Next generation sequencing identifies differentially expressed genes between breast cancer with diabetes and breast cancer without diabetes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE150586 | GEO | 2020/05/16
REPOSITORIES: GEO
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Project description:Diabetes commonly affects cancer patients. As a comorbidity, it may modify tumor biology and therapy response. Yet, we still lack an understanding of the diabetes-induced molecular changes in human breast tumors and their implication for therapy. The goal of this study was aimed to identify diabetes induced phenotypes and molecular signatures in breast cancer. Here, we investigated the effect of diabetes on breast cancer biology using a three-pronged approach that included analysis of orthotopic human tumor xenografts, patient tumors, and breast cancer cells exposed to diabetes and hyperglycemia. Diabetes and hyperglycemia induced a mesenchymal and stem cell-like phenotypes. Further Diabetes and hyperglycemia also associated with oxidative stress and both gene expression and mutational signatures of DNA repair deficiency. Breast cancer cells cultured under hyperglycemia acquired increased DNA damage and sensitivity to DNA damage response inhibitors. Based on these observations, diabetes-associated breast tumors may show an increased drug response to DNA repair pathway inhibitors that are cancer therapeutics.
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Project description:Next generation sequencing identifies differentially expressed genes between breast cancer with diabetes and breast cancer without diabetes
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Project description:Diabetes commonly affects cancer patients. As a comorbidity, it may modify tumor biology and therapy response. Yet, we still lack an understanding of the diabetes-induced molecular changes in human breast tumors and their implication for therapy. The goal of this study was aimed to identify diabetes induced phenotypes and molecular signatures in breast cancer. Here, we investigated the effect of diabetes on breast cancer biology using a three-pronged approach that included analysis of orthotopic human tumor xenografts, patient tumors, and breast cancer cells exposed to diabetes and hyperglycemia. Diabetes and hyperglycemia induced a mesenchymal and stem cell-like phenotypes. Further Diabetes and hyperglycemia also associated with oxidative stress and both gene expression and mutational signatures of DNA repair deficiency. Breast cancer cells cultured under hyperglycemia acquired increased DNA damage and sensitivity to DNA damage response inhibitors. Based on these observations, diabetes-associated breast tumors may show an increased drug response to DNA repair pathway inhibitors that are cancer therapeutics.
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Project description:Diabetes commonly affects cancer patients. As a comorbidity, it may modify tumor biology and therapy response. Yet, we still lack an understanding of the diabetes-induced molecular changes in human breast tumors and their implication for therapy. The goal of this study was aimed to identify diabetes induced phenotypes and molecular signatures in breast cancer. Here, we investigated the effect of diabetes on breast cancer biology using a three-pronged approach that included analysis of orthotopic human tumor xenografts, patient tumors, and breast cancer cells exposed to diabetes and hyperglycemia. Diabetes and hyperglycemia induced a mesenchymal and stem cell-like phenotypes. Further Diabetes and hyperglycemia also associated with oxidative stress and both gene expression and mutational signatures of DNA repair deficiency. Breast cancer cells cultured under hyperglycemia acquired increased DNA damage and sensitivity to DNA damage response inhibitors. Based on these observations, diabetes-associated breast tumors may show an increased drug response to DNA repair pathway inhibitors that are cancer therapeutics.
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Project description:To screen candidate methylation markers for early detection of breast cancer, we performed methylated-CpG island recovery assay combined with CpG island array on 61982 CpG sites across 4162 genes in 10 breast tumor tissues and 10 non-tumor breast tissues. We detected 70 significantly hypermethylated genes in breast tumor tissues, including many novel hypermethylated genes such as ITGA4, NFIX, OTX2 and FGF12. Direct bisulfite sequencing showed widespread methylations occurred in intragenic regions of WT1, PAX6 and ITGA4 genes and promoter region of OTX2 in breast cancer tissue. COBRA assay in independent tumor and non-tumor samples confirmed that WT1, OTX2 and PAX6 genes were hypermethylated in breast cancer tissues. To explore the relationship between methylation and gene expression, gene expression profiling analysis was performed in 8 breast tumor tissues and 8 non-tumor breast tissues. We found that some hypermethylated genes in breast cancer were not expressed in breast tissues. RT-PCR assay showed that WT1 and PITX2 were only weakly expressed in the breast tumor tissues and weren’t expressed in most non-tumor breast tissues. OTX2 and PAX6 weren’t expressed in both breast tumor tissues and non-tumor tissues. Unpaired experiments, breast cancer tissue vs. normal cancer tissue. Biological replicates: 10 breast cancer tissue replicates, 10 normal breast tissue replicates.
2011-11-11 | E-GEOD-33445 | biostudies-arrayexpress
Project description:To screen candidate methylation markers for early detection of breast cancer, we performed methylated-CpG island recovery assay combined with CpG island array on 61982 CpG sites across 4162 genes in 10 breast tumor tissues and 10 non-tumor breast tissues. We detected 70 significantly hypermethylated genes in breast tumor tissues, including many novel hypermethylated genes such as ITGA4, NFIX, OTX2 and FGF12. Direct bisulfite sequencing showed widespread methylations occurred in intragenic regions of WT1, PAX6 and ITGA4 genes and promoter region of OTX2 in breast cancer tissue. COBRA assay in independent tumor and non-tumor samples confirmed that WT1, OTX2 and PAX6 genes were hypermethylated in breast cancer tissues. To explore the relationship between methylation and gene expression, gene expression profiling analysis was performed in 8 breast tumor tissues and 8 non-tumor breast tissues. We found that some hypermethylated genes in breast cancer were not expressed in breast tissues. RT-PCR assay showed that WT1 and PITX2 were only weakly expressed in the breast tumor tissues and weren’t expressed in most non-tumor breast tissues. OTX2 and PAX6 weren’t expressed in both breast tumor tissues and non-tumor tissues. Unpaired experiments, breast tumor tissues vs. breast non-tumor tissues. Biological replicates: 8 breast cancer tissue replicates, 8 breast non-tumor tissue replicates.
2011-11-11 | E-GEOD-33447 | biostudies-arrayexpress