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Pancreatic cancer (PC) is the fourth cause of cancer death in Western countries, the only chance for long term survival is an R0 surgical resection that is feasible in about 10%-20% of all cases. Five years cumulative survival is less than 5% and rises to 25% for radically resected patients. About 40% has locally advanced in PC either borderline resectable (BRPC) or unresectable locally advanced (LAPC). Since LAPC and BRPC have been recognized as a particular form of PC neoadjuvant therapy (NT) has increasingly became a valid treatment option. The aim of NT is to reach local control of disease but, also, it is recognized to convert about 40% of LAPC patients to R0 resectability, thus providing a significant improvement of prognosis for responding patients. Once R0 resection is achieved, survival is comparable to that of early stage PCs treated by upfront surgery. Thus it is crucial to look for a proper patient selection. Neoadjuvant strategies are multiples and include neoadjuvant chemotherapy (nCT), and the association of nCT with radiotherapy (nCRT) given as either a combination of a radio sensitizing drug as gemcitabine or capecitabine or and concomitant irradiation or as upfront nCT followed by nRT associated to a radio sensitizing drug. This latter seem to be most promising as it may select patients who do not go on disease progression during initial treatment and seem to have a better prognosis. The clinical relevance of nCRT may be enhanced by the application of higher active protocols as FOLFIRINOX.

Desmoid tumors (DTs) are neoplasms of fibroblastic origin characterized by lack of a capsule. They are nonmetastatic and locally aggressive. Intraabdominal DTs are often observed in familial adenomatous polyposis and Gardner syndrome or subsequent to localized traumatic injury. Sporadic forms are defined as nontrauma- or nongenetic-related DTs. Isolated, sporadic pancreatic DTs have been considered anecdotal, with only 9 cases described in the literature. We report the case of a 68-year-old man with a case of sporadic cystic DT localized to the pancreatic tail. The tumor was discovered incidentally during computerized tomography performed for an unrelated condition. The patient was asymptomatic; however, biopsy was performed on the clinical suspicion of cystic cancer of the pancreas. Pathology analysis showed fibroblastic proliferation, and the diagnosis of DT was confirmed by immunohistochemical staining for beta-catenin. The patient underwent resection with no further treatment and remain disease-free 60 months after surgery.

The incidence of unsuspected adrenal masses (incidentalomas) based on CT-scan results to be higher than in the past. The aim for our study was to establish some guidelines for an appropriate management.From 1986 to 1995, 61 patients with no history or clinical findings suggestive of adrenal mass or adrenal hyperfunction were discovered by radiologic examination to have an incidentaloma larger than 1 cm. In each patient basal biochemical evaluations were obtained to exclude the presence of adrenal cortical or medullary dysfunction. There were 28 men and 33 (54.1%) women, with a mean age of 53 years (range 16-74). 19 patients underwent CT-guided fine-needle biopsy to exclude metastatic tumors. Furthermore in 29 patients 75-Se-selenomethyl-norcholesterol was performed and 17 were studied by MRI.At CT-scan mean lesion diameter was 5.48 +/- 3.76 cm (range 2-23); 32 adrenal masses were right sided and 3 (4.9%) were bilateral. 17 patients had concordant scintigraphic imaging pattern, 6 bilateral uptake and 6 had discordant imaging. CT-guided FNAB showed malignancy in 9. Adrenalectomy was performed in 45 patients according to a score calculated by 4 parameters: age of the patients, size of the mass, scintigraphic pattern, MR imaging. Twenty-four had a score greater than 9 and in the remaining 21 patients in spite of a score lower than 10 adrenalectomy was performed based on: 1) increased size at CT scan follow-up (15 pts); 2) either suspected primitive malignant neoplasm at CT-guided FNAB or history of malignancy (6 pts); 3) elevated 24-hour dopamine (4 pts). In 12 (26.7%) patients a malignant tumor was found. There were not any statistically significant differences (p0.05) between the age of the patients with malignant neoplasms and those with benign masses, and between the size of the masses, which were 7.58 +/- 5.93 cm (range 2-23) and 5.03 +/- 2.81 cm (range 3-17) respectively. The difference in scores between the patients with malignant masses (12.17 +/- 2.95) and those with benign ones (9.09 +/- 1.33) was statistically significant (p0.01).Since adrenal incidentaloma have a malignancy rate higher than the other adrenal tumors, it is crucial to outlinesome criteria to sort out the patients at risk for whom adrenalectomy is to be warranted. Based on our results we believe that patients with a score9 should undergo adrenalectomy.

In 15-20% of the cases pheochromocytoma (pheo) localizes in extraadrenal sites and in about 15% of all cases it seems to be multiple. We analyze our 20-year experience in surgical treatment of pheos, studying the differences between typical and extraadrenal or multiple tumors. From 1977 to 1996 we operated 55 patients (patients) with pheos, 28 (50.9%) males and 27 females (mean age 41 years, range 10-63). Two groups have been distinguished: classic pheos (Group 1, 45 patients) and extraadrenal or multiple pheos (Group 2, 10 patients). Hypertensive crises were present in 37/45 (82.2%) patients of Group 1 and in 7/10 patients of Group 2. Five (11.1%) masses were nonfunctioning and incidentally discovered (4 in Group 1 and one in Group 2). In 4 cases association with familial syndromes was observed (3 MEN IIb, 1 von Recklinghausen syndrome); no further significant differences in clinical features and laboratory data were found between the two Groups. At immunohistochemical analysis 26/26 patients resulted positive for chromogranin A and NSE and 17/26 (11/20 in Group 1 and 4/6 in Group 2) resulted positive for S 100 protein. Five (11.1%) malignant pheos were discovered and removed (Group 1); average survival of these patients was 54.4 months, two patients underwent radioactive iodine (131-I-MIBG) therapy after surgery and only one patient is still alive at 24-month follow-up. Recurrence for benign sporadic pheo (Group 1) occurred in one patient 183 months after adrenalectomy. Ectopic, associated with familial syndromes and multiple pheos are not uncommon and although recovery in surgically treated patients is excellent, lifelong follow-up is necessary also in benign tumors.

The aim of this study was to evaluate CEA and CA 15-3 changes in patients surgically treated for breast cancer. One hundred and three women (median age 59 years, range 31-83 years) with pT1-2, pN0-1, M0 breast cancer were followed up for at least 5 years. CEA and CA 15-3 serum levels were measured before operation and every 6 months during follow-up. The diagnostic sensitivity of CEA and CA 15-3 was 22.3% and 33.3% respectively. There was a significant difference (p0.01) between pre- and post-operative (6 months and 5 years after surgery) mean CEA serum levels independent of TNM staging. During follow-up, 21 (20.4%) patients showed recurrence of cancer and overall CEA and CA 15-3 sensitivity was 38.1% and 61.1%, with 98.8% and 91.2% specificity, respectively. Tumor marker measurement may be useful in post-surgical follow-up, but at present they are neither sensitive nor specific enough for early diagnosis of malignancy.

Primary hyperparathyroidism is the most common cause of hypercalcemia and 80-85% of the patients have parathyroid tumors. The purpose of this retrospective review was to analyse whether differences exist between patients with parathyroid tumors treated in the 1980s and 1990s. Between 1980-1997, 253 patients underwent initial surgical neck exploration for hyperfunctioning parathyroid tumors. Renal (polyuria, nocturia, renal colic due to lithiasis), rheumatologic (bone and joint pain), neurological (fatigue, memory loss, depression) and gastrointestinal (dyspepsia, anorexia, nausea) symptoms were recorded and main biochemical parameters were measured. In all patients one or more preoperative localization procedures were carried out prior to successful parathyroidectomy, and the confirmation of imaging findings was obtained after surgery. The patients were divided in two groups. Group A: 121 (47.8%) patients who underwent surgery from 1980-1989; Group B: 132 (52.2%) patients in whom parathyroidectomy was performed from 1990-1997. There were no differences (p=NS) between the two groups in average age, preoperative serum creatinine and intact-PTH levels. Symptoms were most common in Group A, and pre-operative serum calcium levels were significantly lower in Group B. Ultrasonography (n=191) sensitivity did not improve significantly (82.8% vs 82.9%), but positive predictive value (PPV) was higher (89.8% vs 96.0%). CT-scan (n=73) sensitivity was 79.2% and 82.6%, and PPV was 95.0% and 100% in Groups A and B, respectively. 201Tl/99mTc subtraction scintigraphy (n=111, Group A) was 84.6% sensitive (PPV=92.6%) whereas 99mTc-sestamibi scanning (n=90, Group B) was 85.1% sensitive (PPV=96.1%). In conclusion, the clinical features of parathyroid tumors has changed in the nineties and increasing asymptomatic pHPT rate has been found. Although sensitivity and PPV of preoperative localization procedures has improved moderately, at present noninvasive techniques may offer excellent results and should be used in all patients with suspected parathyroid tumors.

The progress of research on the molecular pathogenesis of liver fibrosis and the consequent discoveries are likely to open new possibilities for therapeutic approaches to the management of this disease in the future. A key step towards this goal is a deeper comprehension of both the complex molecular and cellular mechanisms and the signaling involved in the development of hepatic fibrosis. It is not yet clear, in fact, what role apoptosis, cytokines, oxidants and other molecules play and what relationships exist between them in favouring or delaying the onset of these adverse mechanisms. At present, a unique mechanism is recognized to be the main reason for the cause and development of liver fibrosis: sustained hepatic stellate cell activation and transformation. Therefore, in this review, after considering the cause, development of fibrosis and interrelation between molecular and cellular profibrotic mechanisms, the part played in counteracting both of these actions by some anti-oxidants and anti-fibrotic molecules such as cytokines, prostacyclin and others will be taken into consideration. The gene therapy and the possible therapeutic use of liver stem cells and tissue engineering will also be dealt with briefly. At the moment, however, the efficacy of these novel strategies still needs to be further validated in animal studies and confirmed in clinical trials. Some data that are already available from in vitro and animal studies demonstrating the effectiveness of novel approaches to inhibiting or treating liver fibrosis can only offer moderate hope.