Whole body 18FDG-PET and the response of esophageal cancer to induction therapy: results of a prospective trial.

PURPOSE: Whole-body 18F-fluorodeoxyglucose ([18F]FDG) positron emission tomography (PET) imaging before and after induction therapy was prospectively evaluated in patients with esophageal cancer to determine whether changes in PET images could measure response to therapy. PATIENTS AND METHODS: Between April 1997 and April 1999, 39 patients (34 men and five women; median age, 59 years; range, 36 to 76 years) with esophageal cancer were prospectively enrolled in a single-institution clinical trial of staging, including PET, induction therapy, restaging including PET, and esophagectomy. All patients undergoing esophagectomy after induction therapy (n = 17) were followed either to recurrence, to death, or through a disease-free interval of at least 24 months. RESULTS: PET after standard staging studies and before therapy imaged undetected sites of metastatic disease in six patients (15%). Restaging (including PET) after induction therapy did not identify any patients with disease progression or any patients with loco-regionally unresectable disease at exploration. The median decrease in the standardized uptake value (SUV) during induction therapy was 59%. After R0 esophagectomy, the 2-year disease-free and overall survival was 38% and 63%, respectively, among patients who had a less than 60% decrease in SUV, and 67% and 89%, respectively, among patients who had a greater than 60% decrease in SUV (P =.055 and P =.088, respectively). CONCLUSION: Compared with conventional imaging, PET detects additional sites of metastatic disease at initial evaluation. After induction therapy, PET did not add to the estimation of loco-regional resectability and did not detect new distant metastases. However, changes in [18F]FDG PET may predict disease-free and overall survival after induction therapy and resection in patients with esophageal cancer. Further evaluation in larger trials is warranted.     

SUNCT and SUNA: medical and surgical treatments

Cognitive deficits may contribute to falls in Parkinson’s disease (PD) and these deficits may be risk factors for falls. However, their association with falls has been generally studied in patients with continuous gait problems. There have been few studies in PD patients without postural instability. In addition, the effectiveness of various simple bedside cognitive tests in predicting falls has not been established. In this study, we investigated the effectiveness of three bedside cognitive tests in consecutive patients with PD without postural instability. Of the 119 patients, 39 experienced falls during the follow-up period. Of the bedside cognitive assessment methods examined, only the Montreal Cognitive Assessment (MoCA) score was significantly lower in the group of fallers than in the group of non-fallers. This result suggests that the MoCA is effective as a bedside test for evaluating the risk of falls.     

Effect of neurotensin on amylase secretion from rat pancreasin vivo andin vitro

The effects of neurotensin, a tridecapeptide localized mainly in the gut, on pancreatic secretion are controversial. It is not clear whether the effects are mediated by direct or indirect effects. The present study was done to determine the effect of threshold doses of neurotensinin vivo in the rat as well asin vitro to clarify whether the action is direct or indirect. Forin vivo studies the pancreatic duct of rats was cannulated and threshold doses of neurotensin and CCK-8 alone or in combination were infused as an intravenous bolus and pancreatic juice collected at 10-min intervals for 1 hr. Forin vitro studies dissociated lobules and acini were incubated for 1 hr with 10^–11–10^–6 M neurotensin with or without 10^–9 M CCK-8 (maximally effective dose). Amylase secretion in the pancreatic juice or in the medium was determined. Neurotensin and CCK-8 at a dose of 50 pM/kg increased pancreatic protein secretionin vivo. Neurotensin in combination with CCK-8 did not potentiate protein secretion. In the pancreatic lobules and acini, neurotensin 10^–11–10^–6 M alone or in combination with CCK-8 (10^–9 M) did not stimulate amylase secretion above the basal level or that stimulated with CCK-8. The combined data indicate that the effect of neurotensin is not mediated by a direct action on the pancreatic acinar cells.This work was supported by the Medical Research Service of the Veterans Administration.     

Effect of somatostatin on amylase secretion fromin vivo andin vitro rat pancreas

In the present study the effect of somatostatin on amylase secretion was determined usingin vivo cannulation and isolated acini from rat pancreas.In vivo somatostatin-14 inhibited amylase secretion in basal state and that stimulated with CCK8 and acetylcholine. Somatostatin-14 and somatostatin-28 failed to inhibit amylase secretion from isolated acini in basal state and that stimulated with CCK8 and bethanechol. Somatostatin-14 did not increase⁴⁵Ca uptake or efflux of label from acini preloaded with⁴⁵Ca. Cellular cyclic AMP levels were not significantly increased. Somatostatin-14 did not alter the synthesis of proteinsin vitro, as judged by incorporation of a mixture of fifteen¹⁴C-labeled amino acids. Somatostatin-14 stimulated phosphoprotein phosphatase in higher doses, whereas no effect was observed at lower doses. Inhibition of secretionin vivo and lack of stimulation of amylase secretion in isolated acini suggest that the somatostatin effectin vivo is mediated by an indirect effect similar to other peptides, for example, opiates and neurotensin. Stimulation of phosphoprotein phosphatase suggests that somatostatin may bind to the acinar cells and affect functions other than secretion and synthesis of enzymes.     

Melanoma histopathology reporting: are we complying with the National Minimum Dataset?

BACKGROUND: The Royal College of Pathologists introduced the National Minimum Dataset (NMDS) for the histopathological reporting of cutaneous melanoma in February 2002. AIM: To determine if histological reporting of invasive primary cutaneous melanoma in the West Midlands region of the UK was compliant with the NMDS. METHODS: Reports were identified from March 2002 to March 2003 via the regional Cancer Intelligence Unit, and compared with the NMDS. If all items of the NMDS were adhered to, the report was considered compliant. If not compliant, the report was checked to see if it included selected clinical and staging parameters. RESULTS: 543 cases of invasive cutaneous melanoma were identified, but only 407 reports were analysed. 69/407 (17%) (95% CI 14% to 20%) reports were fully compliant with the NMDS. Of the non-complaint reports, 45/361 (12%) (95% CI 9% to 16%) reported all staging and clinically relevant parameters; 62/361 (17%) (95% CI 59% to 65%) reported all staging parameters. Breslow thickness was reported in all but one of the reports (99.7%), Clark's level was reported in 344/407 (85%), ulceration in 280/407 (69%), and microsatellites in 146/407 (36%). CONCLUSION: There was slow uptake of the NMDS in this region in the year following its introduction. Although major parameters required for staging were more consistently reported, ulceration and microsatellites were less frequently reported.