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Transcriptome analysis of basal and luminal tumor-initiating cells in ErbB2-driven breast cancer.

Borcherding N, Bormann N, Kusner D, Kolb R, Zhang W - Genom Data (2015)

Bottom Line: Several genes were further validated using real-time reverse transcription polymerase chain reaction (RT-PCR).Here we provide further details on the experimental methods and microarray analysis.This data provides a resource to further understanding how different mammary cell populations can initiate ErbB2-driven tumors and the role of these cell populations as putative tumor-initiating cells (TICs).

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Iowa, Iowa City, IA 52242-1109 ; Medical Science Training Program, University of Iowa, Iowa City, IA 52242-1109 ; Holden Comprehensive Cancer Center, University of Iowa, Iowa City, IA 52242-1109 ; Carver College of Medicine, University of Iowa, Iowa City, IA 52242-1109.

ABSTRACT

Breast cancer is the leading cause of cancer-related mortality for females worldwide.(1) Improving early screening strategies and understanding the events that lead to tumor initiation have led to demonstrable improvements in clinical outcome. Our previous work revealed a variance in the tumorigenic capacity between different mammary epithelial cell populations in an MMTV-ErbB2 mouse model. In order to greater understand how different mammary epithelial cells influence the tumorigenic capacity in ErbB2-induced breast cancer, we transplanted different cell populations from pre-neoplastic MMTV-ErbB2 female mice into recipient mice for tumorigenic study. We found that different mammary epithelial cells bear different tumorigenic potential even when induced by the same ErbB2 proto-oncogene. To understand the difference in tumors formed from different epithelial cells, we performed gene expression profiling using these tumors (GSE64487). Several genes were further validated using real-time reverse transcription polymerase chain reaction (RT-PCR). Here we provide further details on the experimental methods and microarray analysis. This data provides a resource to further understanding how different mammary cell populations can initiate ErbB2-driven tumors and the role of these cell populations as putative tumor-initiating cells (TICs).

No MeSH data available.


Related in: MedlinePlus

A. Volcano plot displaying the gene expression fold change and P-value for Myo WT versus MSC WT. Genes with fold-change ≥ 1 and P-value ≤ 0.05 (30 genes) are highlighted in red and fold-change ≤ − 1 and P-value ≤ 0.05 (39 genes) in green. B. Heatmap of the 20 most differentially expressed genes, as measured by absolute fold-change difference. Samples are labeled according to the GSE64487 dataset.
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f0015: A. Volcano plot displaying the gene expression fold change and P-value for Myo WT versus MSC WT. Genes with fold-change ≥ 1 and P-value ≤ 0.05 (30 genes) are highlighted in red and fold-change ≤ − 1 and P-value ≤ 0.05 (39 genes) in green. B. Heatmap of the 20 most differentially expressed genes, as measured by absolute fold-change difference. Samples are labeled according to the GSE64487 dataset.

Mentions: Expression values were compared based on the tumor-initiating cells (TICs) that gave rise to the tumors. Previously, we published the comparison between LP- and MSC-derived tumors, finding that the non-canonical Wnt5a was downregulated in MSC-derived tumors [4]. We also conducted comparisons between the tumors from LP WT versus LP AA to investigate the transcriptional differences with the inactivation of IKK-α (CHUK) in luminal progenitors (Fig. 2A, B). We continued our transcriptional comparisons with the analysis of tumors derived from Myo and MSC, two cell types of the basal compartment that gave rise to ErbB2-driven tumors (Fig. 3A, B). Finally, as another comparison between tumors derived from cells of the basal versus luminal compartments, we compared the transcriptional profiles of the Myo- and LP-derived tumors (Fig. 4A, B).


Transcriptome analysis of basal and luminal tumor-initiating cells in ErbB2-driven breast cancer.

Borcherding N, Bormann N, Kusner D, Kolb R, Zhang W - Genom Data (2015)

A. Volcano plot displaying the gene expression fold change and P-value for Myo WT versus MSC WT. Genes with fold-change ≥ 1 and P-value ≤ 0.05 (30 genes) are highlighted in red and fold-change ≤ − 1 and P-value ≤ 0.05 (39 genes) in green. B. Heatmap of the 20 most differentially expressed genes, as measured by absolute fold-change difference. Samples are labeled according to the GSE64487 dataset.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493742&req=5

f0015: A. Volcano plot displaying the gene expression fold change and P-value for Myo WT versus MSC WT. Genes with fold-change ≥ 1 and P-value ≤ 0.05 (30 genes) are highlighted in red and fold-change ≤ − 1 and P-value ≤ 0.05 (39 genes) in green. B. Heatmap of the 20 most differentially expressed genes, as measured by absolute fold-change difference. Samples are labeled according to the GSE64487 dataset.
Mentions: Expression values were compared based on the tumor-initiating cells (TICs) that gave rise to the tumors. Previously, we published the comparison between LP- and MSC-derived tumors, finding that the non-canonical Wnt5a was downregulated in MSC-derived tumors [4]. We also conducted comparisons between the tumors from LP WT versus LP AA to investigate the transcriptional differences with the inactivation of IKK-α (CHUK) in luminal progenitors (Fig. 2A, B). We continued our transcriptional comparisons with the analysis of tumors derived from Myo and MSC, two cell types of the basal compartment that gave rise to ErbB2-driven tumors (Fig. 3A, B). Finally, as another comparison between tumors derived from cells of the basal versus luminal compartments, we compared the transcriptional profiles of the Myo- and LP-derived tumors (Fig. 4A, B).

Bottom Line: Several genes were further validated using real-time reverse transcription polymerase chain reaction (RT-PCR).Here we provide further details on the experimental methods and microarray analysis.This data provides a resource to further understanding how different mammary cell populations can initiate ErbB2-driven tumors and the role of these cell populations as putative tumor-initiating cells (TICs).

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Iowa, Iowa City, IA 52242-1109 ; Medical Science Training Program, University of Iowa, Iowa City, IA 52242-1109 ; Holden Comprehensive Cancer Center, University of Iowa, Iowa City, IA 52242-1109 ; Carver College of Medicine, University of Iowa, Iowa City, IA 52242-1109.

ABSTRACT

Breast cancer is the leading cause of cancer-related mortality for females worldwide.(1) Improving early screening strategies and understanding the events that lead to tumor initiation have led to demonstrable improvements in clinical outcome. Our previous work revealed a variance in the tumorigenic capacity between different mammary epithelial cell populations in an MMTV-ErbB2 mouse model. In order to greater understand how different mammary epithelial cells influence the tumorigenic capacity in ErbB2-induced breast cancer, we transplanted different cell populations from pre-neoplastic MMTV-ErbB2 female mice into recipient mice for tumorigenic study. We found that different mammary epithelial cells bear different tumorigenic potential even when induced by the same ErbB2 proto-oncogene. To understand the difference in tumors formed from different epithelial cells, we performed gene expression profiling using these tumors (GSE64487). Several genes were further validated using real-time reverse transcription polymerase chain reaction (RT-PCR). Here we provide further details on the experimental methods and microarray analysis. This data provides a resource to further understanding how different mammary cell populations can initiate ErbB2-driven tumors and the role of these cell populations as putative tumor-initiating cells (TICs).

No MeSH data available.


Related in: MedlinePlus