Transanal versus traditional laparoscopic total mesorectal excision for rectal carcinoma.

BACKGROUND: After total mesorectal excision (TME) surgery, patients with an incomplete mesorectum have an increased risk of local and overall recurrence. With the introduction of laparoscopic TME, an improved quality of the specimen was expected. However, the quality-related results were comparable to the results after traditional open surgery. Transanal TME is a new technique in which the rectum is mobilised by using a single-port and endoscopic instruments through the so called 'down to up' procedure. This new technique potentially leads to an improved specimen quality. This study was designed to investigate the pathological quality of specimens after transanal (TME) and to compare these with specimens after traditional laparoscopic TME. METHODS: This matched case control study compared the specimens of a cohort of consecutive patients who underwent transanal TME with the specimens after traditional laparoscopic TME. The pathological quality of the mesorectum was determined by the definitions of Quirke as 'complete', 'nearly complete', or 'incomplete'. RESULTS: From June 2012 until July 2013, 25 consecutive patients underwent transanal TME because of a rectum carcinoma. Within the transanal TME group, 96% of the specimens had a complete mesorectum, while in the traditional laparoscopic group, 72% was deemed complete (p < 0.05). Other pathological characteristics, such as the circumferential resection margin, were comparable between the two groups. CONCLUSIONS: Transanal TME appears associated with a significant higher rate of completeness of the mesorectum. Further studies are necessary to evaluate this novel technique.

EGFR and KRAS mutations in lung carcinomas in the Dutch population: increased EGFR mutation frequency in malignant pleural effusion of lung adenocarcinoma.

BACKGROUND: Frequencies of EGFR and KRAS mutations in non-small cell lung cancer (NSCLC) have predominantly been determined in East Asian and North American populations, showing large differences between these populations. The aim of the present study was to determine the frequency of EGFR and KRAS mutations in NSCLC in the West European Dutch population in primary carcinomas and different metastatic locations. METHODS: EGFR (exons 19, 20 and 21) and KRAS (exons 2 and 3) mutation test results of NSCLC samples of patients in 13 hospitals were collected. The tests were performed on paraffin-embedded tissue or cytological material of primary and metastatic lung carcinomas. RESULTS: EGFR mutations were detected in 71/778 (9.1 %) tested patients; in 66/620 (10.6 %) adenocarcinomas. EGFR mutations were significantly more often detected in female than in male patients (13.4 % vs. 5.5 %, p < 0.001). KRAS mutations were found in 277 out of 832 (33.3 %) tested patients; in 244/662 (36.9 %) adenocarcinomas. A significantly increased frequency of EGFR mutations was observed in patients with malignant pleural/pericardial effusions (26.5 %; odds ratio (OR) 2.80, 95 % confidence interval (CI) 1.22-6.41), whereas the frequency of KRAS mutations was significantly decreased (18.8 %; OR 0.35, 95 % CI 0.14-0.86). CONCLUSIONS: In the investigated Dutch cohort, patients with malignant pleural/pericardial effusion of lung adenocarcinoma have an increased frequency of EGFR mutations. The overall frequency of EGFR mutations in lung adenocarcinomas in this West European population is within the frequency range of North American and South European populations, whereas KRAS mutation frequency is higher than in any population described to date.

Allelic imbalance in hereditary and sporadic prostate cancer.

BACKGROUND: In this study, we evaluate the pattern of allelic imbalance (AI) in both sporadic prostate cancer (SPC) and hereditary prostate cancer (HPC) at loci that frequently show allelic imbalance in sporadic prostate cancer, or are believed to have a putative role in the disease. METHODS: DNA obtained from 35 sporadic tumors and 46 hereditary tumors were tested for AI, by using a panel of 35 microsatellite markers. RESULTS: Chromosomal regions that display high frequencies of AI (>or=30%) in HPC include 1q, 5q, 7q, 8p, 13q, 16q, 17q, 18q, and 20q. In SPC, high frequencies of AI were found at 5q, 7q, 8p, 10q, 13q. Main differences (delta >or= 20%) in AI between HPC and SPC were at 1q, 10q, 17q, 18q, and 20q. CONCLUSION: AI at the prostate cancer susceptibility loci HPC1, PCaP, and HPC20 was seen more often in HPC compared with SPC. It appears that there are marked differences in the pattern of AI between sporadic and hereditary PCa.

Single-nucleotide polymorphism in the E-cadherin gene promoter modifies the risk of prostate cancer.

E-cadherin plays a major role in intercellular adhesion, cell polarity and tissue architecture. We determined the relative risk of PCa associated with a previously reported C/A SNP at -160 bp relative to the transcription-start site of the E-cadherin gene promoter. Eighty-two PCa patients and 188 controls were genotyped. Genotype and allele frequencies differed significantly among cases and controls. A-allele carriers had a higher relative risk of PCa (OR = 3.6, 95% CI 2.0-6.4) compared to C-only carriers. AC and AA genotypes had an increased risk of PCa (OR = 3.8, 95% CI 2.1-6.8 and OR = 1.7, 95% CI 0.4-6.6, respectively) compared to CC genotypes.