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Microarray expression data from follicular lymphoma patients' lymph node biopsies (frozen)

ABSTRACT: Abstract from the associated publication: Although PET allows an accurate staging of disease in follicular lymphoma (FL) patients, the impact of pre-treatment maximum standardized uptake (SUVmax) value in this population remains elusive as well as its real biological significance. A training cohort of 48 FL patients and a validation cohort of 84 patients unpreviously treated were included retrospectively. SUVmax of 18-FDG PET was evaluated by centrally expert review and the optimum threshold of SUVmax value was determined in the training cohort to predict progression free survival (PFS). To explore the biologic meaning of PET results, tumor samples were analyzed from the two cohorts independantly :- the tumor microenvironment immune cartography by immunochemistry , - the cell gene-expression profiles assessed using Sample enrichment score combined to CIBERSORT method and - the tumor cell mutational profile determined by targeted Next Generation Sequencing (t-NGS). At baseline, patients with a SUVmax >14.5 had a significantly lower PFS compared to patients with SUVmax ≤14.5 (2y PFS: 40% vs 86%, HR = 0.16, p = 0.0009). The prognostic value of SUVmax was confirmed in the validation cohort (p= 0.006). Neither immune cell infiltration nor immune checkpoint expression were related to the baseline PET metrics including SUVmax. By constrast, high tumor cell proliferation (assessed by Ki67 staining) was significantly related to high SUVmax level ( p= 0.007). Interestingly FOXO1 mutated patients harbored high SUVmax and high tumor proliferation, that is why FOXO1 status could reflect to proliferation of FL tumor cells through SUVmax and Ki67 staining. So, FL patients with high baseline SUVmax related to high tumor cell proliferation have a poorer PFS despite absence of lymphoma transformation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE148070 | GEO | 2020/12/31

REPOSITORIES: GEO

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Project description:We report the RNA sequencing data from the REPEAT study, in which patients with beyond first-line esophagogastric cancer were treated with regorafenib and paclitaxel. For the RNA sequencing, biopsies from metastatic lesions were obtained on baseline (n=21) and fifteen days following treatment initiation (n=13). PURPOSE: Regorafenib monotherapy, a multikinase-inhibitor of angiogenesis, tumor microenvironment, and oncogenesis, showed promising results in gastric cancer. We aimed to assess the tolerability of regorafenib and paclitaxel in advanced esophagogastric cancer (EGC) patients refractory to first-line treatment, and explore potential biomarkers. METHODS: Patients received paclitaxel (80 mg/m2) on days 1, 8, and 15 of a 28-day cycle and regorafenib (80/120/160 mg) on day 1-21 in the dose-escalation cohort, and the maximum-tolerated dose (MTD) in the dose-expansion cohort. Exploratory, overall- (OS) and progression-free survival (PFS) were compared to a propensity-score matched cohort receiving standard second/third line systemic treatment. Paclitaxel pharmacokinetics were assessed using D1 and D15 samples. We performed ELISA measurements of galectin-1, RNA sequencing and shallow whole-genome sequencing of metastatic tumor biopsies for biomarker analyses. RESULTS: In the dose-escalation cohort (n=14), the MTD of regorafenib was 120 mg. Thirty-four patients were enrolled in the dose-expansion cohort. Most common toxicities (all grades; grade ≥3) were fatigue (79%; 4%) and sensory neuropathy (63%; 4%). Best responses achieved were partial response (28%) and stable disease (54%). Median OS and PFS were 7.8 and 4.2 months, respectively (median follow-up 7.8 months). OS (p=0.08) and PFS (p=0.81) were not significantly improved compared to the matched cohort. Paclitaxel concentrations were significantly increased with regorafenib (D15) compared with paclitaxel only (D1; p<0.05); no associations were observed with toxicity or efficacy. An increase in circulating galectin-1 compared to baseline was associated with shorter OS (p<0.01). Enrichment of angiogenesis-related gene expression was observed in short-survivors measured by RNA sequencing. Chromosome 19q13.12-q13.2 amplification was associated with shorter OS (p=0.02) and PFS (p=0.02). CONCLUSION: Treatment with regorafenib and paclitaxel is tolerable and shows promising efficacy in advanced EGC refractory to first-line treatment. Galectin-1 and chromosome 19q13.12-q13.2 amplification could serve as negative predictive biomarkers for treatment response.

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Microarray expression data from follicular lymphoma patients' lymph node biopsies (frozen)

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