 60% at 60 months; in 69 ALL, 32% and 45% at 82 months. Differences in favour of higher doses and dose rates were observed and are presented. Before autologous BMT, 1000 cGy/1 fx were prescribed to AML and NHL, and 1200 cGy/3 fx/3 d to ALL patients. Disease free survival (DFS) was 71% and 13% at 82 months in 21 AML treated in first R and 9 ALL, respectively; 81% at 32 months in 11 NHL treated in R.
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PMID:Total body irradiation before allogeneic and autologous bone marrow transplantation: a ten year Genoa experience. 224 39

Short term clinical results of bone marrow transplantation on 66 patients conditioned with fractionated total body irradiation (12 Gy in 6 fractions and 3 days) are presented here. An acute toxic effects incident, similar to that obtained previously, a 27.6% interstitial pneumonitis associated with acute severe graft versus host disease in 77% of cases, 19.2% relapses, and 41% total crude survival with an actuarial probability of surviving for more than two years of 46% for ALL, 64% for AML and 28% for CML, are the results obtained since now.
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PMID:Fractionated total body irradiation for bone marrow transplantation: clinical results on 66 patients. 224 43

In May 1979, Memorial Sloan-Kettering embarked on a programme of hyperfractionated TBI (HFTBI), 1320 cGy in 11 fractions over 4 days with partial lung shielding (1 HVL), followed by cyclophosphamide (60 mg/kg/d x 2d) for cytoreduction prior to allogeneic bone marrow transplantation (BMT). Anterior and posterior chest wall electron "boosts" were given to the areas blocked (600 cGy in 2 fractions) on the last two days of treatment. Since then, we have treated over 600 patients with HFTBI, the majority for allogeneic BMT. Several modifications have occurred over the years. We have added a "boost" electron dose of 400 cGy to the testes in all male leukemic patients; this reduced testicular relapses from a rate of 14% (4/28) to 0%. In an attempt to increase engraftment of T-depleted BMTs, we added one additional fraction; since our present dose/fraction was also increased to 125 cGy, we now deliver a total dose of 1500 cGy in 12 fractions over 4 days for allogeneic transplants. Tolerance to HFTBI has been excellent relative to the single dose (SD) regimen utilised prior to May, 1979. The incidence of fatal interstitial pneumonitis (IP) decreased from 50% in the SD regimen to 18% after the introduction of HFTBI. In children, the incidence of IP was only 4% with HFTBI. With the introduction of T-depleted marrows, fatal IP in adults has decreased also, e.g. to less than 10% in CML patients. With conventional BMT after HFTBI, relapse at 5 years has been exceedingly low (e.g. in children, 13% for ALL, 2nd remission and 0% for AML, 1st remission) and engraftment has been 100%. With matched T-depleted BMT, rejections have occurred in 15% overall; the incidence of graft failure has not been reduced by the higher dose of HFTBI. Relapses in this setting are equivalent to relapses with conventional BMT for AML, but appear to be increased for ALL. Radiobiological findings related to HFTBI will also be discussed.
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PMID:Total body irradiation for bone marrow transplantation: the Memorial Sloan-Kettering Cancer Center experience. 224 51

The indications and results of allogeneic bone marrow transplantation are well known by the analyses of European and International registries. In acute non-lymphoblastic leukemia in first complete remission (CR), the disease-free survival (DFS) is 45%, with a risk of relapse (RR) of 15%; in ALL in first CR the DFS is 60% with a RR of 15%; in ALL in second CR the DFS in 40%, with a RR of 30%; in CML in chronic phase the DFS is 60%, with a RR of 20%. These results have to be adjusted with other risk factors such as age, sex mismatch, disease status, CMV serology, and GVH. The use of donors different from a genotypically matched related donor is currently under investigation. Mismatched related transplants give disappointing results except in the case of one HLA mismatch. Unrelated HLA matched donor panels have been recently established in various countries with 200 transplants performed with a DFS of approximately 40%. Current research tries to reduce the risk of relapse by intensifying the conditioning or using the GVL effect of allogeneic T cells, to reduce GVH by the use of monoclonal antibodies and to improve the engraftment by the use of growth factors.
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PMID:Recent trends in allogeneic bone marrow transplantation. 225 66

The diagnosis and classification of leukaemia started with simple morphological examination and now embraces use of special stains, cytochemistry and immunophenotyping. Genetic studies have progressed from karyotyping to detection of genetic changes within genes. The methods described in this chapter are still at an early stage of development and, so far, have provided relatively little in the way of an extension of available diagnostic information. Sometimes the methods provide extensions to existing techniques, for example by the detection of bcr rearrangements in patients who have CML or ALL but do not have a detectable Philadelphia chromosome. Another example is retrospective diagnosis of gene rearrangements using DNA from slide preparations. However, it should be noted that it has only very recently been shown that there is likely to be a causal relationship between the Ph chromosome and leukaemia. Daley et al (1990) induced CML in mice by bone marrow transplantation of cells infected with a retrovirus encoding P210bcr/abl and Heisterkamp et al (1990) produced mice transgenic for a BCR/ABL P190 DNA construct and showed that the progeny died of acute leukaemia (mostly ALL). We have not summarized studies of the incidence of activated oncogenes such as RAS in leukaemia and myelodysplasia. Such oncogenes appear to be involved in many tumours and may well indicate either a predisposition to cancer or a particular stage of malignancy, but their analysis does not at present help in making a diagnosis. It is likely that, as we understand more about the nature of the malignant process, we shall be able to use genetic techniques to enhance considerably both diagnostic and prognostic precision.
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PMID:Molecular biology and leukaemia diagnosis. 227 97

The Ph1 chromosome has two molecular subtypes: a bcr-positive seen in CML and some cases of ALL, and the bcr-negative subtype mainly seen in ALL. In CML, because of the restriction of chromosome 22 breakpoints to the bcr, Southern analysis to detect bcr rearrangements also can be used to detect the Ph1 chromosome. In contrast, the translocation breakpoints on the Ph1 chromosome are scattered in ALL, so that other methods such as PFGE and PCR are necessary to detect the Ph1 chromosome. In both CML and ALL, use of these methods to detect molecular abnormalities may be superior to cytogenetics in detecting chromosomal abnormalities. Southern analysis also can be used in CML to map breakpoint locations within the bcr. This may offer prognostic information as to the length of chronic phase, but there is conflicting information as to the validity of this approach. The modified PCR (using cDNA from mRNA) can be used to detect the Ph1 chromosome and to define which of the molecular subtypes are present. The exquisite sensitivity of this method, which is capable of detecting as little as a single abnormal molecule of RNA or DNA, makes it suited for the detection of minimal residual disease in both CML and ALL. This is particularly useful after intensive therapies, such as bone marrow transplantation. Whether these low levels of fusion gene expression are of prognostic significance is still unclear.
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PMID:Molecular methods to detect the Philadelphia chromosome. 227 77

During the stage of blast crisis, the increase in the population of peripheral blasts in one examined untreated CML patient, obeyed an exponential equation of growth that requires a maintained equal proportion of proliferating to quiescent blasts. A model of cell growth at CML blast crisis is presented, which interprets the required constancy of equal-size blast subcompartments in terms of regulation of the G0----G1 flow, the latter involving activation of one cell out of three interacting quiescent blasts in contact. This model is discussed in the light of evidence that G0 blast activation involves membrane-bound interacting sites interfering with growth-promoting pathways. The model-predicted proliferative index (f) value of 0.5 +/- 0.16 is found to be nearly identical to a reported estimate of the 3H-thymidine-labeling index of CML blasts at the crisis stage of the disease. It is also close to corresponding indexes of CML blood and marrow progenitor cells and to labeling indexes of AML and ALL large blasts.
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PMID:Cell growth in chronic myeloid leukemia at blast crisis. 228 42


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