ABSTRACT
Background: The purpose of the study was to analyze the expression of nucleophosmin (NPM1), CCAT/enhancer-binding protein alpha (CEBPA), and FMS-like tyrosine kinase 3 (FLT3) with immunohistochemistry and evaluate the relationship with clinicopathologic data with special emphasis on prognosis in bone marrow biopsy specimens diagnosed with acute myeloid leukemia (AML). Materials and Methods: Bone marrow biopsies of 104 patients who were diagnosed with AML were re-evaluated for diagnosis and subclassification. Immunohistochemically, anti-NPM1, anti-CEBPA, and anti-FLT3 antibodies were applied to slides prepared from formalin-fixed paraffin-embedded tissues. Sixty-three of these patients had their follow-up in our institutional hematology clinic and these patients' clinical, biochemical, and radiological data were obtained and analyzed from patient files. These data were analyzed with survival times statistically. Results: Except for age, no significant effect of clinical data on prognosis was detected. Immunohistochemical results were also statistically compared with clinical data. No correlation was found between overall survival and disease-free survival with the expression of anti-CEBPA or anti-NPM1 antibodies. However, immunohistochemical reactivity for anti-FLT3 antibody was found to be a poor prognostic factor and statistically significant. Also, when the expression of FLT3 was analyzed with that of NPM1 or CEBPA, a correlation (dependent on the expression of FLT3) was found with disease-free survival. Conclusions: FLT3 is an independent prognostic factor for AML. CEBPA and NPM1 should be considered as good prognostic factors only in the absence of FLT3 abnormalities.
Subject(s)
Leukemia, Myeloid, Acute , Nucleophosmin/metabolism , fms-Like Tyrosine Kinase 3 , CCAAT-Enhancer-Binding Proteins/genetics , DNA-Binding Proteins , Humans , Leukemia, Myeloid, Acute/diagnosis , Leukemia, Myeloid, Acute/pathology , Mutation , Nuclear Proteins/genetics , Prognosis , fms-Like Tyrosine Kinase 3/geneticsABSTRACT
OBJECTIVE: The aim of this study is to evaluate the effects of intraarticular insulin on the treatment of chondral defects. DESIGN: Twenty-four mature New Zealand rabbits were randomly divided into 3 groups as control (Group 1), microfracture (Group 2), and microfracture and insulin (Group 3). Four-millimeter full-thickness cartilage defects were created to the weight-bearing surface on the medial femoral condyles of each rabbit. In the first group, any additional interventions were not performed. Microfracture was performed on defects in groups 2 and 3. Additionally, 10 IU of insulin glargine was administrated into the knee joints of the third group. Three months after surgery, the knee joints were harvested and cartilage quality was assessed according to Wakitani and ICRS (International Cartilage Repair Society) scores histopathologically. Insulin injections were performed into the knees of 2 additional rabbits without creating a cartilage defect to evaluate the potential adverse effects of insulin on healthy cartilage (Group 4). RESULTS: The total ICRS and Wakitani scores of the insulin group were found to be significantly lower than the microfracture group but similar to the control group. No negative effects of insulin on healthy cartilage were detected. Intraarticular insulin after surgery has led to a statistically significant decrease in systemic blood sugar levels whereas the decrease observed after administration to intact tissues was not statistically significant. CONCLUSIONS: Insulin had a negative influence on the quality of cartilage regeneration and had no effect on healthy cartilage. Intraarticular insulin administration does not cause significant systemic effects in intact tissue.
