Multiple observational studies suggest an increased risk of colon cancer in patients with diabetes mellitus (DM). This can theoretically be the result of an influence of the diabetic environment on carcinogenesis or the tumor biologic behavior. To gain insight into the influence of a diabetic environment on colon cancer characteristics and outcomes. Retrospective analysis of clinical records in an academic tertiary care hospital with detailed analysis of 81 diabetic patients diagnosed of colon cancer matched with 79 non-diabetic colon cancer patients. The impact of streptozotocin-induced diabetes on the growth of colon cancer xenografts was studied in mice. The incidence of DM in 1,137 patients with colorectal cancer was 16%. The diabetic colon cancer cases and non-diabetic colon cancer controls were well matched for demographic and clinical variables. The ECOG Scale Performance Status was higher (worse) in diabetics (ECOG ≥1, 29.1% of controls vs 46.9% of diabetics, p = 0.02), but no significant differences were observed in tumor grade, adjuvant therapy, tumor site, lymphovascular invasion, stage, recurrence, death or cancer-related death. Moreover, no differences in tumor variables were observed between patients treated or not with metformin. In the xenograft model, tumor growth and histopathological characteristics did not differ between diabetic and nondiabetic animals. Our findings point towards a mild or negligible effect of the diabetes environment on colon cancer behavior, once cancer has already developed.

To provide effective and accurate radiotherapy (RT) for advanced cancer patients who experience breakthrough pain (BP) due to positioning manoeuvres, through the use of FPNS. Secondary endpoints were the dose and time required to achieve a 50% numeric rating scale (NRS) reduction and conduction of a pharmacoeconomic analysis. Twenty-seven advanced cancer patients with moderate-severe BP associated with routine radiotherapy procedures and manoeuvres were selected to receive FPNS. Most patients (20/27) had bone metastases. The patients showed a low Karnovsky performance status (mean 54%; range: 30-80). BP intensity was scored with the NRS before and after the procedures that triggered it. All patients were already receiving opioid baseline treatment at a total dose equivalent to 40-160mg oral morphine. Before the procedure, BP was treated with 100-400μg of FPNS. Data related to tolerance, pain relief, onset of the relief and efficient dose to allow RT to proceed were collected. In 26 patients the BP score was reduced by at least 50% as determined in 15.5min (range 8-35min) after fentanyl pectin intranasal administration, and pain relief started after 7min (range 3-15min); p<0.05 in both cases. The duration of pain reduction facilitated the proceeding of RT. The Mean NRS score before the procedure was 9 (95%CI: 8.6-9.4) and decreased during procedure to 3 (95%CI: 2.5-3.8). The average dose of FPNS for most patients was 100-200μg to achieve pain control, except in three patients who required progressive doses of up to 300-400μg. After receiving 300μg, one patient dropped out of the study due to severe adverse effects (nausea). Seven patients reported minor undesirable effects related to FPNS administration. Certain necessary RT procedures in advanced cancer patients can cause severe BP episodes. A simple, safe, fast acting and strong analgesic is needed. FPNS is a rapidly absorbed opioid analgesic with a pain relief profile that would be particularly well suited for this patient population. By reducing BP, the drug enables the completion of necessary RT procedures without needless patient discomfort. When BP is attenuated, Department productivity is maintained and unnecessary delays are avoided. Further studies and clinical trials are needed to assess therapeutic FPNS dosages with a view to defining efficacy in the correct clinical context.