Fyn

Saito, Yoshihito; Jensen, Ana R.; Salgia, Ravi; Posadas, Edwin M.

doi:10.1002/cncr.24879

Cited by 173 publications

(105 citation statements)

References 46 publications

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“…Moreover, FYN is a Proto-oncogene tyrosine-protein kinase of the Src family of kinases, typically associated with T-cell and neuronal signaling in development and normal cell physiology. Disruptions FYN signaling pathways often have implications in the formation of a variety of cancers (Saito et al, 2010). …”

Section: Resultsmentioning

confidence: 99%

The Genome Conformation As an Integrator of Multi-Omic Data: The Example of Damage Spreading in Cancer

Tordini¹,

Aldinucci²,

Milanesi

et al. 2016

Front. Genet.

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Publicly available multi-omic databases, in particular if associated with medical annotations, are rich resources with the potential to lead a rapid transition from high-throughput molecular biology experiments to better clinical outcomes for patients. In this work, we propose a model for multi-omic data integration (i.e., genetic variations, gene expression, genome conformation, and epigenetic patterns), which exploits a multi-layer network approach to analyse, visualize, and obtain insights from such biological information, in order to use achieved results at a macroscopic level. Using this representation, we can describe how driver and passenger mutations accumulate during the development of diseases providing, for example, a tool able to characterize the evolution of cancer. Indeed, our test case concerns the MCF-7 breast cancer cell line, before and after the stimulation with estrogen, since many datasets are available for this case study. In particular, the integration of data about cancer mutations, gene functional annotations, genome conformation, epigenetic patterns, gene expression, and metabolic pathways in our multi-layer representation will allow a better interpretation of the mechanisms behind a complex disease such as cancer. Thanks to this multi-layer approach, we focus on the interplay of chromatin conformation and cancer mutations in different pathways, such as metabolic processes, that are very important for tumor development. Working on this model, a variance analysis can be implemented to identify normal variations within each omics and to characterize, by contrast, variations that can be accounted to pathological samples compared to normal ones. This integrative model can be used to identify novel biomarkers and to provide innovative omic-based guidelines for treating many diseases, improving the efficacy of decision trees currently used in clinic.

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Section: Resultsmentioning

confidence: 99%

The Genome Conformation As an Integrator of Multi-Omic Data: The Example of Damage Spreading in Cancer

Tordini¹,

Aldinucci²,

Milanesi

et al. 2016

Front. Genet.

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show abstract

“…It has been demonstrated that it is involved in the regulation of T-cell development and activation, factor and cytokine receptor signaling, cell–cell adhesion, integrin-mediated signaling, ion channel function, platelet activation, T- and B-cell receptor signaling, axon guidance, mitosis, differentiation of NK cells (Palacios and Weiss, 2004; Salmond et al, 2009; Saito et al, 2010). …”

Section: Introdutionmentioning

confidence: 99%

A Pyrazolo[3,4-d]pyrimidine Compound Reduces Cell Viability and Induces Apoptosis in Different Hematological Malignancies

et al. 2016

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Molecular targeted therapies are based upon drugs acting on tumors by interfering with specific targets involved in growth and spread of cancer. Many targeted therapies were approved by Food and Drug Administration as standard treatment, others were introduced into preclinical or clinical studies on hematological malignancies (HMs). The development of drug-resistance in some HMs and the lack of effective treatments in other ones emphasized the need for searching new molecular targets and therapeutic agents. The aim of this study was to evaluate the effects of 4c pyrazolo[3,4-d]pyrimidine compound, a Src inhibitor, on lymphoid and myeloid neoplasms. Here, we demonstrated its ability to reduce cell viability, induce apoptosis and cell cycle arrest in lymphoid cell lines such as Jurkat, SKMM1, Derl-2/7, and myeloid cell lines, such as Jurl-MK1. Moreover, we reported a high expression of a Src kinase, Fyn, in these cell lines compared to healthy subjects. This study was a starting point to investigate 4c pyrazolo[3,4-d]pyrimidine compound as a drug for HMs and Src kinases as its potential molecular targets.

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“…Fyn is up-regulated in prostate cancer where it exhibits tumorigenic potential in processes of cellular motility. Its interaction with several signal molecules, including focal adhesion kinase (FAK), Akt and paxillin, that play an essential role in prostate cancer progression, might account for the described cell transformations and possibly lends credence to its role in both cancer progression and metastasis [10-12]. …”

Section: Introductionmentioning

confidence: 99%

MicroRNA miR-125a-3p modulates molecular pathway of motility and migration in prostate cancer cells

et al. 2014

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Fyn

Cited by 173 publications

References 46 publications

The Genome Conformation As an Integrator of Multi-Omic Data: The Example of Damage Spreading in Cancer

The Genome Conformation As an Integrator of Multi-Omic Data: The Example of Damage Spreading in Cancer

A Pyrazolo[3,4-d]pyrimidine Compound Reduces Cell Viability and Induces Apoptosis in Different Hematological Malignancies

MicroRNA miR-125a-3p modulates molecular pathway of motility and migration in prostate cancer cells

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