ABSTRACT
Cancer of the body-tail of the pancreas often involves adjacent structures. Thus, surgical treatment may be extended to other organs or vessels in order to achieve radical resection. The aim of this study is to evaluate the safety and efficacy of extended distal pancreatectomy for ductal adenocarcinoma of the body and tail of the pancreas. Between January 2000 and December 2016, 101 patients underwent distal pancreatectomy (DP) for pancreatic cancer: 65 patients underwent standard-DP and 36 extended-DP, including the resection of the partial stomach (n = 12), adrenal gland (n = 7), liver (n = 7), colon (n = 8), celiac axis (n = 6), portal vein (n = 5), jejunum (n = 4) and kidney (n = 4). The two groups were compared in terms of their TNM classification, pathological grade, nodal status, state of resection margins, age, sex and levels of preoperative serum carbohydrate antigen 19-9 (CA 19.9). The morbidity and mortality were not statistically different in the two groups. The two groups disease-free and overall survival rates were significantly influenced by the tumor's stage, nodal status, pathological features and resection margins. Survival was not influenced by the extent of the surgical resection. However, when patients were stratified according to the type of extended resection, survival was worse in the group of patients undergoing vascular resection. Multivariate analysis showed that the stage and resection margins are independent predictors of disease-free and overall survival. Extended distal pancreatectomy may be performed with acceptable morbidity and mortality rates. Survival is not significantly different after standard or extended resection. However, the rate of tumor recurrence is high, and long-term survival is a rare event, especially in those patients who undergo distal pancreatectomy associated with vascular resection.
ABSTRACT
BACKGROUND: Colon cancer in young patients is often associated with hereditary syndromes; however, in early-onset rectal cancer, mutations of these genes are rarely observed. The aim of this study was to analyse the features of the local immune microenvironment and the mutational pattern in early-onset rectal cancer. METHODS: Commonly mutated genes were analysed within a rectal cancer series from the University Hospital of Padova. Mutation frequency and immune gene expression in a cohort from The Cancer Genome Atlas ('TCGA') were compared and immune-cell infiltration levels in the healthy rectal mucosa adjacent to rectal cancers were evaluated in the IMMUNOlogical microenvironment in REctal AdenoCarcinoma Treatment 1 and 2 ('IMMUNOREACT') series. RESULTS: In the authors' series, the mutation frequency of BRAF, KRAS, and NRAS, as well as microsatellite instability frequency, were not different between early- and late-onset rectal cancer. In The Cancer Genome Atlas series, among the genes with the most considerable difference in mutation frequency between young and older patients, seven genes are involved in the immune response and CD69, CD3, and CD8ß expression was lower in early-onset rectal cancer. In the IMMUNOlogical microenvironment in REctal AdenoCarcinoma Treatment 1 and 2 series, young patients had a lower rate of CD4+ T cells, but higher T regulator infiltration in the rectal mucosa. CONCLUSION: Early-onset rectal cancer is rarely associated with common hereditary syndromes. The tumour microenvironment is characterized by a high frequency of mutations impairing the local immune surveillance mechanisms and low expression of immune editing-related genes. A constitutively low number of CD4 T cells associated with a high number of T regulators indicates an imbalance in the immune surveillance mechanisms.
