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)

We investigated the origin of the fibroblastic compartment of stromal hematopoietic microenvironment in eight chronic myeloid leukemia (CML) patients following allogeneic BMT. At the time of the study, all eight CML patients showed complete and long-lasting (14-87 months) engraftment of donor hematopoiesis and absence of clonal Ph-positive hematopoiesis. The study was carried out using in vitro amplification of informative DNA sequences: a Y chromosome specific DNA fragment in three patients who received a sex-mismatched allograft, and locus D1S80, a variable number of tandem repeats polymorphism, in five patients who received a sex-matched allograft. In all cases bone marrow fibroblasts were of recipient origin. These data indicate that with current BMT procedures the stromal compartment of hematopoiesis is not transplantable in humans.
Bone Marrow Transplant 1992 Sep
PMID:Host origin of bone marrow fibroblasts following allogeneic bone marrow transplantation for chronic myeloid leukemia. 142 79

Donor leukocyte infusions were administered to a patient who had relapsed with chronic myelogenous leukemia after having failed two successive HLA-matched allogeneic bone marrow transplants. Serial cytogenetic, restriction fragment length polymorphism, and polymerase chain reaction studies of the patient's marrow and blood after receiving donor leukocyte infusions revealed disappearance of the leukemic clone and the establishment of complete donor chimerism. An antileukemic response in this patient occurred initially in the absence of clinically evident graft-versus-host disease (GVHD), but complete eradication of the leukemic clone did not occur until after the onset of GVHD. The patient is now 48 weeks post infusion and remains in complete remission. This case demonstrates that leukocyte infusions are an effective form of adoptive immunotherapy which can result in a sustained molecular remission.
Bone Marrow Transplant 1992 Sep
PMID:Molecular remission occurring after donor leukocyte infusions for the treatment of relapsed chronic myelogenous leukemia after allogeneic bone marrow transplantation. 142 83

We report a patient who underwent two allogeneic bone marrow transplants for chronic myelogenous leukemia, initially in 1984 and again after relapse in 1990, who developed an identical pulmonary syndrome at a similar interval following each transplant. The patient presented with a non-productive cough, bilateral inspiratory crackles, and multiple patchy infiltrates on chest X-ray. Pulmonary function testing revealed a restrictive abnormality but no obstructive defects. The appearance of this pulmonary disorder after each transplant coincided with the development of chronic graft-versus-host disease. In both instances, this pulmonary syndrome completely reversed with corticosteroid therapy. The patient's chest computed tomographic scan and lung biopsy specimens were consistent with the diagnosis of bronchiolitis obliterans with organizing pneumonia (BOOP). While bronchiolitis obliterans has been reported following allogeneic transplant, BOOP has not previously been reported in this setting.
Bone Marrow Transplant 1992 Sep
PMID:Bronchiolitis obliterans organizing pneumonia as a complication of allogeneic bone marrow transplantation. 768 3

Renal and electrolyte disturbances in 91 patients with chronic myelogenous leukemia (CML) were analyzed over a period of these twenty years. At diagnosis, renal and electrolytes were studied in 72 patients including 65 in chronic cases, 5 in accelerated phase and 2 in blastic crisis. There were 8 cases of hypocalcemia among 62 patients and 5 cases of hyperphosphatemia among 48 patients. The cases of hyperphosphatemia and renal dysfunction had short median survival. There were no significant differences of renal and electrolyte disturbances between before and after chemotherapy. Various electrolyte disturbances, that is, hyponatremia, hypo-, hyperkalemia, hypocalcemia, hypo-, hyperphosphatemia, were found in the blastic crisis of CML. In the last admission, renal dysfunction and various electrolyte disturbances were present in almost half of the cases. Pathological studies were performed in 18 autopsy cases. Acute tubular insufficiency or necrosis, hypercalcemic nephropathy, and renal infiltration of leukemic cells were recognized in patients who had renal dysfunction.
Rinsho Ketsueki 1992 Sep
PMID:[Renal and electrolyte disturbances in chronic myelogenous leukemia]. 143 33

Urinary excretion of parathyroid hormone-related protein (PTH-rP) was measured by radioimmunoassay in 25 patients with adult T-cell leukemia (ATL), in 68 patients with other hematologic disorders and in 13 asymptomatic individuals seropositive for human T-cell leukemia virus type I (HTLV-I). The mean levels of urinary PTH-rP in ATL patients with hypercalcemia (11.01 micrograms/g.Cr) were higher than in ATL patients with normocalcemia (5.16 micrograms/g.Cr). The mean levels in patients with acute type (8.84 micrograms/g.Cr), lymphoma type (4.18 micrograms/g.Cr) and crisis ATL (18.20 micrograms/g.Cr) were significantly higher than in urine of healthy controls. However, all asymptomatic carriers of HTLV-I and patients with chronic and smoldering ATL had normal urinary PTH-rP levels. In 7 patients with acute myelogenous leukemia, 1 patient with blastic crisis of chronic myelogenous leukemia and 3 patients with malignant lymphoma, the urinary levels of PTH-rP were above the normal range. Urinary levels of PTH-rP of the ATL patients with hypercalcemia correlated with the serum calcium levels. Urinary levels of PTH-rP of the all ATL correlated with serum lactic dehydrogenase level. These findings suggest that the measurement of urinary levels of PTH-rP is useful for evaluation of ATL and that some tumor cells of other hematologic diseases may produce PTH-rP.
Rinsho Ketsueki 1992 Sep
PMID:[Urinary excretion of parathyroid hormone-related protein in patients with adult T-cell leukemia and other hematologic disorders]. 143 36

Serum aldolase A (ALD-A) levels were determined in patients with leukemia using a radioimmunoassay method. The method is a double antibody radioimmunoassay consisting of purified ALD-A as ligand, chicken antisera to ALD-A and rabbit antibodies to chicken IgG. Serum ALD-A levels of 41 normal healthy subjects ranged from 130 to 210 ng/ml (mean +/- 2 SD; 171 +/- 39 ng/ml). Serum ALD-A levels ranged from 90 to 200 ng/ml in patients with 42 non-neoplastic hematological diseases with the exception of hemolytic anemia. In contrast, 61 patients with acute leukemia before treatment exhibited increased serum ALD-A levels ranging from 125 to 1,550 ng/ml, with a mean value of 480 ng/ml. Serum ALD-A levels in 24 patients with chronic myelocytic leukemia (CML) during the chronic phase also exhibited high mean values of 481 ng/ml in a range of 270 to 1,100 ng/ml. Serum ALD-A levels were higher than 210 ng/ml in 85.2% of the patients with acute leukemia and in all patients with CML. Serum ALD-A levels tended to be decreased within the normal range, if those patients could achieve complete remission. In contrast, serum ALD-A levels showed a tendency to increase if those patients experienced a relapse of leukemia. These results suggest that the measurement of serum ALD-A levels by radioimmunoassay is useful for diagnosis and prediction of relapse in patients with leukemia.
Rinsho Ketsueki 1992 Sep
PMID:[Clinical significance of aldolase A in sera of patients with leukemia]. 143 40

The authors report a rare case of chronic myelogenous leukemia (CML) in which the Ph1 clone disappeared after remission induction of lymphoid crisis. A 58-year-old man was admitted to our hospital because of fever in July 1988. The white cell count was elevated. Bone marrow aspirate showed hypercellularity with myeloid hyperplasia. In the chromosomal analysis, Ph1 chromosomes were detected in 100% of bone marrow cells analysed. Diagnosis of CML was made and treatment was initiated with recombinant interferon-alpha 2a. Hematological remission without cytogenetic improvement was achieved. In March 1990 he developed lymphoid crisis with proliferation of CD10-positive cells. The chromosomal analysis revealed additional abnormalities including, 45, X, -Y, t(9;22) (q34;q11), +1, -8. With vincristine 0.6 mgX4, pirarubicin 15 mgX4, dexamethasone 40 mgX4 therapy complete remission was obtained. In December 1990 the Ph1 positive clone completely disappeared judging from normal karyotypes in the chromosomal analysis and the disappearance of M-bcr gene rearrangement.
Rinsho Ketsueki 1992 Sep
PMID:[Disappearance of Philadelphia chromosomes after remission induction in lymphoid crisis of chronic myelogenous leukemia]. 143 45

A 42-year-old male was diagnosed as having Ph-positive chronic myelogenous leukemia (CML) in 1988. He had been treated with ranimustine and interferon alpha. In April 1990, he was admitted to our hospital because of hemorrhagic diathesis. Blood counts revealed a white blood cell count of 319,200/microliters with 12 per cent blasts, a hemoglobin level of 9.2 g/dl, and a platelet count of 48,000/microliters. The bone marrow aspiration revealed hypercellularity with 68.2 per cent blasts, and chromosomal analysis showed 48, XY, +8, double Ph. A combination chemotherapy containing vindesine, cytarabine and prednisolone was administered. Four days later, he suddenly complained of headache and vertigo. CT scan of the brain showed a high density area at the cerebellar vermis. He was then treated with intensive combination chemotherapy including enocitabine, daunomycin, 6-mercaptopurine and prednisolone. He attained a hematological response and clinical improvement temporarily, as the cerebellar tumor regressed. In September he had headache and vertigo again, and CT scan revealed a rapid increase in size of the cerebellar tumor. Local irradiation with total doses of 19 Gy brought about a partial resolution of the lesion, and relief from the symptoms. In November, his hematological conditions deteriorated gradually and he died of brain hemorrhage on November 22, 1990. Post-mortem examination disclosed a 1 x 1 cm sized mass in the cerebellar vermis which showed a fibrous change surrounded with hemosiderin-laden macrophages microscopically. We reviewed the eight reported cases of CML with intracranial tumors, and discussed the factors which had contributed to the prolongation of survival in our patient.
Rinsho Ketsueki 1992 Sep
PMID:[Isolated cerebellar tumor formation in a patient with blastic crisis of chronic myelogenous leukemia]. 143 48

Forty-three-year-old man with schizophrenia, who had been diagnosed as chronic myelogenous leukemia (CML) and had been treated with hydroxyurea for 3 months, developed blastic crisis. The cytochemical study of the blastic cells showed POX (+), SBB (+) and TdT (+). The surface marker analysis revealed that the blastic cells expressed both myeloid (CD13, 33) and lymphoid (CD10, 19) markers. In the chromosomal analysis, additional chromosomal abnormality (11q+) was detected in all cells analysed (20/20) in addition to the standard type Ph1 chromosome. He was diagnosed as bi-phenotypic blastic crisis, and vincristine-prednisolone therapy was started. Initially, he responded to VP therapy well, but gradually became refractory to the therapy after 5 courses of VP. As many myeloblasts containing azurophilic granules were seen in the bone marrow after VP therapy, low dose Ara-C therapy was combined to VP. After 21 days of low dose Ara-C and VP, the percentage of the blast in the BM was significantly decreased and normal myeloid differentiation was observed after transient BM suppression. The chromosomal analysis showed the partial reappearance of standard Ph1 chromosome in 55% of the cells analyzed (11/20). Taken together, our data suggested that the combination of VP and low-dose Ara-C therapy might have some therapeutic benefit for the treatment of the CML with blastic crisis.
Rinsho Ketsueki 1992 Sep
PMID:[Treatment of CML with blastic crisis by the combination therapy of VP and low-dose Ara-C]. 143 49

We examined the fluorescence intensity of CD16 antigen, which represents the density of CD16 antigen, on granulocytes by flow cytometry in 15 healthy subjects and 15 patients with neutrophilia due to inflammatory diseases and 10 patients with chronic myeloid leukemia (CML). The fluorescence intensity of CD16 antigen was significantly lower in patients with CML than in healthy subjects and also than in patients with neutrophilia. These data indicate that 1) density of CD16 antigen on granulocytes decrease in CML, and 2) analysis on the density of granulocyte CD16 antigen is useful for differential diagnosis of CML from inflammatory diseases with neutrophilia.
Rinsho Byori 1992 Sep
PMID:[Decrease of CD16 antigen density on granulocytes in chronic myeloid leukemia]. 143 38


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