The prognostic role of tumor size in early breast cancer in the era of molecular biology.

BACKGROUND: The prognosis of early breast cancer (EBC) depends on patient and tumor characteristics. The association between tumor size, the largest diameter in TNM staging, and prognosis is well recognized. According to TNM, tumors classified as T2, could have very different volumes; e.g. a tumor of 2.1 cm has a volume of 4500 mm3, while a tumor of 4.9 cm has a volume of 60.000 mm3 even belonging to the same class. The aim of the study is to establish if the prognostic role of tumor size, expressed as diameter and volume, has been overshadowed by other factors. METHODS: The primary objective is to evaluate the association between tumor dimensions and overall survival (OS) / disease free survival (DFS), in our institution from January 1st 2005 to September 30th 2013 in a surgical T1-T2 population. Volume was evaluated with the measurement of three half-diameters of the tumor (a, b and c), and calculated using the following formula: 4/3π x a x b x c. RESULTS: 341 patients with T1-T2 EBC were included. 86.5% were treated with conservative surgery. 85.1% had a Luminal subtype, 9.1% were Triple negative and 7.4% were HER2 positive. Median volume was 942 mm3 (range 0.52-31.651.2). 44 patients (12.9%) relapsed and 23 patients died. With a median follow-up of 6.5 years, the univariate analysis for DFS showed an association between age, tumor size, volume, histological grading and molecular subtype. The multivariate analysis confirmed the statistically significant association only for molecular subtype (p 0.005), with a worse prognosis for Triple negative and HER2 positive subtypes compared with Luminal (HR: 2.65; 95%CI: 1.34-5.22). Likewise for OS, an association was shown by the multivariate analysis solely for molecular subtype (HER2 and Triple negative vs. Luminal. HR: 2.83; 95% CI:1.46-5.49; p 0.002). CONCLUSIONS: In our study, the only parameter that strongly influences survival is molecular subtype. These findings encourage clinicians to choose adjuvant treatment not based on dimensional criteria but on biological features.

Sporadic desmoid tumors of the abdominal wall: the results of surgery.

PURPOSE: Before the wait-and-see policy became the standard approach in abdominal wall desmoid tumors, surgery was performed on a systematic basis. Surgery remains indicated for progressing tumors but its extent is debatable. The abdominal wall is a common site of origin of sporadic desmoids, usually associated with a favorable prognosis. We analyzed the results of surgery at this specific site. METHODS: Data from 33 patients affected by sporadic desmoid tumors of the abdominal wall (31 primary, 2 recurrent) consecutively treated at our cancer center between January 2000 and September 2013 were retrospectively studied. RESULTS: Twenty-nine patients underwent surgery upfront and 1 after progression during the initial wait-and-see period. Prosthetic reconstruction of the abdominal wall was required in 28 patients. The average hospital stay was 5 days. Three patients developed surgical complications. Local recurrence-free survival was 90% at 5 and 10 years. Three patients had an uneventful childbirth during the follow-up after surgery. CONCLUSIONS: Desmoid tumors of the abdominal wall have a favorable prognosis after surgical resection, which remains a safe and effective treatment. Wild-type tumors are common, whereas the incidence of S45F mutation in the beta-catenin gene is lower than in other anatomic sites. Upfront surgery may be considered in selected women who wish to bear a child.

Experimental evidence on the immunopathogenesis of primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease for which an autoimmune pathogenesis is supported by clinical and experimental data, including the presence of autoantibodies and autoreactive T cells. The etiology remains to be determined, yet data suggest that both a susceptible genetic background and unknown environmental factors determine disease onset. Multiple infectious and chemical candidates have been proposed to trigger the disease in a genetically susceptible host, mostly by molecular mimicry. Most recently, several murine models have been reported, including genetically determined models as well as models induced by immunization with xenobiotics and bacteria.