A5085885299- PI3K/AKT/mTOR signaling in cancer
- Infectious Diseases and Mycology
- Fungal Plant Pathogen Control
- Lipid metabolism and biosynthesis
- Cancer, Lipids, and Metabolism
- Adipose Tissue and Metabolism
- Cancer-related Molecular Pathways
- Metabolism, Diabetes, and Cancer
- Protein Kinase Regulation and GTPase Signaling
- Autophagy in Disease and Therapy
- HER2/EGFR in Cancer Research
- Click Chemistry and Applications
- Effects of Radiation Exposure
- Melanoma and MAPK Pathways
- Cancer Mechanisms and Therapy
- RNA Research and Splicing
- Ocular Oncology and Treatments
- Microtubule and mitosis dynamics
- Cancer, Hypoxia, and Metabolism
- Prostate Cancer Treatment and Research
- Inflammatory mediators and NSAID effects
- Cancer Research and Treatments
- Cancer Cells and Metastasis
- Epigenetics and DNA Methylation
- NF-κB Signaling Pathways
The University of Texas MD Anderson Cancer Center
2005-2023
Scripps MD Anderson Cancer Center
2011
Mudanjiang Medical University
2010
Sanford Burnham Prebys Medical Discovery Institute
2010
Abstract Small GTPase Ras homologue enriched in brain (RHEB) binds and activates the key metabolic regulator mTORC1, which has an important role cancer cells, but of RHEB pathogenesis not been shown. By performing a meta-analysis published cytogenetic transcriptome databases, we defined gain chromosome 7q36.1-q36.3 containing locus, overexpression mRNA several different carcinoma histotypes, association between upregulation poor prognosis breast head neck cancers. To model function...
Immunohistochemical analysis has consistently shown that cyclin E is up-regulated in human malignant melanomas vivo. Here we analyzed such expression more detail and show overexpressed present low molecular weight (LMW) isoforms metastatic melanoma a subset of primary invasive tumor tissues, but not benign nevi. Human cell lines, normal melanocytes, also expressed the LMW forms. The biological significance these findings was established by showing overexpression two forms named truncated 1...
Lipid metabolism plays a central role in prostate cancer. To date, the major focus has centered on de novo lipogenesis and lipid uptake cancer, but inhibitors of these processes have not benefited patients. A better understanding how cancer cells access lipids once they are created or taken up stored could uncover more effective strategies to perturb treat Here, we identified that expression adipose triglyceride lipase (ATGL), an enzyme controls droplet homeostasis previously suspected tumor...
AbstractAnti-HER2 antibody trastuzumab (Herceptin®) has been used effectively to treat patients with breast cancer that overexpresses HER2. We have demonstrated p27Kip1 upregulation is one of the key events cause G1 arrest upon treatment. Here, we examined effect on CDK2, Rb, E2F1, NPAT, histone H4, and their associated signaling pathway. Results showed was able dramatically inhibit kinase activity expression whereas CDK4 were not affected by Unlike occurs primarily through...
Despite early studies linking calcium-calmodulin protein kinase 2 (CAMKK2) to prostate cancer cell migration and invasion, the role of CAMKK2 in metastasis vivo remains unclear. Moreover, while is known regulate systemic metabolism, whether CAMKK2’s effects on whole-body metabolism would impact progression and/or related comorbidities not known. Here, we demonstrate that germline ablation Camkk2 slows, but does stop, primary tumorigenesis TRansgenic Adenocarcinoma Mouse Prostate (TRAMP)...
Abstract Previously, we reported that breast cancer cells with retinoblastoma (pRb) pathway–defective checkpoints can be specifically targeted chemotherapeutic agents, following staurosporine-mediated reversible growth inhibition in normal cells. Here set out to determine if the kinetics of is G1 phase cells, and such arrest requires activity wild-type pRb. Normal human mammary epithelial immortalized intact pRb treated low concentrations staurosporine arrested cell cycle, whereas...
Chemotherapeutic agents have been the mainstay of cancer therapy for years. However, their effectiveness has limited by toxicities they impart on normal cells. Staurosporine (ST) shown to arrest normal, but not breast cancer, cells in G 1 . Therefore, ST may become a chemoprotective agent, arresting while allowing tumor enter cell cycle phases where are sensitive chemotherapeutic agents. Understanding mechanism ST-mediated allow beneficial treatment strategy patients. We utilized 76NE6...
<p>28 supplementary figures supporting the main text and figures.</p>
<p>IP/MS summary table describing the ATGL interactome in C4-2 cells.</p>
<p>28 supplementary figures supporting the main text and figures.</p>
<p>IP/MS summary table describing the ATGL interactome in C4-2 cells.</p>
<div>Abstract<p>Lipid metabolism plays a central role in prostate cancer. To date, the major focus has centered on <i>de novo</i> lipogenesis and lipid uptake cancer, but inhibitors of these processes have not benefited patients. A better understanding how cancer cells access lipids once they are created or taken up stored could uncover more effective strategies to perturb treat Here, we identified that expression adipose triglyceride lipase (ATGL), an enzyme controls...
<p>Supplementary Dataset of Phosphoproteomics Analyses Patient Samples</p>
<p>Supplementary Dataset of Phosphoproteomics Analyses Patient Samples</p>
<div>Abstract<p>Lipid metabolism plays a central role in prostate cancer. To date, the major focus has centered on <i>de novo</i> lipogenesis and lipid uptake cancer, but inhibitors of these processes have not benefited patients. A better understanding how cancer cells access lipids once they are created or taken up stored could uncover more effective strategies to perturb treat Here, we identified that expression adipose triglyceride lipase (ATGL), an enzyme controls...
Abstract Despite early studies linking calcium-calmodulin protein kinase 2 (CAMKK2) to prostate cancer cell migration and invasion, the role of CAMKK2 in metastasis vivo remains unclear. Moreover, while is known regulate systemic metabolism, whether CAMKK2’s effects on whole body metabolism would impact progression and/or related comorbidities not known. Here, we demonstrate that germline ablation Camkk2 slows, but does stop, primary tumorigenesis TR ansgenic A denocarcinoma M ouse P rostate...
Supplementary Figure 5 from Mammalian Target of Rapamycin Activator RHEB Is Frequently Overexpressed in Human Carcinomas and Critical Sufficient for Skin Epithelial Carcinogenesis