The Impact of Sidedness on the Efficacy of Anti-EGFR-Based First-Line Chemotherapy in Advanced Colorectal Cancer Patients in Real-Life Setting-A Nation-Wide Retrospective Analysis (RACER).

Anti-EGFR antibodies combined with chemotherapy doublets are a cornerstone of the upfront treatment of colorectal cancer. RAS and BRAF mutations are established negative predictive factors for such therapy. The primary tumour located in the proximal colon has recently emerged as another negative predictive factor. We have conducted a retrospective multicentre study to collect data on real-world population characteristics, practice patterns, and outcomes in patients with metastatic colorectal cancer treated in a first-line setting with either cetuximab or panitumumab in combination with either FOLFOX or FOLFIRI chemotherapy. The presented analysis focuses on the impact of the primary tumour location. 126 of 842 patients analysed (15.0%) had proximal primary. It was associated with a lower BMI at diagnosis, mucinous histology, and peritoneal metastases. It was also associated with inferior treatment outcomes in terms of response ratio: 59.4% vs. 74.22% (odds ratio [OR] 0.51, 95% CI 0.33-0.78, p = 0.010), and median depth of response: -36.7% vs. -50.0% (p = 0.038). There was only a borderline non-significant trend for inferior PFS in patients with proximal tumours. OS data was incomplete. The presented analysis confirms the negative impact of tumour sidedness on the efficacy of an upfront anti-EGFR-chemotherapy combination and provides valuable data on real-world population characteristics.

[To know more about the Prader-Willi syndrome. Diagnosis]. / Wiedziec wiecej o zespole Pradera-Williego. Diagnostyka.

Prader-Willi syndrome, induced by a function changes of paternal genes in the subcentrometric region of the chromosome 15 (q11.2q13), is the most common genetic cause of obesity resulting from hyperphagia. Behavioural disturbancies with compulsions in which psychiatric interventions are necessary, are relatively frequently seen. In this paper we reviewed the recent data of the clinical diagnosis verified by molecular studies.

[To know more about the Prader-Willi syndrome. Multidisciplinary support]. / Wiedziec wiecej o zespole Pradera-Williego. Opieka wielospecjalistyczna.

Prader-Willi syndrome, induced by a loss of function of paternal genes in the subcentrometric region of the chromosome 15 (q11.2q13), is a complex neurodevelopmental disorder with characteristic obesity resulting from hyperphagia. In addition behavioural disturbancies with obsessive-compulsive features, aggression, temper tantrums included, are relatively frequently seen and they often require psychiatric intervention. In this part of the paper we reviewed the recent data of behavioural phenotype the correlations of phenotype-genotype and possibilities of the multidisciplinary support for the affected persons and theirs families.

Capecitabine and temozolomide combination for treatment of high-grade, well-differentiated neuroendocrine tumour and poorly-differentiated neuroendocrine carcinoma - retrospective analysis.

INTRODUCTION: Many retrospective studies have confirmed that capecitabine combined with temozolomide is effective in neuroendocrine neoplasms. Most of the studies focused on grade 1 and grade 2 neuroendocrine tumours, mainly of pancreatic origin. There are limited data regarding the efficacy capecitabine with temozolomide in grade 3 neuroendocrine tumours. The new World Health Organisation 2017 classification distinguished well-differentiated grade 3 neuroendocrine tumours from poorly differentiated grade 3 neuroendocrine carcinomas. Treatment options for grade 3 neuroendocrine neoplasms are limited, and the overall prognosis is better in the subgroup of patients with grade 3 neuroendocrine tumours. MATERIAL AND METHODS: It was a retrospective study in the population of patients with diagnosed grade 3 neuroendocrine neoplasms of different origin treated with capecitabine and temozolomide. Data on clinical and demographic characteristics of the population were collected from four Polish clinical centres. This study aimed to evaluate response and survival parameters and compare outcomes of treatment of neuroendocrine tumours and carcinomas. RESULTS: The study included 32 patients with grade 3 neuroendocrine tumours treated with capecitabine and temozolomide. The disease control rate was twice as high in the group of patient with neuroendocrine tumours in comparison to carcinomas (70 vs. 30%). The progression-free survival for patients with neuroendocrine tumours was 15.3 months (95% CI: 3.9-30.4), and for patients with neuroendocrine carcinomas it was 3.3 months (95% CI: 2.5-7.1). Median overall survival was 22 months (95% CI: 11.8-22.0) and 4.6 months (95% CI: 2.2-5.9) for patients with tumours and carcinomas, respectively. The treatment regimen was generally well tolerated. CONCLUSIONS: The combination of capecitabine and temozolomide is an effective treatment for patients with grade 3 neuroendocrine tumours with Ki-67 index ranging between 20 and 54%. The treatment did not overcome the aggressive character of neuroendocrine carcinomas and resulted in low response and survival outcomes in comparison to those achieved in tumour therapy.