RISK OF PANCREATIC CANCER FOLLOWING BREAST CANCER

Abstract

Background and aim: About 10% of pancreatic cancers (PaCa) are caused by an inherited disorder. In particular, mutations in the BRCA1 and BRCA2 tumour suppressor gene, which are responsible for the hereditary breast and ovarian cancer syndrome, have been associated with excess risk of PaCa. The aims of the study were a) to assess whether PaCa risk is increased in breast cancer patients, b) to establish whether it is more frequently associated with specific breast cancer characteristics. Material and methods: We retrieved information from a computerized database on all consecutive patients treated for invasive breast cancer at the European Institute of Oncology (EIO) in Milan during 1997-2006. Follow-up was obtained through the patients' follow-up visit to the hospital. The number of PaCa cases observed during follow-up was compared with that expected calculated using age- and sex-specific population-based incidence data. Results: Of the 16,016 patients included in the database, 4706 (29%) had no follow-up. The remaining 11,310 patients (11,246 women, 64 men, median age 53) contributed to 38,193 patient-years of observation. During a median follow-up of 3.2 years (range 0.1 to 10 years), 6 women developed PaCa (1.6 per 10,000 patient-year) against 6.3 expected. Non-significant excess risks of PaCa were observed in women treated for breast cancer before age 50 (O = 2, E = 0.5) in those with high-grade (O = 4, E = 1.7), ER and PgR negative (O = 3, E = 1.0), high proliferative index (ki67 ≥ 20%) (O = 4, E = 2.8) breast tumors. A significant excess of pancreas cancer was observed in women with more "aggressive" tumors (G3, ER/PgR negative, Ki67 ≥ 20%) (O = 3; E = 0.6; SIR = 5.0; 95% CI = 1.0-14.6). Of interest, 1 of the 2 women diagnosed with PaCa before age 50 had a 1st degree relative with breast cancer and diabetes. Discussion: Since many patients came from distant parts of Italy, it was difficult to maintain durable contact with them. Possibly, development of PaCa could have interfered with routine breast cancer follow-up visit at the EIO, leading to under-estimation of the risk of PaCa. Still, our limited results are compatible with an excess of PaCa in younger breast cancer patients, possibly related to common genetic predisposition. Conclusion: Despite common genetic predisposition, PaCa does not constitute a major concern in breast cancer patients. Overall, the risk is similar to that of the general population, although younger patients and those with aggressive tumors are at higher risk.