Abstract. Objectives:The aims of this study are to (1) study the influence of polymorphisms in adiponectin gene on adiponectin levels and potential associations with breast, prostate and colon cancer; (2) investigate the associations of adiponectin levels with other adipokines and breast, prostate and colon cancers. Subjects: We measured fasting adiponectin, leptin, insulin, Sex steroids in 132 (66 females, 66 males) cancer patients and 68 age and sex matched apparently healthy subjects. Body Mass Index (BMI) and waist circumference were used as indices of obesity. Insulin Resistance was assessed using Homeostasis Model Assessment (HOMA). Three single nucleotide polymorphisms (SNP rs182052 (G-10066-A), SNP rs1501299 (276G > T), SNP rs224176 (45T > G) in adiponectin gene were studied using Real Time Polymerase Chain Reaction. Results: GG genotype of SNP rs1501299 was significantly associated with higher levels of adiponectin (OR = 1.2, 95%CI(1.03-1.3), p = 0.02); breast (OR = 8.6, 95%CI(1.03-71), p = 0.04), colon cancers (OR = 12, 95%CI(1.2-115), p = 0.03). GT genotype was also associated significantly with colon cancer (OR = 2.6, 95%CI (1.1-6), p = 0.03). However SNP rs224176 was associated with only breast cancer. Conclusion: Our results demonstrate that adiponectin gene SNP rs1501299 and SNP rs224176 may be the predisposing factors in some cancers but our results differ from what has been reported in other populations suggesting a complex relationship between genetic variations and phenotypic adiponectin levels.
10711 Background: TAC confers significant disease free and overall survival benefits vs FAC for patients with node positive breast cancer. However TAC is associated with higher incidence of febrile neutropenia. In our study prophylactic G-CSF was used in patients, who developed grade 4 neutropenia with ANC < 100 or febrile neutropenia to prior cycle of TAC. Methods: Following surgery, patients with operable, 1–9 nodes positive breast cancer, ECOG 0–1, and adequate hematologic and organ function were enrolled on to the study, and were to receive TAC day 1 every 3 weeks for 6 cycles . All patients received prophylactic Ciprofloxacin 500-mg bid from days 5–14 after each cycle of chemotherapy unless prophylactic G-CSF was given. Eighty three patients were enrolled during the period 13–1-04 to 30–12–05. Patients who had received at least 2 cycles of TAC were eligible for evaluation. Patients were given prophylactic G-CSF if they had profound neutropenia (ANC < 100) or febrile neutropenia in prior cycle. Results: At the cut-off date for this analysis 79 patients were evaluable. 68 patients had completed the planned 6 cycles of TAC. Three, 2, 3 and 3 patients completed 2, 3, 4 and 5 cycles respectively. Sixty one patients required prophylactic G-CSF - 21 after febrile neutropenia in prior cycle, 39 after profound neutropenia in prior cycle and 1 received from first cycle itself because of post operative seroma with diabetes mellitus. 23 patients developed febrile neutropenia (29.1%) - 3, 8, and 12 after 3, 2 and 1 cycles respectively. Only two patients (3.2%) who received prophylactic G-CSF developed febrile neutropenia. Full dose of TAC could be maintained in 98.6% cycles. Conclusions: The use of G-CSF prophylaxis based on risk assessment could prevent febrile neutropenia in patients, who had profound neutropenia in prior cycle. Also G-CSF could prevent further febrile neutropenia in patients who had developed the same in prior cycle. The above strategy helped in maintaining the dose intensity of TAC. No significant financial relationships to disclose.
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