A Worldwide Support Network For Chronic Myelogenous Leukemia
Posted by rob on November 28, 2010 under Uncategorized | 
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In conclusion, Rakicidin A is a promising compound for targeting TKI?resistant quiescent CML stem cells in the hypoxic BM environment. (Source: Cancer Science)
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Serial quantitation of BCR-ABL mRNA levels is an important indicator of therapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome–positive acute lymphoblastic leukemia, but there is substantial variation in the real-time quantitative polymerase chain reaction methodologies used by different testing laboratories. To help improve the comparability of results between centers we sought to develop accredited reference reagents that are directly linked to the BCR-ABL international scale. After assessment of candidate cell lines, a reference material panel comprising 4 different dilution levels of freeze-dried preparations of K562 cells diluted in HL60 cells was prepared. After performance evaluation, the materials were assigned fixed percent BCR-ABL/co…
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Posted by rob on November 26, 2010 under Uncategorized | Comments are off for this article
Spontaneous remission in acute myelogenous leukemia evidenced by cytogenetic changes.
Ann Hematol. 2010 Nov 24;
Authors: Teng CJ, Yang CF, Gau JP, Liu JH, Hong YC, Liu CY, Yu YB, Hsiao LT, Wang WS, Tzeng CH
PMID: 21107840 [PubMed - as supplied by publisher]
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Pure erythroid leukemia: a reassessment of the entity using the 2008 World Health Organization classification.
Mod Pathol. 2010 Nov 19;
Authors: Liu W, Hasserjian RP, Hu Y, Zhang L, Miranda RN, Medeiros LJ, Wang SA
Pure erythroid leukemia (PEL) is rare, characterized by a neoplastic proliferation of erythroblasts. Given recent incorporation of molecular genetic findings and clinical features in the revised 2008 World Health Organization classification scheme of acute myeloid leukemia, we questioned if PEL still remains as a distinct subtype of acute myeloid leukemia. In this retrospective study, we identified 18 cases of acute leukemia with morphologic and immunophenotypic features of PEL. Following the current World Health Organization classification algorithm, these cases were classified as: 13 acute myeloid leukemia with myelodysplasia-related changes, 3 therapy-related acute myeloid leukemia, and 1 chronic myelogenous leukemia blast crisis, and one unclassifiable due to insufficient clinical information. All 16 cases with cytogenetic data harbored an extremely complex karyotype and the median overall survival of the 18 patients was 3 months (range, 1-7 months). This survival was significantly shorter than that of patients with acute erythroid leukemia, erythroid/myeloid subtype, or acute myeloid leukemia with myelodysplasia-related changes with erythroid predominance (P<0.001). PEL is characterized as a neoplastic erythroid hyperproliferation with maturation arrest. E-cadherin emerged as the most sensitive and specific marker for immature erythroblasts, and was helpful in distinguishing PEL from other erythroid proliferations. Our study showed that the criteria for acute myeloid leukemia in the 2008 World Health Organization system facilitate reclassification of PEL cases into other acute myeloid leukemia categories, mainly of acute myeloid leukemia with myelodysplasia-related changes. These new assigned categories fail to capture the distinct features of PEL, where the phenotype of PEL correlates with a very complex karyotype and an extremely aggressive clinical course.Modern Pathology advance online publication, 19 November 2010; doi:10.1038/modpathol.2010.194.
PMID: 21102413 [PubMed - as supplied by publisher]
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Persistent Activation of the Fyn/ERK Kinase Signaling Axis Mediates Imatinib Resistance in Chronic Myelogenous Leukemia Cells through Upregulation of Intracellular SPARC.
Cancer Res. 2010 Nov 23;
Authors: Fenouille N, Puissant A, Dufies M, Robert G, Jacquel A, Ohanna M, Deckert M, Pasquet JM, Mahon FX, Cassuto JP, Raynaud S, Tartare-Deckert S, Auberger P
SPARC is an extracellular matrix protein that exerts pleiotropic effects on extracellular matrix organization, growth factor availability, cell adhesion, differentiation, and immunity in cancer. Chronic myelogenous leukemia (CML) cells resistant to the BCR-ABL inhibitor imatinib (IM-R cells) were found to overexpress SPARC mRNA. In this study, we show that imatinib triggers SPARC accumulation in a variety of tyrosine kinase inhibitor (TKI)–resistant CML cell lines. SPARC silencing in IM-R cells restored imatinib sensitivity, whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis. Notably, we found that the protective effect of SPARC required intracellular retention inside cells. Accordingly, SPARC was not secreted into the culture medium of IM-R cells. Increased SPARC expression was intimately linked to persistent activation of the Fyn/ERK kinase signaling axis. Pharmacologic inhibition of this pathway or siRNA-mediated knockdown of Fyn kinase resensitized IM-R cells to imatinib. In support of our findings, increased levels of SPARC mRNA were documented in blood cells from CML patients after 1 year of imatinib therapy compared with initial diagnosis. Taken together, our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC. Cancer Res; 70(23); 1-12. ©2010 AACR.
PMID: 21098700 [PubMed - as supplied by publisher]
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Declining lymphoid progenitor fitness promotes aging-associated leukemogenesis.
Proc Natl Acad Sci U S A. 2010 Nov 22;
Authors: Henry CJ, Marusyk A, Zaberezhnyy V, Adane B, Degregori J
Aging is associated with the functional decline of cells, tissues, and organs. At the same time, age is the single most important prognostic factor in the development of most human cancers, including chronic myelogenous and acute lymphoblastic leukemias initiated by Bcr-Abl oncogenic translocations. Prevailing paradigms attribute the association between aging and cancers to the accumulation of oncogenic mutations over time, because the accrual of oncogenic events is thought to be the rate-limiting step in initiation and progression of cancers. Conversely, aging-associated functional decline caused by both cell-autonomous and non-cell-autonomous mechanisms is likely to reduce the fitness of stem and progenitor cell populations. This reduction in fitness should be conducive for increased selection of oncogenic mutations that can at least partially alleviate fitness defects, thereby promoting the initiation of cancers. We tested this hypothesis using mouse hematopoietic models. Our studies indicate that the dramatic decline in the fitness of aged B-lymphopoiesis coincides with altered receptor-associated kinase signaling. We further show that Bcr-Abl provides a much greater competitive advantage to old B-lymphoid progenitors compared with young progenitors, coinciding with restored kinase signaling pathways, and that this enhanced competitive advantage translates into increased promotion of Bcr-Abl-driven leukemias. Moreover, impairing IL-7-mediated signaling is sufficient to promote selection for Bcr-Abl-expressing B progenitors. These studies support an unappreciated causative link between aging and cancer: increased selection of oncogenic mutations as a result of age-dependent alterations of the fitness landscape.
PMID: 21098275 [PubMed - as supplied by publisher]
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Myeloperoxidase-dependent Oxidation of Etoposide in Human Myeloid Progenitor CD34+ Cells.
Mol Pharmacol. 2010 Nov 19;
Authors: Vlasova II, Feng WH, Goff JP, Giorgianni A, Do D, Gollin SM, Lewis DW, Kagan VE, Yalowich JC
Etoposide is a widely used anticancer drug successfully utilized for treatment of many types of cancer in children and adults. Its use, however, is associated with an increased risk of development of secondary acute myelogenous leukemia (t-AML) involving MLL gene (11q23) translocations. Previous studies demonstrated that the phenoxyl radical of etoposide can be produced by action of myeloperoxidase (MPO), an enzyme found in developing myeloid progenitor cells, the likely origin for myeloid leukemias. We hypothesized, therefore, that one-electron oxidation of etoposide by myeloperoxidase (MPO) to its phenoxyl radical is important for converting this anticancer drug to genotoxic and carcinogenic species in human CD34+ myeloid progenitor cells. In the present study, using EPR spectroscopy, we provide conclusive evidence for MPO-dependent formation of etoposide phenoxyl radicals in growth factor mobilized CD34+ cells isolated from human umbilical cord blood and demonstrate that MPO-induced oxidation of etoposide is amplified in the presence of phenol. Formation of etoposide radicals resulted in oxidation of endogenous thiols thus providing evidence for etoposide-mediated MPO-catalyzed redox cycling that may play a role in enhanced etoposide genotoxicity. In separate studies, etoposide-induced DNA damage and MLL gene rearrangements were demonstrated to be dependent in part on MPO activity in CD34+ cells. Together our results are consistent with the idea that MPO-dependent oxidation of etoposide in human hematopoetic CD34+ cells makes these cells especially prone to induction of etoposide-related acute myeloid leukemia.
PMID: 21097707 [PubMed - as supplied by publisher]
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Genetically modified donor leukocyte transfusion and Graft-versus-Leukemia effect after allogeneic stem cell transplantation.
Hum Gene Ther. 2010 Nov 23;
Authors: Borchers S, Provasi E, Benati C, Dammann E, Radrizzani M, Krons A, Kuehnau W, Schmidke J, von Neuhoff N, Stadler M, Ciceri F, Bonini C, Ganser A, Hertenstein B, Mischak-Weissinger EM
Seven patients with acute myeloid leukemia (AML) and two patients with chronic myelogenous leukemia (CML) were transplanted from HLA-identical sibling donors with CD34+-enriched stem cells (HSCT) without further immunosuppression. The myeloablative standard transplantation protocol was adapted to include transfusion of gene-modified donor T-cells after HSCT. Donor T-cells were transduced with the replication-deficient retrovirus SFCMM-3, which expresses the herpes simplex thymidine-kinase (HSV-Tk) and the truncated version of low affinity nerve growth factor receptor (?LNGFR) for selection and characterization of transduced cells. Transduced T-cells were detectable in all patients during follow-up for up to 5 years after transfusion. Proteomic screening for development of acute graft-versus-host disease (aGvHD) was applied to five of seven AML patients. No positivity for the aGVHD grade II specific proteomic pattern was observed. Only one patient developed aGvHD grade I. To date, 3 AML patients relapsed, one responded to the transfusion of 3 untransduced, escalating DLI from the original donor and is in complete remission. Two were re-transplanted with non-T-cell depleted peripheral blood stem cells from their original donors and died post re-transplantation from septic complications or relapse, respectively. In one CML-patient, loss of bcr-abl gene expression was observed following an expansion of transduced cells. Seven of nine patients are alive and in complete remission.
PMID: 21091264 [PubMed - as supplied by publisher]
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Targeted Blockage of Signal Transducer and Activator of Transcription 5 Signaling Pathway with Decoy Oligodeoxynucleotides Suppresses Leukemic K562 Cell Growth.
DNA Cell Biol. 2010 Nov 22;
Authors: Wang X, Zeng J, Shi M, Zhao S, Bai W, Cao W, Tu Z, Huang Z, Feng W
The protein signal transducer and activator of transcription 5 (STAT5) of the JAK/STAT pathway is constitutively activated because of its phosphorylation by tyrosine kinase activity of fusion protein BCR-ABL in chronic myelogenous leukemia (CML) cells. This study investigated the potential therapeutic effect of STAT5 decoy oligodeoxynucleotides (ODN) using leukemia K562 cells as a model. Our results showed that transfection of 21-mer-long STAT5 decoy ODN into K562 cells effectively inhibited cell proliferation and induced cell apoptosis. Further, STAT5 decoy ODN downregulated STAT5 targets bcl-xL, cyclinD1, and c-myc at both mRNA and protein levels in a sequence-specific manner. Collectively, these data demonstrate the therapeutic effect of blocking the STAT5 signal pathway by cis-element decoy for cancer characterized by constitutive STAT5 activation. Thus, our study provides support for STAT5 as a potential target downstream of BCR-ABL for CML treatment and helps establish the concept of targeting STAT5 by decoy ODN as a novel therapy approach for imatinib-resistant CML.
PMID: 21091189 [PubMed - as supplied by publisher]
Posted by rob on November 22, 2010 under Uncategorized | Comments are off for this article
Abstract Imatinib mesylate has become a therapy of interest for the treatment of systemic sclerosis because of its ability to inhibit
c-Abl and platelet-derived growth factor receptor, tyrosine kinases involved in profibrotic pathways. Preclinical data using
in vitro and murine models of fibrosis have demonstrated the antifibrotic properties of imatinib. Imatinib is currently used
widely in the treatment of chronic myelogenous leukemia, gastrointestinal stromal tumors, and other conditions, and a large
amount of information is available regarding the safety of the medication in these patient populations. Whether imatinib will
be tolerable or effective in the treatment of systemic sclerosis is the subject of several investigations. The aim of this
review is to summarize thi…
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Posted by rob on November 20, 2010 under Uncategorized | Comments are off for this article
Unrelated donor transplantation for acute myelogenous leukemia in first remission.
Biol Blood Marrow Transplant. 2010 Nov 15;
Authors: Bashir Q, Andersson BS, Fernandez-Vina M, de Padua Silva L, Giralt S, Chiattone A, Wei W, Sharma M, Anderlini P, Shpall EJ, Popat U, Rodrigues M, Champlin RE, de Lima M
We retrospectively analyzed the outcomes of all AML patients in first remission (n=44; median age=48 years; high-risk cytogenetics=59%) who received unrelated donor hematopoietic cell transplantation with myeloablative conditioning regimen of IV busulfan, fludarabine and anti-thymocyte globulin between January 2002 and November 2009 at our institution. Donor-recipient pairs were matched by high-resolution HLA A, B, C, DRB1 and DQB1 typing (10/10 matches, n=41; 9/10 matches, n=3). With a median follow-up of 34 months, actuarial 3-year event-free survival (EFS) and overall survival (OS) is 70% and 78%, respectively. The 3-year EFS and OS in patients with and without poor risk cytogenetics is similar (63% vs. 82%, p=0.43 and 78% vs. 82%, p=0.89, respectively). The 3-year EFS and OS is also similar in patients above age 55 year versus patients age 55 year or younger (80% vs.67%, p=0.47 and 80% vs. 78%, p=0.81, respectively). One hundred-day and 3-year cumulative incidence of transplant-related mortality is 5% and 15%, respectively. Six patients have relapsed and three of them are alive and in remission after salvage therapy with a median follow up of 23 months. These results indicate that the majority of AML patients eligible for this treatment can achieve long term disease control.
PMID: 21087679 [PubMed - as supplied by publisher]
Posted by rob on November 19, 2010 under Uncategorized | Comments are off for this article
Imatinib and the Treatment of Fibrosis: Recent Trials and Tribulations.
Curr Rheumatol Rep. 2010 Nov 18;
Authors: Gordon J, Spiera R
Imatinib mesylate has become a therapy of interest for the treatment of systemic sclerosis because of its ability to inhibit c-Abl and platelet-derived growth factor receptor, tyrosine kinases involved in profibrotic pathways. Preclinical data using in vitro and murine models of fibrosis have demonstrated the antifibrotic properties of imatinib. Imatinib is currently used widely in the treatment of chronic myelogenous leukemia, gastrointestinal stromal tumors, and other conditions, and a large amount of information is available regarding the safety of the medication in these patient populations. Whether imatinib will be tolerable or effective in the treatment of systemic sclerosis is the subject of several investigations. The aim of this review is to summarize this body of research to date.
PMID: 21086081 [PubMed - as supplied by publisher]
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Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D3.
Cell Cycle. 2010 Nov 15;9(22):4533-4542
Authors: Wang X, Gocek E, Novik V, Harrison JS, Danilenko M, Studzinski GP
Acute myelogenous leukemia (AML) is a disease characterized by dysregulated cell proliferation associated with impaired cell differentiation, and current treatment regimens rarely save the patient. Thus, new mechanism-based approaches are needed to improve prognosis of this disease. We have investigated in preclinical studies the potential anti-leukemia use of the plant-derived polyphenol Silibinin (SIL) in combination with 1,25-dihydroxyvitamin D3 (1,25D). Although most of the leukemic blasts ex vivo responded by differentiation to treatment with this combination, the reasons for the absence of SIL-1,25D synergy in some cases were unclear. Here we report that failure of SIL to enhance the action of 1,25D is likely due to the SIL-induced increase in the activity of differentiation-antagonizing cell components, such as ERK5. This kinase is under the control of Cot1/Tlp2, and inhibition of Cot1 activity by a specific pharmacological inhibitor 4-(3-chloro-4-fluorophenylamino)-6-(pyridin-3-yl-methylamino-3-cyano-[1-7]-naphthyridine, or by Cot1 siRNA, increases the differentiation by SIL/1,25D combinations. Conversely, over-expression of a Cot1 construct increases the cellular levels of P-ERK5, and SIL/1,25D-induced differentiation and cell cycle arrest are diminished. It appears that reduction in ERK5 activity by inhibition of Cot1 allows SIL to augment the expression of 1,25D-induced differentiation promoting factors and cell cycle regulators such as p27Kip1, which leads to cell cycle arrest. This study shows that in some cell contexts SIL/1,25D can promote expression of both differentiation-promoting and differentiation-inhibiting genes, and that the latter can be neutralized by a highly specific pharmacological inhibitor, suggesting a potential for supplementing treatment of AML with this combination of agents.
PMID: 21084834 [PubMed - as supplied by publisher]
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[Effect of Low-Dose Dasatinib in an Elderly Patient with Chronic Myelogenous Leukemia(CML).]
Gan To Kagaku Ryoho. 2010 Nov;37(11):2213-2215
Authors: Takagi Y, Aota Y, Gotoh A, Sakurai M
We experienced a case of chronic myelogenous leukemia(CML)treated successfully with low-dose dasatinib(20mg/day). An 87-year-old man was diagnosed with CML in January 2003 and was given imatinib(200mg/day). Although complete hematologic responses(CHR)were achieved, we replaced imatinib with hydroxycarbamide(HU)because of the renal dysfunction possibly due to imatinib. However, since the blood count was poorly controlled with HU, treatment with dasatinib, one of the second-generation tyrosine kinase inhibitors, was started at the accelerated phase(AP)in June 2009. Dasatinib was given in a daily dose of 20 mg, intending dose escalation after confirmation of its safety. White blood cells and platelets decreased rapidly, and after 18 days, CHR was achieved. Thereafter, daily dasatinib was reduced twice per week because of the cytopenia. However, the patient has continued CHR without developing AP for more than six months. Lowdose dasatinib might be a useful treatment in the control of selected patients with CML.
PMID: 21084830 [PubMed - as supplied by publisher]
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Use of posaconazole in the treatment of invasive fungal infections.
Expert Rev Hematol. 2009 Dec;2(6):619-630
Authors: Mehta AK, Langston AA
The emergence of invasive fungal infections as an increasingly important clinical problem in immunocompromised patients highlights the need for more effective antifungal agents and better strategies for prevention, diagnosis and treatment. Posaconazole is an extended-spectrum triazole with broad activity against a variety of fungal pathogens, both yeasts and molds. In particular, it has activity against several emerging pathogens, such as the Zygomycetes, which are resistant to many currently available antifungals, making it an attractive agent for use in both prophylactic and therapeutic situations. Studies demonstrating the prophylactic utility of posaconazole in neutropenic patients with acute myelogenous leukemia or myelodysplastic syndrome, and in patients with graft-versus-host disease following allogeneic stem cell transplantation has led to the approval of the drug in the USA. These data have been reviewed elsewhere in detail. Published data on posaconazole as primary antifungal therapy are very limited, although there is a considerable amount of experience with the drug in the salvage setting following failure of or intolerance to other antifungal agents. In this review we will focus on the use of posaconazole for treatment of established invasive fungal infections, with a focus on opportunistic infections in immunocompromised patients.
PMID: 21082953 [PubMed - as supplied by publisher]
Posted by rob on November 18, 2010 under Uncategorized | Comments are off for this article
Tubulin-binding dibenz[c,e]oxepines as colchinol analogues for targeting tumour vasculature.
Org Biomol Chem. 2010 Nov 17;
Authors: Edwards DJ, Hadfield JA, Wallace TW, Ducki S
Various methoxy- and hydroxy-substituted dibenz[c,e]oxepines were prepared via the copper(i)-induced coupling of ether-tethered arylstannanes or the dehydrative cyclisation of 1,1′-biphenyl-2,2′-dimethanols, assembled using the Ullmann cross-coupling of ortho-bromoaryl carbonyl compounds. The dibenzoxepines were screened for their ability to inhibit tubulin polymerisation and the in vitro growth of K562 human chronic myelogenous leukemia cells. The most active was 5,7-dihydro-3,9,10,11-tetramethoxydibenz[c,e]oxepin-4-ol, whose tubulin inhibitory and cytotoxicity (IC(50)) values were 1 ?M and 40 nM, respectively.
PMID: 21082139 [PubMed - as supplied by publisher]
Posted by rob on November 17, 2010 under Uncategorized | Comments are off for this article
Nonspecific Capillary Proliferation and Vasculopathy Indicate Skin Hypoxia in Erythromelalgia.
Arch Dermatol. 2010 Nov 15;
Authors: Kalgaard OM, Clausen OP, Mellbye OJ, Hovig T, Kvernebo K
OBJECTIVE: To report on the histopathologic findings of affected skin in consecutively collected biopsy specimens from 49 patients with erythromelalgia (EM). DESIGN: Skin biopsy specimens were obtained from the foot arch and analyzed by light microscopy, immunofluorescence microscopy, and electron microscopy. SETTING: Oslo University Hospital-Gaustad, University of Oslo, Oslo, Norway. PARTICIPANTS: Thirty-one patients had primary EM, 17 patients had secondary EM, and 1 patient had erythromelalgic syndrome. Main Outcome Measure Evidence of microvascular abnormalities in skin biopsy specimens. RESULTS: Light microscopy showed evidence of capillary proliferation in 10 of 31 patients with primary EM and in 1 of 17 patients with secondary EM. The biopsy specimen from the patient with erythromelalgic syndrome showed numerous capillary nests with endothelial cell defects and a slight perivascular inflammatory reaction. Among the 17 secondary EM cases, sparse perivascular lymphocyte infiltrations were observed in the biopsy specimens from 2 patients with chronic myelogenous leukemia and 1 patient with diabetes mellitus. Eleven patients also had signs of vasculopathy based on findings of immunodeposits of C3 and fibrin. Six of 30 patients with primary EM showed endothelial abnormalities on electron microscopy. All 3 investigations showed unremarkable biopsy results in 16 cases. CONCLUSIONS: Histopathologic analysis is not useful as a routine diagnostic tool in EM because no morphological changes are specific to EM. The capillary proliferation and vasculopathy are assumed to be a consequence of intermittent skin hypoxia (vascular hypothesis of pathogenesis). Whether the proliferation is a consequence of EM or a pathogenic factor in the development of the disease is uncertain.
PMID: 21079053 [PubMed - as supplied by publisher]
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Correlations between imatinib pharmacokinetics, pharmacodynamics, adherence, and clinical response in advanced metastatic gastrointestinal stromal tumor (GIST): An emerging role for drug blood level testing?
Cancer Treat Rev. 2010 Nov 13;
Authors: von Mehren M, Widmer N
Imatinib is the standard of care for patients with advanced metastatic gastrointestinal stromal tumors (GIST), and is also approved for adjuvant treatment in patients at substantial risk of relapse. Studies have shown that maximizing benefit from imatinib depends on long-term administration at recommended doses. Pharmacokinetic (PK) and pharmacodynamic factors, adherence, and drug-drug interactions can affect exposure to imatinib and impact clinical outcomes. This article reviews the relevance of these factors to imatinib’s clinical activity and response in the context of what has been demonstrated in chronic myelogenous leukemia (CML), and in light of new data correlating imatinib exposure to response in patients with GIST. Because of the wide inter-patient variability in drug exposure with imatinib in both CML and GIST, blood level testing (BLT) may play a role in investigating instances of suboptimal response, unusually severe toxicities, drug-drug interactions, and suspected non-adherence. Published clinical data in CML and in GIST were considered, including data from a PK substudy of the B2222 trial correlating imatinib blood levels with clinical responses in patients with GIST. Imatinib trough plasma levels <1100ng/mL were associated with lower rates of objective response and faster development of progressive disease in patients with GIST. These findings have been supported by other analyses correlating free imatinib (unbound) levels with response. These results suggest a future application for imatinib BLT in predicting and optimizing therapeutic response. Nevertheless, early estimates of threshold imatinib blood levels must be confirmed prospectively in future studies and elaborated for different patient subgroups.
PMID: 21078547 [PubMed - as supplied by publisher]
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Palatal mucormycosis in patients with hematologic malignancy and stem cell transplantation.
Med Mycol. 2010 Nov 15;
Authors: Akhrass FA, Debiane L, Abdallah L, Best L, Mulanovich V, Rolston K, Kontoyiannis DP
We present two patients with acute myelogenous leukemia who developed palatal mucormycosis, as well as a review of 15 well described reported cases of the same condition in patients who had hematologic malignancy and had undergone hematopoietic stem cell transplantation. Early diagnosis of palatal mucormycosis requires high suspicion of the disease along with a thorough oral examination. Mucormycosis is a devastating disease with a high mortality rate, thereby stressing the importance for early appropriate antifungal therapy in immunocompromised patients with palatal lesions while awaiting the results of histopathology and cultures.
PMID: 21077735 [PubMed - as supplied by publisher]
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| Related Articles |
Are chronic myeloid leukemia patients more at risk for second malignancies? A population-based study.
Am J Epidemiol. 2010 Nov 1;172(9):1028-33
Authors: Rebora P, Czene K, Antolini L, Passerini CG, Reilly M, Valsecchi MG
The authors used cancer registry data to assess the incidence rate of second primary cancers among chronic myeloid leukemia (CML) patients and the long-term survival of CML patients before the introduction of tyrosine kinase inhibitors. In the Swedish Cancer Registry, the authors identified 2,753 adult CML patients diagnosed between 1970 and 1995 who were followed through December 2007. Standardized incidence ratios (SIRs) and relative survival ratios were computed. With a total of 145 subsequent primary malignancies, an increased incidence rate of second malignancy was found for stomach cancer (SIR = 2.76, 95% confidence interval (CI): 1.33, 5.08), skin cancer (SIR = 5.36, 95% CI: 3.18, 8.47), urogenital tract cancer (SIR = 1.61, 95% CI: 1.15, 2.21), and lymphoid leukemia (SIR = 5.53, 95% CI: 1.79, 12.89). Long-term relative survival figures showed that CML was related, in the era prior to the introduction of imatinib, to a very steep decline in survival (2 years from diagnosis, relative survival = 51%, 95% CI: 49, 53). This was in spite of a marginal improvement after 1985, possibly related to the introduction of interferon-? for treatment. These estimates constitute a relevant reference for future studies and a benchmark for comparisons with prognosis in CML patients after chronic use of tyrosine kinase inhibitors.
PMID: 20861143 [PubMed - indexed for MEDLINE]
