Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151399 | ENA |
REPOSITORIES: ENA
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Project description:A part of current research has intensively been focused on the proliferation and metabolic processes governing biological systems. Since the advent of high throughput methodologies like microarrays, the load of genomic data has increased geometrically and along with that the need for computational methods which will interpret these data. In the present work we study in vitro the common proliferation and metabolic processes, which are combined to the common oncogenic pathways, as far as gene expression is concerned, between the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational approach, using cDNA microarrays, in order to identify commonalities between diverse biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are the driving forces in the two cell lines. This type of analysis can lead to the understanding of the common mechanisms that transform physiological cells to malignant, as well as it reveals a new holistic way to understandthe the dynamics of tumor onset as well as the mechanistics of oncogenic drivers. The present work is concerned with the common expressional profile of two cell lines: the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. Our investigation was focused on the identification of genes that share a common expression profile between the two cell lines. Both cell lines are characterized by the fact that their differentiation has stopped at an early stage, before they mature to their final cell type. Normally, these cells would have matured and progressed into differentiated cells, constituting blood and muscle cells, respectively. At some unknown point, normal differentiation ceased for these cells and they became malignant. From that point on, to the first manifestation of symptoms of malignancy, there is a lack of knowledge regarding the mechanisms underlying oncogenesis. From these observations, the question whether two distinct cell types destined to fulfill different functions, manifest similar mechanisms of growth and progression due to their malignant character, arises. The present study was focused on the identification of the differential expression profiles underlying the two cell lines. A previous report studied the expression profile of seven ARMS cell lines possessing the PAX3-FKHR fusion gene, along with other cell lines of different tumor types (22). To our knowledge, this is the first time that a comparison between two totally different types of neoplasia, such as the CCRF-CEM and TE-671 cell lines, is attempted. These mechanisms are examined with purpose to identify common drivers that lead to the progression of tumor cells. We hereby propose a new computational approach for the investigation of common oncogenic drivers.
2011-12-20 | E-GEOD-34522 | biostudies-arrayexpress
Project description:A part of current research has intensively been focused on the proliferation and metabolic processes governing biological systems. Since the advent of high throughput methodologies like microarrays, the load of genomic data has increased geometrically and along with that the need for computational methods which will interpret these data. In the present work we study in vitro the common proliferation and metabolic processes, which are combined to the common oncogenic pathways, as far as gene expression is concerned, between the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational approach, using cDNA microarrays, in order to identify commonalities between diverse biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are the driving forces in the two cell lines. This type of analysis can lead to the understanding of the common mechanisms that transform physiological cells to malignant, as well as it reveals a new holistic way to understandthe the dynamics of tumor onset as well as the mechanistics of oncogenic drivers.
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In a healthy person, progastrin is not detectable in the peripheral blood. However, progastrin is abnormally released in the blood of patients with different cancers (colorectal, gastric, ovarian, breast, cervix uterus, melanoma...) The gene GAST coding for progastrin is a direct target gene of the WNT/ß-catenin oncogenic pathway. The activation of this oncogenic pathway is an early event in cancer development.
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Progastrin measured in the peripheral blood of patients on treatments, could be a new powerful marker for diagnosis and prognosis at different stages.
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2012-05-14 | E-GEOD-30516 | biostudies-arrayexpress
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