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MeSH Review:

Leukemia, Myelocytic, Acute

Pelicci, P.G. et al., Schwieger, M. et al., Akashi, K. et al., Blaise, D. et al., Buick, R.N. et al., et al.

Griffith, Black, Faerman, Swenson, Wynn, Lu, Lippke, Saxena,

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Disease relevance of Leukemia, Myelocytic, Acute

Clustering algorithms reveal that lymphoblastic leukemias with MLL translocations can clearly be separated from conventional acute lymphoblastic and acute myelogenous leukemias [1].
Interaction between leukemic-cell VLA-4 and stromal fibronectin is a decisive factor for minimal residual disease of acute myelogenous leukemia [2].
The translocation (8;21), generating the AML1-ETO fusion protein, is one of the most frequent chromosomal abnormalities associated with acute myelogenous leukemia (AML) [3].
Signal transduction and transforming properties of the TEL-TRKC fusions associated with t(12;15)(p13;q25) in congenital fibrosarcoma and acute myelogenous leukemia [4].
Plasma cyclic GMP, in contrast, was significantly elevated in all five types of cancer patients, and urinary cyclic GMP was significantly elevated (five times the normal mean) in patients with acute myelogenous leukemia and Hodgkin's disease [5].

High impact information on Leukemia, Myelocytic, Acute

Ectopic ACTH production with autoantibody formation in a patient with acute myeloblastic leukemia [6].
The role of the c-mos gene in the 8;21 translocation in human acute myeloblastic leukemia [7].
Amplification of the c-myb oncogene in a case of human acute myelogenous leukemia [8].
An improved complete remission rate in acute myelogenous leukemia (AML) has been noted since cytarabine and anthracyclines were introduced into clinical practice [9].
Certain classes of FLT3 mutations cause constitutively activated forms of the receptor that are found in significant numbers of patients with acute myelogenous leukemia (AML) [10].

Chemical compound and disease context of Leukemia, Myelocytic, Acute

Tumor necrosis factor alpha stimulates the growth of the clonogenic cells of acute myeloblastic leukemia in synergy with granulocyte/macrophage colony-stimulating factor [11].
LBN rats bearing acute myelocytic leukemia (AML) were treated with 100 mg Ara-C/kg q.8 h six times beginning on day 0 and on other days in sequence (0,1 through 0,12) [12].
Retinoic acid inhibited the clonal growth of the KG-1, acute myeloblastic leukemia, and the HL-60, acute promyelocytic leukemia, human cell lines [13].
A colony assay available for a subpopulation of acute myeloblastic leukemia blasts with proliferative potential was used to measure adriamycin (adria) and daunorubicin (dauno) dose-response curves following brief exposure to either drug and washing [14].
Lithium reinduction of acute myeloblastic leukemia [15].

Biological context of Leukemia, Myelocytic, Acute

A 19-year-old male developed an acute myeloblastic leukemia 11 months after presenting with an MGCT; karyotypes of the two tumors showed them to be clonally related, both showing an i(12p), a cytogenetic marker of germ cell tumors [16].
Isolation and analysis of the 21q+ chromosome in the acute myelogenous leukemia 8;21 translocation: evidence that c-mos is not translocated [17].
The t(8;21) chromosomal translocation in acute myelogenous leukemia modifies intranuclear targeting of the AML1/CBFalpha2 transcription factor [18].
DNA transfection analyses (tumorigenicity assay) and hybridization to mutation-specific oligonucleotide probes established NRAS mutations in codon 12 or 61 of 4/9 acute myelocytic leukemias (AML) and three AML lines [19].
Novel triterpenoid CDDO-Me is a potent inducer of apoptosis and differentiation in acute myelogenous leukemia [20].

Anatomical context of Leukemia, Myelocytic, Acute

The acute myelogenous leukemia cell line MO7, the Philadelphia BV173 cell line, and the acute promyelocytic leukemia NB4 and HL-60 cell lines were similarly examined [21].
A transforming N-ras gene has been cloned from acute myeloblastic leukemia bone marrow cells, in parallel with the N-ras gene derived from fibroblasts of the same patient [22].
In a previous study, we showed that the blast stem cells of acute myeloblastic leukemia (AML) were more sensitive to cytosine arabinoside (ara-C) when growing in suspension culture than during colony formation in methylcellulose [23].
CD8+ T cells activated during the course of murine acute myelogenous leukemia elicit therapeutic responses to late B7 vaccines after cytoreductive treatment [24].
In the present study, we addressed the role of the c-jun proto-oncogene in the mitogenic response of human fibroblasts and primary acute myelogenous leukemia blasts to tumor necrosis factor alpha (TNF-alpha) [25].

Gene context of Leukemia, Myelocytic, Acute

Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML [26].
Interleukin-1 (IL-1) is spontaneously produced by acute myeloblastic leukemia (AML) cells [27].
Effects of interleukin-4 and interleukin-6 on the proliferation of CD34+ and CD34- blasts from acute myelogenous leukemia [28].
We studied the effects of interleukin-4 (IL-4) and IL-6 on the growth of leukemic blasts from 40 patients with acute myelogenous leukemia (AML) [28].
Acquired FANCA dysfunction and cytogenetic instability in adult acute myelogenous leukemia [29].

Analytical, diagnostic and therapeutic context of Leukemia, Myelocytic, Acute

A complete remission rate of 82% was obtained in a group of 68 patients with acute myelogenous leukemia treated with a high-dose induction chemotherapy (TAD) consisting of 7-day courses of 6-thioguanine, cytarabine, and daunorubicin [30].
Recently, alloreactive NK cells were shown to mediate antileukemic effects against acute myelogenous leukemia (AML) after mismatched transplantation, when KIR ligand incompatibility existed in the direction of graft-versus-host disease (GVHD) [31].
Seventy consecutive adult patients with acute myelogenous leukemia (AML), median age 44 years, received high-dose cytarabine (3 g/m2 every 12 hours for 12 doses) followed by daunorubicin (45 mg/m2 daily for three doses) for remission induction [32].
Treatment of refractory and relapsed acute myelogenous leukemia with combination chemotherapy plus the multidrug resistance modulator PSC 833 (Valspodar) [33].
Long-term follow-up of a randomized trial comparing the combination of cyclophosphamide with total body irradiation or busulfan as conditioning regimen for patients receiving HLA-identical marrow grafts for acute myeloblastic leukemia in first complete remission [34].

References

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