BackgroundTo date, patients with metastasized pancreatic ductal adenocarcinoma (PDAC M1) are regarded as a uniform collective. We hypothesize the existence of oligometastatic disease (OMD): a state of PDAC M1 disease with better tumor biology, limited metastasis, and increased survival.MethodsData of 128 PDAC M1 patients treated at the University of Cologne between 2008 and 2018 was reviewed. Interdependence between clinical parameter was calculated using the Mann-Whitney U-Test. Survival curves were generated using the Kaplan-Meier method and analyzed using the log-rank test.ResultsEighty-one (63%) patients had metastases confined to one organ (single organ metastasis, SOG) whereas the remaining 47 (37%) showed multiple metastatic sites (multi-organ metastasis, MOG). Survival analysis revealed a median overall survival (OS) of 12.2 months for SOG vs 4.5 months for MOG (95% CI 5.7–9.8; p < 0.001). We defined limited disease by the presence of ≤4 metastases in liver or lung. Limited disease together with CA 19–9 baseline < 1000 U/ml and response or stable disease after first-line chemotherapy defined OMD. We identified 8 patients with hepatic metastases and 2 with pulmonary metastases matching all OMD criteria. This group of 10 (7.8%) had a median overall survival of 19.4 vs 7.2 months compared to the remaining patients (95% CI 5.7–9.8; p = 0.009).ConclusionWe propose a definition of oligometastatic disease in PDAC including anatomical criteria and biological criteria reflecting better tumor biology. The 10 OMD patients (7.8%) survived significantly longer and might even benefit from surgical resection in the future.

Expression of HMGA2 is not correlated with the regulatory let7 miRNAs. Interestingly, SLC5A5 was down-regulated in FTC and PTC. Its expression could be modulated by hsa-let-7f-5p. ATC showed a loss of SLC5A5/hsa-let7f-5p correlation. SLC5A5, in ATC, needs further investigation to clarify the genetic/epigenetic mechanism altering its expression.

Valid biomarkers for a better prognostic prediction of the clinical course in esophageal adenocarcinoma (EAC) are still not implemented. Integrin alpha V (ITGAV), a transmembrane glycoprotein responsible for cell-to-matrix binding has been found to enhance tumor progression in several tumor entities. The expression pattern and biological role of ITGAV expression in esophageal adenocarcinoma (EAC) has not been analyzed so far. Aim of the study is to evaluate the expression level of ITGAV in a very large collective of EAC and its impact on individual patients´ prognosis. 585 patients with esophageal adenocarcinoma were analyzed immunohistochemically for ITGAV. The data was correlated with clinical, pathological and molecular data (TP53, HER2/neu, c-myc, GATA6, PIK3CA and KRAS). A total of 85 patients (14.3%) out of 585 analyzable tumors showed an ITGAV expression and intratumoral heterogeneity was low. ITGAV expression was correlated with a shortened overall-survival in the patients´ group that underwent primary surgery (p = 0.014) but not in the group of patients that received neoadjuvant treatment before surgery. No correlation between any of the analyzed molecular marker (mutations or amplifications) (TP53, HER2, c-myc, GATA6, PIK3CA and KRAS) and ITGAV expression could be observed. A multivariate cox-regression model was performed which showed tumor stage, lymph node metastasis and ITGAV expression as independent prognostic markers for overall-survival in the group of patients without neoadjuvant treatment. ITGAV expression is correlated with an impaired patient outcome in the group of patients without neoadjuvant therapy and serves as a prognostic factor in EAC.

No abstract