Gene expression alterations in response to cigarette smoke have been characterized in normal-appearing bronchial epithelium of healthy smokers and it has been suggested that adjacent histologically normal tissue display tumor-associated molecular abnormalities.
Characterizing the molecular spatial and temporal field of injury in early-stage smoker non-small cell lung cancer patients after definitive surgery by expression profiling.
Specimen part, Subject, Time
View SamplesPrevious work has shown that lung tumors and normal-appearing adjacent lung tissues share specific abnormalities that may be highly pertinent to the pathogenesis of lung cancer. However, the global and molecular adjacent airway field cancerization in non-small cell lung cancer (NSCLC) has not been characterized before.
Transcriptomic architecture of the adjacent airway field cancerization in non-small cell lung cancer.
Specimen part
View SamplesLung cancer is still the leading cause of cancer-related deaths in the US and worldwide. Understanding the global molecular profiles or transcriptome of lung cancers would strengthen our understanding of the biology of this malignancy.
ETS2 mediated tumor suppressive function and MET oncogene inhibition in human non-small cell lung cancer.
Specimen part
View SamplesOvarian cancer is the most lethal malignancy in the United States. While studies on ovarian cancer pathogenesis were mainly focused on the epithelial component of the tumor, understanding in the role of cancer associated fibroblasts (CAFs) in ovarian cancer progression is limited. In the present study, we describe the use of microdissected transcriptome profiles for the identification of cancerstroma crosstalk networks with prognostic value, which presents a unique opportunity for developing new treatment strategies for ovarian cancer.
Systematic Identification of Druggable Epithelial-Stromal Crosstalk Signaling Networks in Ovarian Cancer.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesOvarian cancer is the most lethal malignancy in the United States. In the year 2012, there will be an estimated 22,280 new cases and 15,500 deaths from ovarian cancer in the country (Siegel et al., 2012). While studies on ovarian cancer pathogenesis were mainly focused on the epithelial component of the tumor, understanding in the role of cancer associated fibroblasts (CAFs) in ovarian cancer progression is limited. We hypothesized that comparing the gene expression profiles of different components from laser capture microdissected ovarian tissue will allow us to identify an ovarian CAFs specific gene signature which accounts for the supportive role of CAFs in ovarian cancer progression. In this study, gene expression profiling was completed for 31 cancer stroma samples and 32 samples of epithelial component from high grade serous ovarian cancer patients. 8 microdissected normal ovarian stroma and 6 normal human ovarian surface epithelium (HOSE) samples were also included in the study. By comparing the expression data from cancer stroma against that from normal stroma, cancer cells and HOSE, we identified a set of differential expressed genes in ovarian CAFs which showed correlation with cancer patient survival. Further study on these genes can reveal their roles in ovarian cancer progression and pathogenesis. Ultimately, ovarian CAFs specified genes identified in this study may aid in the classification and enhancement of patient outcome.
TGF-β modulates ovarian cancer invasion by upregulating CAF-derived versican in the tumor microenvironment.
Specimen part
View SamplesAs part of a clinical trial of the MDM2 inhibitor DS-3032b, 41 primary tumor samples were obtained before treatment from 38 patients newly diagnosed with AML, or relapsed or refractory to standard induction chemotherapy
Predictive Gene Signatures Determine Tumor Sensitivity to MDM2 Inhibition.
Specimen part, Disease, Disease stage
View SamplesHomologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesDefects in replication stress response (RSR) allow the survival and proliferation of genomically unstable cells, ultimately leading to tumorigenesis. Therefore, the RSR status can potentially serve as a powerful indicator to predict the possibility of early tumorigenesis. Here, we identified an RSR defects (RSRD) gene signature that robustly predicted RSR status. For the clinical benefit, our identification of RSRD gene signature gives the possibility to assess the risk of early tumorigenesis in the precancerous patients.
No associated publication
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer.
Specimen part, Cell line
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