Endovenous laser treatment: is there a clinical difference between using a 1500 nm and a 980 nm diode laser? A multicenter randomised clinical trial.

AIM: We compared the use of two different laser wavelengths in the treatment of great saphenous vein (GSV) reflux: the 1500 nm versus the 980 nm diode laser. We studied the occlusion rates and noted possible side-effects. METHODS: In three centers 180 great saphenous veins were treated with endovenous laser ablation (EVLA). By random selection half of the patients were treated with a 980 nm laser and half with a 1500 nm laser. A Duplex scan was scheduled at one month and six months postoperatively. Ecchymosis was measured at one week using a calculated scale. In addition the need for analgesics, the induration around the treated vein and patient satisfaction rate were noted. At two weeks postoperatively a quality of life score (CIVIQ2) was obtained. RESULTS: The complete occlusion rates at six months were not statistical significant different between both groups (95.5% for 980 nm and 93.1% for 1500 nm). Most of the non-occluded veins had a filiform internal lumen and did not show reflux. There was no significant difference in the postoperative appearance of ecchymosis (P=0.09). Patients treated with a 1500 laser had less induration around the treated vein (P=0.002), less need to take analgetics (1.8 days versus 2.9 days) and had a better postoperative quality of life (P=0.018). The patient satisfaction rate did not differ in the two groups. CONCLUSION: Using a 1500 nm diode laser in the treatment of an incompetent GSV, compared to the use of a 980 nm laser, results in similar occlusion rates at six months, but somewhat less side-effects.

Integrated genomic profiling of endometrial carcinoma associates aggressive tumors with indicators of PI3 kinase activation.

Although 75% of endometrial cancers are treated at an early stage, 15% to 20% of these recur. We performed an integrated analysis of genome-wide expression and copy-number data for primary endometrial carcinomas with extensive clinical and histopathological data to detect features predictive of recurrent disease. Unsupervised analysis of the expression data distinguished 2 major clusters with strikingly different phenotypes, including significant differences in disease-free survival. To identify possible mechanisms for these differences, we performed a global genomic survey of amplifications, deletions, and loss of heterozygosity, which identified 11 significantly amplified and 13 significantly deleted regions. Amplifications of 3q26.32 harboring the oncogene PIK3CA were associated with poor prognosis and segregated with the aggressive transcriptional cluster. Moreover, samples with PIK3CA amplification carried signatures associated with in vitro activation of PI3 kinase (PI3K), a signature that was shared by aggressive tumors without PIK3CA amplification. Tumors with loss of PTEN expression or PIK3CA overexpression that did not have PIK3CA amplification also shared the PI3K activation signature, high protein expression of the PI3K pathway member STMN1, and an aggressive phenotype in test and validation datasets. However, mutations of PTEN or PIK3CA were not associated with the same expression profile or aggressive phenotype. STMN1 expression had independent prognostic value. The results affirm the utility of systematic characterization of the cancer genome in clinically annotated specimens and suggest the particular importance of the PI3K pathway in patients who have aggressive endometrial cancer.