|
|
 Previous Article | Table of Contents | Next Article 
Blood, Vol. 89 No. 9 (May 1), 1997:
pp. 3323-3329
Acute Myeloid Leukemia in the Elderly: Assessment of Multidrug Resistance (MDR1) and Cytogenetics Distinguishes Biologic Subgroups With Remarkably Distinct Responses to Standard Chemotherapy. A Southwest Oncology Group Study
By
Catherine P. Leith,
Kenneth J. Kopecky,
John Godwin,
Thomas McConnell,
Marilyn L. Slovak,
I-Ming Chen,
David R. Head,
Frederick R. Appelbaum, and
Cheryl L. Willman
From the Departments of Pathology and Cancer Center, University of New Mexico School of Medicine, Albuquerque, NM; the Fred Hutchinson Cancer Research Center and the Department of Medicine, University of Washington and the SWOG Statistical Center, Seattle, WA; the Department of Medicine and Cancer Center, Loyola University School of Medicine, Chicago, IL; the Department of Pathology, City of Hope Cancer Center, Duarte, CA; and the Department of Pathology, St Jude Children's Hospital, Memphis, TN.
 |
ABSTRACT |
Compared with younger patients, elderly patients with acute myeloid leukemia (AML) respond poorly to conventional chemotherapy. To determine if this poor response is due to differences in the biologic characteristics of AML in the elderly, we studied 211 patients (161 de novo, 50 secondary AML) over 55 years of age (median, 68 years) registered to a single clinical trial for previously untreated AML (SWOG 9031, Phase III randomized trial of standard dose cytosine arabinoside and daunomycin ± rhG-CSF ). Pretreatment leukemic blasts were karyotyped and were also analyzed for intrinsic drug resistance by quantitating expression of the multidrug resistance glycoprotein MDR1 and functional drug efflux using sensitive flow cytometric techniques. Results were correlated with clinical variables and outcome. These elderly AML patients had a high frequency of unfavorable cytogenetics (32%), MDR1 protein expression (71%), and functional drug efflux (58%); each of these factors occurred at high frequencies in both de novo and secondary AML patients and was associated with a significantly poorer complete remission (CR) rate. In multivariate analysis, secondary AML (P = .0035), unfavorable cytogenetics (P = .0031), and MDR1 (P = .0041) were each significantly and independently associated with lower CR rates. Resistant disease was associated with unfavorable cytogenetics (P = .017) and MDR1 expression (P = .0007). Strikingly, elderly MDR1(-) de novo AML patients with favorable/intermediate cytogenetics had a CR rate of 81%; with increasing MDR1 expression, CR rate decreased in this cytogenetic group. MDR1(+) secondary AML patients with unfavorable cytogenetics had a CR rate of only 12%. Thus, AML in the elderly is associated with an increased frequency of unfavorable cytogenetics and MDR1 expression, both of which independently contribute to poor outcomes. The high frequencies of these features in both de novo and secondary elderly AML patients suggest a common biologic mechanism for these leukemias distinct from that in younger patients. Investigation of biologic parameters at diagnosis in AML in the elderly may help identify patients with a high likelihood of achieving CR with conventional regimens, as well as those who may require alternate regimens designed to overcome therapy resistance.
| |
INTRODUCTION |
THE AGE-SPECIFIC INCIDENCE of acute myeloid leukemia (AML) increases exponentially after 50 years, resulting in a median age for AML onset of 63 to 65 years.1 Thus, the largest proportion of AML cases are those that occur in elderly individuals. In contrast to younger patients with AML, AML in the elderly is frequently highly resistant to chemotherapy and overall outcomes remain extremely poor. AML patients under 50 years of age, treated with curative intent chemotherapy, have complete remission (CR) rates that average 70%; median relapse free survival (RFS) in this group is nearly 2 years with a 5-year RFS of 25% to 40%.2-4 In contrast, in AML in the elderly patient, CR rates average 30% to 50%; median RFS in these patients is only 9 to 12 months, and very few elderly patients survive beyond 2 years.2,5-8
The poor outcome of AML in the elderly may result from reduced patient tolerance to chemotherapy, differences in the biology of the leukemic blasts in older versus younger patients, or a combination of these factors. Several recent clinical trials have sought to improve patient tolerance to therapy by incorporating hematopoietic growth factors into chemotherapeutic regimens; unfortunately, while faster hematologic recoveries and a reduced incidence of infection were frequently seen, there has been no consistent benefit in CR rate or survival.5,9-11 These results suggest that intrinsic biologic differences in the leukemic cells may play a more important role than host factors in conferring the poor outcomes observed in AML in the elderly.
A variety of evidence suggests that AML in the elderly may be biologically different from AML in younger patients. As the frequency of myelodysplasia (MDS) increases with age, so does the frequency of AML evolving from MDS; such "secondary" AML cases are frequently highly therapy resistant.4,12,13 The frequency of "poor prognosis" cytogenetic abnormalities, such as -5/del(5q) and/or -7/del(7q), also increases with age.14-18 A third potentially important biologic factor that might account for the therapeutic resistance of AML in the elderly is an increase in the incidence of intrinsic drug resistance in leukemic blasts, mediated by expression of the multidrug resistance glycoprotein MDR1 (also known as p-glycoprotein) or other alternative resistance mechanisms. MDR1 encodes a transmembrane efflux pump that actively extrudes chemotherapeutic compounds from leukemic cells, such as the anthracyclines that are commonly employed in AML therapy. MDR1 expression has been extensively studied in AML and has been shown to be associated with poorer outcomes,19-25 although no prior study has focused on elderly AML patients.
The aim of our study was to investigate the biologic characteristics of AML in the elderly using pretreatment samples from a large number of uniformly treated elderly patients with newly diagnosed AML registered to a single recently completed clinical trial (SWOG 9031) to determine if biologic characteristics might be useful in predicting outcome and in providing insight into the overall poor therapeutic response of AML in the elderly.
| |
MATERIALS AND METHODS |
Patients
All biologic samples were obtained at initial diagnosis before therapy from patients registered to a single Southwest Oncology Group study, SWOG 9031, a randomized, double-blind, placebo-controlled trial of daunomycin (45 mg/m2, days 1 through 3) and standard dose cytosine arabinoside (200 mg/m2 days 1 through 7) with or without recombinant human granulocyte colony-stimulating factor (rhG-CSF) for previously untreated AML patients over 55 years of age (Godwin et al, in preparation).11 Patients with clinical de novo AML and secondary AML were eligible for this trial; however patients with acute promyelocytic leukemia (French-American-British [FAB] M3/M3v) were excluded. The diagnosis of AML was confirmed by central histopathologic review by the SWOG Leukemia Pathology Committee using standard FAB criteria as modified by SWOG.26,27
Biologic Studies
Analysis of MDR1 expression and functional efflux.
Blasts from pretreatment bone marrow/peripheral blood samples were enriched by density gradient separation and assays were performed either on fresh cells or after cryopreservation and thawing; our previous studies have reported successful assessment of MDR and functional dye/drug efflux on appropriately cryopreserved samples.28 MDR1 expression by leukemic blasts was measured using the MDR1-specific antibody MRK16 (Kamiya, Thousand Oaks, CA) in three-color flow cytometric assays where blasts were costained with MRK16, the hematopoietic stem/progenitor cell antigen CD34, and the pan-myeloid antigen CD33, as previously described.28 This approach allows accurate analysis of MRK16 staining in a phenotypically gated myeloid blast population and correlation of MDR1 protein, CD34, and CD33 expression.28 Appropriately matched isotype controls were used in all assays. To assess functional drug efflux and correlate efflux with MDR1 expression, the ability of leukemic blasts to efflux a fluorescent dye, DiOC2 , was measured in single-color flow cytometric assays, as described.28 The fluorescent dye, DiOC2 , is an MDR1 substrate, but unlike other MDR1 substrates such as doxorubicin and Rhodamine 123, it does not appear to be transported by the multidrug resistance protein (MRP), one of the more recently identified drug transporters, and thus may be more specific than these other drugs/dyes for MDR1-mediated transport.29,30 Briefly, leukemic blasts were incubated in media containing DiOC2 to allow uptake for 30 minutes; the blasts were then washed, baseline dye uptake measured, and resuspended in fresh dye-free media with or without the MDR1-modulator cyclosporine A (CsA; 2500 ng/mL; Sandoz Pharmaceuticals, Basel, Switzerland) and incubated for 90 minutes at 37°C to allow efflux. Cells were then resuspended in fresh 4°C media for immediate flow cytometric analysis. The MDR1(+) DOX cell lines and MDR1(-) 8226/S parental line (kindly provided by W.S. Dalton, University of Arizona, Tucson) were used as controls in all experiments.31
Analysis of MDR1 expression and efflux data.
Analyses were performed on a FACScan flow cytometer using Lysis II software (Becton Dickinson, Thousand Oaks, CA). MRK16 staining of gated leukemic blasts compared with control cells was measured using the Kolmogorov-Smirnov (KS) statistic, denoted D, which measures the difference between two distribution functions and generates a value ranging from -1.0 to 1.0.32 This method accurately identifies small differences in fluorescence and is useful in detection of low level MDR1 expression, which frequently occurs in primary patient samples.28,33 MRK16 staining intensity was categorized for descriptive purposes as follows: bright (D  0.25), moderate (0.15  D > 0.25), dim (0.10 D < 0.15), and negative (D < 0.10); however, correlations with clinical outcome were largely performed using the D value as a continuous variable. DiOC2 efflux was assessed by analyzing cellular fluorescence of gated leukemic blasts after efflux in the presence/absence of CsA; differences in fluorescence were analyzed with KS statistics and a D value of 0.25 was used to define a case as efflux (+).
Cytogenetic analysis.
Cytogenetic studies on pretreatment bone marrow or unstimulated blood samples were performed using standard G-banding with trypsin-Giemsa or trypsin-Wright's staining in SWOG-approved cytogenetics laboratories. Karyotypes were interpreted using International System for Cytogenetic Nomenclature (ISCN) criteria (1995).34 Karyotypes were considered normal diploid if no clonal abnormalities were detected in a minimum of 20 metaphases examined and if two growth/harvesting methods were used. Each karyotype was independently reviewed by at least three members of the SWOG Cytogenetics Committee.
Statistical Analysis
Demographic and clinical data for patients in this study were collected with quality control review according to standard procedures of the SWOG. MDR1 expression and efflux were represented as either quantitative variables using the KS statistic D, or were dichotomized as positive versus negative. Unweighted least squares (LS) and logistic regression (LR) analyses were performed to identify variables predictive of MDR1 expression or functional efflux.35,36 The two methods gave similar results, so only LS results are reported here. Standard criteria were used to define CR and relapse.37 Overall survival (OS) was measured from randomization until death from any cause, with observation censored for patients last known alive. RFS was measured from establishment of CR until relapse or death from any cause, with observation censored for patients last known alive without report of relapse. Distributions of OS and RFS were estimated by the method of Kaplan and Meier.38 Analyses of prognostic factors for treatment outcomes were based on LR models for CR and proportional hazards (PH) regression models for OS and RFS.36,39 Prognostic factors considered in the analysis included the clinical parameters listed in Tables 1 and 2, MDR1 and CD34 expression, functional efflux, and cytogenetics. Statistical significance is represented by two-tailed P values. Analyses were based on clinical and biologic data available September 23, 1996.
| |
RESULTS |
Patient and Disease Characteristics
A total of 234 patients entered SWOG study 9031 between January 1992 and February 1994. In 23 cases (10%) the initial diagnosis of AML was not confirmed by central pathology review; these patients were excluded from the present analysis. The 211 remaining patients included 89 women and 122 men with a median age at study entry of 68 years (range, 56 to 88). AML cases were most frequently classified as FAB M1 or M2 (Table 1). Fifty patients (24%) were considered to have secondary AML based on a history of antecedent MDS or exposure to potentially leukemogenic drug/radiation therapy, while 161 patients (76%) were considered clinically as de novo AML. Sufficient pretreatment biologic samples were available to examine one or more of the following in these 211 patients: MDR1 protein expression on leukemic blasts, functional efflux, cytogenetics and CD34 expression. All four parameters were examined in 130 cases. Data was not available for all four parameters in 81 cases either because the specimens received contained insufficient blasts for all analyses or because the analyses performed were deemed unsatisfactory after review (for flow cytometric assays: low viability; for cytogenetic analysis: no metaphases detected or < 20 normal metaphases detected or normal metaphases detected when only a single growth/harvesting time was used).
Cytogenetics
Among 164 cases classified cytogenetically, abnormalities were found in 90 cases (55%) including 54 (33%) with two or more abnormalities. The most common cytogenetic abnormalities in these elderly AML cases were those associated with MDS, as well as AML, including -7/7q- (24 cases [15%]), -5/5q- (21 cases [13%]), +8 (25 cases [15%]). In contrast, abnormalities associated with de novo AML were uncommon: t(8; 21) was found in only three cases (2%), while inv(16)/t(16; 16) was found in only seven cases (4%). As the number of patients with any single abnormality was small, karyotypic abnormalities were grouped into favorable, intermediate, or unfavorable categories based on published literature for correlation with clinical outcome (Table 3).14-18,40-42 Using this scheme, the cytogenetics in 52 cases (32%) were classified as unfavorable, while only nine patients (5%) had a favorable karyotype. The remaining 103 cases (63%) had cytogenetic abnormalities considered intermediate in prognosis. Because of the small number of favorable cases, this category was combined with the intermediate category for most analyses with clinical outcome. Although the unfavorable cytogenetic category included abnormalities such as -7/7q-, which are associated with MDS-related secondary AML, the correlation between secondary AML and unfavorable cytogenetics was only marginal (P = .059) in multivariate analysis after accounting for a significant association between unfavorable cytogenetics and both increasing CD34 expression (P = .0032) and decreasing platelet count (P = .0001).
MDR1 Expression and Functional Efflux
MDR1 protein expression on selected leukemic blasts was examined using multiparameter flow cytometry in 189 cases and detected in 135 (71%) including 69 (37%) staining brightly with the MDR1-specific antibody, MRK16. Moderate or dim positive staining was seen in 33 (17%) each. Functional dye/drug efflux, inhibited by cyclosporine (an MDR1 efflux inhibitor), was detected in 101 (58%) of 175 samples studied (Table 4). As expected, functional efflux was strongly correlated with MDR1 expression: 82 (67%) of 122 MDR1(+) cases were efflux(+), while 32 (67%) of 48 MDR1(-) cases were efflux(-) (P < 0.0001). However, as we and others have previously described,28,43,44 discrepant cases were identified including 16 MDR1(-)/efflux(+) cases and 40 MDR1(+)/efflux(-) cases. In multiple LS regression analyses performed to identify factors predictive of MDR1 expression or efflux, MDR1 expression was found to be significantly and independently associated with efflux (P < .0001) and FAB subtype (P = .0037). Associations of MDR1 and FAB subtype were largely due to lower MDR1 expression in the M4 and M5 categories; 14 of 36 (39%) M4 or M5 cases were MDR1(+) in contrast to 121 of 153 (79%) non-M4/M5 cases. In addition to its significant association with MDR1 expression, functional efflux was also independently associated with CD34 (P < .0001), but not with any other factor measured. Surprisingly, although CD34 expression was associated with MDR1 expression in univariate analysis (P = .0001), after accounting for all other factors in multiple LS regression analysis including the significant effects of functional efflux and FAB type on MDR1 expression, there was no longer an association between these variables (P = 0.60). Similarly, multiple LS regression analysis failed to find an independent association of MDR1 expression with secondary disease (P = .76) or unfavorable cytogenetics (P = .28).
Prognostic Factors for Response to Therapy
Overall 95 (45%) of the 211 elderly patients with AML achieved a complete remission (CR). The CR rate after the first induction attempt was 86 of 211 (41%) patients. Of the remaining 125 patients, 48 received the second protocol induction attempt and 9 (19%) achieved CR. In univariate analysis, disease onset (de novo v secondary AML) was the only clinical parameter strongly predictive for achievement of CR (P = .0005; Table 4); no other clinical parameter including age, white blood count, blast count, or platelet count at presentation, or treatment arm (G-CSF v placebo) was correlated with CR rate. Among laboratory parameters, there was a marginally significant association between CR rate and FAB subtype (P = .048) with CR rates ranging from 34% (24 of 70) for M2 to 65% (26 of 40) for M4 and M5 combined. However, as shown in Table 4, in univariate analysis the CR rate was highly significantly associated with CD34 and MDR1 expression and with functional efflux. CR rate significantly decreased with increasing expression of CD34 (P = .0027) or MDR1 expression (P = .0019) and with increasing strength of efflux (P = .0039). The CR rate was also significantly worse in patients with unfavorable cytogenetics (P < .0001).
In multiple LR analysis, CR rate was highly significantly and independently associated with each of three factors: secondary AML (P = .0035), MDR1 expression (P = .0041), and unfavorable cytogenetics (P = .0031). After accounting for these three factors, there was no significant association of CR rate with CD34 expression (P = .80), functional efflux (P = .75), or FAB subtype (P = .081), or any of the other factors in Table 1. Only 2 (12%) of 17 MDR1(+) patients with secondary AML and unfavorable karyotype achieved CR. In contrast, 22 of 27 (81%) patients with de novo MDR1(-) AML and favorable/intermediate cytogenetics achieved CR (Table 5).
Of the 116 patients who failed to achieve CR, 73 (63%) had documented resistant disease, including 41 patients who received one and 32 patients who received two induction courses. The remaining 43 patients included 19 who died during aplasia, 19 who died before marrow examination was performed, and five who were unevaluable for various reasons. Resistant disease was significantly and independently associated with unfavorable cytogenetics (P = .017) and MDR1 expression (P = .0007), but not with secondary AML status (P = .11).
Prognostic Factors for OS and RFS
Of the 211 patients, 180 have died. The remaining 31 were alive between 18 and 53 months (median, 33 months) after registration. Multivariate proportional hazards regression analysis of OS identified three significant independent prognostic factors: OS was significantly poorer for patients with unfavorable cytogenetics (P < .0001) and decreased significantly with increasing age (P = .014) and increasing white blood cell count (WBC) (P = .029). After accounting for these factors, none of the other variables considered had independent prognostic significance, including secondary AML (P = .29), MDR1 expression (P = .93), efflux (P = .10), or CD34 (P = .45).
Of the 95 patients who achieved CR, 78 relapsed and 4 others died without report of relapse (all 4 from consolidation toxicities). In multivariate analysis, only one marginally significant prognostic factor was identified: RFS was poorer for patients with unfavorable cytogenetic status (P = .028).
None of the other variables considered had independent prognostic significance for RFS, including secondary AML (P = .44), efflux (P = .73), CD34 (P = .27), or MDR1 expression (P = .19).
| |
DISCUSSION |
Our studies indicate that the consistently poor outcomes achieved with conventional chemotherapeutic regimens in elderly AML patients may result predominantly from the distinct biologic features of the leukemic blasts in older patients. In our studies, we observed a notably high frequency of: (1) secondary AML (24% of our cases), (2) cytogenetic features traditionally associated with an unfavorable outcome (32%), and (3) MDR1 protein expression by leukemic blasts (71%). Each of these factors was independently and significantly linked to lower CR rates in elderly patients treated with the conventional regimen employed in SWOG trial 9031. Additionally, we demonstrate that assessment of these biologic parameters at diagnosis can be used to identify groups of patients with quite different responses to therapy. Using these factors, we could identify elderly AML patients with de novo MDR1(-) AML and favorable or intermediate cytogenetics who had a very high likelihood of achieving CR, over 80% in our study. This unusually high CR rate achieved in elderly patients who lack the typical elderly AML biologic profile is comparable to that seen in younger AML patients with "good risk" features.6,17 At the other extreme, we could identify patients with de novo or secondary MDR1(+) AML and unfavorable karyotypes who had very poor CR rates. Our studies suggest that these patients rarely benefit from current conventional chemotherapeutic regimens.
Comparison of the biologic features that we have described herein in elderly AML patients with those historically associated with younger patients strongly supports the hypothesis that AML in the elderly is a biologically distinct disease. In our trial, 24% of the elderly patients had documented secondary AML; however, we found that most of the elderly patients who presented clinically with de novo disease shared similar biologic features with these secondary AML patients. In particular, our studies indicate that many cases of de novo AML occurring in the elderly are strikingly similar to secondary AML cases occurring after alkylating agent therapy or myelodysplasia.14,16,45-49 There was a similarly high frequency of unfavorable cytogenetic abnormalities such as -7/7q- or -5/5q- (which are frequently detected in MDS and secondary AML) in both our de novo, as well as secondary AML patients, while in contrast, the frequency of cytogenetic abnormalities more traditionally associated with de novo AML in younger patients [such as inv(16) or t(8; 21)] was strikingly low.14-18,45,46 The frequency of MDR1 expression was also extremely high in our study (71%) and moreover occurred at similar frequencies in patients with de novo or secondary disease. This high frequency of MDR1 expression detected in elderly AML patients stands in striking contrast to the frequency of 30% that we have found in a recent study of 400 younger AML patients registered to SWOG study 8600 (median age, 45 years) using the identical sensitive methodology reported herein (C. Leith et al, in preparation). Thus, our studies show that most cases of de novo AML in elderly patients show a similar constellation of biologic features more traditionally associated with secondary AML; these features are quite distinct from those associated with true de novo AML in younger patients. We thus speculate that the majority of AML cases arising in elderly patients that present clinically with de novo disease actually arise from a setting of prior bone marrow injury or clinically undetected antecedent MDS.
The identification of biologic and clinical features associated with a poor prognosis is an essential first step for developing a rational approach to overcome the poor therapeutic outcome of AML in elderly patients. Our identification of MDR1 expression as an important independent predictor of response to therapy is particularly interesting, as it suggests that therapies that incorporate MDR1 modulators may be potentially beneficial to many elderly patients with AML. The use of MDR1 reversing agents might have a large impact on those elderly patients who have MDR1(+) leukemic cells, but otherwise favorable prognostic indicators for CR (including a de novo disease presentation and intermediate/favorable cytogenetics); such patients constituted 38% of the elderly AML patients entering our trial.
In our study, although MDR1 expression was associated with a lower CR rate and resistant disease, it did not predict for OS or RFS. These results differ from previous studies in predominantly younger AML patients, in which MDR1 expression was associated with both CR rate and OS.19,21,23 This lack of correlation between MDR1 expression and OS and RFS may, in part, be because the small number of survivors in this study precluded identification of all biologic parameters associated with outcome in statistical analysis. In addition, other as yet unidentified biologic factors may contribute to disease resistance in AML in elderly patients. Patterns of drug resistance in elderly AML are particularly complex: the MDR1(-)/efflux(+) cases identified by us and others suggest that alternative efflux pumps (such as the more recently recognized multidrug resistance associated protein (MRP) or the lung resistance protein (LRP), may be important in conferring resistance. 22,30,43,44,50,51 The relative expression of these resistance proteins in older versus younger AML patients is currently unknown. The poor OS even among patients who achieved CR points out the need for better postremission therapies in these elderly patients with AML.
In conclusion, we have identified biologic disease characteristics that can be used to help identify those elderly AML patients with a high likelihood of response, as well as those with a poor response to current conventional chemotherapeutic regimens. Recognition of these disease characteristics leads the way to the development of risk adapted therapies designed to circumvent these biologic disease factors. The incorporation of MDR1 modulators into therapeutic regimens represents a first step in this direction.49,52
| |
FOOTNOTES |
Submitted October 21, 1996;
accepted December 5, 1996.
Supported by Department of Health and Human Services (DHHS NIH, Bethesda, MD) grants to the Southwest Oncology Group and SWOG Leukemia Biology and Cytogenetics Programs (Grants No. CA32102, CA60433), and the State of New Mexico Dedicated Health Research Fund (University of New Mexico School of Medicine, Albuquerque).
Address reprint requests to Southwest Oncology Group Operations Office, 14980 Omicron Dr, San Antonio, TX 78245-3218.
The publication costs of this article were defrayed in part by page
charge payment. This article must therefore be hearly marked
``advertisment'' in accordance with 18 U.S.C. section 1734 solely to
indicate this fact.
| |
REFERENCES |
1. Henderson SH: Acute leukemia: General considerations, in Williams WJ, Beutler E, Erslav HA, Lichtman MA (eds): Hematology (ed 4). New York, NY, McGraw Hill, 1990, p 237
2. Estey EH, Kantarjian H, Keating MJ: Therapy for acute myeloid leukemia, in Hoffman R, Benz EJ, Shattil SJ, Furie B, Cohen HJ, Silberstein LE (eds): Hematology Basic Principles and Practice (ed 2). New York, NY, Churchill Livingstone, 1995, p 1014
3.
Rees JKH,
Gray RG,
Swirsky D,
Hayhoe FGJ:
Principal results of the Medical Research Council's 8th acute myeloid leukaemia trial.
Lancet
2:1236,
1986[Medline]
[Order article via Infotrieve]
4.
Champlin R,
Gale RP:
Acute myelogenous leukemia: Recent advances in therapy.
Blood
69:1551,
1987[Abstract/Free Full Text]
5. Rowe JM, Anderson JW, Mazza JJ, Bennett JM, Paietta E, Hayes FA, Oette D, Cassileth PA, Stadtmauer EA, Wiernik PH: A randomized placebo-controlled phase III study of granulocyte-macrophage colony-stimulating factor in adult patients (>55 to 70 years of age) with acute myelogenous leukemia: A study of the Eastern Cooperative Oncology Group (E1490) Blood 86:457, 1995
6.
Mayer RJ,
Davis RB,
Schiffer CA,
Berg DT,
Powell BL,
Schulman P,
Omura GA,
Moore JO,
McIntyre OR,
Frei E:
Intensive postremission chemotherapy in adults with acute myeloid leukemia.
N Engl J Med
331:896,
1994[Abstract/Free Full Text]
7.
Bishop JF,
Matthews JP,
Young GA,
Szer J,
Gillett A,
Joshua D,
Bradstock K,
Enno A,
Wolf MM,
Fox R,
Cobcroft R,
Herrmann R,
Van Der Weyden M,
Lowenthal RM,
Page F,
Garson OM,
Juneja S:
A randomized study of high-dose cytarabine in induction in acute myeloid leukemia.
Blood
87:1710,
1996[Abstract/Free Full Text]
8.
Taylor PRA,
Reid MM,
Stark AN,
Brown N,
Hamilton PJ,
Proctor SJ:
De novo acute myeloid leukaemia in patients over 55-years-old: A population based study of incidence, treatment and outcome.
Leukemia
9:231,
1995[Medline]
[Order article via Infotrieve]
9.
Stone RM,
Berg DT,
George SL,
Dodge RK,
Paciucci PA,
Schulman P,
Lee EJ,
Moore JO,
Powell BL,
Schiffer CA:
Granulocyte-macrophage colony-stimulating factor after initial chemotherapy for elderly patients with primary acute myelogenous leukemia.
N Engl J Med
332:1671,
1995[Abstract/Free Full Text]
10.
Dombret H,
Chastang C,
Fenaux P,
Reiffer J,
Bordessoule D,
Bouabdallah R,
Mandelli F,
Ferrant A,
Auzanneau G,
Tilly H,
Yver A,
Degos L:
A controlled study of recombinant human granulocyte colony-stimulating factor in elderly patients after treatment for acute myelogenous leukemia.
New Engl J Med
332:1678,
1995[Abstract/Free Full Text]
11. Godwin JE, Kopecky KJ, Head DR, Hynes HE, Balcerzak SP, Appelbaum FR: A double blind placebo controlled trial of G-CSF in elderly patients with previously untreated acute myeloid leukemia. A Southwest Oncology Group study. Blood 86:434a, 1995 (abstr, suppl 1)
12.
Foucar K,
Langdon RM,
Armitage JO,
Olson DB,
Carroll TJ:
Myelodysplastic syndromes: A clinical and pathologic analysis of 109 cases.
Cancer
56:553,
1985[Medline]
[Order article via Infotrieve]
13.
Aul C,
Getterman N,
Schneider W:
Age-related incidence and other epidemiological aspects of myelodysplastic syndromes.
Br J Haematol
82:358,
1992[Medline]
[Order article via Infotrieve]
14. Fourth International Workshop on Chromosomes in Leukemia, 1982, Clinical significance of chromosomal abnormalities in acute non-lymphoblastic leukemia. Cancer Genet Cytogenet 11:332, 1984
15.
Schiffer CA,
Lee EJ,
Takafumi T,
Wiernik PH,
Testa JR:
Prognostic impact of cytogenetic abnormalities in patients with de novo acute nonlymphocytic leukemia.
Blood
73:263,
1989[Abstract/Free Full Text]
16.
Yunis JJ,
Lobell M,
Arnesen MA,
Oken MM,
Mayer MG,
Rydell RE,
Brunning RD:
Refined chromosome study helps define prognostic subgroups in most patients with primary myelodysplastic syndrome and acute myelogenous leukaemia.
Br J Haematol
68:189,
1988[Medline]
[Order article via Infotrieve]
17.
Dastugue N,
Payen C,
Lafage-Pochitaloff M,
Bernard P,
Lerous D,
Huguet-Rigal F,
Stoppa A-M,
Marit G,
Molina L,
Michallet M,
Maraninchi D,
Attal Reiffers J:
Prognostic significance of karyotype in de novo adult acute myeloid leukemia.
Leukemia
9:1491,
1995[Medline]
[Order article via Infotrieve]
18.
Fenaux P,
Preudhomme C,
Lai JL,
Morel P,
Beuscart R,
Bauters F:
Cytogenetics and their prognostic value in de novo acute myeloid leukaemia: A report on 283 cases.
Br J Haematol
73:61,
1989[Medline]
[Order article via Infotrieve]
19.
Pirker R,
Wallner J,
Geissler K,
Linkesch W,
Haas OA,
Bettelheim P,
Hopfner M,
Scherrer R,
Valent P,
Havelec L,
Ludwig H,
Lechner K:
MDR1 gene expression and treatment outcome in acute myeloid leukemia.
J Natl Cancer Inst
83:708,
1991[Abstract/Free Full Text]
20.
Musto P,
Melillo L,
Lombardi G,
Matera R,
Di Giorgio G Carotenuto M:
High risk of early resistant relapse for leukaemic patients with presence of multidrug resistance associated P-glycoprotein positive cells in complete remission.
Br J Haematol
77:50,
1991[Medline]
[Order article via Infotrieve]
21.
Wood P,
Burgess R,
MacGregor A,
Liu JA:
P-glycoprotein expression on acute myeloid leukaemia blast cells at diagnosis predicts response to chemotherapy and survival.
Br J Haematol
87:509,
1994[Medline]
[Order article via Infotrieve]
22.
Guerci A,
Merlin JL,
Missoum N,
Feldmann L,
Marchal S,
Witz F,
Rose C,
Guerci O:
Predictive value for treatment outcome in acute myeloid leukemia of cellular daunorubicin accumulation and P-glycoprotein expression simultaneously determined by flow cytometry.
Blood
8:2147,
1995
23.
Campos L,
Guyotat D,
Archimbaud E,
Calmard-Oriol P,
Tsuruo T,
Troncy J,
Treille D,
Fiere D:
Clinical significance of multidrug resistance P-glycoprotein expression on acute nonlymphoblastic leukemia cells at diagnosis.
Blood
79:473,
1992[Abstract/Free Full Text]
24.
Zochbauer S,
Gsur A,
Brunner R,
Kryle PA,
Lechner K,
Pirker R:
P-glycoprotein expression as unfavorable prognostic factor in acute myeloid leukemia.
Leukemia
8:974,
1994[Medline]
[Order article via Infotrieve]
25. Willman CL, Kopecky K, Weick J, Appelbaum F, Grever MR, Head DR, Elias L, Balcerzak SP, Mills GM, Hynes HE: Biologic parameters that predict treatment response in de novo acute myeloid leukemia: CD34, but not multidrug resistant (MDR) gene expression, is associated with a decreased complete remission rate and CD-34+ patients more frequently achieved CR with high-dose cytosine arabinoside. Proc ASCO 11:262A, 1992 (abstr)
26.
Bennett JM,
Catovsky D,
Daniel MT,
Flandrin G,
Galton DAG,
Gralnick HR,
Sultan C:
Proposals for the classification of the acute leukemias.
Br J Haematol
33:451,
1976[Medline]
[Order article via Infotrieve]
27.
Head DR,
Cerezo L,
Savage RA,
Craven CM,
Bickers JN,
Hartsock R,
Hosty TA,
Saiki JH,
Wilson HE,
Morrison FS,
Coltman CA,
Hutton JJ:
Institutional performance in application of the FAB classification of acute leukemia, the Southwest Oncology Group experience.
Cancer
55:1979,
1985[Medline]
[Order article via Infotrieve]
28.
Leith CP,
Chen I-M,
Kopecky KJ,
Appelbaum FR,
Head DR,
Godwin JE,
Weick JK,
Willman CL:
Correlation of multidrug resistance (MDR1) protein expression with functional dye/drug efflux in acute myeloid leukemia by multiparameter flow cytometry: Identification of discordant CD34+/MDR1-/Efflux+ and MDR1+/Efflux- cases.
Blood
86:2329,
1995[Abstract/Free Full Text]
29.
Minderman H,
Vanhoefer U,
Toth K,
Yin M-B,
Minderman MD,
Wrzosek C,
Slovak ML,
Rustum YM:
DiOC2(3) is not a substrate for multidrug resistance protein (MRO)-mediated drug efflux.
Cytometry
25:14,
1996[Medline]
[Order article via Infotrieve]
30.
Cole SPC,
Bhardwaj G,
Gerlach JH,
Mackie JE,
Grant CE,
Almquist KC,
Stewart AJ,
Kurz EU,
Duncan AMV,
Deeley RG:
Overexpression of a transporter gene in a multidrug-resistant human lung cancer cell line.
Science
258:1650,
1992[Abstract/Free Full Text]
31.
Dalton WS,
Durie BGM,
Alberts DS,
Gerlach JH,
Cress AE:
Characterization of a new drug-resistant human myeloma cell line that expresses p-glycoprotein.
Cancer Res
46:5125,
1986[Abstract/Free Full Text]
32.
Young IT:
Proof without prejudice: Use of the Kolmogorov-Smirnov test for the analysis of histograms from flow systems and other sources.
J Histochem Cytochem
25:935,
1977[Abstract]
33.
Beck WT,
Grogan TM,
Willman CL,
Cordon-Cardo C,
Parham DM,
Kuttesch JF,
Andreeff M,
Bates SE,
Berard CW,
Boyett JM,
Brophy NA,
Broxterman HJ,
Chan HSL,
Dalton WS,
Dietl M,
Fojo AT,
Gascoyne RD,
Head D,
Houghton PJ,
Kumar Srivastava D,
Lehnert M,
Leith CP,
Paietta E,
Pavelic ZP,
Rimsza L,
Roninson IB,
Sikic BI,
Twentyman PR,
Warnke R,
Weinstein R:
Methods to detect P-glycoprotein-associated multidrug resistance in patient tumors: Consensus recommendations.
Cancer Res
56:3010,
1996[Abstract/Free Full Text]
34. ISCN (1995): An International System for Human Cytogenetic Nomenclature, Mitelman F (ed). Basel, Switzerland, Karger, 1995
35. Neter J, Wasserman W: Applied linear statistical models. Homewood, IL, Richard D. Irwin, 1974
36. Cox DR: The analysis of binary data. London, UK, Chapman & Hall, 1970
37.
Cheson BD,
Cassileth PA,
Head DR,
Schiffer CA,
Bennett JM,
Bloomfield CD,
Brunning R,
Gale RP,
Grever MR,
Keating MJ,
Sawitsky A,
Stass S,
Weinstein H,
Woods W:
Report of the National Cancer Institute-sponsored workshop on definitions of diagnosis and response in acute myeloid leukemia.
J Clin Oncol
8:813,
1990[Abstract]
38.
Kaplan EL,
Meier P:
Nonparametric estimate from incomplete observations.
J Am Stat Assoc
53:457,
1958
39.
Cox DR:
Regression models and life tables (with discussion).
J Royal Stat Soc B
34:187,
1972
40.
Arthur DC,
Berger R,
Golomb HM,
Swansbury GJ,
Reeves BR,
Alimena G,
Van Den Berghe H,
Bloomsfield CD,
de la Chapelle A,
Dewald GW,
Garson OM,
Hagemeijer A,
Kaneko Y,
Mitelman F,
Pierre RV,
Ruutu T,
Sakurai M,
Lawler SD,
Rowley JD:
The clinical significance of karyotype in acute myelogenous leukemia.
Cancer Genet Cytogenet
40:203,
1989[Medline]
[Order article via Infotrieve]
41.
Keating MJ,
Cork A,
Broach Y,
Smith T,
Walters RS,
McCredie KB,
Trujillo J,
Freireich EJ:
Toward a clinically relevant cytogenetic classification of acute myelogenous leukemia.
Leuk Res
11:119,
1987[Medline]
[Order article via Infotrieve]
42. Le Beau ML: The role of cytogenetics in the diagnosis and classification of hematopoietic neoplasms, in Knowles DM (ed): Neoplastic Hematopathology. Baltimore, MD, Williams & Wilkins, 1992, p 299
43.
Lamy T,
Drenou B,
Grulois I,
Fardel O,
Jacquelinet C,
Goasguen J,
Dauriac C,
Amiot L,
Bernard M,
Fauchet R,
Le Prise PY:
Multi-drug resistance (MDR) activity in acute leukemia determined by rhodamine 123 efflux assay.
Leukemia
9:1549,
1995[Medline]
[Order article via Infotrieve]
44.
Ross DD,
Wooten PJ,
Sridhara R,
Ordóñez JV,
Lee EJ,
Schiffer CA:
Enhancement of daunorubicin accumulation, retention, and cytotoxicity by verapamil or cyclosporin A in blast cells from patients with previously untreated acute myeloid leukemia.
Blood
82:1288,
1993[Abstract/Free Full Text]
45.
Pedersen-Bjergaard J,
Pedersen M,
Roulston D,
Philip P:
Different genetic pathways in leukemogenesis for patients presenting with therapy-related myelodysplasia and therapy-related acute myeloid leukemia.
Blood
86:3542,
1995[Abstract/Free Full Text]
46. Johansson B, Mertens F, Heim S, Kristoffersson U, Mitelman F: Cytogenetics of secondary myelodysplasia (sMDS) and acute nonlymphocytic leukemia (sANLL) Eur J Haematol 47:17, 1991
47.
Sonneveld P,
van Dongen JJM,
Hagemeijer A,
van Lom K,
Nooter K,
Schoester M,
Adriaansen HJ,
Tsuruo T,
de Leeuw K:
High expression of the multidrug resistance P-glycoprotein in high-risk myelodysplasia is associated with immature phenotype.
Leukemia
7:963,
1993[Medline]
[Order article via Infotrieve]
48.
List AF,
Spier CM,
Cline A,
Doll DC,
Garewal H,
Morgan R,
Sandberg AA:
Expression of the multidrug resistance gene product (P-glycoprotein) in myelodysplasia is associated with a stem cell phenotype.
Br J Haematol
78:28,
1991[Medline]
[Order article via Infotrieve]
49.
List AF,
Spier C,
Greer J,
Wolff S,
Hutter J,
Dorr R,
Salmon S,
Futscher B,
Baier M,
Dalton W:
Phase I/II trial of cyclosporine as a chemotherapy-resistance modifier in acute leukemia.
J Clin Oncol
11:1652,
1993[Abstract/Free Full Text]
50.
Scheffer GL,
Wijngaard PLJ,
Flens MJ,
Izquierdo MA,
Slovak ML,
Pinedo HM,
Meijer CJLM,
Clever HC,
Scheper RJ:
The drug resistance-related protein LRP is the human major vault protein.
Nature Med
1:578,
1995[Medline]
[Order article via Infotrieve]
51.
List AF,
Spier SC,
Grogan TM,
Johnson C,
Roe DJ,
Gree JP,
Wolff SN,
Broxterman HJ,
Scheffer GL,
Scheper RJ,
Dalton WS:
Overexpression of the major vault transporter protein lung-resistance protein predicts treatment outcome in acute myeloid leukemia.
Blood
87:2464,
1996[Abstract/Free Full Text]
52.
Marie JP,
Bastie JN,
Coloma F,
Suberville AMF,
Delmer A,
Rio B,
Delmas-Marsalet B,
Leroux G,
Casassus P,
Baumelou E,
Catalin J,
Zittoun R:
Cyclosporin A as a modifier agent in the salvage treatment of acute leukemia (AL).
Leukemia
7:821,
1993[Medline]
[Order article via Infotrieve]
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
A. R. Derolf, S. Y. Kristinsson, T. M.-L. Andersson, O. Landgren, P. W. Dickman, and M. Bjorkholm
Improved patient survival for acute myeloid leukemia: a population-based study of 9729 patients diagnosed in Sweden between 1973 and 2005
Blood,
April 16, 2009;
113(16):
3666 - 3672.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. D. Klepin and L. Balducci
Acute Myelogenous Leukemia in Older Adults
Oncologist,
March 1, 2009;
14(3):
222 - 232.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. S. Becker, K. J. Kopecky, A. N. Wilks, S. Chien, J. M. Harlan, C. L. Willman, S. H. Petersdorf, D. L. Stirewalt, T. Papayannopoulou, and F. R. Appelbaum
Very late antigen-4 function of myeloblasts correlates with improved overall survival for patients with acute myeloid leukemia
Blood,
January 22, 2009;
113(4):
866 - 874.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Buchner, W. E. Berdel, C. Haferlach, T. Haferlach, S. Schnittger, C. Muller-Tidow, J. Braess, K. Spiekermann, J. Kienast, P. Staib, et al.
Age-Related Risk Profile and Chemotherapy Dose Response in Acute Myeloid Leukemia: A Study by the German Acute Myeloid Leukemia Cooperative Group
J. Clin. Oncol.,
January 1, 2009;
27(1):
61 - 69.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. D. Shah and J. E. Lancet
Frontline Treatment of Acute Myeloid Leukemia: Are We Making Progress?
ASCO Educational Book,
January 1, 2009;
2009(1):
372 - 377.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Laubach and A. V. Rao
Current and Emerging Strategies for the Management of Acute Myeloid Leukemia in the Elderly
Oncologist,
October 1, 2008;
13(10):
1097 - 1108.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Langer, M. D. Radmacher, A. S. Ruppert, S. P. Whitman, P. Paschka, K. Mrozek, C. D. Baldus, T. Vukosavljevic, C.-G. Liu, M. E. Ross, et al.
High BAALC expression associates with other molecular prognostic markers, poor outcome, and a distinct gene-expression signature in cytogenetically normal patients younger than 60 years with acute myeloid leukemia: a Cancer and Leukemia Group B (CALGB) study
Blood,
June 1, 2008;
111(11):
5371 - 5379.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Walsby, V. Walsh, C. Pepper, A. Burnett, and K. Mills
Effects of the aurora kinase inhibitors AZD1152-HQPA and ZM447439 on growth arrest and polyploidy in acute myeloid leukemia cell lines and primary blasts
Haematologica,
May 1, 2008;
93(5):
662 - 669.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Fianchi, L. Pagano, F. Leoni, S. Storti, M. T. Voso, C. G. Valentini, S. Rutella, A. Scardocci, M. Caira, G. Gianfaldoni, et al.
Gemtuzumab ozogamicin, citosine arabinoside, G-CSF combination (G-AraMy) in the treatment of elderly patients with poor-prognosis acute myeloid leukemia
Ann. Onc.,
January 1, 2008;
19(1):
128 - 134.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. R. Baer, H. D. Klepin, and A. S. Artz
Acute Leukemia in Older Adults: Are We Treating Too Much or Too Little?
ASCO Educational Book,
January 1, 2008;
2008(1):
216 - 223.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. L. Sorror, B. M. Sandmaier, B. E. Storer, M. B. Maris, F. Baron, D. G. Maloney, B. L. Scott, H. J. Deeg, F. R. Appelbaum, and R. Storb
Comorbidity and Disease Status Based Risk Stratification of Outcomes Among Patients With Acute Myeloid Leukemia or Myelodysplasia Receiving Allogeneic Hematopoietic Cell Transplantation
J. Clin. Oncol.,
September 20, 2007;
25(27):
4246 - 4254.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. B. Walter, T. A. Gooley, V. H. J. van der Velden, M. R. Loken, J. J. M. van Dongen, D. A. Flowers, I. D. Bernstein, and F. R. Appelbaum
CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy
Blood,
May 15, 2007;
109(10):
4168 - 4170.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Estey
Acute Myeloid Leukemia and Myelodysplastic Syndromes in Older Patients
J. Clin. Oncol.,
May 10, 2007;
25(14):
1908 - 1915.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Kuptsova, K. J. Kopecky, J. Godwin, J. Anderson, A. Hoque, C. L. Willman, M. L. Slovak, and C. B. Ambrosone
Polymorphisms in DNA repair genes and therapeutic outcomes of AML patients from SWOG clinical trials
Blood,
May 1, 2007;
109(9):
3936 - 3944.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X. Thomas, S. Suciu, B. Rio, G. Leone, G. Broccia, G. Fillet, U. Jehn, W. Feremans, G. Meloni, M. Vignetti, et al.
Autologous stem cell transplantation after complete remission and first consolidation in acute myeloid leukemia patients aged 61 70 years: results of the prospective EORTC GIMEMA AML 13 study
Haematologica,
March 1, 2007;
92(3):
389 - 396.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Meshinchi and R. J. Arceci
Prognostic Factors and Risk-Based Therapy in Pediatric Acute Myeloid Leukemia
Oncologist,
March 1, 2007;
12(3):
341 - 355.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. R. Appelbaum, D. Rosenblum, R. J. Arceci, W. L. Carroll, P. P. Breitfeld, S. J. Forman, R. A. Larson, S. J. Lee, S. B. Murphy, S. O'Brien, et al.
End points to establish the efficacy of new agents in the treatment of acute leukemia
Blood,
March 1, 2007;
109(5):
1810 - 1816.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. E. Lancet, I. Gojo, J. Gotlib, E. J. Feldman, J. Greer, J. L. Liesveld, L. M. Bruzek, L. Morris, Y. Park, A. A. Adjei, et al.
A phase 2 study of the farnesyltransferase inhibitor tipifarnib in poor-risk and elderly patients with previously untreated acute myelogenous leukemia
Blood,
February 15, 2007;
109(4):
1387 - 1394.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. P. Erba
Prognostic Factors in Elderly Patients with AML and the Implications for Treatment
Hematology,
January 1, 2007;
2007(1):
420 - 428.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Marzac, I. Teyssandier, O. Calendini, J.-Y. Perrot, A.-M. Faussat, R. Tang, N. Casadevall, J.-P. Marie, and O. Legrand
Flt3 Internal Tandem Duplication and P-Glycoprotein Functionality in 171 Patients with Acute Myeloid Leukemia
Clin. Cancer Res.,
December 1, 2006;
12(23):
7018 - 7024.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Frohling, R. F. Schlenk, S. Kayser, M. Morhardt, A. Benner, K. Dohner, H. Dohner, and for the German-Austrian AML Study Group
Cytogenetics and age are major determinants of outcome in intensively treated acute myeloid leukemia patients older than 60 years: results from AMLSG trial AML HD98-B
Blood,
November 15, 2006;
108(10):
3280 - 3288.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. S. Farag, K. J. Archer, K. Mrozek, A. S. Ruppert, A. J. Carroll, J. W. Vardiman, M. J. Pettenati, M. R. Baer, M. B. Qumsiyeh, P. R. Koduru, et al.
Pretreatment cytogenetics add to other prognostic factors predicting complete remission and long-term outcome in patients 60 years of age or older with acute myeloid leukemia: results from Cancer and Leukemia Group B 8461
Blood,
July 1, 2006;
108(1):
63 - 73.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. R. Appelbaum, H. Gundacker, D. R. Head, M. L. Slovak, C. L. Willman, J. E. Godwin, J. E. Anderson, and S. H. Petersdorf
Age and acute myeloid leukemia
Blood,
May 1, 2006;
107(9):
3481 - 3485.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Becton, G. V. Dahl, Y. Ravindranath, M. N. Chang, F. G. Behm, S. C. Raimondi, D. R. Head, K. C. Stine, N. J. Lacayo, B. I. Sikic, et al.
Randomized use of cyclosporin A (CsA) to modulate P-glycoprotein in children with AML in remission: Pediatric Oncology Group Study 9421
Blood,
February 15, 2006;
107(4):
1315 - 1324.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Latagliata, V. Bongarzoni, I. Carmosino, A. Mengarelli, M. Breccia, P. A. Borza, M. D'Andrea, G. M. D'Elia, S. Mecarocci, S. G. Morano, et al.
Acute myelogenous leukemia in elderly patients not eligible for intensive chemotherapy: the dark side of the moon
Ann. Onc.,
February 1, 2006;
17(2):
281 - 285.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. J. Jabbour, E. Estey, and H. M. Kantarjian
Adult Acute Myeloid Leukemia
Mayo Clin. Proc.,
February 1, 2006;
81(2):
247 - 260.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
U. Hegenbart, D. Niederwieser, B. M. Sandmaier, M. B. Maris, J. A. Shizuru, H. Greinix, C. Cordonnier, B. Rio, A. Gratwohl, T. Lange, et al.
Treatment for Acute Myelogenous Leukemia by Low-Dose, Total-Body, Irradiation-Based Conditioning and Hematopoietic Cell Transplantation From Related and Unrelated Donors
J. Clin. Oncol.,
January 20, 2006;
24(3):
444 - 453.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. A. Mehta, T. A. Alonzo, R. B. Gerbing, J. S. Elliott, T. A. Wilke, R. J. Kennedy, J. A. Ross, J. P. Perentesis, B. J. Lange, and S. M. Davies
XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report
Blood,
January 1, 2006;
107(1):
39 - 45.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Tauro, C. Craddock, K. Peggs, G. Begum, P. Mahendra, G. Cook, J. Marsh, D. Milligan, A. Goldstone, A. Hunter, et al.
Allogeneic Stem-Cell Transplantation Using a Reduced-Intensity Conditioning Regimen Has the Capacity to Produce Durable Remissions and Long-Term Disease-Free Survival in Patients With High-Risk Acute Myeloid Leukemia and Myelodysplasia
J. Clin. Oncol.,
December 20, 2005;
23(36):
9387 - 9393.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. B. Walter, J. L. Pirga, M. R. Cronk, S. Mayer, F. R. Appelbaum, and D. E. Banker
PK11195, a peripheral benzodiazepine receptor (pBR) ligand, broadly blocks drug efflux to chemosensitize leukemia and myeloma cells by a pBR-independent, direct transporter-modulating mechanism
Blood,
November 15, 2005;
106(10):
3584 - 3593.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Z. Benderra, A. M. Faussat, L. Sayada, J.-Y. Perrot, R. Tang, D. Chaoui, H. Morjani, C. Marzac, J.-P. Marie, and O. Legrand
MRP3, BCRP, and P-Glycoprotein Activities are Prognostic Factors in Adult Acute Myeloid Leukemia
Clin. Cancer Res.,
November 1, 2005;
11(21):
7764 - 7772.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. van der Holt, B. Lowenberg, A. K. Burnett, W. U. Knauf, J. Shepherd, P. P. Piccaluga, G. J. Ossenkoppele, G. E. G. Verhoef, A. Ferrant, M. Crump, et al.
The value of the MDR1 reversal agent PSC-833 in addition to daunorubicin and cytarabine in the treatment of elderly patients with previously untreated acute myeloid leukemia (AML), in relation to MDR1 status at diagnosis
Blood,
October 15, 2005;
106(8):
2646 - 2654.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. S. Tallman, D. G. Gilliland, and J. M. Rowe
Drug therapy for acute myeloid leukemia
Blood,
August 15, 2005;
106(4):
1154 - 1163.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C.-C. Chen, C.-F. Yang, M.-H. Yang, K.-D. Lee, W.-K. Kwang, J.-Y. You, Y.-B. Yu, C.-H. Ho, C.-H. Tzeng, W.-K. Chau, et al.
Pretreatment prognostic factors and treatment outcome in elderly patients with de novo acute myeloid leukemia
Ann. Onc.,
August 1, 2005;
16(8):
1366 - 1373.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Amadori, S. Suciu, U. Jehn, R. Stasi, X. Thomas, J.-P. Marie, P. Muus, F. Lefrere, Z. Berneman, G. Fillet, et al.
Use of glycosylated recombinant human G-CSF (lenograstim) during and/or after induction chemotherapy in patients 61 years of age and older with acute myeloid leukemia: final results of AML-13, a randomized phase-3 study
Blood,
July 1, 2005;
106(1):
27 - 34.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Qadir, K. L. O'Loughlin, S. M. Fricke, N. A. Williamson, W. R. Greco, H. Minderman, and M. R. Baer
Cyclosporin A Is a Broad-Spectrum Multidrug Resistance Modulator
Clin. Cancer Res.,
March 15, 2005;
11(6):
2320 - 2326.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. P. Alyea, H. T. Kim, V. Ho, C. Cutler, J. Gribben, D. J. DeAngelo, S. J. Lee, S. Windawi, J. Ritz, R. M. Stone, et al.
Comparative outcome of nonmyeloablative and myeloablative allogeneic hematopoietic cell transplantation for patients older than 50 years of age
Blood,
February 15, 2005;
105(4):
1810 - 1814.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. S. Tallman
New Strategies for the Treatment of Acute Myeloid Leukemia Including Antibodies and Other Novel Agents
Hematology,
January 1, 2005;
2005(1):
143 - 150.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Z. Benderra, A.-M. Faussat, L. Sayada, J.-Y. Perrot, D. Chaoui, J.-P. Marie, and O. Legrand
Breast Cancer Resistance Protein and P-Glycoprotein in 149 Adult Acute Myeloid Leukemias
Clin. Cancer Res.,
December 1, 2004;
10(23):
7896 - 7902.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. E. Kolitz, S. L. George, R. K. Dodge, D. D. Hurd, B. L. Powell, S. L. Allen, E. Velez-Garcia, J. O. Moore, T. C. Shea, E. Hoke, et al.
Dose Escalation Studies of Cytarabine, Daunorubicin, and Etoposide With and Without Multidrug Resistance Modulation With PSC-833 in Untreated Adults With Acute Myeloid Leukemia Younger Than 60 Years: Final Induction Results of Cancer and Leukemia Group B Study 9621
J. Clin. Oncol.,
November 1, 2004;
22(21):
4290 - 4301.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Mahadevan and A. F. List
Targeting the multidrug resistance-1 transporter in AML: molecular regulation and therapeutic strategies
Blood,
October 1, 2004;
104(7):
1940 - 1951.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Kang, M. H. Fisher, D. Xu, Y. J. Miyamoto, A. Marchand, A. Van Aerschot, P. Herdewijn, and R. L. Juliano
Inhibition of MDR1 gene expression by chimeric HNA antisense oligonucleotides
Nucleic Acids Res.,
August 17, 2004;
32(14):
4411 - 4419.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Saussoy, J.-L. Vaerman, N. Straetmans, V. Deneys, G. Cornu, A. Ferrant, and D. Latinne
Differentiation of Acute Myeloid Leukemia from B- and T-Lineage Acute Lymphoid Leukemias by Real-Time Quantitative Reverse Transcription-PCR of Lineage Marker mRNAs
Clin. Chem.,
July 1, 2004;
50(7):
1165 - 1173.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. R. Sperr, M. Piribauer, F. Wimazal, C. Fonatsch, R. Thalhammer-Scherrer, I. Schwarzinger, K. Geissler, P. Knobl, U. Jager, K. Lechner, et al.
A Novel Effective and Safe Consolidation for Patients Over 60 Years with Acute Myeloid Leukemia: Intermediate Dose Cytarabine (2 x 1 g/m2 on Days 1, 3, and 5)
Clin. Cancer Res.,
June 15, 2004;
10(12):
3965 - 3971.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. B. Walter, B. W. Raden, M. R. Cronk, I. D. Bernstein, F. R. Appelbaum, and D. E. Banker
The peripheral benzodiazepine receptor ligand PK11195 overcomes different resistance mechanisms to sensitize AML cells to gemtuzumab ozogamicin
Blood,
June 1, 2004;
103(11):
4276 - 4284.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. L. Greenberg, S. J. Lee, R. Advani, M. S. Tallman, B. I. Sikic, L. Letendre, K. Dugan, B. Lum, D. L. Chin, G. Dewald, et al.
Mitoxantrone, Etoposide, and Cytarabine With or Without Valspodar in Patients With Relapsed or Refractory Acute Myeloid Leukemia and High-Risk Myelodysplastic Syndrome: A Phase III Trial (E2995)
J. Clin. Oncol.,
March 15, 2004;
22(6):
1078 - 1086.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Argiris, Y. Li, B. A. Murphy, C. J. Langer, and A. A. Forastiere
Outcome of Elderly Patients With Recurrent or Metastatic Head and Neck Cancer Treated With Cisplatin-Based Chemotherapy
J. Clin. Oncol.,
January 15, 2004;
22(2):
262 - 268.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. M. Rowe, D. Neuberg, W. Friedenberg, J. M. Bennett, E. Paietta, A. Z. Makary, J. L. Liesveld, C. N. Abboud, G. Dewald, F. A. Hayes, et al.
A phase 3 study of three induction regimens and of priming with GM-CSF in older adults with acute myeloid leukemia: a trial by the Eastern Cooperative Oncology Group
Blood,
January 15, 2004;
103(2):
479 - 485.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. Stone, M. R. O'Donnell, and M. A. Sekeres
Acute Myeloid Leukemia
Hematology,
January 1, 2004;
2004(1):
98 - 117.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Steinbach, S. Wittig, G. Cario, S. Viehmann, A. Mueller, B. Gruhn, R. Haefer, F. Zintl, and A. Sauerbrey
The multidrug resistance-associated protein 3 (MRP3) is associated with a poor outcome in childhood ALL and may account for the worse prognosis in male patients and T-cell immunophenotype
Blood,
December 15, 2003;
102(13):
4493 - 4498.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. H. Lewis, M. L. Kilgore, D. P. Goldman, E. L. Trimble, R. Kaplan, M. J. Montello, M. G. Housman, and J. J. Escarce
Participation of Patients 65 Years of Age or Older in Cancer Clinical Trials
J. Clin. Oncol.,
April 1, 2003;
21(7):
1383 - 1389.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. El-Osta, M. Lubbert, P. W. Wijermans, T. Licht, and P. A. Jones
On the use of DNA methylation inhibitors and the reversal of transcriptional silencing
Blood,
February 15, 2003;
101(4):
1656 - 1657.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Itoh, T. Kitano, M. Watanabe, T. Kondo, T. Yabu, Y. Taguchi, K. Iwai, M. Tashima, T. Uchiyama, and T. Okazaki
Possible Role of Ceramide as an Indicator of Chemoresistance: Decrease of the Ceramide Content via Activation of Glucosylceramide Synthase and Sphingomyelin Synthase in Chemoresistant Leukemia
Clin. Cancer Res.,
January 1, 2003;
9(1):
415 - 423.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Mufti, A. F. List, S. D. Gore, and A. Y.L. Ho
Myelodysplastic Syndrome
Hematology,
January 1, 2003;
2003(1):
176 - 199.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. E. Anderson, K. J. Kopecky, C. L. Willman, D. Head, M. R. O'Donnell, F. W. Luthardt, T. H. Norwood, I-M. Chen, S. P. Balcerzak, D. B. Johnson, et al.
Outcome after induction chemotherapy for older patients with acute myeloid leukemia is not improved with mitoxantrone and etoposide compared to cytarabine and daunorubicin: a Southwest Oncology Group study
Blood,
December 1, 2002;
100(12):
3869 - 3876.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. Stone
The Difficult Problem of Acute Myeloid Leukemia in the Older Adult
CA Cancer J Clin,
November 1, 2002;
52(6):
363 - 371.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. W. Vardiman, N. L. Harris, and R. D. Brunning
The World Health Organization (WHO) classification of the myeloid neoplasms
Blood,
September 18, 2002;
100(7):
2292 - 2302.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. S. Farag, S. L. George, E. J. Lee, M. Baer, R. K. Dodge, B. Becknell, T. Fehniger, L. R. Silverman, J. Crawford, C. D. Bloomfield, et al.
Postremission Therapy with Low-dose Interleukin 2 with or without Intermediate Pulse Dose Interleukin 2 Therapy Is Well Tolerated in Elderly Patients with Acute Myeloid Leukemia: Cancer and Leukemia Group B Study 9420
Clin. Cancer Res.,
September 1, 2002;
8(9):
2812 - 2819.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. F. List, K. J. Kopecky, C. L. Willman, D. R. Head, M. L. Slovak, D. Douer, S. R. Dakhil, and F. R. Appelbaum
Cyclosporine inhibition of P-glycoprotein in chronic myeloid leukemia blast phase
Blood,
August 13, 2002;
100(5):
1910 - 1912.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. R. Baer, S. L. George, R. K. Dodge, K. L. O'Loughlin, H. Minderman, M. A. Caligiuri, J. Anastasi, B. L. Powell, J. E. Kolitz, C. A. Schiffer, et al.
Phase 3 study of the multidrug resistance modulator PSC-833 in previously untreated patients 60 years of age and older with acute myeloid leukemia: Cancer and Leukemia Group B Study 9720
Blood,
July 30, 2002;
100(4):
1224 - 1232.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Menzin, K. Lang, C. C. Earle, D. Kerney, and R. Mallick
The Outcomes and Costs of Acute Myeloid Leukemia Among the Elderly
Arch Intern Med,
July 22, 2002;
162(14):
1597 - 1603.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Tafuri, C. Gregorj, M. T. Petrucci, M. R. Ricciardi, M. Mancini, G. Cimino, C. Mecucci, A. Tedeschi, G. Fioritoni, F. Ferrara, et al.
MDR1 protein expression is an independent predictor of complete remission in newly diagnosed adult acute lymphoblastic leukemia
Blood,
July 18, 2002;
100(3):
974 - 981.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. R. Wolman, H. Gundacker, F. R. Appelbaum, and M. L. Slovak
Impact of trisomy 8 (+8) on clinical presentation, treatment response, and survival in acute myeloid leukemia: a Southwest Oncology Group study
Blood,
June 17, 2002;
100(1):
29 - 35.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Garcia-Manero, C. Bueso-Ramos, J. Daniel, J. Williamson, H. M. Kantarjian, and J.-P. J. Issa
DNA Methylation Patterns at Relapse in Adult Acute Lymphocytic Leukemia
Clin. Cancer Res.,
June 1, 2002;
8(6):
1897 - 1903.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. J. Giles, A. Keating, A. H. Goldstone, I. Avivi, C. L. Willman, and H. M. Kantarjian
Acute Myeloid Leukemia
Hematology,
January 1, 2002;
2002(1):
73 - 110.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
A. D. Schimmer, D. W. Hedley, L. Z. Penn, and M. D. Minden
Receptor- and mitochondrial-mediated apoptosis in acute leukemia: a translational view
Blood,
December 15, 2001;
98(13):
3541 - 3553.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. F. List, K. J. Kopecky, C. L. Willman, D. R. Head, D. L. Persons, M. L. Slovak, R. Dorr, C. Karanes, H. E. Hynes, J. H. Doroshow, et al.
Benefit of cyclosporine modulation of drug resistance in patients with poor-risk acute myeloid leukemia: a Southwest Oncology Group study
Blood,
December 1, 2001;
98(12):
3212 - 3220.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. M. Galmarini, K. Graham, X. Thomas, F. Calvo, P. Rousselot, A. El Jafaari, E. Cros, J. R. Mackey, and C. Dumontet
Expression of high Km 5'-nucleotidase in leukemic blasts is an independent prognostic factor in adults with acute myeloid leukemia
Blood,
September 15, 2001;
98(6):
1922 - 1926.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. H. Goldstone, A. K. Burnett, K. Wheatley, A. G. Smith, R. M. Hutchinson, and R. E. Clark
Attempts to improve treatment outcomes in acute myeloid leukemia (AML) in older patients: the results of the United Kingdom Medical Research Council AML11 trial
Blood,
September 1, 2001;
98(5):
1302 - 1311.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Grimwade, H. Walker, G. Harrison, F. Oliver, S. Chatters, C. J. Harrison, K. Wheatley, A. K. Burnett, and A. H. Goldstone
The predictive value of hierarchical cytogenetic classification in older adults with acute myeloid leukemia (AML): analysis of 1065 patients entered into the United Kingdom Medical Research Council AML11 trial
Blood,
September 1, 2001;
98(5):
1312 - 1320.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. L. Linenberger, T. Hong, D. Flowers, E. L. Sievers, T. A. Gooley, J. M. Bennett, M. S. Berger, L. H. Leopold, F. R. Appelbaum, and I. D. Bernstein
Multidrug-resistance phenotype and clinical responses to gemtuzumab ozogamicin
Blood,
August 15, 2001;
98(4):
988 - 994.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. Stone, D. T. Berg, S. L. George, R. K. Dodge, P. A. Paciucci, P. P. Schulman, E. J. Lee, J. O. Moore, B. L. Powell, M. R. Baer, et al.
Postremission therapy in older patients with de novo acute myeloid leukemia: a randomized trial comparing mitoxantrone and intermediate-dose cytarabine with standard-dose cytarabine
Blood,
August 1, 2001;
98(3):
548 - 553.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Pallis, M. Grundy, J. Turzanski, R. Kofler, and N. Russell
Mitochondrial membrane sensitivity to depolarization in acute myeloblastic leukemia is associated with spontaneous in vitro apoptosis, wild-type TP53, and vicinal thiol/disulfide status
Blood,
July 15, 2001;
98(2):
405 - 413.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. L. Sievers, R. A. Larson, E. A. Stadtmauer, E. Estey, B. Lowenberg, H. Dombret, C. Karanes, M. Theobald, J. M. Bennett, M. L. Sherman, et al.
Efficacy and Safety of Gemtuzumab Ozogamicin in Patients With CD33-Positive Acute Myeloid Leukemia in First Relapse
J. Clin. Oncol.,
July 1, 2001;
19(13):
3244 - 3254.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. L. Stirewalt, K. J. Kopecky, S. Meshinchi, F. R. Appelbaum, M. L. Slovak, C. L. Willman, and J. P. Radich
FLT3, RAS, and TP53 mutations in elderly patients with acute myeloid leukemia
Blood,
June 1, 2001;
97(11):
3589 - 3595.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. M. van den Heuvel-Eibrink, E. A. C. Wiemer, M. J. de Boevere, B. van der Holt, P. J. M. Vossebeld, R. Pieters, and P. Sonneveld
MDR1 gene-related clonal selection and P-glycoprotein function and expression in relapsed or refractory acute myeloid leukemia
Blood,
June 1, 2001;
97(11):
3605 - 3611.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Toyota, K. J. Kopecky, M.-O. Toyota, K.-W. Jair, C. L. Willman, and J.-P. J. Issa
Methylation profiling in acute myeloid leukemia
Blood,
May 1, 2001;
97(9):
2823 - 2829.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Legrand, J.-Y. Perrot, G. Simonin, M. Baudard, and J.-P. Marie
JC-1: a very sensitive fluorescent probe to test Pgp activity in adult acute myeloid leukemia
Blood,
January 15, 2001;
97(2):
502 - 508.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Head
Problematic WHO Reclassification of Myelodysplastic Syndromes
J. Clin. Oncol.,
October 19, 2000;
18(19):
3447 - 3452.
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. H. Estey
How I treat older patients with AML
Blood,
September 1, 2000;
96(5):
1670 - 1673.
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Legrand, J.-Y. Perrot, M. Baudard, A. Cordier, R. Lautier, G. Simonin, R. Zittoun, N. Casadevall, and J.-P. Marie
The immunophenotype of 177 adults with acute myeloid leukemia: proposal of a prognostic score
Blood,
August 1, 2000;
96(3):
870 - 877.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
U. Tidefelt, J. Liliemark, A. Gruber, E. Liliemark, B. Sundman-Engberg, G. Juliusson, L. Stenke, A. Elmhorn-Rosenborg, L. Mollgard, S. Lehman, et al.
P-Glycoprotein Inhibitor Valspodar (PSC 833) Increases the Intracellular Concentrations of Daunorubicin In Vivo in Patients With P-Glycoprotein-Positive Acute Myeloid Leukemia
J. Clin. Oncol.,
May 9, 2000;
18(9):
1837 - 1844.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. V. Dahl, N. J. Lacayo, N. Brophy, K. Dunussi-Joannopoulos, H. J. Weinstein, M. Chang, B. I. Sikic, and R. J. Arceci
Mitoxantrone, Etoposide, and Cyclosporine Therapy in Pediatric Patients With Recurrent or Refractory Acute Myeloid Leukemia
J. Clin. Oncol.,
May 9, 2000;
18(9):
1867 - 1875.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Pallis and N. Russell
P-glycoprotein plays a drug-efflux-independent role in augmenting cell survival in acute myeloblastic leukemia and is associated with modulation of a sphingomyelin-ceramide apoptotic pathway
Blood,
May 1, 2000;
95(9):
2897 - 2904.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Hellstrom-Lindberg, C. Willman, A. J. Barrett, and Y. Saunthararajah
Achievements in Understanding and Treatment of Myelodysplastic Syndromes
Hematology,
January 1, 2000;
2000(1):
110 - 132.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. F. Hutchins, J. M. Unger, J. J. Crowley, C. A. Coltman, and K. S. Albain
Underrepresentation of Patients 65 Years of Age or Older in Cancer-Treatment Trials
N. Engl. J. Med.,
December 30, 1999;
341(27):
2061 - 2067.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. Hiddemann, W. Kern, C. Schoch, C. Fonatsch, A. Heinecke, B. Wormann, and T. Buchner
Management of Acute Myeloid Leukemia in Elderly Patients
J. Clin. Oncol.,
November 1, 1999;
17(11):
3569 - 3576.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Lowenberg, J. R. Downing, and A. Burnett
Acute Myeloid Leukemia
N. Engl. J. Med.,
September 30, 1999;
341(14):
1051 - 1062.
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. J. Lee, S. L. George, M. Caligiuri, T. P. Szatrowski, B. L. Powell, S. Lemke, R. K. Dodge, R. Smith, M. Baer, and C. A. Schiffer
Parallel Phase I Studies of Daunorubicin Given With Cytarabine and Etoposide With or Without the Multidrug Resistance Modulator PSC-833 in Previously Untreated Patients 60 Years of Age or Older With Acute Myeloid Leukemia: Results of Cancer and Leukemia Group B Study 9420
J. Clin. Oncol.,
September 1, 1999;
17(9):
2831 - 2831.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Legrand, G. Simonin, A. Beauchamp-Nicoud, R. Zittoun, and J.-P. Marie
Simultaneous Activity of MRP1 and Pgp Is Correlated With In Vitro Resistance to Daunorubicin and With In Vivo Resistance in Adult Acute Myeloid Leukemia
Blood,
August 1, 1999;
94(3):
1046 - 1056.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. P. Leith, K. J. Kopecky, I-M. Chen, L. Eijdems, M. L. Slovak, T. S. McConnell, D. R. Head, J. Weick, M. R. Grever, F. R. Appelbaum, et al.
Frequency and Clinical Significance of the Expression of the Multidrug Resistance Proteins MDR1/P-Glycoprotein, MRP1, and LRP in Acute Myeloid Leukemia. A Southwest Oncology Group Study
Blood,
August 1, 1999;
94(3):
1086 - 1099.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y.-M. Zhu, E.P. Das-Gupta, and N.H. Russell
Microsatellite Instability and p53 Mutations Are Associated With Abnormal Expression of the MSH2 Gene in Adult Acute Leukemia
Blood,
July 15, 1999;
94(2):
733 - 740.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. M. Kornblau, P. F. Thall, Z. Estrov, M. Walterscheid, S. Patel, A. Theriault, M. J. Keating, H. Kantarjian, E. Estey, and M. Andreeff
The Prognostic Impact of BCL2 Protein Expression in Acute Myelogenous Leukemia Varies with Cytogenetics
Clin. Cancer Res.,
July 1, 1999;
5(7):
1758 - 1766.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. McCoy, S. B. McGee, and M. M. Cornwell
The Wilms' Tumor Suppressor, WT1, Inhibits 12-O-Tetradecanoylphorbol-13-acetate Activation of the Multidrug Resistance-1 Promoter
Cell Growth Differ.,
June 1, 1999;
10(6):
377 - 386.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
R. Advani, H. I. Saba, M. S. Tallman, J. M. Rowe, P. H. Wiernik, J. Ramek, K. Dugan, B. Lum, J. Villena, E. Davis, et al.
Treatment of Refractory and Relapsed Acute Myelogenous Leukemia With Combination Chemotherapy Plus the Multidrug Resistance Modulator PSC 833 (Valspodar)
Blood,
February 1, 1999;
93(3):
787 - 795.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. A. Cassileth, D. P. Harrington, F. R. Appelbaum, H. M. Lazarus, J. M. Rowe, E. Paietta, C. Willman, D. D. Hurd, J. M. Bennett, K. G. Blume, et al.
Chemotherapy Compared with Autologous or Allogeneic Bone Marrow Transplantation in the Management of Acute Myeloid Leukemia in First Remission
N. Engl. J. Med.,
December 3, 1998;
339(23):
1649 - 1656.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Nakayama, M. Wada, T. Harada, J. Nagayama, H. Kusaba, K. Ohshima, M. Kozuru, H. Komatsu, R. Ueda, and M. Kuwano
Hypomethylation Status of CpG Sites at the Promoter Region and Overexpression of the Human MDR1 Gene in Acute Myeloid Leukemias
Blood,
December 1, 1998;
92(11):
4296 - 4307.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. E. Hogge, C. L. Willman, R. J. Kreitman, M. Berger, P. D. Hall, K. J. Kopecky, C. McLain, E. P. Tagge, C. J. Eaves, and A. E. Frankel
Malignant Progenitors From Patients With Acute Myelogenous Leukemia Are Sensitive to a Diphtheria Toxin-Granulocyte-Macrophage Colony-Stimulating Factor Fusion Protein
Blood,
July 15, 1998;
92(2):
589 - 595.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Stasi, G. Del Poeta, A. Venditti, M. Masi, E. Stipa, M. Christina Cox, S. Amadori;, F. R. Appelbaum, K. J. Kopecky, and C. L. Willman
Prognostic Value of Cytogenetics and Multidrug Resistance (MDR1) in Elderly Patients With Acute Myeloid Leukemia
Blood,
July 15, 1998;
92(2):
695 - 697.
[Full Text]
[PDF]
|
|
|
|
|
Abstract
Introduction
Abstract