Homo sapiens strain:SAEC
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB16238 | ENA |
REPOSITORIES: ENA
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Project description:Lung cancer is the leading cause of cancer-related mortality. The two main lung cancer types are small cell lung cancer (SCLC) and non-SCLC (NSCLC), where NSCLC comprises about 80-85% of all lung cancer. Despite the introduction of improved treatments, the overall survival rate of lung cancer patients remains low. Further elucidation of the regulatory network perturbations between cancer-related genes and proteins is one promising route to alter this mortality trend. The deregulation of the DNA replication, cell cycle, proliferation and migration are the common factors that are involved in cancer development and progression, and therefore logical targets for analysis. Minichromosome maintenance 2(MCM2) is a DNA replication licensing factor, which belongs to the heterohexameric MCM2-7 complex. MCM2 has been proposed as an excellent proliferation marker in many types of cancer. Our study will establish a global functional distribution of identified proteins in silenced-MCM2 in H1299 NSCLC by the means of iTRAQ. Understanding the molecular basis of MCM2 in lung cancer cells enables us to discover alternative target for lung cancer therapy.
2018-10-26 | PXD003743 | Pride
Project description:We are investigating the molecular development of squamous cell lung carcinoma based upon analysis of global gene expression profiles representing progressive stages of cancer development, consisting of precancerous, carcinoma-in-situ, and invasive cancer. Keywords: global gene expression analysis, lung cancer development
2010-03-05 | GSE7898 | GEO
Project description:We are investigating the molecular development of squamous cell lung carcinoma based upon analysis of global gene expression profiles representing progressive stages of cancer development, consisting of precancerous, carcinoma-in-situ, and invasive cancer. Keywords: global gene expression analysis, lung cancer development In this study, we have generated 13 SAGE libraries, consisting of five carcinoma-in-situ libraries, six early invasive squamous cell carcinoma libraries, and two reference libraries representing precancerous squamous development.
2010-03-04 | E-GEOD-7898 | biostudies-arrayexpress
Project description:Lung cancer remains the leading cause of cancer death. Genome sequencing of lung tumors from patients with Squamous Cell Carcinoma has identified SMAD4 to be frequently mutated. Here we used a novel mouse model to determine the molecular mechanisms regulated by loss of Smad4 which lead to lung cancer progression. Mice with ablation of Pten and Smad4 in airway epithelium developed metastatic adenosquamous tumors. Comparative transcriptomic and in vivo cistromic analyses determined that loss of PTEN and SMAD4 resulted in activation of the ELF3 and the ErbB2 pathway due to decreased ERRFI1M-bM-^@M-^Ys expression, a negative regulator of ERBB2 in mice and human cells. The combinatorial inhibition of ErbB2 and Akt signaling attenuated tumor progression and cell invasion, respectively. Expression profiles analysis of human lung tumors substantiated the importance of the ErbB2/Akt/ELF3 signaling pathway as both prognostic biomarkers and therapeutic drug targets for treating lung cancer. Examination of genome-wide SMAD4 binding in 7-month-old Ptend/d mouse lung.
2015-03-05 | E-GEOD-57177 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer, but the underlying molecular mechanisms are unknown. We hypothesized that lung stromal cells activate pathological gene expression programs supporting oncogenesis. To identify molecular mechanisms operating in the lung stroma that support development of lung cancer. Study subjects included patients with- or without- lung cancer across a spectrum of lung function. We conducted multi-omics analysis of non-malignant lung tissue to quantify the transcriptome, translatome and proteome. Cancer-associated gene expression changes predominantly manifested as alterations in the efficiency of mRNA translation modulating protein levels in the absence of corresponding changes in mRNA levels. The molecular mechanisms driving these cancer-associated translation programs differed based on lung function. In subjects with normal to mildly impaired lung-function, the mammalian target of rapamycin (mTOR) pathway served as an upstream driver; whereas in severe airflow obstruction, pathways downstream of pathological extracellular matrix (ECM) emerged. Consistent with a role during cancer initiation, both the mTOR and ECM gene expression programs paralleled activation of previously identified pro-cancer secretomes. Furthermore, in situ examination of lung tissue documented that stromal fibroblasts express cancer-associated proteins from the two pro-cancer secretomes including IL6 in mild or no airflow obstruction and BMP1 in severe airflow obstruction. Two distinct stromal gene expression programs promoting cancer initiation are activated in lung cancer patients depending on lung function. Our work has implications both for screening strategies and personalized approaches to cancer treatment.
2019-03-05 | GSE103404 | GEO
Project description:The proteomics analysis of circulating exosomes derived from cancer cells represents a promising approach to the elucidation of cell-cell communication and the discovery of putative biomarker candidates for cancer diagnosis and treatment. Nonetheless, the proteome of exosomes derived from cell lines with different metastatic capabilities still warrants further investigation. Here, we present a comprehensive quantitative proteomics investigation of exosomes isolated from im-mortalized mammary epithelial cells and matched tumor lines with different metastatic potential, in an attempt to discover exosome markers specific to breast cancer (BC) metastasis. A total of 2,135 unique proteins were quantified with a high confidence level from 20 isolated exosome samples, including 94 of the TOP 100 exosome markers archived by ExoCarta, e.g., CD9, HSPa8, and PDCD6IP. Moreover, 344 altered proteins were observed, among which several metastasis-specific markers, including CATW, MRS2, SDCB2, RTN4, and RAD23B, were also identified. Notably, the abundance of these metastasis-specific corresponds well with the overall survival of BC patients in clinical settings. Together, these data provide a valuable dataset for BC exosome proteomics in-vestigation and prominently facilitate the elucidation of the molecular mechanisms underlying primary tumor development and progression.
2023-03-11 | PXD038553 | Pride
Project description:The present project will follow our previous phaseⅡ study of FOLFOX regimens for the treatment of stage Ⅳ colorectal cancer. We will recruit at least 200 patients for this study. The selection of patients will be based on rigorous eligibility criteria. The patients will be allocated based on the expression of each molecular marker (MSI, TS, DPD, MVD and EGFR) and the implementation of chemotherapy. For example, in the examination for the clinical implications of EGFR, the patients will be classified into four groups: EGFR（＋） chemotherapy（＋）; EGFR（＋） chemotherapy（-）; EGFR（-） chemotherapy（＋）; EGFR（-） chemotherapy（-）. Base on the analysis of this 2×2 table, we will clarify the prognostic significance of a specific molecular marker is due to whether the specific molecular marker predicts biological invasiveness and/or chemosensitivity. We believe the present study will have the following significance: （1）To further clarify the mechanisms for the carcinogenesis and progression of CRC; （2）To facilitate the development of novel chemotherapeutic agents; and （3） To gain the experience for the practice of evidence-based medicine.
| 2017518 | ecrin-mdr-crc
Project description:Microarray analysis of serum microRNAs for the detection of urothelial cancer and for the elucidation of cancer development mechanisms
| PRJNA830981 | ENA