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M Robin,
R Porcher, L Adès,
N Boissel,
E Raffoux,
A Xhaard,
J Larghero,
C Gardin,
C Himberlin,
A Delmer,
P Fenaux,
H Dombret,
G Socié,
R Peffault de Latour
[show abstract]
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ABSTRACT: The impact of allelic HLA matching in patients with AML and myelodysplastic syndrome (MDS) who receive allogeneic PBSC after a reduced-intensity conditioning (RIC) regimen is unclear. From January 2000 to December 2010, 108 consecutive patients with AML (n=63) and MDS (n=45) received PBSC after RIC in our center, either from siblings (n=70) or from matched unrelated donors (MUD; 10/10 high resolution, n=38). Conditioning regimen was fludarabine based in 95% of patients and GvHD prophylaxis was mostly cyclosporine plus mycophenolate. Patient characteristics were similar between sibling and MUD for age (median 57 years), gender and disease distribution. Conditioning regimen (more anti-thymocyte globulin (ATG) in MUD), donor age (younger for MUD) and number of CD34+ cells infused (higher in MUD) were different. The median follow-up was 36 months (range 2-72). Engraftment, GvHD, TRM, relapse rate and OS at 3 years were comparable between sibling and MUD. After adjustment for age, cytogenetic risk, ATG and number of CD34+ cells infused, donor type still did not influence OS. In patients with AML or MDS, HSCT from MUD using PBSC after a RIC regimen led to similar outcomes than from Siblings.Bone Marrow Transplantation advance online publication, 15 April 2013; doi:10.1038/bmt.2013.50.
Bone marrow transplantation 04/2013; · 3.00 Impact Factor
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C Kelaidi,
O Beyne-Rauzy,
T Braun,
R Sapena,
P Cougoul, L Adès,
F Pillard,
C Lamberto,
J C Charniot,
A Guerci, [......],
F Boyer,
M P Chaury,
L Legros,
S Cheze,
A Testu,
E Gyan,
M C Béné,
C Rose,
F Dreyfus,
P Fenaux
Annals of Hematology 03/2013; · 2.62 Impact Factor
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C Kelaidi,
O Beyne-Rauzy,
T Braun,
R Sapena,
P Cougoul, L Adès,
F Pillard,
C Lambert,
J C Charniot,
A Guerci, [......],
F Boyer,
M P Chaury,
L Legros,
S Cheze,
A Testu,
E Gyan,
M C Béné,
C Rose,
F Dreyfus,
P Fenaux
[show abstract]
[hide abstract]
ABSTRACT: Darbepoetin (DAR), with or without granulocyte colony-stimulating factor (G-CSF), has proved effective in treating anemia in patients with lower-risk myelodysplastic syndrome (MDS), but its effects on quality of life (QoL) and exercise functioning are less well established. In this phase II study (no. NCT00443339), lower-risk MDS patients with anemia and endogenous erythropoietin (EPO) level <500 IU/L received DAR 500 μg once every 2 weeks for 12 weeks, with G-CSF added at week 12 in non-responders. Physical performance was assessed with the 6-min walking test and, for fit patients, maximal oxygen consumption (VO(2max)). QoL was evaluated using SF-36 and FACT-An tests. In 99 patients, erythroid response rate according to IWG 2006 criteria was 48 and 56 % at 12 and 24 weeks, respectively. Addition of G-CSF rescued 22 % of non-responders. In 48 % of the responders, interval between darbepoetin injections could be increased for maintenance treatment. Serum EPO level was the only independent predictive factor of response at 12 weeks, and its most discriminant cutoff value was 100 IU/L. QoL and VO(2max) showed improvement over time in responders, compared with non-responders. With a median follow-up of 52 months, median response duration was not reached, and 3-year cumulative incidence of acute myeloid leukemia and overall survival (OS) was 14.5 and 70 %, respectively. Baseline transfusion dependence, International Prognostic Score System (IPSS), and Revised IPSS accurately predicted OS from treatment onset. Tolerance of darbepoetin was good. In conclusion, this regimen of darbepoetin every 2 weeks yielded high response rates and prolonged response duration. Objective improvement in exercise testing and in patient-reported QoL confirms the clinical relevance of anemia correction with erythropoiesis-stimulating agents.
Annals of Hematology 01/2013; · 2.62 Impact Factor
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C Kelaidi,
S Park,
R Sapena,
O Beyne-Rauzy,
V Coiteux,
N Vey,
A Stamatoullas,
B Choufi,
J Delaunay,
M-P Gourin,
S Cheze,
C Ravoet,
A Ferrant,
M Escoffre-Barbe,
L Aljassem,
E Raffoux,
R Itzykson, L Adès,
F Dreyfus,
P Fenaux
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ABSTRACT: A large proportion of lower-risk myelodysplastic syndromes (MDS) respond to erythropoiesis-stimulating agents (ESA), but most responses are transient. We updated a previously reported cohort of lower-risk MDS patients treated with ESA and analyzed outcomes after ESA failure. In 120 patients with primary resistance and 66 patients with relapse after an initial response to ESA, the 5-year cumulative incidence of acute myeloid leukemia (AML) after failure was 18.9% and 11.6%, respectively (P=0.20). Median overall survival (OS) after failure was 40.1 and 44.9 months (P=0.35), respectively. We further categorized patients as 'early failures' (including resistance and relapse after <6 months of response), or 'later failures' (that is, relapse after 6 months). The 5-year cumulative incidence of AML and median OS after failure in early and later failure were 21.6% and 9% (P=0.02) and 36.7 and 54.3 months (P=0.02), respectively. Early failure to ESA and a baseline diagnosis of refractory anemia with excess blasts (RAEB)-1 were independent prognostic factors for AML progression and, along with trisomy 8, for shorter OS. Median OS from treatment onset was 40, 90.7 and 65.8 months in early failure, later failure and no relapse, respectively (P=0.001). Lower-risk MDS with early failure to ESA have a relatively unfavorable outcome, and should be offered alternative treatments.Leukemia advance online publication, 1 February 2013; doi:10.1038/leu.2013.16.
Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 01/2013; · 8.30 Impact Factor
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L Faivre,
G Collod-Beroud, L Adès,
E Arbustini,
A Child,
B L Callewaert,
B Loeys,
C Binquet,
E Gautier,
K Mayer, [......],
P Coucke,
U Francke,
O Bouchot,
J E Wolf,
C Stheneur,
N Hanna,
D Detaint,
A De Paepe,
C Boileau,
G Jondeau
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ABSTRACT: The diagnosis of Marfan syndrome (MFS) is challenging and international criteria have been proposed. The 1996 Ghent criteria were adopted worldwide, but new diagnostic criteria for MFS were released in 2010, giving more weight to aortic root aneurysm and ectopia lentis. We aimed to compare the diagnosis reached by applying this new nosology vs the Ghent nosology in a well-known series of 1009 probands defined by the presence of an FBN1 mutation. A total of 842 patients could be classified as MFS according to the new nosology (83%) as compared to 894 (89%) according to the 1996 Ghent criteria. The remaining 17% would be classified as ectopia lentis syndrome (ELS), mitral valve prolapse syndrome or mitral valve, aorta, skeleton and skin (MASS) syndrome, or potential MFS in patients aged less than 20 years. Taking into account the median age at last follow-up (29 years), the possibility has to be considered that these patients would go on to develop classic MFS with time. Although the number of patients for a given diagnosis differed only slightly, the new nosology led to a different diagnosis in 15% of cases. Indeed, 10% of MFS patients were reclassified as ELS or MASS in the absence of aortic dilatation; conversely, 5% were reclassified as MFS in the presence of aortic dilatation. The nosology is easier to apply because the systemic score is helpful to reach the diagnosis of MFS only in a minority of patients. Diagnostic criteria should be a flexible and dynamic tool so that reclassification of patients with alternative diagnosis is possible, requiring regular clinical and aortic follow-up.
Clinical Genetics 05/2011; 81(5):433-42. · 3.13 Impact Factor
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R Itzykson,
O Kosmider,
T Cluzeau,
V Mansat-De Mas,
F Dreyfus,
O Beyne-Rauzy,
B Quesnel,
N Vey,
V Gelsi-Boyer,
S Raynaud,
C Preudhomme, L Adès,
P Fenaux,
M Fontenay
[show abstract]
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ABSTRACT: The impact of ten-eleven-translocation 2 (TET2) mutations on response to azacitidine (AZA) in MDS has not been reported. We sequenced the TET2 gene in 86 MDS and acute myeloid leukemia (AML) with 20-30% blasts treated by AZA, that is disease categories wherein this drug is approved by Food and Drug Administration (FDA). Thirteen patients (15%) carried TET2 mutations. Patients with mutated and wild-type (WT) TET2 had mostly comparable pretreatment characteristics, except for lower hemoglobin, better cytogenetic risk and longer MDS duration before AZA in TET2 mutated patients (P=0.03, P=0.047 and P=0.048, respectively). The response rate (including hematological improvement) was 82% in MUT versus 45% in WT patients (P=0.007). Mutated TET2 (P=0.04) and favorable cytogenetic risk (intermediate risk: P=0.04, poor risk: P=0.048 compared with good risk) independently predicted a higher response rate. Response duration and overall survival were, however, comparable in the MUT and WT groups. In higher risk MDS and AML with low blast count, TET2 status may be a genetic predictor of response to AZA, independently of karyotype.
Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 04/2011; 25(7):1147-52. · 8.30 Impact Factor
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R Itzykson,
S Thépot,
V Eclache,
B Quesnel,
F Dreyfus,
O Beyne-Rauzy,
P Turlure,
N Vey,
C Recher,
S Boehrer,
C Gardin, L Adès,
P Fenaux
Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 04/2011; 25(7):1207-9. · 8.30 Impact Factor
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[show abstract]
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ABSTRACT: Acute promyelocytic leukemia (APL) with WBC above 10 G/L has long been considered, even in the all-trans retinoic acid (ATRA) era, to carry a relatively poor prognosis (compared to APL with WBC below 10 G/L), due to increased early mortality and relapse. However, early deaths can to a large extent be avoided if specific measures are rapidly instigated, including prompt referral to a specialized center, immediate onset of ATRA and chemotherapy, treatment of coagulopathy with adequate platelet transfusional support, and prevention and management of differentiation syndrome. Strategies to reduce relapse rate include chemotherapy reinforcement with cytarabine and/or arsenic trioxide during consolidation, prolonged maintenance treatment, especially with ATRA and low dose chemotherapy, and possibly, although this is debated, intrathecal prophylaxis to prevent central nervous system relapse. By applying those measures, outcomes of patients with high risk APL have considerably improved, and have become in many studies almost similar to those of standard risk APL patients.
Mediterranean Journal of Hematology and Infectious Diseases 01/2011; 3(1):e2011038.
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Bone marrow transplantation 09/2009; 45(4):791-2. · 3.00 Impact Factor
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S Boehrer, L Adès,
N Tajeddine,
W K Hofmann,
S Kriener,
G Bug,
O G Ottmann,
M Ruthardt,
L Galluzzi,
C Fouassier,
M Tailler,
K A Olaussen,
C Gardin,
V Eclache,
S de Botton,
S Thepot,
P Fenaux,
G Kroemer
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ABSTRACT: The molecular mechanisms responsible for the evolution from the preleukemic entities of low-risk myelodysplastic syndrome (MDS) to the less favorable forms of high-risk MDS, as well as those enabling transformation to acute myeloid leukemia (AML), are still incompletely understood. Abundant evidence from solid tumors demonstrates that preneoplastic lesions activate signaling pathways of a DNA damage response (DDR), which functions as an 'anticancer barrier' hindering tumorigenesis. Testing the hypothesis that subgroups of MDS and AML differ with respect to DDR, we first assessed markers of DDR (phosphorylation of ATM, Chk-1, Chk-2 and H2AX) in cell lines representing different entities of MDS (P39, MOLM-13) and AML (MV4-11, KG-1) before and after gamma-irradiation. Although gamma-irradiation induced apoptosis and G(2)/M arrest and a concomitant increase in the phosphorylation of ATM, Chk-1 and H2AX in MDS-derived cell lines, this radiation response was attenuated in the AML-derived cell lines. It is noteworthy that KG-1, but not P39 cells exhibit signs of an endogenous activation of the DDR. Similarly, we found that the frequency of P-ATM(+) cells detectable in bone marrow (BM) biopsies increased in samples from patients with AML as compared with high-risk MDS samples and significantly correlated with the percentage of BM blasts. In contrast, the frequency of gamma-H2AX(+) cells was heterogeneous in all subgroups of AML and MDS. Whereas intermediate-1 MDS samples contained as little P-Chk-1 and P-Chk-2 as healthy controls, staining for both checkpoint kinases increased in intermediate-2 and high-risk MDS, yet declined to near-to-background levels in AML samples. Thus the activation of Chk-1 and Chk-2 behaves in accord with the paradigm established for solid tumors, whereas ATM is activated during and beyond transformation. In conclusion, we demonstrate the heterogeneity of the DDR response in MDS and AML and provide evidence for its selective suppression in AML because of the uncoupling between activated ATM and inactive checkpoint kinases.
Oncogene 05/2009; 28(22):2205-18. · 6.37 Impact Factor
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L. Faivre,
G. Collod-Beroud,
B. Callewaert,
A. Child,
B.L. Loeys,
C. Binquet,
E. Gautier,
E. Arbustini,
K. Mayer,
M. Arslan-Kirchner, [......],
O. Bouchot,
J.E. Wolf,
P.N. Robinson, L. Adès,
J. De Backer,
P. Coucke,
U. Francke,
A. De Paepe,
C. Boileau,
G. Jondeau
[show abstract]
[hide abstract]
ABSTRACT: Mutations in the FBN1 gene cause Marfan syndrome (MFS) and have been associated with a wide range of milder overlapping phenotypes. A proportion of patients carrying a FBN1 mutation does not meet diagnostic criteria for MFS, and are diagnosed with “other type I fibrillinopathy.” In order to better describe this entity, we analyzed a subgroup of 146 out of 689 adult propositi with incomplete “clinical” international criteria (Ghent nosology) from a large collaborative international study including 1,009 propositi with a pathogenic FBN1 mutation. We focused on patients with only one major clinical criterion, [including isolated ectopia lentis (EL; 12 patients), isolated ascending aortic dilatation (17 patients), and isolated major skeletal manifestations (1 patient)] or with no major criterion but only minor criteria in 1 or more organ systems (16 patients). At least one component of the Ghent nosology, insufficient alone to make a minor criterion, was found in the majority of patients with isolated ascending aortic dilatation and isolated EL. In patients with isolated EL, missense mutations involving a cysteine were predominant, mutations in exons 24–32 were underrepresented, and no mutations leading to a premature truncation were found. Studies of recurrent mutations and affected family members of propositi with only one major clinical criterion argue for a clinical continuum between such phenotypes and classical MFS. Using strict definitions, we conclude that patients with FBN1 mutation and only one major clinical criterion or with only minor clinical criteria of one or more organ system do exist but represent only 5% of the adult cohort. © 2009 Wiley-Liss, Inc.
American Journal of Medical Genetics Part A 04/2009; 149A(5):854 - 860. · 2.39 Impact Factor
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[show abstract]
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ABSTRACT: The anti-apoptotic transcription factor nuclear factor-kappaB (NF-kappaB) is constitutively activated in CD34(+) myeloblasts from high-risk myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) patients. Inhibition of NF-kappaB by suppressing the canonical NF-kappaB activation pathway, for instance by knockdown of the three subunits of the inhibitor of NF-kappaB (I kappaB) kinase (IKK) complex (IKK1, IKK2 and NEMO) triggers apoptosis in such cells. Here, we show that an MDS/AML model cell line exhibits a constitutive interaction, within the nucleus, of activated, S1981-phosphorylated ataxia telangiectasia mutated (ATM) with NEMO. Inhibition of ATM with two distinct pharmacological inhibitors suppressed the activating autophosphorylation of ATM, blocked the interaction of ATM and NEMO, delocalized NEMO as well as another putative NF-kappaB activator, PIDD, from the nucleus, abolished the activating phosphorylation of the catalytic proteins of the IKK complex (IKK1/2 on serines 176/180), enhanced the expression of I kappaB alpha and caused the relocalization of NF-kappaB from the nucleus to the cytoplasm, followed by apoptosis. Knockdown of ATM with small-interfering RNAs had a similar effect that could not be enhanced by knockdown of NEMO, PIDD and the p65 NF-kappaB subunit, suggesting that an ATM inhibition/depletion truly induced apoptosis through inhibition of the NF-kappaB system. Pharmacological inhibition of ATM also induced the nucleocytoplasmic relocalization of p65 in malignant myeloblasts purified from patients with high-risk MDS or AML, correlating with the induction of apoptosis. Altogether, these results support the contention that constitutively active ATM accounts for the activation of NF-kappaB in high-risk MDS and AML.
Oncogene 01/2009; 28(8):1099-109. · 6.37 Impact Factor
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L Faivre,
G Collod-Beroud,
B Callewaert,
A Child,
C Binquet,
E Gautier,
B L Loeys,
E Arbustini,
K Mayer,
M Arslan-Kirchner, [......],
M Claustres,
C Bonithon-Kopp,
P N Robinson, L Adès,
J De Backer,
P Coucke,
U Francke,
A De Paepe,
G Jondeau,
C Boileau
[show abstract]
[hide abstract]
ABSTRACT: Mutations in the FBN1 gene cause Marfan syndrome (MFS) and a wide range of overlapping phenotypes. The severe end of the spectrum is represented by neonatal MFS, the vast majority of probands carrying a mutation within exons 24-32. We previously showed that a mutation in exons 24-32 is predictive of a severe cardiovascular phenotype even in non-neonatal cases, and that mutations leading to premature truncation codons are under-represented in this region. To describe patients carrying a mutation in this so-called 'neonatal' region, we studied the clinical and molecular characteristics of 198 probands with a mutation in exons 24-32 from a series of 1013 probands with a FBN1 mutation (20%). When comparing patients with mutations leading to a premature termination codon (PTC) within exons 24-32 to patients with an in-frame mutation within the same region, a significantly higher probability of developing ectopia lentis and mitral insufficiency were found in the second group. Patients with a PTC within exons 24-32 rarely displayed a neonatal or severe MFS presentation. We also found a higher probability of neonatal presentations associated with exon 25 mutations, as well as a higher probability of cardiovascular manifestations. A high phenotypic heterogeneity could be described for recurrent mutations, ranging from neonatal to classical MFS phenotype. In conclusion, even if the exons 24-32 location appears as a major cause of the severity of the phenotype in patients with a mutation in this region, other factors such as the type of mutation or modifier genes might also be relevant.
European journal of human genetics: EJHG 12/2008; 17(4):491-501. · 3.56 Impact Factor
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C Kelaidi,
S Park,
S Brechignac,
L Mannone,
N Vey,
H Dombret,
L Aljassem,
A Stamatoullas, L Adès,
S Giraudier,
S de Botton,
S Raynaud,
P Lepelley,
F Picard,
G Leroux,
M T Daniel,
D Bouscary,
F Dreyfus,
P Fenaux
[show abstract]
[hide abstract]
ABSTRACT: Anemia in MDS with 5q deletion was generally considered, until the advent of lenalidomide, unresponsive to available treatments. We analyzed erythroid response to erythropoetin (EPO) or darbepoetin (DAR) and thalidomide in MDS with 5q deletion treated by French centers (GFM) and in whom karyotype was successfully performed. Of 345 patients treated with EPO or DAR+/-G-CSF, 48 had 5q deletion. The response rate was 46% (31% major, 15% minor) according to International Working Group (IWG) 2000 criteria versus 64% in patients without 5q deletion (p=0.03). According to IWG 2006 criteria, the response rate in patients with 5q deletion was 39% versus 52% in patients without 5q deletion (p=0.10). Mean duration of response was 14 months versus 25 months (IWG 2000) and 13 months versus 27 months (IWG 2006) in 5q deletion and non-5q deletion patients (p=0.019 and 0.003, respectively). Of 120 MDS treated with thalidomide, all of whom had successful cytogenetic analysis, 37% of the 24 patients with 5q deletion responded (IWG 2000 criteria, 20% major, 17% minor) with a mean duration of 9.5 months, versus 32% (18% major, 14% minor) in MDS without 5q deletion and a mean response duration of 9 months (p=NS). Our results confirm that response rates to EPO or DAR and thalidomide are clearly inferior to those obtained with lenalidomide.
Leukemia Research 08/2008; 32(7):1049-53. · 2.92 Impact Factor
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L Faivre,
G Collod-Beroud,
A Child,
B Callewaert,
B L Loeys,
C Binquet,
E Gautier,
E Arbustini,
K Mayer,
M Arslan-Kirchner, [......],
M Claustres,
H Plauchu,
P N Robinson, L Adès,
J De Backer,
P Coucke,
U Francke,
A De Paepe,
C Boileau,
G Jondeau
[show abstract]
[hide abstract]
ABSTRACT: The diagnosis of Marfan syndrome (MFS) is usually initially based on clinical criteria according to the number of major and minor systems affected following international nosology. The number of FBN1 mutation carriers, at risk of aortic complications who would not be properly diagnosed based only on clinical grounds, is of growing importance owing to the increased availability of molecular screening. The aim of the study was to identify patients who should be considered for FBN1 mutation screening.
Our international series included 1009 probands with a known FBN1 mutation. Patients were classified as either fulfilling or not fulfilling "clinical" criteria. In patients with unfulfilled "clinical" criteria, we evaluated the percentage of additional patients who became positive for international criteria when the FBN1 mutation was considered. The aortic risk was evaluated and compared in patients fulfilling or not fulfilling the "clinical" international criteria.
Diagnosis of MFS was possible on clinical grounds in 79% of the adults, whereas 90% fulfilled the international criteria when including the FBN1 mutation. Corresponding figures for children were 56% and 85%, respectively. Aortic dilatation occurred later in adults with unfulfilled "clinical criteria" when compared to the Marfan syndrome group (44% vs 73% at 40 years, p<0.001), but the lifelong risk for ascending aortic dissection or surgery was not significantly different in both groups.
Because of its implications for aortic follow-up, FBN1 molecular analysis is recommended in newly suspected MFS when two systems are involved with at least one major system affected. This is of utmost importance in patients without aortic dilatation and in children.
Journal of Medical Genetics 06/2008; 45(6):384-90. · 6.36 Impact Factor
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C Fabre,
G Carvalho,
E Tasdemir,
T Braun, L Adès,
J Grosjean,
S Boehrer,
D Métivier,
S Souquère,
G Pierron,
P Fenaux,
G Kroemer
[show abstract]
[hide abstract]
ABSTRACT: CD34(+) bone marrow blasts from high-risk myelodysplastic syndrome (MDS) patients as well as MDS patient-derived cell lines (P39 and MOLM13) constitutively activate the nuclear factor-kappaB (NF-kappaB) pathway and undergo apoptosis when NF-kappaB is inhibited. Here, we show that the combination of conventional chemotherapeutic agents (daunorubicin, mitoxantrone, 5-azacytidine or camptothecin) with the NF-kappaB inhibitor BAY11-7082 did not yield a synergistic cytotoxicity. In contrast, BAY11-7082 (which targets the NF-kappaB-activating I-kappaB kinase (IKK) complex) or knockdown of essential components of the NF-kappaB system (such as the IKK1 and IKK2 subunits of the IKK complex and the p65 subunit of NF-kappaB), by small interfering RNAs sensitized MDS cell lines to starvation-induced apoptosis. The combination of BAY11-7082 and nutrient depletion synergistically killed the acute myeloid leukemia (AML) cell line U937 as well as primary CD34(+) bone marrow blasts from AML and high-risk MDS patients. The synergistic killing by BAY11-7082, combined with nutrient depletion, led to cell death accompanied by all hallmarks of apoptosis, including an early loss of the mitochondrial transmembrane potential, the release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, activation of caspase-3, phosphatidylserine exposure on the plasma membrane surface and nuclear chromatin condensation. Transmission electron microscopy revealed the presence of numerous autophagic vacuoles in the cytoplasm before cells underwent nuclear apoptosis. Nonetheless, cell death was neither inhibited by the pan-caspase inhibitor z-VAD-fmk nor by knockdown of AIF or of essential components of the autophagy pathway (ATG5, ATG6/Beclin-1, ATG10, ATG12). In contrast, external supply of glucose, insulin or insulin-like growth factor-I could retard the cell death induced by BAY11-7082 combined with starvation. These results suggest that in MDS cells, NF-kappaB inhibition can precipitate a bioenergetic crisis that leads to an autophagic stress response followed by apoptotic cell death.
Oncogene 07/2007; 26(28):4071-83. · 6.37 Impact Factor
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L Faivre,
G Collod-Beroud,
B Callewaert,
A Child,
C Binquet,
E Gautier,
B L Loeys,
E Arbustini,
K Mayer,
M Arslan-Kirchner, [......],
M Claustres,
C Bonithon-Kopp,
P N Robinson, L Adès,
J De Backer,
P Coucke,
U Francke,
A De Paepe,
G Jondeau,
C Boileau
