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Abstract 768: A kinome-wide siRNA screen identifies modifiers of sensitivity to the EGFR T790M-targeted tyrosine kinase inhibitor (TKI), AZD9291, in EGFR mutant lung adenocarcinoma
In conclusion, through a kinome wide siRNA screen, we identified that gene products in the MAP kinase signaling pathway modify sensitivity to AZD9291. Such sensitivity may be associated with ERK re-phosphorylation within 96h of drug treatment. Collectively, these data suggest rational drug combinations that could be used to forestall resistance to AZD9291. Additional hits from the screen are currently under investigation.This study is supported by AstraZeneca Oncology Innovative Medicines, National Institutes of Health (NIH) NCI grants R01-CA121210, P01-CA129243, U54-CA143798, and the Uehara Memorial Foundation.Citation Fo...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Ichihara, E., Bauer, J. A., Lu, P., Ye, F., Cross, D., Pao, W., Lovly, C. M. Tags: Experimental and Molecular Therapeutics Source Type: research

Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters
Conclusion In summary, this study is the first to combine metabolomics, transcriptomics, and genome-wide association studies in a porcine model. Our results improve understanding of the genetic regulation of metabolites which link to transcripts and finally biochemical-clinical parameters. Further, high-performance profiling of metabolites as intermediate phenotypes is a potentially powerful approach to uncover how genetic variation affects metabolic and health status. Our results advance knowledge in areas of biomedical and agricultural interest and identify potential correlates of biomarkers, SNPs-metabolites, SNPs-tran...
Source: Frontiers in Genetics - April 16, 2019 Category: Genetics & Stem Cells Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

High Expression of DEPDC1 Promotes Malignant Phenotypes of Breast Cancer Cells and Predicts Poor Prognosis in Patients With Breast Cancer
In this study, the immunohistochemistry results demonstrated that DEPDC1 was high-expressed in breast cancer tissues compared with the paired adjacent normal breast tissues, and its tendency at protein level was consistent with mRNA level from TCGA data. Moreover, DEPDC1 mRNA level revealed the strongest association with poor prognosis and development in breast cancer. In vitro assays showed that DEPDC1 overexpression resulted in significant promotion of proliferation by regulating cell cycle in MCF-7 cells, whilst an opposite effect was found in the MDA-MB-231 cells with DEPDC1 deletion. Notably, further investigation ind...
Source: Frontiers in Oncology - April 11, 2019 Category: Cancer & Oncology Source Type: research

The JAK/STAT Pathway in Skeletal Muscle Pathophysiology
Conclusion and Perspectives The IL-6/JAK/STAT signaling cascade plays a dominant role in skeletal muscle pathophysiology. IL-6 autocrine, paracrine, and endocrine functions assign to its downstream effectors pivotal importance in skeletal muscle-wasting-associated diseases and other multiple system diseases where muscle acts in communication with other organs. Targeting the components of the JAK/STAT pathway recently emerged as a strategic approach for the treatment of inflammatory diseases and human cancer. This review highlights the opposite outcomes on muscle biology caused by the amount of local and systemic release ...
Source: Frontiers in Physiology - April 29, 2019 Category: Physiology Source Type: research

DDR1 and MT1-MMP Expression Levels Are Determinant for Triggering BIK-Mediated Apoptosis by 3D Type I Collagen Matrix in Invasive Basal-Like Breast Carcinoma Cells
In conclusion, and in agreement with the other studies (Ford et al., 2007; Koh et al., 2015; Toy et al., 2015; Takai et al., 2018), our data suggest that during the acquisition of mesenchymal features, the level of full-length DDR1 expression should be considered, in addition to the other markers, as an important biomarker in the prognosis of aggressive breast carcinomas. As summarized in Figure 9, the regulation of cell proliferation and apoptosis by the collagen/DDR1 axis involves a differential activation of DDR1 signaling pathway and thus BIK expression. In the case of the basal-like bre...
Source: Frontiers in Pharmacology - May 2, 2019 Category: Drugs & Pharmacology Source Type: research

Abstract 2330: Transcription factor MAZ promotes cell growth and aggressive behavior of human pancreatic cancer cells
Pancreatic ductal adenocarcinoma (PDAC) is the fourth most common cancer in the United States and the eighth worldwide. PDAC is most aggressive type of cancer that spreads rapidly and is seldom detected in its early stages as signs and symptoms may not appear until pancreatic cancer is quite advanced. MAZ (Myc-associated zinc-finger protein) or SAF1 (Serum amyloid A activating factor 1) gene is a member of multiple Cys2-His2-type zinc finger proteins that are activated in response to various inflammatory signals and may act as a transcription factor with dual roles in transcription initiation and termination. Deregulation ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Maity, G., Sarkar, S., Dhar, K., Dhar, G., Haque, I., Banerjee, S. K., Banerjee, S. Tags: Molecular and Cellular Biology Source Type: research

Abstract 3152: Integrin {alpha}6{beta}1 dependent collective cell migration in prostate cancer metastasis
In this study, we optimized the growth and retrieval of tumor cells from 3-dimensional matrigel cultures, to determine the role of integrin α6β1, α6pβ1 and α3β1 in DU145 prostate tumor cell collective migration. The DU145 prostate tumor cells embedded in growth factor reduced matrigel, grew robust networks within 24 hours and contained extensive branching structures. The network formation was shown to be dependent on integrin α6β1 expression as determined by specific knockdown of α6β1 over a 24 hour period using 25nM siRNA targeting. Interestingly, the knockdown of α3β1 integrin had no observable effect on the ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Rubenstein, C. S., Gard, J., Nagle, R. B., Landowski, T. H., Cress, A. E. Tags: Tumor Biology Source Type: research