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

A 31-year-old woman with Philadelphia chromosome-positive chronic myeloid leukaemia (CML) was treated intermittently with high-dose busulphan over a 6-yr period (total dose 1320 mg). 3 yr later (after receiving no further cytotoxic drugs) she developed pancytopenia and marrow aplasia of relatively abrupt onset. Transfusion of reconstituted blood-derived stem cells (collected 7 yr previously) re-established chronic phase CML. These events are more consistent with 'stem cell exhaustion' than with an acquired marrow microenvironmental defect occurring in the course of CML. The contribution of busulphan is uncertain.
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PMID:Marrow aplasia developing 3 years after treatment with busulphan for chronic myeloid leukaemia. 256 49

Bone marrow transplantation is impossible without effective support with blood components during the period of pancytopenia before graft function appears. We analyzed 39 patients with leukemia and three patients with severe aplastic anemia with regard to the pre- and postgrafting requirements for RBC and PLT transfusions. Overall a median of eight RBC and four PLT concentrates were necessary in all 42 patients after allogeneic BMT (ranges, 1-32 RBC and 1-11 PLT units). Requirements were identical irrespective of the underlying disease (ALL, AML, CML, SAA). Transfusion need for RBC and PLT concentrates increased in patients over 30 years old and with a major red blood group AB0 barrier between marrow donor and recipient. The presence of grade II-IV GvHD increased RBC requirements significantly, but not PLT requirements. In addition these patients were dependent on RBC transfusions for significantly longer periods. Only one patient required therapeutic granulocyte transfusions. In a CMV-negative patient with a CMV-negative marrow donor, who died of veno-occlusive disease, cytomegalovirus was transmitted inadvertently by a seropositive PLT concentrate in his final course. Our transfusion strategy included frozen deglycerolized RBC concentrates and single donor PLT concentrates, collected mainly from the marrow donor by a cell separator. All blood products were irradiated in vitro with 1500 cGy before transfusion. An optimal transfusion policy starting before BMT can contribute to successful bone marrow transplantation.
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PMID:Hematological support in patients undergoing allogenetic bone marrow transplantation. 305 Dec 11

Patients in the stable phase of chronic myelogenous leukemia (CML) are usually treated with busulfan. The bone marrow of patients with CML may be exquisitely sensitive to busulfan, and occasionally such patients develop pancytopenia, secondary to hypoplasia or aplasia of the bone marrow, which is presumed to be due to busulfan-induced marrow toxicity. We report a case of Philadelphia chromosome-positive CML who developed pancytopenia while being treated with busulfan; however, the patient's bone marrow was not hypoplastic or aplastic but rather hyperplastic with sideroblastic changes. Busulfan is not known to cause sideroblastic changes, so this was considered to herald a transformation into acute leukemia. Busulfan was stopped, and only supportive treatment was given. To our surprise approximately 22 weeks after busulfan was stopped, the sideroblastic changes had disappeared and the bone marrow again showed features of CML. This case suggests that busulfan may cause sideroblastic anemia.
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PMID:Busulfan-induced sideroblastic anemia. 316 1

We report a case of a female patient with chronic myelogenous leukemia who presented, 8 yr after initial diagnosis, with pancytopenia, encephalopathy, and myalgia. The tentative diagnosis was accelerated phase of chronic myelogenous leukemia. However, because the patient had been treated with cimetidine for 7 months we first omitted this drug. When cimetidine was stopped, bone marrow recovered, and myalgia and encephalopathy subsided. Immunological studies showed stimulation of the patient's lymphocyte blastogenesis by cimetidine and a marked increase in the proportion of cytotoxic/suppressor T lymphocytes after incubation of peripheral blood lymphocytes with cimetidine for 6 days. These findings indicate a role for cell-mediated immunity in the pathogenesis of cimetidine-induced pancytopenia in this patient.
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PMID:Immune basis for cimetidine-induced pancytopenia. 347 Oct 83

A case of epidermotropic cutaneous toxoplasmosis is reported. The patient, a 53-year-old man with chronic myelogenous leukemia in blast crisis, received a bone marrow allograft but continued to have severe pancytopenia. Numerous diffuse, palpable, purpuric nodules appeared 21 days after the transplant. Organisms were found within the epidermal keratinocytes--both singularly and in cysts. Dermal and neural infiltration was also present. Toxoplasma gondii was identified on the basis of the ultrastructural features of the parasite. Possible sources of infection include reactivation of a previous latent infection, transmission through a bone marrow allograft, or nosocomial acquisition.
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PMID:Cutaneous toxoplasmosis. 351 6

Trisomy 14 was demonstrated on four occasions over a 2-year period in the bone marrow cells of a 63-year-old patient with refractory anemia with excess of blasts in transformation (RAEB-t). Trisomy 14 as the sole karyotype abnormality has been documented in only six malignancies, namely, in two cases of acute leukemias, one Philadelphia-negative chronic myeloid leukemia, one pancytopenia, and in two colonic polyps. In hematologic neoplasms, this rare primary change preferentially occurs in elderly adults and seems exclusively associated with the myeloid cell lineage.
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PMID:Trisomy 14 in refractory anemia with excess of blasts in transformation. 367 48

Diaziquone (AZQ), a new lipid-soluble antitumor agent, was given by 15-30-minute infusion on a daily X 5 schedule to 47 children with refractory solid tumors and leukemia. The starting daily dose of 6 mg/m2 was escalated to 10 and 35 mg/m2 in patients with solid tumors and leukemia, respectively. In patients with solid tumors, myelosuppression was dose-limiting at a daily dose of 10 mg/m2. In patients with leukemia, prolonged pancytopenia and bone marrow hypoplasia were observed at daily doses greater than or equal to 25 mg/m2. At these higher doses, significant hyperbilirubinemia associated with sepsis was also seen. Corresponding increases of transaminases or alkaline phosphatase and significant hemolysis were not noted. The maximum tolerated dose for this daily dose schedule was 9 mg/m2 in children with solid tumors and 25 mg/m2 in children with relapsed leukemia. Responses to AZQ included stabilization of disease in osteosarcoma, neurofibrosarcoma, pinealoma, and ependymoma. A patient with juvenile chronic myelocytic leukemia in blast crisis converted back to the chronic phase. A patient with acute lymphoblastic leukemia had a substantial decrease in cerebrospinal fluid blast count. Bone marrow aplasia was achieved in children with acute lymphoblastic leukemia and acute nonlymphoblastic leukemia; however, remissions were not achieved. A phase II study of AZQ in children with refractory malignancies is now being performed by the Childrens Cancer Study Group.
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PMID:Phase I clinical evaluation of diaziquone in childhood cancer. 385 80

Chromosome studies may be of value in determining the diagnosis or prognosis in leukemia and related states. They are rarely helpful with solid neoplasms. Special technical problems associated with such investigations in tumor material must be appreciated. In cases where the diagnosis of acute leukemia is in doubt, demonstration of a chromosome change in the immature cells of blood or marrow is strong evidence of neoplasia; however, the absence of a cytogenetic abnormality does not rule out the diagnosis. The Philadelphia chromosome (Ph) is present in nearly every typical case of chronic granulocytic leukemia (CGL) and may confirm the diagnosis. Absence of the Ph chromosome in CGL or the appearance of additional cytogenetic changes in the neoplastic cells are indications of a poor prognosis. In "preleukemic" myeloproliferative disorders (except polycythemia vera) or unexplained pancytopenia, a clone of chromosomally abnormal marrow cells commonly indicates that clinical leukemia will soon become manifest; conversely, normal marrow chromosomes in these states are often correlated with a prolonged indolent course.
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PMID:Diagnostic and prognostic value of chromosome studies in cancer. 453 99

Quantitative whole-body linear profile scans of 59Fe, obtained by a whole-body counter, conventional ferrokinetics and hematological parameters are investigated in patients (n = 208) with various hematological-oncological diseases. Linear whole-body profile scans in controls, obtained 24 h after i.v. injection of 59Fe-transferrin, give quantitative information about sites of the erythropoietic system. Early profile scans (1 h p.i.) in patients with anemia show a typical 'iron-suction' corresponding to the fast outflow of 59Fe from the blood compartment. We found no typical change of iron distribution in Hodgkin and Non-Hodgkin lymphomas, even in patients with anemia or hemolysis there was no evidence of expansion of erythropoiesis to distal marrow sites. Our investigation does not contribute to staging of patients with Hodgkin's disease. Osteomyelofibrosis is characterized by a centrifugally expanded erythropoiesis. The value of increased iron uptake 24 h p.i. in leg regions for differential diagnosis of hemolytic anemia, chronic myelocytic leukemia, and pancytopenia where a similar pattern of iron distribution is observed will be discussed. Quantitative iron kinetics with one dimensional 59Fe profile scans give additional information in patients with displaced erythropoietic system.
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PMID:[Ferrokinetics in 1-dimensional whole-body profiles in hematologic diseases]. 640 12

Thirty-seven patients with acute leukemia in relapse were treated with a three-drug combination that included a 3- or 4-day course of AMSA with total doses ranging from 600 mg/m2 to 740 mg/m2 I.V., cytosine arabinoside 25 mg/m2 I.V. followed by 200 mg/m2 by continuous infusion daily for 5 days, and thioguanine 100 mg/m2 p.o. q 12h for 5 days. Eight of the 25 patients with acute nonlymphoblastic leukemia achieved a complete remission and 3 a partial remission. None of the five patients with acute lymphoblastic leukemia achieved a response and there was one partial remission in the seven patients with myelodysplastic syndrome or blastic CML. Reversible toxicity included nausea and vomiting (78%), alopecia (100%), pancytopenia (100%), mild stomatitis (63%), and hepatic dysfunction (24%). One patient developed seizures and cardiac arrhythmias. The activity of this combination in heavily treated patients with ANLL is comparable to that of the anthracycline-containing regimens, and its use in previously untreated patients with ANLL should now be explored.
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PMID:Treatment of acute leukemia in relapse with 4'(9-acridinylamino) methanesulfon-m-anisidide (AMSA) in combination with cytosine arabinoside and thioguanine. 689 90


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