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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve new cases of childhood leukemia and neurofibromatosis were ascertained and evaluated in conjunction with 17 previously well-documented cases. The ratio of ALL:nonlymphocytic leukemia was 9:20, markedly different from the 4:1 ratio in children without NF. Rarer subtypes predominated: 8 CML and 8 AMML. The peculiar distribution of leukemia by cell type and the number of cases observed in the United States indicate that the risk of childhood leukemia in NF is increased. Two possible variants were noted: NF with "transient leukemia," and multiple skin xanthomas with nonlymphocytic leukemia.
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PMID:Neurofibromatosis and childhood leukemia. 9 39

44 patients suffering from myelomonocytic leukemia (MML) have been observed over the last four years. They have been subclassified in acute myelomonocytic and acute monoblastic leukemias (AMML, n = 12; AMoL, n = 10), subacute myelomonocytic leukemias (SMML, n = 13), and chronic myelomonocytic leukemias (CMML, n = 9) on the basis of bone marrow cytology(blast and promonocyte counts, maturation of granulopoesis) and cytochemical findings (peroxydase and unspecific esterase reaction). This subclassification has been proved to be of prognostic relevance by its good correlation with the mean survival times (AMML : 4.5 months, AMoL : 2.4 months, SMML : 8 months, CMML : 18 months). The acute forms have been treated in general with combined cytostatic chemotherapy, whereas SMML and CMML have been treated this way only in case of progression to an acute phase. These progressions to an AMML have been observed more often and earlier in subacute forms than in chronic forms. The diagnosis of SMML and CMML is supported by the finding of sea-blue histiocytes in the bone marrow, increased lysozyme levels in serum and urine and by the absence of the Philadelphia-Chromosome.
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PMID:[Myelomonocytic leukemia: clinical, cytological, and cytogenetic studies of acute, subacute, and chronic forms (author's transl)]. 26 23

Acute myelomonocytic leukemia developed in a patient 18 months after treatment with cyclophosphamide, vincristine, adriamycin, and DTIC, a chemotherapeutic regimen used for the treatment of metastatic sarcoma. The patient had had no prior history of radiation. More than 400 patients received this treatment and none of them developed leukemia. The occurrence of leukemia in this relatively short period of time may have been caused by the combined chemotherapeutic agents. However, confirmation of this will require long-term followup studies in cancer patients receiving chemotherapy to determine the true risk of second malignancies.
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PMID:Acute myelomonocytic leukemia following a chemotherapeutic regimen for metastatic sarcoma. 28 Apr 18

The ultrastructural analysis of the leukemic cells in twelve cases with AMML was considered a valuable tool in the diagnosis of this type of leukemia. Furthermore intracytoplasmic structure resembling virus like particles were observed in three bone marrow and one eye sample of the patients studied. The role of C-type RNA viruses in the etiology of leukemia was discussed.
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PMID:Ultrastructural studies on AMML and ocular granulocytic sarcoma. 28 78

The phenomenon of premature chromosome condensation (PCC) was used to compare the bone marrow proliferation characteristics of 163 patients with various forms of leukemia prior to the initiation of new therapy. The proliferative potential index (PPI, or fraction of G1 cells in late G1 phase) and the fraction of cells in S phase was determined and compared to the type of disease and the bone marrow blast infiltrate for each patient. Previously untreated patients with acute leukemia exhibited an average PPI value three times that of normal bone marrow (37.5% for acute myeloblastic leukemia [AML], acute monomyeloblastic leukemia [AMML], or acute promyelocytic leukemia [APML] and 42% for acute lymphocytic leukemia [ALL] or acute undifferentiated leukemia [AUL]). Untreated chronic myelogenous leukemia (CML) patients showed intermediate PPI values (25.2%), whereas CML patients with controlled disease exhibited nearly normal PPI values (14.6%). On the other hand, blastic-phase CML patients exhibited PPI values closer to that observed in patients with acute leukemia (35.4%). Seven patients with chronic lymphocytic leukemia (CLL) exhibited even higher PPI values. No correlations were observed between PPI values, fraction of cells in S phase, and marrow blast infiltrate. For untreated acute disease patients, PPI values were prognostic for response only at low and high PPI values. These results suggest that the PCC-determined proliferative potential is a biologic reflection of the degree of malignancy within the bone marrow.
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PMID:Premature chromosome condensation studies in human leukemia. I. Pretreatment characteristics. 29 41

Acute myelomonocytic leukemia occurred in a 69-year-old man with malignant lymphoma and macroglobulinemia. Fluorescent staining demonstrated the macroglobulin in plasma and leukemic cells. Plasma cells seemed to be producing paraproteins, while leukemic cells appeared to be engulfing them as seen with transmission electron microscopy. The sequence of events ruled out the possibility that myelomonocytic leukemia developed following the use of cytotoxic drugs. The case presented in this report is a rare example of malignant lymphoma, macroglobulinemia, and acute myelomonocytic leukemia occurring in the same patient.
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PMID:Acute myelomonocytic leukemia in a patient with macroglobulinemia and malignant lymphoma. 41 Apr 95

The author describes a 20-year-old patient with leukaemia and with meningoradicular symptoms. The first neurological symptoms developed 2 years after disclosure of haematological changes. Despite treatment with steroids, intrathecal Methotrexate and radiotherapy the patient died 3 years after the diagnosis of leukaemia had been established. Myeloblastic leukaemia was confirmed on autopsy. The importance of early intrathecal Methotrexate treatment is stressed.
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PMID:[Diagnostic difficulties in a case of leukemia with radicular symptoms]. 106 49

According to criteria established by the French-American-British (FAB) classification, a diagnosis of acute myelomonoblastic leukemia (FAB M4) is based on the presence of 20% bone marrow monocytes or a serum lysozyme level that exceeds the reference value by three times. Reported here is a case of acute myelogenous leukemia with eosinophilia and a cytogenetic inversion of chromosome 16 (inv 16) that lacks morphologic, cytochemical, and immunophenotypic features of monocytic differentiation, but which is associated with an elevated serum lysozyme value. The authors used an immunoelectron microscope to localize lysozyme to both normal and abnormal eosinophil granules, in addition to the secondary granules of myeloid precursors and monocytes. This enzyme could not be demonstrated within the myeloblasts of the patient studied. Postfixation with osmium tetroxide greatly reduced the staining intensity within the crystalloids of normal eosinophils, but only minimally affected that of monocytes, neutrophils, normal eosinophil granule matrix, and the abnormal granules of the leukemic eosinophils. These results demonstrate that lysozyme is present in both normal and leukemic eosinophils and that elevation of serum lysozyme in patients with acute myelogenous leukemia with eosinophilia is not a reliable indicator of monocytic differentiation. Furthermore, an occasional case of acute leukemia with inv 16 is classifiable as acute myelogenous leukemia with differentiation (FAB M2).
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PMID:The significance of an elevated serum lysozyme value in acute myelogenous leukemia with eosinophilia. 154 87

Acute myelomonocytic leukemia develops in 10-30% of irradiated (300 rad) SJL/J mice, after a lag period of around one year. Additional treatment with dexamethasone shortly after irradiation increased leukemia incidence up to 50%. Experiments were conducted in order to demonstrate the existence of preleukemic cells in irradiated mice and to explore the possible role of dexamethasone, cyclophosphamide, and different hemopoietic growth factors on their promotion to overt leukemia. Transplantation of bone marrow cells from mice exposed to 300 rad plus dexamethasone into appropriate recipients, performed 4-5 months after leukemogenic treatment, resulted in acute myeloid leukemia (AML) development of donor origin in 70% of the recipients. Transfer of fractionated preleukemic bone marrow showed that the highest AML incidence developed in the recipients of fractions enriched in early hemopoietic precursors. The promoting effect of dexamethasone on preleukemic cells was confirmed by demonstrating its similar coleukemogenic effect whether administered within several hours or 130 days after radiation. Treatment with cyclophosphamide shortly after radiation could not replace the dexamethasone effect but was found to be complementary to the coleukemogenic effect of dexamethasone. Early administration of hemopoietic growth factors (starting 14 days after radiation and dexamethasone) showed that colony-stimulating factor (CSF) 1 increased the AML incidence (75%) and reduced its latency. Treatment with recombinant granulocyte-CSF (rG-CSF) had a reduced effect and recombinant granulocyte-macrophage CSF (rGM-CSF) had no promoting effect. However, administration of different factors several months after the leukemogenic treatment revealed that rGM-CSF increased AML incidence (75%) and shortened its latency, whereas rG-CSF and CSF-1 had no effect. In contrast, the late administration of recombinant interleukin 6 reduced AML incidence significantly (23%). The present results indicate that murine radiation induced AML is a multiphase process involving radiation induced preleukemia that can be promoted by different treatments.
Leukemia 1992 Jul
PMID:Initiation and promotion in radiation-induced myeloid leukemia. 162 87

Chromosome studies were carried out after a 24-hour harvest of unstimulated bone marrow aspirate cell cultures from a 75-year-old male with a clinical diagnosis of acute myelomonocytic leukemia (FAB M4). Analysis of nine cells after trypsin-Giemsa banding (GTG) revealed two cell lines with a mosaic chromosome pattern, 46,XY/46,XY,t(7;19)(q22;p13.3). A review of the recent literature reveals one case of childhood ALL with a 46,XY/46,XY,t(7;19)(q11;q13) chromosome pattern [1] and a 46,XY,t(3q;11q),t(7q;19p),t(15;17)(q26;q22) in one patient with ANLL (FAB M3) [2]. The t(7;19)(q22;p13.3) seen in our case has not been reported as the sole specific clonal chromosome rearrangement in myeloid neoplasia. Interestingly, the plasminogen activator inhibitor type I, multi-drug resistance, and erythropoietin genes are located at band 7q22 and the insulin receptor gene is located at band 19p13.3. Both sites contain fragile site loci. The possible role of these fragile sites, genes, or other genes in the rearrangement can only be surmised.
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PMID:Atypical (7;19) translocation in acute myelomonocytic leukemia. 175 94


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