This SuperSeries is composed of the SubSeries listed below.
Combined inhibition of receptor tyrosine and p21-activated kinases as a therapeutic strategy in childhood ALL.
Specimen part, Disease, Disease stage, Time
View SamplesThe purpose of this study was the principal investigation and frequency of RTK expression in primary T-ALLs. Primary initial T-ALLs were assessed regarding their transcriptome-wide expression profiles and screend for prominent RTK expression.
Combined inhibition of receptor tyrosine and p21-activated kinases as a therapeutic strategy in childhood ALL.
Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.
Specimen part, Disease stage, Time
View SamplesLymph node metastasis is a poor prognosis indicator in esophageal cancer. Although tumor spreading currently forms the main basis for therapy selection, the molecular mechanisms underlying the metastatic pathway remain insufficiently understood. Several studies aimed to investigate these mechanisms but focused mainly on regulatory patterns in the tumors themselves and/or the invaded lymph nodes. To date no study has yet investigated the potential changes on transcription level, which take place within the yet non-invaded niche. Here we provide a comprehensive description of these regulations in patients. In this study the transcriptomic profiles of regional lymph nodes were determined for two patient groups: patients classified as pN1 (metastasis) or pN0 (no metastasis) respectively. All investigated lymph nodes, also those from pN1 patients, were still free of metastasis. The gene expression data was obtained via microarray analysis. Top candidates were validated via PCR and immunohistochemistry. The results show that regional lymph nodes of pN1 patients differ decisively from those of pN0 patients even before metastasis has taken place. In the pN0 group distinct immune response patterns were observed. In contrast, lymph nodes of the pN1 group exhibited a clear profile of reduced immune response and reduced proliferation, but increased apoptosis, enhanced hypoplasia and morphological conversion processes. DKK1 was the most significant gene associated with the molecular mechanisms taking place in lymph nodes of patients suffering from metastasis (pN1). We assume that the two molecular profiles observed constitute two different stages of a progressive disease. Finally we suggest that DKK1 might play an important role within the mechanisms leading to lymph node metastasis.
Molecular changes in pre-metastatic lymph nodes of esophageal cancer patients.
Specimen part, Subject
View SamplesTransgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis.
Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.
Specimen part, Disease stage
View SamplesDeregulated RTK activity has been implicated as a causal leukemogenic factor in the context of molecular aberrations that perturb differentiation in the hematopoietic lineage such as in childhood ALL. A deeper understanding of RTK signaling processes on a system-wide scale will be key in defining critical components of signaling networks. To link RTK activity with in vivo output in primary ALL we took a functional approach, which combined SH2 domain binding, mass spectrometry, and transcriptome analyses. Structure and composition of evolving networks were highly diverse with few generic features determined by receptor and cell type. A combinatorial assembly of varying context-dependent and few generic signaling components at multiple levels likely generates output specificity. PAK2 was identified as a phosphoregulated FLT3 target, whose allosteric inhibition resulted in apoptosis of ALL cells. Our studies provide evidence that a functional approach to leukemia signaling may yield valuable information for a network-directed intervention.
Combined inhibition of receptor tyrosine and p21-activated kinases as a therapeutic strategy in childhood ALL.
Specimen part, Time
View SamplesThe cytotoxic drug edelfosine is a synthetic analog of 2-lysophosphatidylcholine. Edelfosine is incorporated by highly proliferating cells, e.g. activated immune cells. It is unknown if the described mechanisms for edelfosine action attained by in vitro approaches exclusively contribute to the observed EAE-amelioration or if edelfosine may exert additional, probably more general and possibly immunoablative effects within the setting of autoimmunity.
The orally available, synthetic ether lipid edelfosine inhibits T cell proliferation and induces a type I interferon response.
Specimen part, Treatment
View SamplesWe have investigated whether the early dissemination of tumor cells into bone marrow is associated with a specific molecular pattern in primary lung cancer
Genomic profiles associated with early micrometastasis in lung cancer: relevance of 4q deletion.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Differential effects of α-catenin on the invasion and radiochemosensitivity of human colorectal cancer cells.
Cell line
View SamplesMutations in the CLN3 gene lead to juvenile neuronal ceroid lipofuscinosis, a pediatric neurodegenerative disorder characterized by visual loss, epilepsy and psychomotor deterioration. Although most CLN3 patients carry the same 1 kb deletion in the CLN3 gene, their disease phenotype can be variable. The aims of this study were (1) to identify genes that are dysregulated in CLN3 disease regardless of the clinical course that could be useful as biomarkers, and (2) to find modifier genes that affect the progression rate of the disease.
Analysis of potential biomarkers and modifier genes affecting the clinical course of CLN3 disease.
Sex, Age, Specimen part, Disease, Disease stage
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