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The expression profile of SLC transporter genes in resectable pancreatic cancer

ABSTRACT: Objectives: The aim of this study was to investigate the prognostic significance of thirteen anticancer drug-relevant solute carrier transporters (SLCs) in pancreatic cancer in the context of clinical-pathological characteristics and the KRAS mutation status of tumors. Methods: Tumors and non-neoplastic pancreatic tissues were obtained from 32 histologically verified patients with pancreatic ductal adenocarcinoma. The transcript profile of SLCs was assessed using quantitative real-time PCR. KRAS mutations in exon 2 were assessed by high resolution melting analysis and confirmed by sequencing. Results: SLC22A3 was upregulated and SLC22A1, SLC22A2, SLC22A11, SLC28A1, SLC28A3 and SLC29A1 were downregulated when compared with non-neoplastic pancreatic tissues. Moreover, significantly lower levels of SLC22A1, SLC22A11 and SLC29A1 were found in tumors with angioinvasion. There was also a significantly higher transcript level of SLC28A1 in tumors with regional lymph nodes affected by metastasis. The study found that a high expression of SLC22A1 or SLC28A1was significantly associated with poor overall survival in unselected patients. In contrast, a high expression of SLC22A3 or SLC29A3 was significantly associated with longer overall survival in patients treated with nucleoside analogs. Finally, SLC levels were not found to be associated with KRAS mutation status in exon 2. Conclusions: This study identified a number of associations of SLCs with prognosis of pancreatic cancer patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47368 | GEO | 2013/06/30

SECONDARY ACCESSION(S): PRJNA205297

REPOSITORIES: GEO

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The expression profile of SLC transporter genes in resectable pancreatic cancer

Project description:Objectives: The aim of this study was to investigate the prognostic significance of thirteen anticancer drug-relevant solute carrier transporters (SLCs) in pancreatic cancer in the context of clinical-pathological characteristics and the KRAS mutation status of tumors. Methods: Tumors and non-neoplastic pancreatic tissues were obtained from 32 histologically verified patients with pancreatic ductal adenocarcinoma. The transcript profile of SLCs was assessed using quantitative real-time PCR. KRAS mutations in exon 2 were assessed by high resolution melting analysis and confirmed by sequencing. Results: SLC22A3 was upregulated and SLC22A1, SLC22A2, SLC22A11, SLC28A1, SLC28A3 and SLC29A1 were downregulated when compared with non-neoplastic pancreatic tissues. Moreover, significantly lower levels of SLC22A1, SLC22A11 and SLC29A1 were found in tumors with angioinvasion. There was also a significantly higher transcript level of SLC28A1 in tumors with regional lymph nodes affected by metastasis. The study found that a high expression of SLC22A1 or SLC28A1was significantly associated with poor overall survival in unselected patients. In contrast, a high expression of SLC22A3 or SLC29A3 was significantly associated with longer overall survival in patients treated with nucleoside analogs. Finally, SLC levels were not found to be associated with KRAS mutation status in exon 2. Conclusions: This study identified a number of associations of SLCs with prognosis of pancreatic cancer patients. Transcript levels of thirteen anticancer drug-relevant solute carrier transporters (SLCs) were determined by qPCR in pancreatic ductal adenocarcinomas and non-neoplastic tissue samples from 32 pancreatic cancer patients. MRPL19, ELF1 and POLR2A were used as reference genes for data normalization.

2013-06-30 | E-GEOD-47368 | biostudies-arrayexpress

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Proteogenomic Network Analysis of Context-Specific KRAS Signaling In Mouse-to-Human Cross-Species Translation

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Project description:Damaged tissues have increased risk of cancer development through poorly understood mechanisms. For example, in the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and, ultimately, pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional perturbations in autochthonous tumor models, we show that the combination of Kras mutation and tissue damage promotes a functionally relevant chromatin state in the pancreatic epithelium that distinguishes neoplastic transformation from normal regeneration and is inherited throughout malignant evolution. This cancer-associated epigenetic state emerges remarkably fast, involves chromatin accessibility changes not induced by pancreatic injury alone, and contributes to the early activation of neoplasia specific genes that define advanced human pancreatic cancer. Among the genes activated by injury-facilitated chromatin reprogramming are a series of known and novel cancer-related factors, including the alarmin cytokine IL33, which cooperates with mutant Kras in driving neoplastic transformation in the absence of tissue damage. Collectively, our study demonstrates how gene-environment interactions can rapidly produce gene regulatory programs that dictate early neoplastic commitment and provides a molecular framework for understanding the cooperation between genetics and environmental cues in cancer initiation.

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