The primary objective of this study is to investigate whether two weeks of metformin treatment can activate the tumour microenvironment in patients with stage II and III oesophageal adenocarcinomas.
Worldwide oesophageal adenocarcinoma (OAC) is one of the most deadly cancers. Even in case of non-metastatic disease, when patients are treated with neoadjuvant chemoradiotherapy (nCRT) and a surgical resection, around 50% of patients suffer from recurrent disease which is associated with a poor prognosis. While 23% of OACs have a complete histopathological response after nCRT, 18-35% lack any effect of nCRT. Previously, we have identified that a complete pathological response to nCRT is associated with an active tumour immune microenvironment (TIME) characterized by high intratumoral T cell levels and a higher CD3:CD163 ratio. To improve response to nCRT we need to identify and target the mechanisms OACs use to suppress the TIME. Using spatial transcriptomics to identify differences between OACs with a T cell-dominant and a T cell-excluded microenvironment, we identified fatty acid oxidation (FAO) as central feature of T cell low OACs (unpublished data). This is an interesting observation as lipid metabolism is strongly associated with an immunosuppressive microenvironment. Metabolic re-programming by drugs such as metformin has shown to be a promising strategy to reactivate the anti-tumour immune response in other cancer types. Over the past decade, metformin has been associated with a beneficial effect in cancer treatment as it has shown to decrease the risk of various cancer types in diabetic patients. More recent, metformin treatment has shown to increase the number of CD8+ tumour infiltrating lymphocytes by preventing apoptosis of these lymphocytes in cancers such as oesophageal squamous cell carcinomas. In addition, metformin can reduce M2-like macrophage polarization due to changes in cytokine expression in cancer cells and thereby stimulate a more pro-inflammatory TIME. In this study we want to investigate the effect of metformin on the TIME in patients with OACs using pre- and post-treatment tumour biopsies prior to nCRT.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
14
Twice a day 500mg of metfomrin orally (1000mg/day) during a 2-week period.
Amsterdam UMC
Amsterdam, Netherlands
NOT_YET_RECRUITINGAmsterdam UMC
Amsterdam, Netherlands
RECRUITINGactivation of the tumour immune microenvironment after two week metformin treatment.
Activation of the tumor immune microenvironment measured by M2 to M1 polarization, CD8 intratumoral T cell infiltration and an increase of CD3 to CD163 ratio when comparing tumor biopsies from before and after treatment.
Time frame: at enrollment and at end of metformin treatment at 2 weeks.
Tolerability and toxicity of metformin
Adverse events based on Common Toxicity Criteria for Adverse Events
Time frame: From starting treatment to end of treatment at 7 weeks.
Metabolic change of cancer cells with SCENITH analysis.
To determine whether SCENITH can be used to assay the change in metabolic state.
Time frame: at enrollment and at end of metformin treatment at 2 weeks
Pathological response
According to the Mandard criteria.
Time frame: After surgery, approximately 16 weeks after enrollment.
Progression-free survival (PFS).
Assess the PFS of patients within the study
Time frame: 60 months
Overall survival (OS)
Determine overall survival of patients within the study
Time frame: 60 months
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