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Gene Therapy Leaves a Vicious Cycle
Reena Goswami1, Gayatri Subramanian2, Liliya Silayeva1, Isabelle Newkirk1, Deborah Doctor1, Karan Chawla2, Saurabh Chattopadhyay2, Dhyan Chandra3, Nageswararao Chilukuri1 and Venkaiah Betapudi1,4* 1Neuroscience Branch, Research Division, United States Army Medical Research Institute of Chemical Defense, Aberdeen, MD, United States 2Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, United States 3Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States 4Department of Physiology and Biophysics, Case Western Reserve University, Clev...
Source: Frontiers in Oncology - April 23, 2019 Category: Cancer & Oncology 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

Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Induces Genetic Instability and Can be Therapeutically Targeted
In conclusion, phosphorylation by Aurora Kinase A and ubiquitination by MDM2 contribute to SETD2 non-genomic loss of function in advanced-phase CML. Loss of SETD2/H3K36me3 is associated with increased DNA damage and impaired HR repair. Restoring physiological H3K36me3 levels may help improve the outcome of this critical subset of pts.Acknowledgments: study supported by AIRC (project code 16996) and AIL (Associazione Italiana contro le Leucemia, Linfomi e Mieloma).Figure 1.DisclosuresCastagnetti: Incyte: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Bristol Meyers Squibb: Consultancy, Honoraria; Novartis: Consulta...
Source: Blood - November 21, 2018 Category: Hematology Authors: Mancini, M., De Santis, S., Monaldi, C., Bavaro, L., Martelli, M., Castagnetti, F., Gugliotta, G., Rosti, G., Fontana, M. C., Dan, E., Sinigaglia, B., Iurlo, A., Orofino, N., Abruzzese, E., Salvucci, M., Pregno, P., Gozzini, A., Crugnola, M., Albano, F., Tags: 631. Chronic Myeloid Leukemia: Biology and Pathophysiology, excluding Therapy: Poster I Source Type: research

Down ‐regulating Myoferlin inhibits the vasculogenic mimicry of melanoma via decreasing MMP‐2 and inducing mesenchymal‐to‐epithelial transition
In conclusion, MYOF plays an important role in VM and knockdown of MYOF suppresses VM formation via decreasing MMP‐2 and inducing MET in A375 melanoma cells.
Source: Journal of Cellular and Molecular Medicine - November 22, 2017 Category: Molecular Biology Authors: Wenxue Zhang, Ping Zhou, Ai Meng, Rongxin Zhang, Yan Zhou Tags: Original Article Source Type: research

Down-regulating Myoferlin inhibits the vasculogenic mimicry of  melanoma via decreasing MMP-2 and inducing mesenchymal-to-epithelial transition.
In conclusion, MYOF plays an important role in VM and knockdown of MYOF suppresses VM formation via decreasing MMP-2 and inducing MET in A375 melanoma cells. PMID: 29164766 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - November 22, 2017 Category: Molecular Biology Authors: Zhang W, Zhou P, Meng A, Zhang R, Zhou Y Tags: J Cell Mol Med Source Type: research

NR4A2 Promotes DNA Double-strand Break Repair Upon Exposure to UVR
Exposure of melanocytes to ultraviolet radiation (UVR) induces the formation of UV lesions that can produce deleterious effects in genomic DNA. Encounters of replication forks with unrepaired UV lesions can lead to several complex phenomena, such as the formation of DNA double-strand breaks (DSBs). The NR4A family of nuclear receptors are transcription factors that have been associated with mediating DNA repair functions downstream of the MC1R signaling pathway in melanocytes. In particular, emerging evidence shows that upon DNA damage, the NR4A2 receptor can translocate to sites of UV lesion by mechanisms requiring post-t...
Source: Molecular Cancer Research - August 31, 2017 Category: Cancer & Oncology Authors: Yin, K., Chhabra, Y., Tropee, R., Lim, Y. C., Fane, M., Dray, E., Sturm, R. A., Smith, A. G. Tags: DNA Damage and Repair Source Type: research

Liposomal systems as viable drug delivery technology for skin cancer sites with an outlook on lipid-based delivery vehicles and diagnostic imaging inputs for skin conditions
Publication date: Available online 30 September 2016 Source:Progress in Lipid Research Author(s): Naseem Akhtar, Riaz A. Khan Skin cancer is among one of the most common human malignancies wide-spread world-over with mortality statistics rising continuously at an alarming rate. The increasing frequency of these malignancies has marked the need for adopting effective treatment plan coupled with better and site-specific delivery options for the desired therapeutic agent's availability at the affected site. The concurrent delivery approaches to cancerous tissues are under constant challenge and, as a result, are evolving and...
Source: Progress in Lipid Research - September 30, 2016 Category: Lipidology Source Type: research

Abstract 3027: Investigating the function of NONO, a novel double strand break repair factor, and exploring its potential role as a biomarker for melanoma
We investigated the in vivo function of NONO, a protein that has been shown to promote a distinct sub-pathway of nonhomologous end joining (NHEJ) repair in vitro and in cultured cells. We used a gene trap strategy to create a null mutant for Nono, the mouse homolog of the human NONO gene. We investigated hematopoietic stem cells (HSCs), which are known to be sensitive to deficiencies in other DNA repair proteins. Nono-deficient mice showed reduced bone marrow and spleen cellularity. HSCs from Nono-deficient mice showed severe impairment in competitive repopulation assays in primary and secondary recipients. HSCs from Nono-...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Li, S., Shu, F., Khan, M. K., Pollack, B. P., Li, Z., McLemore, M., Dynan, W. S. Tags: Molecular and Cellular Biology Source Type: research

Radiosensitization and downregulation of heterogeneous nuclear ribonucleoprotein K (hnRNP K) upon inhibition of mitogen/extracellular signal-regulated kinase (MEK) in malignant melanoma cells.
CONCLUSION: Our results indicate that pharmacological interference with MAPK signaling increases vulnerability of NRAS-mutant malignant melanoma cells to ionizing radiation along with downregulation of endogenous hnRNP K and point towards a possible use for combined MEK inhibition and localized radiation therapy of MM in the NRAS-mutant setting where BRAF inhibitors offer no clinical benefit. PMID: 26136337 [PubMed - as supplied by publisher]
Source: Oncotarget - July 5, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Involvement of Polymerase {eta} in Anticancer Drug Resistance
DNA repair processes are a key determinant of the sensitivity of cancer cells to DNA-damaging chemotherapeutics, which may induce certain repair genes as a mechanism to promote resistance. Here, we report the results of a screen for repair genes induced in cancer cells treated with DNA crosslinking agents, which identified the translesion polymerase η (PolH) as a p53-regulated target acting as one defense against interstrand crosslink (ICL)-inducing agents. PolH was induced by fotemustine, mafosfamide, and lomustine in breast cancer, glioma, and melanoma cells in vitro and in vivo, with similar inductions observed in norm...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Tomicic, M. T., Aasland, D., Naumann, S. C., Meise, R., Barckhausen, C., Kaina, B., Christmann, M. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research

GPNMB enhances bone regeneration by promoting angiogenesis and osteogenesis: Potential role for tissue engineering bone
Abstract Bone regeneration is a coordinated process involving the connection between blood vessels and bone cells. Glycoprotein non‐metastatic melanoma protein B (GPNMB) is known to be vital in bone formation. However, the effect of GPNMB on bone regeneration and the underlying molecular mechanism are still undefined. Fibroblast growth factor receptor (FGFR)‐mediating signaling is pivotal in bone formation and angiogenesis. Therefore, we assessed GPNMB function as a communicating molecule between osteoblasts and angiogenesis, and the possible correlation with FGFR‐1 signaling. Recombinant GPNMB dose‐dependently inc...
Source: Journal of Cellular Biochemistry - June 24, 2013 Category: Biochemistry Authors: Xuefeng Hu, Ping Zhang, Zhenjie Xu, Hongdong Chen, Xin Xie Tags: Article Source Type: research

MLN4924 Genome-Wide RNAi Screen
MLN4924 is an investigational small-molecule inhibitor of the NEDD8-activating enzyme (NAE) in phase I clinical trials. NAE inhibition prevents the ubiquitination and proteasomal degradation of substrates for cullin-RING ubiquitin E3 ligases that support cancer pathophysiology, but the genetic determinants conferring sensitivity to NAE inhibition are unknown. To address this gap in knowledge, we conducted a genome-wide siRNA screen to identify genes and pathways that affect the lethality of MLN4924 in melanoma cells. Of the 154 genes identified, approximately one-half interfered with components of the cell cycle, apoptotic...
Source: Cancer Research - January 2, 2013 Category: Cancer & Oncology Authors: Blank, J. L., Liu, X. J., Cosmopoulos, K., Bouck, D. C., Garcia, K., Bernard, H., Tayber, O., Hather, G., Liu, R., Narayanan, U., Milhollen, M. A., Lightcap, E. S. Tags: Molecular and Cellular Pathobiology Source Type: research