Optical Property Stability of Light-Cured versus Precured CAD-CAM Composites.

Objective: The aim of this study was to evaluate the optical property changes after staining of precured (PC) and light-cured (LC) composites. Materials and Methods: Specimens were prepared using different LC composites (GrandioSO-Voco, Filtek Z350-3M/ESPE, Opallis-FGM, and Kalore-GC) and four PC blocks (Grandio Blocs-Voco, Lava Ultimate-3M ESPE, Brava Block-FGM, and Cerasmart-GC) from the same manufacturers (n = 20). Baseline color, gloss, translucency, and fluorescence were evaluated. The staining protocol was performed for 15 days, and the final optical properties were reevaluated. Results: The changes in each property were calculated (ΔGloss, ΔTranslucency, ΔFluorescency, ΔE ∗ 00). Data were analyzed by ANOVA and Tukey's test (α = 5%). Changes in all properties were observed after staining for all materials, with darkening and reduction of gloss, fluorescence, and translucency. Nonsignificant differences were observed between the light-cured and precured materials of the same manufacturer for ΔG and ΔT, but significant differences existed for ΔF and ΔE ∗ 00. For ΔF, the only significant differences were observed between Brava Block and Opallis (smaller). For ΔE ∗ 00, only the light-cured composites GrandioSO and Z350 showed significantly less change than the corresponding blocks. Precured composites were affected the same way as light-cured ones by the staining in relation to the reduction of gloss and translucency. Conclusion: A higher reduction in fluorescence was observed for only one brand of block and was similar for the others. The two brands of light-cured materials showed less staining, while for the others, the staining was similar. The effects of staining vary according to the composite formulation.

Primers on molecular pathways - lipoxygenases: their role as an oncogenic pathway in pancreatic cancer.

Different evidence supports a functional role of enzymes involved in lipid metabolic pathways, such as lipoxygenases (LOXs) and their metabolite derivatives, in carcinogenesis. LOX enzymes catalyze the dioxygenation of arachidonic acid into hydroxyperoxyeicosatetraenoic acids, which is followed by their conversion to their corresponding eicosanoids as hydroxyeicosatetraenoic acids, leukotrienes, lipoxins and hepoxilins, which in turn act as cellular messengers. Subcellular LOX enzyme localization varies according to the LOX and cellular type regulating different cell functions. LOX enzymes or their products may exert their biological effects in different modes, either intracellular or in other cells. Numerous clinical studies on expression of LOXs in human tumors as well as in animal models indicate different roles of distinct LOX isoforms in carcinogenesis. In fact, different LOXs exhibit either protumorigenic or antitumorigenic activities and modulate the tumor response in a tissue-specific manner. Moreover, the LOX pathways are involved in the spread and metastasis of several cancers, including pancreas, through the activation of several cellular signaling pathways which modify gene expression affecting cellular proliferation, survival, migration and extracellular matrix production. In this review we focus on the important role and different mechanisms of action of LOX pathways in the regulation of pancreatic cancer initiation and progression. A novel approach for pancreatic cancer chemoprevention would involve targeting LOX activities, alone or in combination with other pathways as a major anticancer strategy.

A randomised phase II study of oxaliplatin alone versus oxaliplatin combined with 5-fluorouracil and folinic acid (Mayo Clinic regimen) in previously untreated metastatic colorectal cancer patients.

The aim of this study was to examine the efficacy and safety of both oxaliplatin as a single agent and oxaliplatin in combination with dailyx5 bolus 5-fluorouracil and folinic acid (5-FU/FA, Mayo clinic regimen) in the first-line treatment of metastatic colorectal cancer (CRC) patients. 73 advanced CRC patients were randomised to receive either oxaliplatin 85 mg/m(2) every 2 weeks (35 patients), or the same treatment combined with 5-FU 425 mg/m(2)/day and FA 20 mg/m(2)/dayx5 days every 4 weeks (38 patients). Treatment was continued until disease progression or unacceptable toxicity. All patients had documented inoperable disease and no previous chemotherapy for advanced disease. Based on the investigators' assessment of best response, objective response rate was 9% (95% confidence interval (CI) 2-24%) in the oxaliplatin arm, and 45% (95% CI 27-64%) in the oxaliplatin+5-FU/FA arm. Median progression-free survival (PFS) was 2 months (95% CI 1.7-2.4 months) in the oxaliplatin arm and 3.9 months (95% CI 2.9-5 months) in the oxaliplatin+5-FU/FA arm. Severe neutropenia was seen in 23% of patients in the oxaliplatin+5-FU/FA arm, and none in the oxaliplatin arm. There were two treatment-related deaths, both in the oxaliplatin+5-FU/FA arm. In the oxaliplatin+5-FU/FA arm, severe diarrhoea, vomiting and stomatitis were seen in 34, 14 and 14% of the patients, respectively. In conclusion, oxaliplatin at a dose of 85 mg/m(2) given every 2 weeks was well tolerated and has limited activity in metastatic CRC, while the combination of this treatment with the full-dose Mayo clinic regimen (5-FU bolus 425 mg/m(2)/day+FA 20 mg/m(2)/dayx5 days every 4 weeks), although active, was unfeasible due to a high level of myelosuppression and gastrointestinal toxicity. Alternative lower dosing or other regimens are to be explored to ascertain the value of bolus 5-FU/FA combined with oxaliplatin.

Single-agent gemcitabine in pretreated patients with non-small-cell lung cancer: results of an Argentinean multicentre phase II trial.

The activity and mild toxicity profile of single-agent gemcitabine therapy in untreated (chemonaive) patients with non-small-cell lung cancer (NSCLC) is well documented. This phase II trial was conducted to determine the objective tumour response rate and toxicity profile of single-agent gemcitabine in pretreated patients with NSCLC. Patients with histological evidence of advanced NCSLC stage IIIB or IV; at least one prior chemotherapy regimen including a platinum or taxane analogue; an Eastern Cooperative Oncology Group (ECOG) performance status of 0-2; clinically measurable disease; adequate bone marrow reserve; and adequate renal function; received 1000 mg m(-2) gemcitabine administered over 30 min on days 1, 8 and 15 of a 28-day cycle defined as 3 weekly treatments followed by 1 week of rest. Twenty-nine patients were evaluated for efficacy and 32 for toxicity. One patient achieved a complete response and five patients had a partial response resulting in a total response rate of 20.6% (95% confidence interval (CI) 6-34). Median response duration was 7 months (range 4-11 months). Twelve (41%) patients reached stable disease after two cycles of therapy and 11 (38%) patients had disease progression. Median progression-free survival time was 3 months and median overall survival time was 5.5 months. Toxicity was generally mild (grades 0-2). Severe (grade 3 or 4) haematological toxicities included grade 3 anaemia in one patient and grade 3 thrombocytopenia in two patients. Severe non-haematological toxicities included one patient each with grade 3 liver transaminase elevations, nausea/vomiting and diarrhoea. This study confirms the activity and safety of single-agent gemcitabine in pretreated patients with advanced NSCLC who are refractory or sensitive to first-line therapy.

Hemodynamic effects of chronic 4'epi-adriamycin administration.

Adriamycin (ADM) is an effective antineoplastic drug. However, the amount of ADM that can be administered must be limited because of the risk of developing a severe dose-dependent cardiomyopathy. 4'Epi-adriamycin (4'ADM) is a new anthracycline analog with similar antineoplastic properties as ADM, but with perhaps less cardiac toxicity. To determine myocardial performance after a chronic treatment with 4'ADM, we studied 17 patients (mean age 36.6 years) suffering from lymphomas by means of 24-hour ambulatory ECG, x-ray, M-mode echocardiogram, and rest-exercise gated radionuclide ventriculography (RNV), performed prior to and 2 months after the end of the treatment. Pretreatment and post-treatment shortening fractions, basal pretreatment and post-treatment ejection fractions, and postexercise pretreatment and post-treatment ejection fractions, were tested for correlation with individual 4'ADM doses and pretreatment with ADM. No association was noted among them, showing the lack of correlation between doses and impairment of ventricular performance. 4'ADM doses ranged from 400 to 1100, x 748 +/- 174 mg/m2; all noninvasive studies including RNV were normal. No correlation was found between 4'ADM doses and RNV (Pearson's correlation coefficient, p = ns). No deterioration of ventricular performance could be demonstrated. Conversely, the basal pretreatment ejection fraction changed from 56.17 +/- 7.6% to 61.52 +/- 8.3% in post-treatment (p less than 0.0001). Surprisingly, the post-exercise pretreatment ejection fraction also increased from 55.47 +/- 7.7% to 63.35 +/- 10% in post-treatment (p less than 0.03). The shortening fraction changed from 35.47 +/- 4.8% to 36.47 +/- 4.2% after 4'ADM treatment (ns). No impairment of cardiac function could be shown in patients previously treated with ADM or radiotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)