Adult acute leukemia

Cripe, Larry D.

doi:10.1016/s0147-0272(97)80006-2

Cited by 25 publications

(21 citation statements)

References 141 publications

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“…Previous investigations have generally been based on smaller, and usually more selected materials, and have reported rather wide frequency ranges, varying from a few percent to 27%. [15][16][17][18][19][20][21][22]25,26,28 In addition, some studies do not distinguish between AML secondary to MDS and AML secondary to prior treatment, 23,24,27 making it even more difficult to draw firm conclusions regardLeukemia ing the impact of previous iatrogenic genotoxic exposure on the incidence of AML. Merging the cases with abnormal karyotype in our own series with data from previously published unselected series of cytogenetically abnormal AML and MDS 32 yielded frequencies of 14% t-AML among a total of 4230 AML and 15% t-MDS among 1629 MDS (Tables 2 and 3).…”

Section: Discussionmentioning

confidence: 99%

“…None had received topo II alone. The used compounds in decreasing frequency were melphalan (22 patients), cyclophosphamide (21), chlorambucil (18), vincristine (17), doxorubicin (14), azathioprine (8), procarbazine (8), vinblastine (8), busulfan (7), cisplatin (6), CCNU (5), methotrexate (5), BCNU (4), mustine (4), 5-fluorouracil (2), (2) (8) (12) …”

Section: Analyses Of the Present Materialsmentioning

confidence: 99%

“…13,14 Another issue that needs to be clarified concerns the true frequency of treatment-related cases among AML and MDS. In the literature, quite variable frequencies, from a few percent to 27%, have been reported, [15][16][17][18][19][20][21][22][23][24][25][26][27][28] discrepancies that may well be due to the fact that few of the series were populationbased. Furthermore, detailed statistical analyses comparing cytogenetic findings in larger series of t-AML/t-MDS and de novo AML/MDS have not been performed.…”

Section: Introductionmentioning

confidence: 99%

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Pooled analysis of clinical and cytogenetic features in treatment-related and de novo adult acute myeloid leukemia and myelodysplastic syndromes based on a consecutive series of 761 patients analyzed 1976–1993 and on 5098 unselected cases reported in the literature 1974–2001

et al. 2002

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To ascertain the frequency of treatment-related acute myeloid leukemias and myelodysplastic syndromes (t-AML/t-MDS) in an unselected series, we have identified all adult cases analyzed in our department from 1976 to 1993. Further aims were to compare karyotypic features of t-AML/t-MDS with de novo AML/MDS, in our material as well as in 5098 unselected, cytogenetically abnormal, published cases, and to analyze associations between type of prior therapy and karyotype. Among our 372 AML and 389 MDS, 47 (13%) were t-AML and 62 (16%) were t-MDS. Clonal abnormalities were significantly more common in t-AML and t-MDS than in de novo disease (68% vs 50%, P Ͻ 0.05 and 84% vs 45%, P Ͻ 0.001, respectively). Among the available 4230 AML and 1629 MDS (the present series and published cases), 14% were t-AML and 15% were t-MDS. In t-AML/t-MDS, the number of anomalies and the ploidy levels differed significantly from de novo cases, with complex and hypodiploid karyotypes being more common in t-AML/t-MDS. In t-AML, unbalanced changes in general, t(1;3), der(1;7), 3p−, −5, 5q−, −7, 7q−, t(9;11), t(11;19), t(11q23), der(12p), −17, der(17p), −18, and −21 were significantly more frequent than in de novo AML. In t-MDS, −5, −7, 7q−, 13q−, der(17p), and −18 were significantly more common. Type of prior treatment correlated significantly with number of anomalies in t-AML and with ploidy levels in t-AML/t-MDS. The frequencies of several aberrations varied with type of therapy, eg, 5q− was more frequent in radiotherapyassociated t-MDS, monosomy 7 was more common in t-AML and t-MDS after treatment with alkylators, and t(11q23) in t-AML was associated with topoisomerase II inhibitors. Abnormalities significantly more common in de novo disease were +8 as a sole anomaly, balanced changes in general, t(8;21), t(9;22), t(15;17), inv(16), and t(21q22) in AML, and −Y, 5q−, and 20q− as sole anomalies and +8 in MDS. The results emphasize the strong association between previous genotoxic exposure and karyotypic features. Leukemia (2002) IntroductionEver since the mid-1970s, when the first case reports describing chromosomal abnormalities in treatment-related acute myeloid leukemias (t-AML) were published, 1,2 the cytogenetic features of t-AML and of therapy-associated myelodysplastic syndromes (t-MDS) have received much attention. 3,4 To date, two distinct karyotypic patterns that correlate with specific types of chemotherapeutic agents have emerged. Previous chemotherapy (CT) with alkylators (alk) has been strongly linked to the development of t-MDS/t-AML harboring unbal- anced changes, mainly whole or partial losses of chromosomes 5 and 7, often in complex, hypodiploid karyotypes, 5-9 whereas prior CT with DNA topoisomerase II inhibitors (topo II) has been associated with t-AML characterized by, in particular, translocations involving chromosome band 11q23 resulting in MLL gene rearrangements. 4,[10][11][12] It has been debated, but remains to be settled, whether prior radiotherapy (RT) alone or exposure to CT other than alk/topo II may correla...

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Section: Discussionmentioning

confidence: 99%

Section: Analyses Of the Present Materialsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pooled analysis of clinical and cytogenetic features in treatment-related and de novo adult acute myeloid leukemia and myelodysplastic syndromes based on a consecutive series of 761 patients analyzed 1976–1993 and on 5098 unselected cases reported in the literature 1974–2001

et al. 2002

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“…Because leukemic blasts are readily obtained from the blood or BM of patients at diagnosis 69 and because a-GalCer has been used safely in early-phase clinical trials, [70][71][72] vaccination with a-GalCer-pulsed irradiated leukemia cells may represent a feasible postremission immunotherapy. We are aware that other approaches to adjuvanting autologous tumor cell vaccines have been described for hematologic malignancies, including toll-like receptor ligands.…”

Section: Discussionmentioning

confidence: 99%

An autologous leukemia cell vaccine prevents murine acute leukemia relapse after cytarabine treatment

Gibbins

Ancelet

Weinkove

et al. 2014

Blood

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“…The subtypes are denoted as M0-M7 [2,4,10,13]. The grouping is made based on the degree of granulocytic maturation (M1, M2, M3) or monocytic differentiation (M4 & M5) or presence of large number of erythroblasts (M6) or magakaryoblasts (M7) *Address correspondence to this author at the Clinical Research Cancer, Division of Experimental Cancer Research, Lund University, Malmö University Hospital, 205 02, Malmö, Sweden; Tel: +46-40-391106; Fax: +46-40-391222; E-mail: jenny_l.persson@med.lu.se [10,13]. The individual subtypes of this heterogenous disease can be identified using multiple methods such as cellular morphology, cytochemistry, immunophenotypes and molecular analysis [14].…”

Section: Introductionmentioning

confidence: 99%

The Common Leukemic Fusions in Pathogenesis and in Treatment Response in Acute Myeloid Leukemia

Fufan¹,

.²,

Persson

2010

TOLEUKEMIAJ

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Chromosomal abnormalities are the most common alterations in acute myeloid leukemia (AML). Among those abnormalities, chromosomal translocations that produce the oncogenic fusion proteins have been frequently observed in different subtypes of AML. Although molecular mechanisms underlying the consequences of the oncogenic transformation resulted from the fusion proteins have been extensively studied, little is known about the molecular events cooperative with the oncogenic fusion proteins in the pathogenesis of leukemia and the cellular mechanisms with regard to the predictive roles of the fusions in treatment response. In this article, we will present an overview of the important aspects of AML-associated fusion proteins and their regulated transcriptional networks in pathogenesis and prognosis of AML. We will also discuss the recent findings pertaining to the functional link between the oncogenic fusions and response of leukemic cells to the treatment. Understanding the regulation of AML-associated fusions and their association with disease characteristics, patient outcome and treatment response will be of fundamental importance for predicting the effectiveness of the treatment and design the specific therapeutic strategies.

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Adult acute leukemia

Cited by 25 publications

References 141 publications

Pooled analysis of clinical and cytogenetic features in treatment-related and de novo adult acute myeloid leukemia and myelodysplastic syndromes based on a consecutive series of 761 patients analyzed 1976–1993 and on 5098 unselected cases reported in the literature 1974–2001

Pooled analysis of clinical and cytogenetic features in treatment-related and de novo adult acute myeloid leukemia and myelodysplastic syndromes based on a consecutive series of 761 patients analyzed 1976–1993 and on 5098 unselected cases reported in the literature 1974–2001

An autologous leukemia cell vaccine prevents murine acute leukemia relapse after cytarabine treatment

The Common Leukemic Fusions in Pathogenesis and in Treatment Response in Acute Myeloid Leukemia

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