Bennett JM, Catovsky D, Daniel MT, Flandrin G, Galton DA, Gralnick HR, Sultan CProposed revised criteria for the classification of acute myeloid leukemia. A report of the French-American-British Cooperative Group. Ann Intern Med 103: 620-625
Available from: Zohreh Sanaat
- "Twenty-seven (14 female and 13 male) patients with newly diagnosed AML who were referred to Shahid Ghazi Tabatabai Hospital in Tabriz from September 2009 to July 2010 were enrolled in this study. The initial diagnosis of AML and its subtypes were determined according to the French-American-British classification . AML smears were routinely investigated at the same hospital, and subtyping was confirmed by flow cytometry. "
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ABSTRACT: Objective: The crucial role of angiogenesis in the pathophysiology of acute myeloid leukemia (AML) has been proposed. One of the key regulators of angiogenesis is the vascular endothelial growth factor (VEGF). Among the VEGF family, it has been observed that VEGF-A and VEGF-C are expressed by AML cells and mediate leukemic cell proliferation, survival, and resistance to chemotherapy. Emerging evidence, however, suggests that elevated levels of VEGF or a proangiogenic phenotype may impede, rather than promote, early tumor development and progression. As the significance of VEGF-A and VEGF-C levels in the pathogenesis of AML has not been clarified well, the aim of this study is to evaluate gene expression of these angiogenesis promoters and its possible prognostic value in peripheral blood mononuclear cells of Iranian patients with AML.
Materials and Methods: We investigated the mRNA expression of VEGF-A and VEGF-C in peripheral blood mononuclear cells of 27 patients with newly diagnosed AML and 28 healthy controls by quantitative real-time PCR.
Results: Expression of VEGF-C mRNA was significantly lower in AML patients than in healthy controls (p<0.001). However, there was no significant decrement in expression of VEGF-A mRNA of AML patients compared to the control group (p=0.861). VEGF-A and VEGF-C expression were not able to predict clinical outcome.
Conclusion: Our data showed that AML is associated with a decreased expression of VEGF-C mRNA. However, expression levels did not influence the clinical outcome in our study. It seems that angiogenesis is affected by different cytokines other than VEGF-C or VEGF-A, and VEGF is also affected by different cytokines. Taken together, these findings help to provide new insights into the investigation of other angiogenic factors and cytokines that may play roles in the pathogenesis of AML.
Conflict of interest:None declared.
Available from: June-Won Cheong
- "Diagnosis of AML was established on the basis of bone marrow (BM) aspiration findings. AML was classified according to the morphological French-American-British (FAB) criteria, and the diagnosis was confirmed on the basis of cytochemical and immunological analyses findings . At diagnosis and relapse, samples of BM or blood were examined for cytogenetic abnormalities using standard banding techniques and were classified according to the International System for Human Cytogenetic Nomenclature . "
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ABSTRACT: Only a few patients who experience AML relapse derive lasting benefit from re-induction therapy. The utility of reassessing the disease karyotype at relapse is unclear. The main goals of this study were to identify prognostic factors for AML relapse and to determine the prognostic utility of karyotypic change between diagnosis and relapse as a variable for predicting response to salvage therapy for relapsed AML.
This retrospective study included 58 patients with relapsed AML treated at the Yonsei University College of Medicine between 2005 and 2010. Karyotypes at both diagnosis and relapse were available for 45 patients (77%). A change in karyotype at relapse was observed in 17 of 45 cases (37%), and no change was noted in 28 of 45 cases (62%).
Karyotypic changes between diagnosis and relapse were associated with the response rate (RR) to salvage therapy (P=0.016). Overall survival (OS) and event-free survival (EFS) in the group with karyotypic changes between diagnosis and relapse were significantly different from those with no karyotypic changes (P=0.004 and P=0.010, respectively). We applied multiple multivariate Cox regression analyses to identify independent prognostic factors for overall response (OR), OS, and EFS. A change in karyotype between diagnosis and relapse was significantly associated with OS (P=0.023; RR=2.655) and EFS (P=0.033; RR=2.831).
Karyotypic changes between the diagnosis and relapse of AML could be used to predict outcomes and tailor clinical and biological therapeutic strategies for relapsed AML patients.
Available from: Xiao-yang Jiao
- "The initial diagnosis of ALL/AML and its subtypes were determined according to the French-American-British (FAB) classification . There were 7 cases with AML- M3, 1 patient with M4, 1 patient with M5, and 25 patients with ALL in our study. "
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ABSTRACT: Over-expression of vascular endothelial growth factor A (VEGF-A) is correlated with leukemia metastasis. VEGF-A acts by binding to its membrane receptors R1 and R2 present in soluble forms (sVEGFR1, sVEGFR2) with different functions. sVEGFR could inhibit VEGF-A bioactivities, associated with favorable prognosis in solid tumors. However, its role is obscure in central nervous system leukemia (CNSL). The aim of this study was to investigate sVEGFR1, R2 as biomarkers in CNSL. Paired cerebrospinal fluid (CSF) and serum samples were collected from 35 leukemia cases with or without CNS metastasis. Levels of sVEGFR1 and sVEGFR2 in both CSF (sVEGFR1(CSF), sVEGFR2(CSF)) and serum (sVEGFR1(Serum), sVEGFR2(Serum)) were detected by ELISA. Other risk factors related to CNSL prognosis were also analyzed. sVEGFR(Serum) levels were 2.54-fold (sVEGFR1) and 25.6-fold (sVEGFR2) higher than sVEGFR(CSF) in both leukemic groups. sVEGFR1(CSF) in CNSL were 33 % higher than in the non-CNSL, and the levels of sVEGFR2(CSF) and sVEGFR2(Serum) had the same trend. Elevated sVEGFR1(CSF) and sVEGFR2(CSF) is closely correlated with blood-brain barrier (BBB) values and WBC(CSF) that is an indicator of CNSL disease burden. Cox regression analysis showed that the sVEGFR2(CSF) had a positive effect on event-free survival. Our data suggest that sVEGFR2(CSF) may be more potent than sVEGFR1(CSF) in predicting the outcome of leukemia patients, the balance between sVEGFR2(CSF) and VEGF-A(CSF) levels might be crucial for the progression of CNSL.
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