Olatoyosi Odenike

University of Chicago, Chicago, Illinois, United States

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Publications (70)456.73 Total impact

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    Kristen Pettit · Olatoyosi Odenike
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    ABSTRACT: Although acute myeloid leukemia (AML) is primarily a disease of older adults (age ≥60 years), the optimal treatment for older adults remains largely undefined. Intensive chemotherapy is rarely beneficial for frail older adults or those with poor-risk disease, but criteria that define fitness and/or appropriateness for intensive chemotherapy remain to be standardized. Evaluation of disease-related and patient-specific factors in the context of clinical decision making has therefore been largely subjective. A uniform approach to identify those patients most likely to benefit from intensive therapies is needed. Here, we review currently available objective measures to define older adults with AML who are ineligible for intensive chemotherapy, and discuss promising investigational approaches.
    Preview · Article · Dec 2015 · Frontiers in Oncology
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    ABSTRACT: Imetelstat, a 13-mer oligonucleotide that is covalently modified with lipid extensions, competitively inhibits telomerase enzymatic activity. It has been shown to inhibit megakaryocytic proliferation in vitro in cells obtained from patients with essential thrombocythemia. In this phase 2 study, we investigated whether imetelstat could elicit hematologic and molecular responses in patients with essential thrombocythemia who had not had a response to or who had had unacceptable side effects from prior therapies. A total of 18 patients in two sequential cohorts received an initial dose of 7.5 or 9.4 mg of imetelstat per kilogram of body weight intravenously once a week until attainment of a platelet count of approximately 250,000 to 300,000 per cubic millimeter. The primary end point was the best hematologic response. Imetelstat induced hematologic responses in all 18 patients, and 16 patients (89%) had a complete hematologic response. At the time of the primary analysis, 10 patients were still receiving treatment, with a median follow-up of 17 months (range, 7 to 32 [ongoing]). Molecular responses were seen in 7 of 8 patients who were positive for the JAK2 V617F mutation (88%; 95% confidence interval, 47 to 100). CALR and MPL mutant allele burdens were also reduced by 15 to 66%. The most common adverse events during treatment were mild to moderate in severity; neutropenia of grade 3 or higher occurred in 4 of the 18 patients (22%) and anemia, headache, and syncope of grade 3 or higher each occurred in 2 patients (11%). All the patients had at least one abnormal liver-function value; all persistent elevations were grade 1 or 2 in severity. Rapid and durable hematologic and molecular responses were observed in patients with essential thrombocythemia who received imetelstat. (Funded by Geron; ClinicalTrials.gov number, NCT01243073.).
    No preview · Article · Sep 2015 · New England Journal of Medicine

  • No preview · Article · Sep 2015

  • No preview · Article · Aug 2015 · Cancer Research
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    ABSTRACT: Safe and effective treatments are urgently needed for patients with relapsed or refractory acute myeloid leukaemia. We investigated the efficacy and safety of vosaroxin, a first-in-class anticancer quinolone derivative, plus cytarabine in patients with relapsed or refractory acute myeloid leukaemia. This phase 3, double-blind, placebo-controlled trial was undertaken at 101 international sites. Eligible patients with acute myeloid leukaemia were aged 18 years of age or older and had refractory disease or were in first relapse after one or two cycles of previous induction chemotherapy, including at least one cycle of anthracycline (or anthracenedione) plus cytarabine. Patients were randomly assigned 1:1 to vosaroxin (90 mg/m(2) intravenously on days 1 and 4 in a first cycle; 70 mg/m(2) in subsequent cycles) plus cytarabine (1 g/m(2) intravenously on days 1-5) or placebo plus cytarabine through a central interactive voice system with a permuted block procedure stratified by disease status, age, and geographical location. All participants were masked to treatment assignment. The primary efficacy endpoint was overall survival and the primary safety endpoint was 30-day and 60-day all-cause mortality. Efficacy analyses were done by intention to treat; safety analyses included all treated patients. This study is registered with ClinicalTrials.gov, number NCT01191801. Between Dec 17, 2010, and Sept 25, 2013, 711 patients were randomly assigned to vosaroxin plus cytarabine (n=356) or placebo plus cytarabine (n=355). At the final analysis, median overall survival was 7·5 months (95% CI 6·4-8·5) in the vosaroxin plus cytarabine group and 6·1 months (5·2-7·1) in the placebo plus cytarabine group (hazard ratio 0·87, 95% CI 0·73-1·02; unstratified log-rank p=0·061; stratified p=0·024). A higher proportion of patients achieved complete remission in the vosaroxin plus cytarabine group than in the placebo plus cytarabine group (107 [30%] of 356 patients vs 58 [16%] of 355 patients, p<0·0001). Early mortality was similar between treatment groups (30-day: 28 [8%] of 355 patients in the vosaroxin plus cytarabine group vs 23 [7%] of 350 in the placebo plus cytarabine group; 60-day: 70 [20%] vs 68 [19%]). Treatment-related deaths occurred at any time in 20 (6%) of 355 patients given vosaroxin plus cytarabine and in eight (2%) of 350 patients given placebo plus cytarabine. Treatment-related serious adverse events occurred in 116 (33%) and 58 (17%) patients in each group, respectively. Grade 3 or worse adverse events that were more frequent in the vosaroxin plus cytarabine group than in the placebo plus cytarabine group included febrile neutropenia (167 [47%] vs 117 [33%]), neutropenia (66 [19%] vs 49 [14%]), stomatitis (54 [15%] vs 10 [3%]), hypokalaemia (52 [15%] vs 21 [6%]), bacteraemia (43 [12%] vs 16 [5%]), sepsis (42 [12%] vs 18 [5%]), and pneumonia (39 [11%] vs 26 [7%]). Although there was no significant difference in the primary endpoint between groups, the prespecified secondary analysis stratified by randomisation factors suggests that the addition of vosaroxin to cytarabine might be of clinical benefit to some patients with relapsed or refractory acute myeloid leukaemia. Sunesis Pharmaceuticals. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · Jul 2015 · The Lancet Oncology
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    ABSTRACT: Gain-of-function mutations of FLT3 (FLT3-ITD), comprises up to 30% of normal karyotype acute myeloid leukemia (AML) and is associated with an adverse prognosis. Current FLT3 kinase inhibitors have been tested extensively, but have not yet resulted in a survival benefit and novel therapies are awaited. Here we show that T-LAK cell-originated protein kinase (TOPK), a mitotic kinase highly expressed in and correlated with more aggressive phenotype in several types of cancer, is expressed in AML but not in normal CD34+ cells and that TOPK knockdown decreased cell viability and induced apoptosis. Treatment of AML cells with TOPK inhibitor (OTS514) resulted in a dose-dependent decrease in cell viability with lower IC50 in FLT3-mutated cells, including blasts obtained from patients relapsed after FLT3-inhibitor treatment. Using a MV4-11-engrafted mouse model, we found that mice treated with 7.5 mg/kg IV daily for 3 weeks survived significantly longer than vehicle treated mice (median survival 46 vs 29 days, P < 0.001). Importantly, we identified TOPK as a FLT3-ITD and CEBPA regulated kinase, and that modulating TOPK expression or activity resulted in significant decrease of FLT3 expression and CEBPA phosphorylation. Thus, targeting TOPK in FLT3-ITD AML represents a novel therapeutic approach for this adverse risk subset of AML.
    No preview · Article · Jul 2015 · Oncotarget
  • Olatoyosi Odenike · Francesco Onida · Eric Padron
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    ABSTRACT: Myelodysplastic syndromes are a heterogeneous group of clonal hematopoietic stem cell disorders characterized by ineffective hematopoiesis, peripheral cytopenias, and a variable propensity for leukemic transformation. In recent years there has been an explosion of information on the molecular genetic changes underlying these disorders. This information has substantial prognostic implications, and the influence on therapeutic approaches and the treatment of patients is evolving. Allogeneic hematopoietic stem cell transplantation (alloSCT) is the only known cure for these diseases, but appropriate patient selection is of utmost importance from a risk-benefit perspective. This review focuses on the factors influencing risk stratification in MDS and optimal choice of front-line therapy in the current era, including the interplay of clinical factors and molecular genetic factors, and factors that determine eligibility for alloSCT. The myelodysplastic/myeloproliferative diseases also will be discussed, including the increasing effort to understand the molecular genetics and natural history of these disorders and treatment approaches.
    No preview · Article · May 2015
  • Michael Tallarico · Olatoyosi Odenike
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    ABSTRACT: The classic Philadelphia chromosome negative myeloproliferative neoplasms including primary myelofibrosis, polycythemia vera, and essential thrombocythemia are associated with a variable propensity for transformation into acute myeloid leukemia. Leukemic transformation in these disorders, so called MPN-blast phase, is uniformly associated with a poor prognosis. In recent years, there has been an increasing understanding of the molecular complexity underlying Philadelphia chromosome negative myeloproliferative neoplasms (Ph- MPNs), and this has spurred efforts to investigate the molecular risk factors associated with clinical outcome in these disorders, including the risk of leukemic transformation. At the same time, there is an ongoing and significant need for new approaches which have the potential to change the natural history of these disorders. This review will focus on the risk factors associated with the development of MPN in blast phase (MPN-BP) including clinical and molecular risk factors, current treatment strategies, and emerging investigational approaches.
    No preview · Article · Apr 2015 · Current Hematologic Malignancy Reports
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    ABSTRACT: At present, allo-SCT is the only curative treatment for patients with myelofibrosis (MF). Unfortunately, a significant proportion of candidate patients are considered transplant ineligible due to their poor general condition and advanced age at the time of diagnosis. The approval of the first JAK inhibitor, ruxolitinib, for patients with advanced MF in 2011 has had a qualified impact on the treatment algorithm. The drug affords substantial improvement in MF-associated symptoms and splenomegaly but no major effect on the natural history. There has, therefore, been considerable support for assessing the drug's candidacy in the peritransplant period. The drug's precise impact on clinical outcome following allo-SCT is currently not known; nor are the drug's long-term efficacy and safety known. Considering the rarity of MF and the small proportion of patients who undergo allo-SCT, well designed collaborative efforts are required. In order to address some of the principal challenges, an expert panel of laboratory and clinical experts in this field was established, and an independent workshop held during the 54th American Society of Hematology Annual Meeting in New Orleans, USA on 6 December 2013, and the European Hematology Association's Annual Meeting in Milan, Italy on 13 June 2014. This document summarizes the results of these efforts.Bone Marrow Transplantation advance online publication, 9 February 2015; doi:10.1038/bmt.2014.323.
    No preview · Article · Feb 2015 · Bone Marrow Transplantation
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    ABSTRACT: Background We hypothesized that targeting two mechanisms of epigenetic silencing would be additive or synergistic with regard to expression of specific target genes. The primary objective of the study was to establish the maximum tolerated dose (MTD) of belinostat in combination with a fixed dose of azacitidine (AZA). Methods In Part A of the study, patients received a fixed dose of AZA, with escalating doses of belinostat given on the same days 1–5, in a 28 day cycle. Part B was designed to evaluate the relative contribution of belinostat to the combination based on analysis of pharmacodynamic markers, and incorporated a design in which patients were randomized during cycle 1 to AZA alone, or the combination, at the maximally tolerated dose of belinostat. Results 56 patients with myeloid neoplasia were enrolled. Dose escalation was feasible in part A, up to 1000 mg/m2 dose level of belinostat. In Part B, 18 patients were assessable for quantitative analysis of specific target genes. At day 5 of therapy, MDR1 was significantly up-regulated in the belinostat/AZA arm compared with AZA alone arm (p = 0.0023). There were 18 responses among the 56 patients. Conclusions The combination of belinostat and AZA is feasible and associated with clinical activity. The recommended phase II dose is 1000 mg/m2 of belinostat plus 75 mg/m2 of AZA on days 1–5, every 28 days. Upregulation in MDR1 was observed in the combination arm at day 5 compared with the AZA alone arm, suggesting a relative biologic contribution of belinostat to the combination.
    No preview · Article · Dec 2014 · Investigational New Drugs
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    A Yacoub · O Odenike · S Verstovsek
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    ABSTRACT: Considerable clinical experience regarding the long-term efficacy and safety of ruxolitinib has been gathered since the drug was approved in the USA for patients with intermediate or high-risk myelofibrosis (MF) in November 2011. Findings from the pivotal phase 3 COMFORT studies showed that ruxolitinib-associated reductions in MF-related splenomegaly and symptom burden occur rapidly and in the majority of patients. Two- and 3-year follow-up data further suggest that the benefits of ruxolitinib are durable and associated with a survival advantage compared with conventional therapies. However, careful management of treatment-related thrombocytopenia and anemia with dose modifications and supportive care is critical to allow chronic therapy. Based on preliminary evidence, ruxolitinib also allows spleen size and symptom reduction before allogeneic stem cell transplantation without negative effect on engraftment or outcomes. In recent studies, ruxolitinib provided effective management of hematologic parameters and symptoms in patients with polycythemia vera refractory to or intolerant of hydroxyurea.
    Preview · Article · Aug 2014 · Current Hematologic Malignancy Reports
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    ABSTRACT: Allogeneic hematopoietic cell transplantation is increasingly utilized in older adults. This study prospectively evaluated the prognostic utility of geriatric assessment domains prior to allogeneic transplantation in recipients 50 years and older. Geriatric assessment was performed prior to transplant, and included validated measures across domains of function and disability, comorbidity, frailty, mental health, nutritional status, and systemic inflammation. 203 patients completed geriatric assessment and underwent transplant. The median age was 58 years (range, 50-73). After adjusting for established prognostic factors, limitations in instrumental activities of daily living (HR 2.38, 95% CI 1.59-3.56; P < .001), slow walk speed (HR 1.80, 95% CI 1.14-2.83; P = .01), high comorbidity by hematopoietic cell transplantation-specific comorbidity index (HR 1.56, 95% CI 1.07-2.28; P = .02), low mental health by short-form-36 mental component summary (HR 1.67, 95% CI 1.13-2.48; P = .01), and elevated serum C-reactive protein (HR 2.51, 95% CI 1.54-4.09; P < .001) were significantly associated with inferior overall survival. These associations were more pronounced in the cohort 60 years and older. Geriatric assessment measures confer independent prognostic utility in older allogeneic transplant recipients. Implementation of geriatric assessment prior to allogeneic transplantation may aid in appropriate selection of older adults.
    Full-text · Article · May 2014 · Haematologica
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    ABSTRACT: Myeloid neoplasms and eosinophilia with rearrangements of PDGFRB are uncommon Philadelphia negative myeloproliferative neoplasms. Patients are typically male, with morphologic features of a Ph- chronic myeloproliferative syndrome or chronic myelomonocytic leukemia with eosinophilia. Reciprocal translocations involving PDGFRB result in fusion genes with constitutively activated receptor tyrosine kinase sensitive to inhibition with imatinib. We present an updated and expanded analysis of a cohort of 26 such patients treated with imatinib. After a median follow-up of 10.2 (range 1.8 - 17) years, the 10-year overall survival rate was 90% (95%CI 64-97%); after median imatinib duration of 6.6 (range 0.1 - 12) years the 6-year progression-free survival rate was 88% (95% CI; 65-96%). 96% patients responded; no patients who achieved a complete cytogenetic (n=13) or molecular (n=8) remission lost their response or progressed to blast crisis. Imatinib is well tolerated and achieves excellent long-term responses in patients with PDGFRB rearrangements.
    Full-text · Article · Mar 2014 · Blood
  • Olatoyosi Odenike
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    ABSTRACT: Myelofibrosis (MF), including primary MF, postpolycythemia vera MF, and postessential thrombocythemia MF, is a clonal stem cell disorder characterized by BM fibrosis, extramedullary hematopoiesis, and a variable propensity to transform into acute leukemia. Allogeneic stem cell transplantation is the only known cure for MF, but its applicability is limited by the advanced age of most patients and by comorbid conditions. In the past decade, there has been an explosion of information on the molecular-genetic features associated with these diseases, fueled recently by the discovery of the JAK2V617F mutation. The development of JAK inhibitors has represented a significant therapeutic advance for these diseases; however, their use in MF has not yet been associated with eradication or a significant suppression of the malignant clone. In this era, much remains to be understood about MF, but it is likely that the identification of key pathogenetic drivers of the disease, coupled with the availability of novel molecularly targeted agents, will result in the discovery of new agents that significantly alter the natural history of the disease. This review focuses on recent and ongoing efforts in the development of novel agents in MF that go beyond the field of JAK inhibitors.
    No preview · Article · Dec 2013 · Hematology
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    ABSTRACT: The clinical relevance of targeting RAS/RAF/MEK/ERK pathway, activated in 70-80% of acute myeloid leukemia (AML) patients, is unknown. Selumetinib is an oral small molecule inhibitor of MEK1/2 kinase. Forty-seven patients with relapsed/refractory AML or ≥60 years old with untreated AML were enrolled on a phase II study. Patients were stratified by FLT3 ITD mutation status. The primary endpoint was response rate (complete, partial and minor). Leukemia cells were analyzed for ERK and mTOR phosphorylation. Common drug-related toxicities were grade I-II diarrhea, fatigue, nausea, vomiting and skin rash. In the FLT3 wild type cohort, 6/36 (17%) patients had a response [1 partial response, 3 minor responses, 2 unconfirmed minor responses (uMR)]. No patient with FLT3 ITD responded. NRAS and KRAS mutations were detected in 7% and 2% patients, respectively. The sole patient with KRAS mutation had uMR with hematologic improvement in platelets. Baseline p-ERK activation was observed in 85% of patients analyzed but did not correlate with a response. A single nucleotide polymorphism (SNP) rs3733542 in exon 18 of KIT gene was detected in significantly higher number of patients with response/stable disease compared with non-responders (60% vs 23%; p=0.027). Selumetinib is associated with modest single agent antileukemic activity in advanced AML. However, given its favorable toxicity profile, combination with drugs that target other signaling pathways in AML should be considered. The potential association of SNP rs3733542 in exon 18 of KIT gene with antileukemic activity of selumetinib is intriguing, but will require validation in larger trials.
    No preview · Article · Oct 2013 · Clinical Cancer Research
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    ABSTRACT: Ruxolitinib, a Janus kinase 1 and 2 inhibitor, demonstrated improvements in spleen volume, symptoms, and survival over placebo and best available therapy in intermediate-2 or high-risk myelofibrosis patients with baseline platelet counts ≥100 ×109/L in phase III studies. The most common adverse events were dose-dependent anemia and thrombocytopenia, which were anticipated because thrombopoietin and erythropoietin signal through JAK2. These events were manageable, rarely leading to treatment discontinuation. Because approximately one-quarter of MF patients have platelet counts <100 ×109/L consequent to their disease, ruxolitinib was evaluated in this subset of patients using lower initial doses. Interim results of a phase II study of ruxolitinib in myelofibrosis patients with baseline platelet counts of 50-100 ×109/L are reported. Ruxolitinib was initiated at a dose of 5 mg twice daily (BID), and doses could be increased by 5 mg once daily every 4 weeks to 10 mg BID if platelet counts remained adequate. Additional dosage increases required evidence of suboptimal efficacy. Assessments included measurement of spleen volume by MRI, MF symptoms by MF Symptom Assessment Form v2.0 Total Symptom Score [TSS]), Patient Global Impression of Change (PGIC); EORTC QLQ-C30, and safety/tolerability. By week 24, 62% of patients achieved stable doses ≥ 10 mg BID. Median reductions in spleen volume and TSS were 24.2% and 43.8%, respectively. Thrombocytopenia necessitating dose reductions and dose interruptions occurred in 12 and 8 patients, respectively, and occurred mainly in patients with baseline platelet counts ≤75 ×109/L. Seven patients experienced platelet count increases ≥15 ×109/L. Mean hemoglobin levels remained stable over the treatment period. Two patients discontinued for adverse events: 1 for grade 4 retroperitoneal hemorrhage secondary to multiple and suspected pre-existing renal artery aneurysms and 1 for grade 4 thrombocytopenia. Results suggest that a low starting dose of ruxolitinib with escalation to 10 mg BID may be appropriate in myelofibrosis patients with low platelet counts.
    Preview · Article · Oct 2013 · Journal of Hematology & Oncology
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    ABSTRACT: Patients with relapsed/refractory leukemias or advanced myelodysplastic syndrome (MDS) fare poorly following allogeneic hematopoietic cell transplant (HCT). We report prospective phase II study results of 29 patients given clofarabine 30 mg/m(2)/day i.v. × 5 days followed immediately by HCT conditioning while at the cytopenic nadir. A total of 15/29 patients (52%) were cytoreduced according to pre-defined criteria (cellularity <20% and blasts <10%). Marrow cellularity (P<0.0001) and blast% (P=0.03) were reduced. Toxicities were acceptable, with transient hyperbilirubinemia (48%) and gr3-4 infections (10%). In all, 28/29 proceeded to transplant; 27 received ATG or alemtuzumab. Post HCT, 180 day non-relapse mortality (NRM) was 7% (95% confidence interval (CI): 1-21), relapse was 29% (95% CI: 13-46) and OS was 71% (95% CI: 51-85), comparing favorably to published data for high-risk patients. Two-year graft vs host disease incidence was 40% (95% CI: 21-58) and 2 year OS was 31% (95% CI: 14-48). Disease at the nadir correlated with inferior OS after HCT (HR=1.22 for each 10% marrow blasts, 95% CI: 1.02-1.46). For AML/MDS patients, there was a suggestion that successful cytoreduction increased PFS (330 vs 171 days, P=0.3) and OS (375 vs 195 days, P=0.31). Clofarabine used as a bridge to HCT reduces disease burden, is well tolerated, and permits high-risk patients to undergo HCT with acceptable NRM. Late relapses are common; thus, additional strategies should be pursued. NCT-00724009.Bone Marrow Transplantation advance online publication, 17 June 2013; doi:10.1038/bmt.2013.79.
    Full-text · Article · Jun 2013 · Bone marrow transplantation
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    ABSTRACT: Background: Angiogenesis is implicated in the pathophysiology and progression of myelodysplastic syndromes (MDS). Vatalanib (PTK787/ZK222584; Novartis and Schering AG) inhibits receptor tyrosine kinases of vascular endothelial growth factor, platelet derived growth factor and c-Kit. We examined whether vatalanib induces hematological responses in MDS and/or delays progression to acute myeloid leukemia (AML) or death. Methods: Two cohorts were studied. Vatalanib 1250 mg orally was given once daily (cohort 1) or 750-1250 mg once daily in an intra-patient dose escalating schedule (cohort 2) in 28-day cycles to 155 patients with MDS; 142 patients were evaluable for response and 153 for toxicity. Results: The median age was 70.5 years; 51 % had low risk (International Prognostic Scoring System {IPSS} Low/Intermediate-1) and 32 % had high risk (IPSS Intermediate-2/High) MDS. Hematological improvement was achieved in 7/142 (5 %) patients; all 7 were among the 47 patients able to remain on vatalanib for at least 3 months (hematological improvement achieved in 15 % of these 47 patients). For patients with low risk and high risk MDS, respectively, median progression-free survivals were 15 and 6 months, median times to transformation to AML were 28 and 6 months, and median overall survivals were 36 and 10 months. The most frequent non-hematological adverse events grade ≥ 2 were fatigue, nausea or vomiting, dizziness, anorexia, ataxia, diarrhea, and pain. Two deaths (one intra-cerebral hemorrhage and one sudden death) were possibly related to vatalanib. Conclusions: Vatalanib induces improvement in blood counts in a small proportion of MDS patients. Clinical applicability is limited by side effects.
    No preview · Article · May 2013 · Investigational New Drugs
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    ABSTRACT: Summary The natural history and prognosis for young patients with polycythemia vera (PV) in the post-JAK2 V617F era is not well defined; therefore, we retrospectively analyzed disease characteristics and clinical outcomes in 120 patients ≤45 years and 84 patients ≥65 years at diagnosis. Despite lower white blood counts (9.2 vs. 13.4 x 10(9)/L, p=0.004) and a lower JAK2 V617F allele burden (51% vs. 66%, p=0.015), younger PV patients had comparable rates of vascular complications compared to older patients (27% vs. 31%, p=0.64). However, splanchnic vein thrombosis occurred more frequently in younger patients (13% vs. 2%, p=0.0056). Myelofibrotic and leukemic transformation, the most serious complications of myeloproliferative neoplasms (MPN), occurred with similar frequencies in young vs. older patients (15% vs. 10%, p=0.29). Prevention or delay of these complications is currently the most urgent challenge in the care of younger patients with PV.
    No preview · Article · Dec 2012 · Leukemia & lymphoma

  • No preview · Article · Dec 2012 · Chest

Publication Stats

1k Citations
456.73 Total Impact Points

Institutions

  • 2004-2015
    • University of Chicago
      • • Department of Medicine
      • • Section of Hematology/Oncology
      Chicago, Illinois, United States
  • 2008-2010
    • The University of Chicago Medical Center
      • • Department of Medicine
      • • Section of Hematology/Oncology
      Chicago, Illinois, United States
  • 2005
    • Duke University
      Durham, North Carolina, United States