The aim of present study was to evaluate the impact of primary tumour location and other factors on the outcome of preoperative chemoradiation followed by surgery in adenocarcinomas of distal oesophagus, gastro-oesophageal junction and stomach. We retrospectively reviewed the institutional patient database. The therapeutic response was re-evaluated as a percentage of residual tumor cells in surgical resection specimens. Overall survival (OS) and disease-free survival (DFS) were assessed. The effect primary tumour location, clinical and pathological TNM stage, and histopathological factors (histological type, grade, angioinvasion, perineural invasion, tumour response) on treatment outcome were evaluated. A total of 108 patients underwent preoperative chemoradiation for adenocarcinoma of distal oesophagus, gastro-oesophageal junction or stomach. The median prescribed dose of radiation was 45 Gy. The concurrent chemotherapy consisted of 5-fluorouracil +/- cisplatin +/- taxanes. R0 resection was achieved in 80 patients (74%). The complete response was observed in 19%. The median follow-up was 50.8 months. Three-year and 5-year OS and DFS were 36.2% and 25.3%; and 28.1% and 23.7%, respectively. Pretreatment T-stage, pathological N-stage, radicality of resection, histological subtype, grade, angioinvasion and perineural invasion, were identified as statistical significant OS predictors in univariate analysis; pathological N-stage, radicality of resection and angioinvasion, in multivariate analysis. The primary tumor location did not influence the prognosis. The pathologic response to chemoradiation had borderline significance. In conclusion, no prognostic impact of primary tumour location, in contrast to other investigated factors, was evident in the present study. The most important predictors of prognosis were angioinvasion status and pN-stage.

• Klíčová slova
• Distal oesophageal cancer, Gastric cancer, Gastro-oesophageal junction cancer, Preoperative chemoradiation, Prognostic factor,
• MeSH
• adenokarcinom mortalita   patologie   terapie   MeSH
• adjuvantní chemoradioterapie MeSH
• chirurgie trávicího traktu MeSH
• dospělí MeSH
• gastroezofageální junkce patologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• nádory jícnu mortalita   patologie   terapie   MeSH
• nádory žaludku mortalita   patologie   terapie   MeSH
• neoadjuvantní terapie MeSH
• přežití bez známek nemoci MeSH
• prognóza MeSH
• retrospektivní studie MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• výsledek terapie MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

The KRAS gene (Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogene that encodes a small GTPase transductor protein called KRAS. KRAS is involved in the regulation of cell division as a result of its ability to relay external signals to the cell nucleus. Activating mutations in the KRAS gene impair the ability of the KRAS protein to switch between active and inactive states, leading to cell transformation and increased resistance to chemotherapy and biological therapies targeting epidermal growth factor receptors. This review highlights some of the features of the KRAS gene and the KRAS protein and summarizes current knowledge of the mechanism of KRAS gene regulation. It also underlines the importance of activating mutations in the KRAS gene in relation to carcinogenesis and their importance as diagnostic biomarkers, providing clues regarding human cancer patients' prognosis and indicating potential therapeutic approaches.

• MeSH
• lidé MeSH
• nádory * genetika   metabolismus   terapie   MeSH
• protoonkogenní proteiny p21(ras) MeSH
• protoonkogenní proteiny * MeSH
• Ras proteiny * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• KRAS protein, human MeSH Prohlížeč
• protoonkogenní proteiny p21(ras) MeSH
• protoonkogenní proteiny * MeSH
• Ras proteiny * MeSH