Synchronous gastrointestinal stromal tumors (GIST) and other primary cancers: case series of a single institution experience.

BACKGROUND: Gastrointestinal stromal tumors (GISTs) are rare mesenchymal neoplasm affecting the gastrointestinal tract. The incidental occurrence of mesenchymal tumors and other primary tumors has not been well described in literature. OBJECTIVE: The aim of this study was to evaluate the clinical and pathologic features of GIST occurring synchronously with other primary tumors. METHODS: Forty-three patients with diagnosis of GIST treated surgically with curative intent at our institution from 1998 to 2006 were included. The patient clinical data and pathological reports were reviewed. RESULTS: Of the 43 patients, there were 6 (14%) cases of synchronous GIST and other primary tumors discovered as coincidental findings. The synchronous GISTs analyzed were located in the stomach (50%) and small intestine (50%), size ranging from 0.7 to 7.6 cm (median 3.35 cm). Five (83%) of the concurrent primary tumors were from gastrointestinal origin and only one (17%) patient presented with concurrent breast cancer and GIST. The synchronous GISTs immunofenotype shows positivity for CD117 and CD34 (100%), smooth-muscle actin (SMA) (67%), S100 (50%) and desmin (33%). Whereas staining for cytokeratin AE1/AE3 and PDGF were all negative. According to GIST risk category for aggressive behavior three were classified as very low, one intermediate and two high. CONCLUSIONS: The synchronous occurrence of GISTs and other primary neoplasm is not an uncommon entity and usually they are discovery incidentally. Epithelial tumors of the gastrointestinal tract are the most associated with concomitant GISTs. Further studies are required to clarify the molecular and genetic mechanisms of carcinogenesis and progression associating GIST and synchronous tumors.

Role of plasma DNA as a predictive marker of fatal outcome following severe head injury in males.

The prediction of outcome is one of the major problems associated with traumatic brain injury. Recently, investigations have been performed on the potential use of circulating cell-free DNA in plasma for clinical diagnosis and prognosis of a variety of conditions. In this study, we investigated DNA plasma concentrations after severe traumatic brain injury (TBI) and its correlation with primary outcome. We studied 41 male victims of TBI, with isolated severe TBI or severe TBI with associated exracranial injuries. Control samples were obtained from 13 healthy male volunteers. Plasma DNA was measured by a real-time PCR assay for the beta-globin gene. The mean time for first sampling (study entry) was 11.7 +/- 5.2 h after injury; subsequent DNA determinations were performed 24 h after study entry. Mean plasma DNA concentrations were significantly increased in TBI patients (366,485 and 131,708 kilogenomes-equivalents/L, at study entry and 24 h later, respectively) compared with the control group (3031 kilogenomes-equivalents/L). Additionally, a significant correlation between higher plasma DNA concentrations, determined 24 h after study entry, and fatal outcome was observed. However, at second sampling, there was no significant correlation between plasma DNA concentrations and the presence of associated extracranial injuries. High plasma DNA concentrations at second sampling time predicted fatal outcome with a sensitivity of 67% and specificity of 76%, considering a cut-off value of 77,883 kilogenomes-equivalents/L. Thus, this study showed that severe TBI is associated with elevated DNA plasma levels and suggests that persistent DNA elevations correlate with mortality.

Radioresistance is associated to increased Hsp70 content in human glioblastoma cell lines.

Radiation therapy is routinely prescribed for high-grade malignant gliomas. However, the efficacy of this therapeutic modality is often limited by the occurrence of radioresistance, reflected as a diminished susceptibility of the irradiated cells to undergo apoptosis. Heat-shock proteins (Hsps) synthesis can be increased by cellular insults, such as radiation-induced damage. Inducible Hsp70 has been suggested to have multiple roles in cytoprotection against apoptosis. Accordingly, high levels of Hsp70 prevent stress-induced apoptosis. In the present study, we investigated whether the content of Hsp70 is associated to glioblastoma cell radioresistance. To this end, the U-87MG, U-251MG and MO59J human glioblastoma cell lines were irradiated at 2, 5 and 10 Gy and their relative radioresistance and Hsp70 were determined. Following 5 Gy irradiation, in MO59J and U-251MG a significant decrease in colony formation was found, whereas the U-87MG was relatively radioresistant. Three hours after the irradiation (at 5 Gy) Hsp70 contents increased 110% in the U-87 MG cells, but did not significantly change in the U-251MG and MO59J cells. Thus, our results suggest that Hsp70 protection against radiation-induced apoptosis might underlie glioblastoma radioresistance.