Specifically, CD91 is phosphorylated in response to HSPs in a uni

Specifically, CD91 is phosphorylated in response to HSPs in a unique pattern and phospho-CD91 triggers signalling

cascades to activate nuclear factor-kappa B. Each HSP-CD91 interaction on APCs stimulates a unique cytokine profile, which dictates priming of specific Th cell subsets. Thus, in a transforming growth factor-beta tumour microenvironment, immunization with CRT, but not gp96 or hsp70, primes Th17-cell responses in a CD91-dependent manner. These results are important for development of T-cell responses in situ in tumour-bearing hosts and for vaccination against cancer and infectious disease.”
“Previous PXD101 mw studies demonstrated that chemotherapy-induced changes in tumor glucose metabolism measured with F-18-FDG PET identify patients who benefit from preoperative chemotherapy and those who do not. The prognosis for chemotherapy metabolic nonresponders is poorer than for metabolic responders. Therefore, we initiated this prospective trial to improve the clinical outcome of metabolic nonresponders using a salvage neoadjuvant radiochemotherapy. buy CH5183284 Methods: Fifty-six patients

with locally advanced adenocarcinomas of the esophagogastric junction were included. Tumor glucose uptake was assessed by F-18-FDG PET before chemotherapy and 14 d after initiation of chemotherapy. PET nonresponders received salvage neoadjuvant radiochemotherapy, whereas metabolic responders received neoadjuvant chemotherapy for 3 mo before surgery. Results: Thirty-three patients were metabolic responders, and 23 were nonresponders. Resection was performed on 54 patients. R0 resection rate was 82% (95% confidence interval [CI], 66%-91%) in metabolic responders and 70% (95% CI, 49%-84%) in metabolic nonresponders (P = 0.51). Major histologic remissions were observed in 12 metabolic responders (36%; 95% CI, 22%-53%) and 6 nonresponders HIF pathway (26%; 95% CI, 13%-46%). One-year progression-free rate was 74% +/- 8% in PET responders and 57% +/- 10% in metabolic nonresponders (log rank test, P = 0.035). One-year overall survival was comparable between the

groups (similar to 80%), and 2-y overall survival was estimated to be 71% +/- 8% in metabolic responders and 42% +/- 11% in PET nonresponders (hazard ratio, 1.9; 95% CI, 0.87-4.24; P = 0.10). Conclusion: This prospective study showed the feasibility of a PET-guided treatment algorithm. However, by comparing the groups of nonresponding patients in the current trial and the previous published MUNICON (Metabolic response evalUatioN for Individualisation of neoadjuvant Chemotherapy in Esophageal and esophagogastric adeNocarcinoma) I trial, increased histopathologic response was observed after salvage radiochemotherapy, but the primary endpoint of the study to increase the R0 resection rate was not met. The prognosis of the subgroup of PET nonresponders remains poor, indicating their different tumor biology.

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