Posted by rob on September 30, 2009 under Uncategorized | 
Autophagy is an important event for megakaryocytic differentiation of the chronic myelogenous leukemia K562 cell line.
Autophagy. 2009 Nov 24;5(8)
Authors: Colosetti P, Puissant A, Robert G, Luciano F, Jacquel A, Gounon P, Cassuto JP, Auberger P
Autophagy is a highly conserved catabolic process for the elimination and recycling of organelles and macromolecules, characterized by the formation of double-membrane vesicles called autophagosomes. To date, the function of autophagy in cell differentiation is poorly documented. Here, we investigated the possibility that megakaryocytic differentiation of the Chronic Myelogenous Leukemia (CML) cell line K562, a process known to be accompanied by accumulation of vacuoles inside the cells, might involve autophagy. Using various complementary approaches, we show that the combination of the phorbol ester PMA and the p38(MAPK) inhibitor SB202190 (SB), which engaged a majority of K562 cells towards the megakaryocytic lineage, also triggered vacuolization and autophagy. The combination of PMA + SB appears to induce both increase in autophagic fluxes and an autophagic degradation blockage. Induction of autophagy was accompanied also by increased expression of Beclin 1 and p62/SQSTM1 and was found to precede the onset of megakaryocytic differentiation. Moreover, knockdown of LC3 and Beclin 1 by specific siRNAs impaired PMA + SB-mediated vacuolization, LC3-II accumulation and megakaryocytic differentiation, as well. To the best of our knowledge, this is the first description that induction of autophagy is involved in megakaryocytic differentiation of K562 CML cells.
PMID: 19786835 [PubMed - as supplied by publisher]
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Impact of Antifungal Prophylaxis on Colonization and Azole Susceptibility of Candida species.
Antimicrob Agents Chemother. 2009 Sep 28;
Authors: Mann PA, McNicholas PM, Chau AS, Patel R, Mendrick C, Ullmann AJ, Cornely OA, Patino H, Black TA
Two large studies compared posaconazole vs. fluconazole or itraconazole for prophylaxis in subjects undergoing allogeneic hematopoietic stem cell transplantation or with acute myelogenous leukemia. To assess the impact of prophylaxis on colonization and development of resistance in yeasts, identification and susceptibility testing were performed on yeasts cultured at regular intervals from mouth/throat/stool samples. Prior to therapy 34-50% of subjects were colonized with yeasts. For all three drugs, the number of positive Candida albicans cultures decreased during drug therapy. In contrast, the proportion of subjects with positive C. glabrata cultures increased by two- and four-fold in the posaconazole and itraconazole arms, respectively. Likewise, in the fluconazole arm the proportion of subjects with positive C. krusei cultures increased two-fold. C. glabrata was the species that most frequently exhibited decreases in susceptibility and this trend did not differ significantly between the prophylactic regimens. For the subset of subjects with colonizing C. glabrata isolated at baseline and end of treatment approximately, 40% of isolates exhibited a >four-fold increase in MIC while on therapy. Molecular typing of C. albicans and C. glabrata isolates confirmed that the majority of the baseline and end of treatment isolates were closely related to suggesting that they were persistent colonizers and not newly acquired. Overall breakthrough infections by Candida species were very rare ( approximately 1%) and C. glabrata was the colonizing species most frequently associated with breakthrough infections.
PMID: 19786600 [PubMed - as supplied by publisher]
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Hematopoietic Stem Cell Origin of Human Fibroblasts: Cell Culture Studies of Female Recipients of Gender Mismatch Stem Cell Transplantation and Patients with Chronic Myelogenous Leukemia.
Exp Hematol. 2009 Sep 25;
Authors: Shirai K, Sera Y, Bulkeley W, Mehrotra M, Moussa O, Larue AC, Watson DK, Stuart RK, Lazarchick J, Ogawa M
OBJECTIVES: Our series of studies using transplantation of single hematopoietic stem cells (HSCs) demonstrated that mouse fibroblasts/myofibroblasts are derived from HSCs. In order to determine the origin of human fibroblasts, we established a method for culturing fibroblasts from human peripheral blood (PB) mononuclear cells and studied fibroblasts from gender mismatch HSC transplant recipients and patients with untreated Philadelphia chromosome-positive chronic myelogenous leukemia (CML). METHODS: We cultured PB cells from three female subjects who showed near complete hematopoietic reconstitution from transplantation of granulocyte-colony stimulating factor (G-CSF)-mobilized male PB cells and examined the resulting fibroblasts using fluorescent in situ hybridization (FISH) for Y chromosome. Because the mobilized PB cells may contain mesenchymal stem cells (MSCs), we could not determine the HSC or MSC origin of the fibroblasts seen in culture. To further document the HSC origin of human fibroblasts, we next examined fibroblasts from two patients with untreated CML, a known clonal disorder of HSCs. RESULTS: All cultured fibroblasts from female recipients of male cells showed the presence of Y-chromosome, indicating the donor origin of fibroblasts. Cultured fibroblasts from the CML patients revealed the presence of BCR-ABL translocation. This demonstration provided strong evidence for the HSC origin of human fibroblasts, because CML is a clonal disorder of the HSC. CONCLUSIONS: These studies strongly suggest that human fibroblasts are derived from HSCs. In addition, the results suggest that fibrosis seen in patients with CML may be a part of the clonal process.
PMID: 19786066 [PubMed - as supplied by publisher]
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A new technique to remove a “stuck” totally implantable venous access catheter.
J Pediatr Surg. 2009 Jul;44(7):1465-7
Authors: Huang SC, Tsai MS, Lai HS
Removal of a totally implantable venous access device (port) is usually a simple procedure; however, if a catheter has been in place for a very long period, it may adhere firmly to the vessel wall. We report a new technique to facilitate removal of a stuck catheter. A 16-year-old girl was admitted for removal of her port, which had been inserted for chemotherapy 11 years earlier. After her disease was controlled, the catheter could not be pulled out during surgery. To remove the catheter, we inserted a guidewire to straighten the catheter and then applied a “push-in” force to detach the adherence from the central vein. The catheter was then removed successfully. We believe that this is a new and simple method for removing a “stuck” catheter.
PMID: 19573682 [PubMed - indexed for MEDLINE]
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Chronic myeloid leukemia (CML) with P190 BCR-ABL: analysis of characteristics, outcomes, and prognostic significance.
Blood. 2009 Sep 10;114(11):2232-5
Authors: Verma D, Kantarjian HM, Jones D, Luthra R, Borthakur G, Verstovsek S, Rios MB, Cortes J
The most common BCR-ABL transcripts in chronic myeloid leukemia (CML) are e13a2(b2a2) and e14a2(b3a2). Other transcripts such as e1a2 are rare and their outcome with tyrosine kinase inhibitors (TKI) therapy is undefined. We analyzed 1292 CML patients and identified 14 with only e1a2 transcripts, 9 in chronic phase (CP), 1 in accelerated phase (AP), and 4 in blast phase (BP). Of the CP, 4 achieved complete hematologic response (CHR); 2, complete cytogenetic response (CCyR); 2, partial cytogenetic response (PCyR), and 1 did not respond to imatinib. Five patients progressed to myeloid BP (3), lymphoid BP (1), or AP (1). The AP patient received various TKIs sequentially and achieved only CHR. BP patients received hyper-CVAD (hyperfractionated cyclophosphamide, vincristine, adriamycin, dexamethasone) plus imatinib/dasatinib or idarubicin plus cytarabine (Ara-C); 2 did not respond, 1 had CCyR, and 1 short-lasting complete molecular response (CMR). Overall, cytogenetic responses lasted 3 to 18 months; only 2 achieved major molecular response (MMR) on TKI. P190(BCR-ABL) CML is rare and is associated with an inferior outcome to therapy with TKI. These patients need to be identified as high-risk patients.
PMID: 19531657 [PubMed - indexed for MEDLINE]
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Posted by rob on September 29, 2009 under Uncategorized |
Arsenic trioxide downregulates the expression of annexin II in bone marrow cells from patients with acute myelogenous leukemia.
Chin Med J (Engl). 2009 Sep 5;122(17):1969-73
Authors: Zhang XH, Hu Y, Bao L, Jiang Q, Yang LH, Lu XJ, Hong M, Xia LH, Guo T, Shen GX, Zhu HH, Zhao T, Song SJ
BACKGROUND: Most patients with acute myelogenous leukemia (AML) suffer from disordered hemostasis. We have previously shown that annexin II (Ann II), a high-affinity co-receptor for plasminogen/tissue plasminogen activator, plays a central role in primary hyperfibrinolysis in patients with acute promyelocytic leukemia (APL). The expression of Ann II in cells from patients with major subtypes of AML and the effect of arsenic trioxide (As2O3) on Ann II expression in AML cells were investigated to determine whether As2O3-mediated downregulation of Ann II could restore hemostatic stability. METHODS: A total of 103 patients (48 females and 55 males; age, 19 – 58 years) were included. Plasma samples were collected before and after treatment as well as after complete remission. Ann II and plasminogen activation were measured in leukemic cells during treatment with 1 micromol/L As2O3. RESULTS: Before As2O3 treatment, Ann II mRNA expression (real-time PCR) was the highest in M3 cells (P < 0.05), higher in M5 cells than that in M1, M2, M4, and M6 cells (P < 0.001), and positively correlated with Ann II protein expression (flow cytometry) (r = 0.752, P < 0.01). Exposure for up to 120 hours to As2O3 (1 micromol/L) had no significant effect on Ann II protein in M1 and M2 leukemic cells, but decreased Ann II protein expression twofold within 48 hours of exposure in M3 cells (P < 0.05) and twofold within 96 hours in M5 cells (P < 0.05). The rate of plasmin generation was higher in APL, M5, and M4 cells than in M1, M2, and M6 cells. CONCLUSIONS: As2O3 may reduce hyperfibrinolysis in AML by downregulation of Ann II. Furthermore, As2O3 affects more than one form of AML (APL, M4 and M5), suggesting its potential role in their management.
PMID: 19781379 [PubMed - in process]
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Neratinib: an oral, irreversible dual EGFR/HER2 inhibitor for breast and non-small cell lung cancer.
Expert Opin Investig Drugs. 2009 Sep 28;
Authors: Bose P, Ozer H
Background: The revolutionary success of imatinib, a specific inhibitor of the BCR-ABL tyrosine kinase (TK) in the treatment of chronic myelogenous leukemia ushered in the era of targeted therapies in cancer. The erythroblastic leukemia viral oncogene homolog family of receptor TKs, to which EGFR (HER1) and human epidermal growth factor receptor 2 (HER2)/neu TKs belong, has been implicated in a variety of cancers, and several agents that inhibit these TKs are in clinical use, with many more in various stages of development. Objectives: To summarize current knowledge about neratinib (HKI-272), an oral, irreversible dual inhibitor of EGFR and HER2 and to define its future clinical role, especially in the context of related agents that are either available or in the pipeline. Methods: A Medline search using Pubmed was conducted using the keywords neratinib, HKI-272, EGFR, HER2, lapatinib, trastuzumab, erlotinib, gefitinib, cetuximab and panitumumab. Relevant abstracts presented at the American Society of Clinical Oncology and San Antonio Breast Cancer Symposium meetings were also reviewed. Conclusions: Both preclinical and human studies have shown that neratinib has promising activity in both advanced breast cancer and NSCLC with an acceptable safety profile. The data support its continued clinical development.
PMID: 19780706 [PubMed - as supplied by publisher]
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Clinical relevance of a pharmacogenetic approach using multiple candidate genes to predict response and resistance to imatinib therapy in chronic myeloid leukemia.
Clin Cancer Res. 2009 Jul 15;15(14):4750-8
Authors: Kim DH, Sriharsha L, Xu W, Kamel-Reid S, Liu X, Siminovitch K, Messner HA, Lipton JH
PURPOSE: Imatinib resistance is major cause of imatinib mesylate (IM) treatment failure in chronic myeloid leukemia (CML) patients. Several cellular and genetic mechanisms of imatinib resistance have been proposed, including amplification and overexpression of the BCR/ABL gene, the tyrosine kinase domain point mutations, and MDR1 gene overexpression. EXPERIMENTAL DESIGN: We investigated the impact of 16 single nucleotide polymorphisms (SNP) in five genes potentially associated with pharmacogenetics of IM, namely ABCB1, multidrug resistance 1; ABCG2, breast-cancer resistance protein; CYP3A5, cytochrome P450-3A5; SLC22A1, human organic cation transporter 1; and AGP, alpha1-acid glycoprotein. The DNAs from peripheral blood samples in 229 patients were genotyped. RESULTS: The GG genotype in ABCG2 (rs2231137), AA genotype in CYP3A5 (rs776746), and advanced stage were significantly associated with poor response to IM especially for major or complete cytogenetic response, whereas the GG genotype at SLC22A1 (rs683369) and advanced stage correlated with high rate of loss of response or treatment failure to IM therapy. CONCLUSIONS: We showed that the treatment outcomes of imatinib therapy could be predicted using a novel, multiple candidate gene approach based on the pharmacogenetics of IM.
PMID: 19584153 [PubMed - indexed for MEDLINE]
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Partially matched related donor transplantation can achieve outcomes comparable with unrelated donor transplantation for patients with hematologic malignancies.
Clin Cancer Res. 2009 Jul 15;15(14):4777-83
Authors: Xiao-Jun H, Lan-Ping X, Kai-Yan L, Dai-Hong L, Yu W, Huan C, Yu-Hong C, Wei H, Jing-Zhi W, Yao C, Xiao-Hui Z, Hong-Xia S, Feng-Rong W, Fei-Fei T
PURPOSE: The study aimed to compare the outcomes of patients undergoing hematopoietic stem cell transplantation (HSCT) from partially matched related donors (PMRD) and unrelated donors (URD) for hematologic malignancies without the use of in vitro T cell depletion. EXPERIMENTAL DESIGN: HSCT was done on 297 consecutive patients from URDs (n = 78) and PMRDs (n = 219) during the same time period. Incidences of graft-versus-host disease (GVHD), relapse, nonrelapse mortality, overall survival, and leukemia-free survival between the PMRD and URD groups were compared. RESULTS: All patients achieved full engraftment. The cumct65ulative incidences of grades II to IV acute GVHD in the PMRD and URD cohorts were 47% [95% confidence interval (95% CI), 33-62%] versus 31% (CI, 20-42%; P = 0.033), with a relative risk of 1.72 (95% CI, 1.01-2.94; P = 0.046). The incidence of chronic GVHD did not differ significantly between the two cohorts (P = 0.17). The 2-year incidences of nonrelapse mortality and relapse were 20% (CI, 15-26%) versus 18% (CI, 10-27%), with P = 0.98, and 12% (CI, 8-16%) versus 18% (CI, 10-27%), with P = 0.12, for the PMRD versus the URD cohort, respectively. The 4-year overall survival and leukemia-free survival were 74% (CI, 67-80%) versus 74% (CI, 62-85%), with P = 0.98, and 67% (CI, 59-75%) versus 61% (CI, 47-74%), with P = 0.74, respectively. CONCLUSIONS: Our comparisons show that every major end point, including relapse, nonrelapse mortality, overall survival, and leukemia-free survival, was comparable between the PMRD and the URD groups.
PMID: 19584148 [PubMed - indexed for MEDLINE]
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Deletion of the der(9q) in chronic myeloid leukemia: the controversy continues.
Leuk Lymphoma. 2009 Jun;50(6):871-2
Authors: Godley LA
PMID: 19479615 [PubMed - indexed for MEDLINE]
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Previous best responses can be re-achieved by resumption after imatinib discontinuation in patients with chronic myeloid leukemia: implication for intermittent imatinib therapy.
Leuk Lymphoma. 2009 Jun;50(6):944-51
Authors: Goh HG, Kim YJ, Kim DW, Kim HJ, Kim SH, Jang SE, Lee J, Kim D, Kim WS, Park SH, Kweon IY
Although imatinib is considered as a front line therapy in patients with chronic myeloid leukemia (CML), it is still unclear whether transient imatinib discontinuation may adversely affect the outcome. This study was conducted to investigate long-term outcome after discontinuation and resumption of imatinib, and to determine whether intermittent imatinib therapy can be employed in patients with CML. Twenty six Philadelphia chromosome positive (Ph+) patients with CML discontinued imatinib when they achieved complete cytogenetic response (CCyR) or complete molecular response (CMR), and they were retreated with imatinib in case of hematologic, cytogenetic or molecular relapse. Except one patient who progressed and two patients who are in persistent molecular remission without imatinib resumption, all of 23 patients are maintaining the best response achieved after imatinib resumption with a median follow-up of 44 months. This study shows that although imatinib cannot be discontinued completely, intermittent therapy can be considered for the treatment of patients with CML in particular situations.
PMID: 19479613 [PubMed - indexed for MEDLINE]
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Karyotype changes during long-term targeted therapy of chronic myeloid leukemia with imatinib.
Leuk Lymphoma. 2009 Jun;50(6):952-65
Authors: Pieńkowska-Grela B, Rygier J, Woroniecka R, Grygalewicz B, Pastwińska A, Krawczyk P, Ceglerek B, Seferyńska I, Sikorska A, Konopka L
The main risk factors during imatinib therapy of chronic myeloid leukemia are still subject to discussion. A group of 39 patients was cytogenetically examined and monitored before and during long-term treatment with imatinib. The cytogenetic response was investigated using karyotype analysis and fluorescence in situ hybridisation method. Different therapy effects were shown for three subgroups distinguished before the start of treatment: patients with the sole translocation t(9;22) with a typical pattern of BCR/ABL fusion vs. patients with submicroscopic deletion in the fusion region ABL/BCR of the sole t(9;22) vs. patients with aberrations additional to t(9;22) and without submicroscopic deletion. Of the two group with sole t(9;22) the group with deletion in the ABL/BCL region suffered a poorer treatment outcome than the group without deletion. The risk of progression of cytogenetic changes in group with deletion was more than nine times higher than in patients with sole t(9;22) without deletion (statistically significant).
PMID: 19479611 [PubMed - indexed for MEDLINE]
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Discontinuing imatinib in chronic myeloid leukemia: don’t try this at home.
Leuk Lymphoma. 2009 Jun;50(6):868-70
Authors: Mattison R, Larson RA
PMID: 19455466 [PubMed - indexed for MEDLINE]
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Posted by rob on September 28, 2009 under Uncategorized |
We report outcomes of 932 recipients of unrelated donor peripheral blood stem cell hematopoietic cell transplantation (URD-PBSC HCT) for acute myeloid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome enrolled on a prospective National Marrow Donor Program trial from 1999 through 2003. Preparative regimens included myeloablative (MA; N = 611), reduced-intensity (RI; N = 160), and nonmyeloablative (NMA; N = 161). For MA recipients, CD34+ counts greater than 3.8 x 106/kg improved neutrophil and platelet engraftment, whereas improved overall survival (OS) and reduced transplant-related mortality (TRM) were seen for all preparative regimens when CD34+ cell doses exceeded 4.5 x 106/kg. Higher infused doses of CD34+ cell dose did not result in inc…
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Role of Hematopoietic Stem Cell Transplantation in Acute Myelogenous Leukemia and Myelodysplastic Syndrome.
Cancer Treat Res. 2009;144:1-25
Authors: Tallman MS, Mathews V, Dipersio JF
PMID: 19779880 [PubMed - as supplied by publisher]
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[Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line.]
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009 Sep;34(9):886-91
Authors: Tang X, Long C, Wang C, Xiao G
Objective To determine the expression of DLK1 gene in acute leukemias (AL) and its function in erythroid differentiation of K562 cells. Methods We detected the expression of DLK1 gene in 65 different acute leukemia categories (a test group) and 34 normal bone marrow controls (a control group) with RT-PCR. DLK1 protein in 20 out of the 65 AL patients and 13 of the 34 controls was assayed by Western blot. The K562 cell line was induced to erythroid differentiation by hemin. We observed the relationship between its expression and erythroid differentiation.Results Both leukemia cells and normal marrow cells expressed DLK1. The expression of DLK1mRNA in patients in the test group was higher than that in the control group (P=0.018), while there was no significance between acute lymphoblastic leukemia and acute myelogenous leukemia (P>0.05).The expression of DLK1 mRNA in the test group at onset had no relation with the WBC and platelet count in the total peripheral blood, and the same was true for blast cell rates in bone marrow cells.The level of DLK1 protein in the test group was higher than that in the control group, which was consistent with the mRNA expression (P=0.042). The expression of DLK1 mRNA decreased gradually with K562 cells towards hemin-induced erythroid differentiation.Conclusion DLK1 gene may be involved in leukemia,but the mRNA level of DLK1 has no relation with some clinical characteristics of AL patients at onset. DLK1 may inhibit the erythroid differentiation of K562 cells.
PMID: 19779261 [PubMed - in process]
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Nonmyeloablative Allogeneic Stem Cell Transplantation for Chronic Myelogenous Leukemia in the Imatinib Era.
Clin Lymphoma Myeloma. 2009 Sep 1;9:S261-S265
Authors: Champlin R, Lima MD, Kebriaei P, Rondon G, Fisher T, Jabbour E, Cortés JE, Kantarjian H, Anderlini P, Alousi A, Hosing C, Shpall E, Popat U, Qazilbash M, Andersson B, Giralt S
Allogeneic stem cell transplantation (ASCT) is a potentially curative treatment for patients with chronic myelogenous leukemia (CML) and was previously considered the preferred treatment for newly diagnosed CML. The success of imatinib has changed treatment recommendations, and allogeneic transplants are now reserved for imatinib treatment failures. Previous imatinib treatment does not compromise the results of ASCT, but patients with overt transformed disease have poor results. It is unclear whether patients whose disease is considered to have failed imatinib should be referred immediately for ASCT or receive treatment with a second-generation tyrosine kinase inhibitors (TKI). Patients whose disease fails 2 TKIs should receive ASCT if possible. Nonmyeloablative preparative regimens reduce the toxicity and treatment-related mortality associated with the transplantation procedure and allow transplantations to be performed in older and medically infirm patients. This approach, including posttransplantation treatment with TKIs and donor lymphocyte infusion, produces a high fraction of durable molecular complete remissions.
PMID: 19778850 [PubMed - as supplied by publisher]
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Molecular cytogenetic characterization of variant Philadelphia translocations in chronic myeloid leukemia: genesis and deletion of derivative chromosome 9.
Cancer Genet Cytogenet. 2009 Oct;194(1):30-7
Authors: Bennour A, Sennana H, Laatiri MA, Elloumi M, Khelif A, Saad A
The mechanisms for the formation of variant Philadelphia (Ph) translocations that occur in 5-10% of patients with chronic myeloid leukemia (CML) are not fully characterized. Studies on the prognosis of these variant translocations have yielded conflicting results, especially regarding imatinib outcome and the status of deletions on the derivative chromosome 9. To shed light on these controversial subjects, we sought to analyze all variant translocation cases presented at diagnosis and identified in our institution between the years 2001 and 2008. Of 336 CML patients who presented at diagnosis and were studied by conventional cytogenetics and fluorescence in situ hybridization (FISH), 25 patients (7.44%) exhibited variant Ph-rearrangements. All chromosomes could be implicated in variant Ph rearrangements, with 32 breakpoints defined. Their distribution was located preferentially in the CG-richest regions of the genome. Deletions on der(9) were observed in 15 of the 25 cases (60%), a greater proportion in typical Ph translocations (12-15%). Both one- and two-step mechanisms were encountered in our series, as well as multiple-step mechanisms, which originate more complex rearrangements. Higher prevalence was observed for the two-step mechanism (56%). Proper assessment of the prognostic significance of variant translocations requires better categorization of these translocations based on their mechanisms of genesis and 9q34 deletion status.
PMID: 19737651 [PubMed - indexed for MEDLINE]
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Asymptomatic eosinophilic colitis in a patient with previous allogeneic bone marrow transplantation for chronic myeloid leukaemia.
Acta Gastroenterol Belg. 2009 Apr-Jun;72(2):267-8
Authors: Shindano A, Geubel A, Fervaille C, Azzouzi K
PMID: 19637788 [PubMed - indexed for MEDLINE]
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Sustained durability of responses and improved progression-free and overall survival with imatinib treatment for accelerated phase and blast crisis chronic myeloid leukemia: long-term follow-up of the STI571 0102 and 0109 trials.
Haematologica. 2009 May;94(5):743-4
Authors: Silver RT, Cortes J, Waltzman R, Mone M, Kantarjian H
PMID: 19407320 [PubMed - indexed for MEDLINE]
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