No abstract

Many different pathologies derived from the notochord can be observed: some are remnants, some may be precursors of chordomas and some have similar features but are probably not genuine chordomas. To-day, immuno-histological studies should permit to differentiate them from real chordomas. Improving knowledge of molecular biology raises hopes for complementary treatments but to date the quality of surgical resection is still the main factor of prognosis. Complementary protontherapy seems useful, especially in skull base chordomas, which have better overall results than those of the craniocervical junction and of the cervical spine. However, we are still lacking an intrinsic marker of evolution to differentiate the slow growing chordomas with an indolent evolution from aggressive types leading rapidly to recurrence and death on which more aggressive treatments should be applied.

Primary tumors of the epididymis are rare. Adenomatoid tumors are benign, usually found within the wall of fallopian tubes or beneath the uterine serosa. They are most frequently diagnosed as benign tumors of the epididymis and represent 30% of paratesticular tumors. The origin of this tumor is mesothelial cells. Leiomyoma are less common in the paratesticular localization. The origin of this tumor is smooth muscle cells. Clinically, these tumors are indistinctive with a painless mass of the scrotum. Here, we reported a case of combined leiomyoadenomatoid tumor. The histogenesis of this lesion remains unknown. This entity can be the result of a collision of the two tumors, or it can be a subtype of adenomatoid tumors with smooth muscle hyperplasia. This case showed the difficulty that occurs in the identification of this kind of lesion. Only one case of this entity in the epididymis was described in the literature. Leiomyoadenomatoid tumor is a benign neoplasm. In our case, this lesion was surgically removed in toto and no recurrence was observed.

Polycystic echinococcosis due to Echinococcus vogeli is a rare parasitic infection that occurs in rural areas of Central and South America. Only molecular identification performed on formalin-fixed paraffin-embedded liver tissue samples gave an unequivocal diagnosis of this disease in a Paraguayan immigrant in Argentina.

Biliopancreatic cancer is one of the most aggressive solid neoplasms, and incidence is rising worldwide. It is known that ATF6α is one of the transmembrane proteins that acts crucially in endoplasmic reticulum stress response, and knockdown induces apoptosis of pancreatic cells. Apart from this, p-p38 has been previously correlated with better outcome in pancreatic cancer. Interestingly, ATF6α knockdown pancreatic cells showed increased p-p38. The aim of this study was to evaluate the expression of these 2 proteins, p-p38 and ATF6α, and their correlation with the outcome of biliopancreatic adenocarcinoma patients.Samples from patients with biliopancreatic adenocarcinoma that underwent pancreaticoduodenectomy from 2007 to 2013 were used to construct a tissue microarray to evaluate p-p38 and ATF6α proteins by immunohistochemistry.We observed that both markers showed a tendency to impact in the time to recurrence; then a combination of these 2 proteins was analyzed. Combination of ATF6αhigh and p-p38low was strongly associated with a higher risk of recurrence (hazard ratio 2.918, P = 0.013). This 2-protein model remained significant after multivariate adjustment.We proposed a 2-protein signature based on ATF6αhigh and p-p38low as a potential biomarker of risk of recurrence in resected biliopancreatic adenocarcinoma patients.