Aim of the present study was to assess the prevalence of atrial fibrillation (AF) in patients with two different types of cancer. Recent epidemiologic and clinical studies support the hypothesis that AF is promoted and maintained by a broad spectrum of modulating factors. A total of 2,339 patients admitted to the Surgery Department of "Luigi Sacco Hospital, Milan," over the period 1987-2004 were eligible for the study. One thousand three hundred and seventeen patients were admitted consecutively with a first diagnosis of colorectal or breast cancer (cases). The remaining 1,022 were patients admitted to undergo non-neoplastic surgery (controls). Routine pre-surgery electrocardiogram available in patient charts was analysed by a cardiologist who was not aware of the present study to evaluate the presence of atrial fibrillation or other arrhythmias. Overall, AF was present in 3.6% cases and 1.6% controls. This corresponded to at least two times higher likelihood of having AF in cases compared to controls. Prevalence of AF increased with age both in cases and controls. Our study describes an increased prevalence of AF in two different types of cancer. Autonomic, endocrine, coagulation, and inflammatory alterations were previously described in both AF and cancer, and can provide the physiopathological basis to our clinical observation.
Patient 1179 relapsed 13 months after initial diagnosis, whereas patient 2112 is in continued complete remission (CCR; 61 ϩ ). Interestingly, patient 1179 showed no FLT3/ITD mutation at relapse ( Figure 1C), possibly due to loss of the mutated allele during therapy, or, alternatively, the FLT3/ITD-positive clone was eliminated during chemotherapy with a subsequent relapse from a non-FLT3-mutated parental clone.In conclusion, we confirm the presence of FLT3 mutations in pediatric T-ALL (2/72; 2.7%). Although both immature, the immunophenotypes of the FLT3-mutated pediatric and adult 2 T-ALL cases differed. In addition, a link between mRNA expression of cKIT/CD117 and FLT3 mutations could not be demonstrated. Since patient 2112 is in CCR and relapse material of patient 1179 did not show evidence for FLT3 mutation, the FLT3-mutated T-ALL subclone seems to be effectively eradicated by current chemotherapy. This suggests that the application of FLT3 inhibitors for FLT3-mutated T-ALL, as suggested by Paietta et al, 2 may not further improve treatment outcome in pediatric T-ALL.
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