Publications by authors named "Zerrin Isık"

Metastatic colorectal cancer (CRC) is still in need of effective treatments. This study applies a holistic approach to propose new targets for treatment of primary and liver metastatic CRC and investigates their therapeutic potential in-vitro. An integrative analysis of primary and metastatic CRC samples was implemented for alternative target and treatment proposals.

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This paper aims to elucidate the differentially coexpressed genes, their potential mechanisms, and possible drug targets in low-grade invasive serous ovarian carcinoma (LGSC) in terms of the biologic continuity of normal, borderline, and malignant LGSC. We performed a bioinformatics analysis, integrating datasets generated using the GPL570 platform from different studies from the GEO database to identify changes in this transition, gene expression, drug targets, and their relationships with tumor microenvironmental characteristics. In the transition from ovarian epithelial cells to the serous borderline, the FGFR3 gene in the "Estrogen Response Late" pathway, the ITGB2 gene in the "Cell Adhesion Molecule", the CD74 gene in the "Regulation of Cell Migration", and the IGF1 gene in the "Xenobiotic Metabolism" pathway were upregulated in the transition from borderline to LGSC.

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Combining omics data from different layers using integrative methods provides a better understanding of the biology of a complex disease such as cancer. The discovery of biomarkers related to cancer development or prognosis helps to find more effective treatment options. This study integrates multi-omics data of different cancer types with a network-based approach to explore common gene modules among different tumors by running community detection methods on the integrated network.

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Computational drug repositioning approaches are important, as they cost less compared to the traditional drug development processes. This study proposes a novel network-based drug repositioning approach, which computes similarities between disease-causing genes and drug-affected genes in a network topology to suggest candidate drugs with highest similarity scores. This new method aims to identify better treatment options by integrating systems biology approaches.

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Computational drug repurposing aims to discover new treatment regimens by analyzing approved drugs on the market. This study proposes previously approved compounds that can change the expression profile of disease-causing proteins by developing a network theory-based drug repurposing approach. The novelty of the proposed approach is an exploration of module similarity between a disease-causing network and a compound-specific interaction network; thus, such an association leads to more realistic modeling of molecular cell responses at a system biology level.

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Adenomatous polyps of the colon are the most common neoplastic polyps. Although most of adenomatous polyps do not show malign transformation, majority of colorectal carcinomas originate from neoplastic polyps. Therefore, understanding of this transformation process would help in both preventive therapies and evaluation of malignancy risks.

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Identification of common molecular mechanisms in interrelated diseases is essential for better prognoses and targeted therapies. However, complexity of metabolic pathways makes it difficult to discover common disease genes underlying metabolic disorders; and it requires more sophisticated bioinformatics models that combine different types of biological data and computational methods. Accordingly, we built an integrative network analysis model to identify shared disease genes in metabolic syndrome (MS), type 2 diabetes (T2D), and coronary artery disease (CAD).

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Leukemia is a fatal cancer and has two main types: Acute and chronic. Each type has two more subtypes: Lymphoid and myeloid. Hence, in total, there are four subtypes of leukemia.

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Identification of effective drug combinations for patients is an expensive and time-consuming procedure, especially for experiments. To accelerate the synergistic drug discovery process, we present a new classification model to identify more effective anti-cancer drug pairs using network biology approach. Based on the hypotheses that the drug synergy comes from the collective effects on the biological network, therefore, we developed six network biology features, including overlap and distance of drug perturbation network, that were derived by using individual drug-perturbed transcriptome profiles and the relevant biological network analysis.

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Objectives: To investigate gene expression differences and related functions between primary tumor, malignant cells in ascites, and metastatic peritoneal implant in high-grade serous ovarian cancer.

Methods: Biopsies from primary tumor, peritoneal implant, and ascites were collected from 10 patients operated primarily for high-grade, advanced-staged serous ovarian cancer. Total RNA isolation was performed from collected tissue biopsy and fluid samples, and RNA expression profile was measured.

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Integration of several types of patient data in a computational framework can accelerate the identification of more reliable biomarkers, especially for prognostic purposes. This study aims to identify biomarkers that can successfully predict the potential survival time of a cancer patient by integrating the transcriptomic (RNA-Seq), proteomic (RPPA), and protein-protein interaction (PPI) data. The proposed method -RPBioNet- employs a random walk-based algorithm that works on a PPI network to identify a limited number of protein biomarkers.

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During a cell state transition, cells travel along trajectories in a gene expression state space. This dynamical systems framework complements the traditional concept of molecular pathways that drive cell phenotype switching. To expose the structure that hinders cancer cells from exiting robust proliferative state, we assessed the perturbation capacity of a drug library and identified 16 non-cytotoxic compounds that stimulate MCF7 breast cancer cells to exit from proliferative state to differentiated state.

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Drugs bind to their target proteins, which interact with downstream effectors and ultimately perturb the transcriptome of a cancer cell. These perturbations reveal information about their source, i.e.

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Disease progression in cancer can vary substantially between patients. Yet, patients often receive the same treatment. Recently, there has been much work on predicting disease progression and patient outcome variables from gene expression in order to personalize treatment options.

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Determination of cell signalling behaviour is crucial for understanding the physiological response to a specific stimulus or drug treatment. Current approaches for large-scale data analysis do not effectively incorporate critical topological information provided by the signalling network. We herein describe a novel model- and data-driven hybrid approach, or signal transduction score flow algorithm, which allows quantitative visualization of cyclic cell signalling pathways that lead to ultimate cell responses such as survival, migration or death.

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