Posted by rob on November 8, 2005 under Uncategorized | 
Th?rn I, Olsson-Str?mberg U, Ohlsen C, Jonsson AM, Klangby U, Simonsson B, Barbany G
Haematologica. 2005 Nov ; 90(11): 1471-6
BACKGROUND AND OBJECTIVES: Accurate quantification of BCR-ABL mRNA is of critical importance for managing patients with chronic myeloid leukemia (CML) who are receiving imatinib therapy. RNA degradation thus constitutes a potential problem for laboratories quantifying minimal residual disease (MRD). Patients’ samples that take a long time to be transported from the hospital to the analyzing laboratory may be subject to RNA degradation with a corresponding loss in sensitivity and possible generation of false negative results. Recently, RNA preservation systems have been developed in order to improve RNA stability. The aim of the present study was to investigate such a system. DESIGN AND METHODS: We evaluated the performance of the PAXgene Blood RNA Kit in follow-up CML peripheral blood samples and compared the results to those from unstabilized parallel Trizol extracted samples. The different sample processing methods were evaluated by real-time polymerase chain reaction (PCR) analysis. RESULTS: RNA isolated with the PAXgene system gave a superior yield per milliliter of blood than did the routine Trizol extraction method. However, although of comparable quality, the RNA did not PCR-amplify as efficiently as equal amounts of RNA from routinely processed samples. Therefore, RNA processed with the PAXgene system showed decreased sensitivity for MRD detection, resulting in false negative results. The sensitivity was comparable to that of samples processed routinely 20-30 hours after phlebotomy. INTERPRETATION AND CONCLUSIONS: We conclude that routinely processed, i.e. unstabilized, peripheral blood that reaches the laboratory and is processed within 30 hours is preferable for MRD detection. Optimal results were achieved with fresh samples processed within 5 hours with the Trizol method. However, RNA stabilization may be useful if sample transit is expected to exceed 30 hours.
The impact of RNA stabilization on minimal residual disease assessment in chronic myeloid leukemia.
Posted by rob on under Uncategorized |
Ferrand H, Tamburini J, Mouly S, Bouscary D, Bergmann JF
Clin Infect Dis. 2005 Dec 1; 41(11): 1684-5
No abstract yet
Listeria monocytogenes meningitis following imatinib mesylate-induced monocytopenia in a patient with chronic myeloid leukemia.
Posted by rob on under Uncategorized |
Tchirkov A, Couderc JL, P?rissel B, Goumy C, Regnier A, Uhrhammer N, Verrelle P, Berger M
Leukemia. 2005 Nov 3;
No abstract yet
Major molecular response to imatinib in a patient with chronic myeloid leukemia expressing a novel form of e8a2 BCR-ABL transcript.
Posted by rob on under Uncategorized |
Rumpold H, Wolf AM, Wolf D
Leukemia. 2005 Nov 3;
No abstract yet
The role of P-glycoporotein in imatinib resistance.
Posted by rob on under Uncategorized |
Cilloni D, Messa F, Arruga F, Defilippi I, Morotti A, Messa E, Carturan S, Giugliano E, Pautasso M, Bracco E, Rosso V, Sen A, Martinelli G, Baccarani M, Saglio G
Leukemia. 2005 Nov 3;
Imatinib represents at present the most attractive therapy for BCR-ABL positive leukemias, even though a percentage of CML patients develop resistance to this compound. For these resistant patients a therapeutic approach based on a combination of drugs is more likely to be effective. In the last years, constitutive NF-kappaB/Rel activity has been demonstrated in several hematological malignancies. As a result, NFkB/Rel-blocking approaches have been proposed as antineoplastic strategies. Furthermore, the identification of specific kinases within the NF-kappaB activation pathway offers a selective target to address tailored therapies. In the current study, we show that the IKK inhibitor PS1145 is able to inhibit the proliferation of CML cell lines and primary BM cells. Moreover, the addition of Imatinib increases the effects of PS1145 in resistant cell lines and BM cells from resistant patients, with a further increase of apoptosis and inhibition of proliferation and colony growth. Our data provide the rational for a new therapeutic approach, which combines Imatinib and the IKK inhibitor PS1145 in CML resistant patients.Leukemia advance online publication, 3 November 2005; doi:10.1038/sj.leu.2403998.
The NF-kappaB pathway blockade by the IKK inhibitor PS1145 can overcome Imatinib resistance.
Posted by rob on under Uncategorized |
Koh TT, Colby TV, Müller NL
Semin Respir Crit Care Med. 2005 Oct ; 26(5): 514-9
Myeloid leukemias are clonal malignancies characterized by the presence of increased numbers of immature myeloid cells in the marrow and peripheral blood. Pulmonary involvement by myeloid leukemia is relatively uncommon and seen mainly in patients with severe disease. The most common form of pulmonary involvement consists of leukemic infiltration along the lymphatics in the peribronchovascular, septal, and pleural interstitial tissue. Less common manifestations include myeloid sarcoma, leukostasis, leukemic cell lysis pneumopathy, and hyperleukocytic reaction. The radiological manifestations of pulmonary leukemic cell infiltration and leukostasis consist mainly of bilateral thickening of the peribronchovascular interstitium and interlobular septa, a pattern that resembles that of interstitial pulmonary edema. The radiological manifestations of leukemic cell lysis pneumopathy and hyperleukocytic reaction consist of symmetric bilateral areas of consolidation. This manuscript reviews the histological and radiological intrathoracic manifestations of myelogenous leukemias.
Myeloid leukemias and lung involvement.
