Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty three patients (pts) received an allogeneic hematopoietic transplant using peripheral blood progenitor cells (PBPC). Diagnosis were acute myeloid leukemia (AML) in 16 pts, acute lymphoblastic leukemia (ALL) in 15, chronic myeloid leukemia (CML) in first chronic phase in 12, aplastic anemia in 4, myelodysplasia in 3 and Hodgkin's disease, major thalasemia and Hunter's syndrome in one each. Mean age was 20 years-old (2-55), 28 males and 25 females. Conditioning regimens were total body irradiation with 1200 cGy and cyclophosphamide 120 mg/kg in 38 pts, busulfan 16 mg/kg and cyclophosphamide 120 mg/kg in 10 pts, total lymphoid irradiation and cyclophosphamide in 3, 2 pts received other chemotherapy based conditionings. PBPC were infused unmanipulated through a central catheter. Graft versus host disease (GVHD) prophylaxis was cyclosporin and short course methotrexate. Donors were 6/6 HLA compatible siblings in 52 cases and 5/6 match in one case. PBPC mobilization was done with G-CSF at a dose of 10 micrograms/kg/day subcutaneously for four days, pheresis started on day 5. Bone marrow harvest was also done in the first thirty cases. Mean cellularities for CD34, CD3, CD4, CD8, CD56, CD19 (cel x 10(6)/kg) were 4.12; 4.59; 2.57; 1.9; 0.55 and 0.68, respectively. Mean recovery of neutrophils > 500/microL was obtained on day +11 and platelets > 20,000/microL on day +13. Patients were hospitalized for a mean period of 26 days (range 18-39) and days with parenteral antibiotics were 12.2 (5-45). Two pts had venoocclusive disease of the liver. Transplant related mortality was 15%. Acute graft versus host disease (GVHD) was observed in 43.4% of pts, only 5 pts had acute GVHD III or IV. Mean time for aGVHD diagnosis was +23 (8-76). Forty three pts were evaluable for chronic GVHD with a mean follow-up of 18 months (4-39). Chronic GVHD was observed in 26.4% by day +240, only 2 pts developed severe cGVHD. The present experience demonstrates an acceptable incidence for cGVHD; however, taking into account recent reports showing an increase of this complication, it seems reasonable not to perform this procedure for non-malignant diseases in which graft versus malignancy effect is not to be expected.
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PMID:[Allogeneic hematopoietic transplantation with stem cells extracted from peripheral blood]. 1096 6

The neural cell adhesion molecule, CD56, is expressed on acute myelogenous leukemia (AML) cells in 17-20% of the patients. However, the clinical and biological significance of its expression in AML has not been well analyzed from the standpoint of CD56 expression and its association with differentiation to a natural killer (NK) cell lineage. Here we present a 78-year-old patient with chronic myelomonocytic leukemia (CMML) whose leukemic cells had features of both monocytes and NK cells. We demonstrated that the leukemic cells were positive for CD4, CD56 and interleukin-2 (IL-2) receptor beta chain (CD112) in addition to myelomonocytic markers such as CD33, CD11b and CD11c. These leukemic cells proliferated well in vitro in response to 10-100 U/ml of IL-2, and functionally showed significant cytotoxicity against K562 target cells in a 4-hour (51) Cr release assay. All the above data indicate that these cells possessed at least some of the biological features of NK cells. Accordingly, we speculate that the leukemic cells in this patient may have been derived from a possible common progenitor of monocytes and NK cells.
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PMID:Chronic myelomonocytic leukemia derived from a possible common progenitor of monocytes and natural killer cells. 1104 23

We report here the case of a woman with acute myeloid leukemia with some blast cells exhibiting acute promyelocytic leukemia (APL)-like hypergranular cytoplasm. The cytologic and cytochemical aspects as well as the mature myeloid phenotype and hemostasis disorders were consistent with the diagnosis of APL. However, no t(15;17), or RARalpha gene, MLL gene or PML gene rearrangement was observed, or any other cytogenetic clonal abnormality. Coexpression on blast cells of CD33 and CD56 without CD34, CD16 or HLA-DR, suggested a myeloid/natural killer cell acute leukemia.
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PMID:Acute myeloid leukemia with hypergranular cytoplasm: a differential diagnosis of acute promyelocytic leukemia. 1108 83

Four patients (three males and one female) were diagnosed as myeloid/natural killer (NK) cell precursor acute leukemia in our department. Two patients showed the extramedullary involvement at initial presentation. Leukemic cells expressed CD7, CD33, CD45 and CD56 in all patients. Additionally, CD13, CD34, HLA-DR, cytoplasmic CD3 and myeloperoxidase were expressed in some patients. Trisomy 10 was found in two patients, which has not been reported in this disease. Therefore, myeloid/NK cell precursor acute leukemia might be rather heterogeneous especially in chromosomal abnormality though it seemed to constitute the distinct clinical entity among acute myeloid leukemia of M0 subtype.
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PMID:Clinicopathological features of myeloid/natural killer (NK) cell precursor acute leukemia. 1116 25

We report on a 30-year-old patient with blast crisis of a chronic myelogenous leukemia (CML) that shows immunophenotypic features similar to those of the myeloid/natural killer (NK) cell precursor leukemia previously described. Expression of CD13/CD33/CD65 as well as MPO+/LF- blasts was classified as a myelogenous blast crisis of a CML. In addition, the blasts were positive for CD7/CD56. Other lymphoid markers were not expressed. Cytogenetic and molecular cytogenetic examinations showed two Philadelphia (Ph-1) chromosomes and a trisomy 8. Similar to expression of the myeloid/NK cell precursor phenotype in acute myelogenous leukemia (AML), it is possible to exhibit this phenotype in Ph-1-positive CML. Only one case report of myeloid/NK precursor phenotype blast crisis of CML was found in the literature. Therefore, it is not clear whether this phenotype is a distinct biologic and clinical disease entity of CML, as is the case in the respective AML phenotype.
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PMID:Myeloid/natural killer cell precursor blast crisis of chronic myelogenous leukemia with two Philadelphia (Ph-1) chromosomes. 1123 79

Idarubicin (IDR) has been used as the main drug in induction chemotherapy for acute myelogenous leukemia (AML) in the USA and Europe. Between May 1995 and October 1998, we treated 41 cases of fresh AML using IDR induction chemotherapy and analyzed the clinical course, remission rate, relapse rate and prognosis. The results obtained in these cases were similar to those in 26 cases treated with daunorubicin (DNR) in our hospital according to JALSG-AML92. The outcome in cases with abnormal chromosomes and cases showing relapse was very poor. In particular, all 5 t(8;21) cases in our series relapsed, suggesting that t(8;21) cannot be considered a favorable prognostic factor in cases treated with IDR-containing regimens. However, 3 of the 5 t(8;21) cases were positive for CD56, which itself is an unfavorable prognostic factor. Thus it is possible that CD56 was related to the poor outcome. Intensive post-remission induction chemotherapies will be required in order to obtain prolonged disease-free survival.
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PMID:[Outcome of acute myelogenous leukemia in 41 patients treated with idarubicin: the prognosis of t(8;21) cases]. 1123 29

A 40-year-old woman, who had suffered from AML (M1) in 1983, developed ovarian cancer (stage IIIc) in December 1996 after long-term remission. She underwent surgical resection of the cancer, 10 courses of standard chemotherapy and tandem PBSCT (total dose: CBDCA 6,750 mg, CDDP 200 mg, CPA 16,000 mg, THP-ADR 450 mg). After receiving the last course of chemotherapy in June 1998, she was referred to our hospital in September 1998 because of pancytopenia. Laboratory findings showed pancytopenia with 34% leukemic cells, which were positive for alpha NBE and negative for POX and CAE. Surface-marker analysis of the leukemic cells showed positivity for CD11c, CD33, CD56, and DR, and chromosome analysis revealed 47, XX, +8. The patient was diagnosed as having AML (M5a), and received induction therapy consisting of IDR and Ara-C, which led to complete remission. As she had not received etoposide, this case was thought to have been therapy-related leukemia due to the platinum agents used for treating the ovarian cancer.
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PMID:[Therapy-related myeloid leukemia following platinum-based chemotherapy for ovarian cancer]. 1128 Sep 24

Here we report a case with precursor natural killer (NK) cell leukemia successfully treated with an unrelated cord blood transplantation. A 7-month-old Japanese boy was diagnosed to have NK cell leukemia based on the existence of abnormal cells in the bone marrow with the phenotype of CD3(-) /CD4(+) /CD7(-) /CD8(-) /CD16(-) /CD33(+) /CD34(-) /CD56(+) /HLA-DR(+) /NKB1(+) / CD94(+). The leukemic cells showed few azurophilic granules in the cytoplasm and weak cytotoxic activity. Although he presented with a huge mass occupying the bilateral paranasal sinuses and hepatosplenomegaly, he achieved complete remission by the conventional chemotherapeutic regimen for acute myelogenous leukemia, followed by an unrelated cord blood transplantation. He has remained in complete remission for 14 months posttransplant. To our knowledge, this is the youngest reported case with precursor NK cell leukemia; cord blood transplantation may thus be the treatment of choice for this disease.
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PMID:An infant with precursor natural killer (NK) cell leukemia successfully treated with an unrelated cord blood transplantation. 1134 48

Multiparameter flow cytometry (MFC) has the potential to allow for sensitive and specific monitoring of residual disease (RD) in acute myeloid leukemia (AML). The use of MFC for RD monitoring assumes that AML cells identified by their immunophenotype at diagnosis can be detected during remission and at relapse. AML cells from 136 patients were immunophenotyped by MFC at diagnosis and at first relapse using 9 panels of 3 monoclonal antibodies. Immunophenotype changes occurred in 124 patients (91%); they consisted of gains or losses of discrete leukemia cell populations resolved by MFC (42 patients) and gains or losses of antigens on leukemia cell populations present at both time points (108 patients). Antigen expression defining unusual phenotypes changed frequently: CD13, CD33, and CD34, absent at diagnosis in 3, 33, and 47 cases, respectively, were gained at relapse in 2 (67%), 15 (45%), and 17 (36%); CD56, CD19, and CD14, present at diagnosis in 5, 16, and 20 cases, were lost at relapse in 2 (40%), 6 (38%), and 8 (40%). Leukemia cell gates created in pretreatment samples using each 3-antibody panel allowed identification of relapse AML cells in only 68% to 91% of cases, but use of 8 3-antibody panels, which included antibodies to a total of 16 antigens, allowed identification of relapse AML cells in all cases. Thus, the immunophenotype of AML cells is markedly unstable; nevertheless, despite this instability, MFC has the potential to identify RD in AML if multiple antibody panels are used at all time points. (Blood. 2001;97:3574-3580)
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PMID:High frequency of immunophenotype changes in acute myeloid leukemia at relapse: implications for residual disease detection (Cancer and Leukemia Group B Study 8361). 1136 53

The occurrence of trisomy 4 or trisomy 10 as the sole chromosomal abnormality in acute myeloid leukemia (AML) is very rare, the reported frequency being less than 1%. We describe two cases of AML-M2 with concomitant trisomy 4 and trisomy 10, a hitherto undescribed phenomenon. They showed two unusual features, including immunoreactivity for CD56 and a short-lived but rapidly progressive myelodysplastic phase preceding the appearance of frank leukemia. These findings raise the possibility that AML with concommitant trisomy 4 and trisomy 10 may constitute a distinctive subtype of AML.
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PMID:Acute myeloid leukemia with concomitant trisomies 4 and 10: a distinctive form of myeloid leukemia? 1140 70


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