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c-Myc, neuroblastoma

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https://www.readbyqxmd.com/read/29505958/wnt-signalling-drives-context-dependent-differentiation-or-proliferation-in-neuroblastoma
#1
Marianna Szemes, Alexander Greenhough, Zsombor Melegh, Sally Malik, Aysen Yuksel, Daniel Catchpoole, Kelli Gallacher, Madhu Kollareddy, Ji Hyun Park, Karim Malik
Neuroblastoma is one of the commonest and deadliest solid tumours of childhood, and is thought to result from disrupted differentiation of the developing sympathoadrenergic lineage of the neural crest. Neuroblastoma exhibits intra- and intertumoural heterogeneity, with high risk tumours characterised by poor differentiation, which can be attributable to MYCN-mediated repression of genes involved in neuronal differentiation. MYCN is known to co-operate with oncogenic signalling pathways such as Alk, Akt and MEK/ERK signalling, and, together with c-MYC has been shown to be activated by Wnt signalling in various tissues...
March 2, 2018: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29464082/myc-family-protein-overexpression-and-prominent-nucleolar-formation-represent-prognostic-indicators-and-potential-therapeutic-targets-for-aggressive-high-mki-neuroblastomas-a-report-from-the-children-s-oncology-group
#2
Risa Niemas-Teshiba, Ryosuke Matsuno, Larry L Wang, Xao X Tang, Bill Chiu, Jasmine Zeki, Jeannine Coburn, Kimberly Ornell, Arlene Naranjo, Collin Van Ryn, Wendy B London, Michael D Hogarty, Julie M Gastier-Foster, A Thomas Look, Julie R Park, John M Maris, Susan L Cohn, Robert C Seeger, Shahab Asgharzadeh, Naohiko Ikegaki, Hiroyuki Shimada
Neuroblastomas with a high mitosis-karyorrhexis index (High-MKI) are often associated with MYCN amplification, MYCN protein overexpression and adverse clinical outcome. However, the prognostic effect of MYC-family protein expression on these neuroblastomas is less understood, especially when MYCN is not amplified. To address this, MYCN and MYC protein expression in High-MKI cases (120 MYCN amplified and 121 non- MYCN amplified) was examined by immunohistochemistry. The majority (101) of MYCN -amplified High-MKI tumors were MYCN(+), leaving one MYC(+), 2 both(+), and 16 both(-)/(+/-), whereas non- MYCN -amplified cases appeared heterogeneous, including 7 MYCN(+), 36 MYC(+), 3 both(+), and 75 both(-)/(+/-) tumors...
January 19, 2018: Oncotarget
https://www.readbyqxmd.com/read/29426276/rare-myc-amplified-neuroblastoma-with-large-cell-histology
#3
Ryosuke Matsuno, Andrew J Gifford, Junming Fang, Mikako Warren, Robyn E Lukeis, Toby Trahair, Tohru Sugimoto, Araz Marachelian, Shahab Asgharzadeh, John M Maris, Naohiko Ikegaki, Hiroyuki Shimada
Background Although MYCN (aka N-myc) amplification is reported in ∼20% of neuroblastomas, MYC (aka C-myc) amplification appears to be a rare event in this disease. As of today, only 2 MYC-amplified neuroblastomas have been briefly mentioned in the literature. Methods We studied here the clinicopathological features of 3 MYC-amplified neuroblastomas. Results All 3 patients (2 females and 1 male) had stage 4 disease. One female is currently alive and well 52 months after the diagnosis, while the other female and male patients died of disease 24 and 20 months after the diagnosis, respectively...
January 1, 2018: Pediatric and Developmental Pathology
https://www.readbyqxmd.com/read/29390274/a-highly-malignant-case-of-neuroblastoma-with-substantial-increase-of-single-nucleotide-variants-and-normal-mismatch-repair-system-a-case-report
#4
Lin-Qing Yuan, Jin-Hu Wang, Kun Zhu, Min Yang, Wei-Zhong Gu, Can Lai, Hao-Min Li, Qiang Shu, Xi Chen
RATIONALE: Neuroblastoma is a common abdominal malignancy in children. The chemoresistant and relapsed cases have poor prognosis. The genetic background and the mechanism of resistance remain unelucidated. Next-generation sequence (NGS) is becoming a popular tool to unravel the genetic background and to guide precision medicine in oncology studies as well as in clinical practice. PATIENT CONCERNS: Here we report a neuroblastoma case of a boy aged 2 years and 8 months when first diagnosed, with multiple metastatic sites found in both lungs...
December 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/29284669/-myc-drives-a-subset-of-high-risk-pediatric-neuroblastomas-and-is-activated-through-mechanisms-including-enhancer-hijacking-and-focal-enhancer-amplification
#5
Mark W Zimmerman, Yu Liu, Shuning He, Adam D Durbin, Brian J Abraham, John Easton, Ying Shao, Beisi Xu, Shizhen Zhu, Xiaoling Zhang, Zhaodong Li, Nina Weichert-Leahey, Richard A Young, Jinghui Zhang, A Thomas Look
The amplified MYCN gene serves as an oncogenic driver in approximately 20% of high-risk pediatric neuroblastomas. Here, we show that the family member MYC is a potent transforming gene in a separate subset of high-risk neuroblastoma cases (∼10%), based on (i) its upregulation by focal enhancer amplification or genomic rearrangements leading to enhancer hijacking, and (ii) its ability to transform neuroblastoma precursor cells in a transgenic animal model. The aberrant regulatory elements associated with oncogenic MYC activation include focally amplified distal enhancers and translocation of highly active enhancers from other genes to within topologically associating domains containing the MYC gene locus...
March 2018: Cancer Discovery
https://www.readbyqxmd.com/read/29207662/tumor-associated-macrophages-promote-neuroblastoma-via-stat3-phosphorylation-and-up-regulation-of-c-myc
#6
Michael D Hadjidaniel, Sakunthala Muthugounder, Long T Hung, Michael A Sheard, Soheila Shirinbak, Randall Y Chan, Rie Nakata, Lucia Borriello, Jemily Malvar, Rebekah J Kennedy, Hiroshi Iwakura, Takashi Akamizu, Richard Sposto, Hiroyuki Shimada, Yves A DeClerck, Shahab Asgharzadeh
Tumor-associated macrophages (TAMs) are strongly associated with poor survival in neuroblastomas that lack MYCN amplification. To study TAM action in neuroblastomas, we used a novel murine model of spontaneous neuroblastoma lacking MYCN amplification, and observed recruitment and polarization of TAMs, which in turn enhanced neuroblastoma proliferation and growth. In both murine and human neuroblastoma cells, we found that TAMs increased STAT3 activation in neuroblastoma cells and transcriptionally up-regulated the MYC oncogene...
October 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/29202477/crispr-cas9-screen-reveals-a-mycn-amplified-neuroblastoma-dependency-on-ezh2
#7
Liying Chen, Gabriela Alexe, Neekesh V Dharia, Linda Ross, Amanda Balboni Iniguez, Amy Saur Conway, Emily Jue Wang, Veronica Veschi, Norris Lam, Jun Qi, W Clay Gustafson, Nicole Nasholm, Francisca Vazquez, Barbara A Weir, Glenn S Cowley, Levi D Ali, Sasha Pantel, Guozhi Jiang, William F Harrington, Yenarae Lee, Amy Goodale, Rakela Lubonja, John M Krill-Burger, Robin M Meyers, Aviad Tsherniak, David E Root, James E Bradner, Todd R Golub, Charles Wm Roberts, William C Hahn, William A Weiss, Carol J Thiele, Kimberly Stegmaier
Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and poor prognosis. Here, we deployed genome-scale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on genes encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12. Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo...
January 2, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29050113/-long-term-follow-up-of-neuroblastoma-in-children-less-than-18-months-of-age
#8
J Zhao, C Pan, M Xu, M Zhou, Y J Gao, W T Hu, J Y Tang
Objective: To assess the clinical features and long-term outcomes of neuroblastoma (NB) in children less than 18 months of age, so as to provide evidence for further improvement of treatment. Method: Clinical data(sex, age, stage, risk group, treatment response, follow-up, etc.) of 155 NB patients under age of 18 months from June 2000 to December 2015 in Shanghai Children's Medical Center were analyzed retrospectively. The clinical features were summarized and the long-term follow-up results were evaluated...
October 2, 2017: Zhonghua Er Ke za Zhi. Chinese Journal of Pediatrics
https://www.readbyqxmd.com/read/28927089/chronic-radiation-exposure-of-neuroblastoma-cells-reduces-nmyc-copy-number
#9
Manu Gnanamony, Reuben Antony, Karen S Fernández, Libes Jaime, Julian Lin, Pushpa A Joseph, Christopher S Gondi
Neuroblastoma accounts for >15% of cancer-associated mortalities of children in the USA. Despite aggressive treatment regimens, the long-term survival for these children remains <40%. The identification of v-Myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (nMYC) gene amplification during diagnosis is associated with poor prognosis in neuroblastoma. There are limited studies examining changes in nMYC copy numbers in response to therapy and its biological effect on cancer cells. The aim of the present study was to evaluate the effect of radiation on nMYC expression and amplification status in high-risk neuroblastoma...
September 2017: Oncology Letters
https://www.readbyqxmd.com/read/28656195/microrna-322-attenuates-aluminum-maltolate-induced-apoptosis-in-the-human-sh-sy5y-neuroblastoma-cell-line
#10
Xinlong Ma, Feng Shang, Qiuxia Zhang, Qingtang Lin, Shuo Han, Yongzhi Shan, Jianxin Du, Feng Ling, Hongqi Zhang, Geng Xu
Aluminum-maltolate (Al‑Malt) is a potent apoptosis inductor, which has been widely reported as an etiologic factor in Alzheimer's disease (AD). MicroRNA-322 (miR‑322) is a vital regulator in various biological processes. The aim of the current study was to identify the role and possible underlying mechanism of miR‑322 in Al‑Malt‑induced apoptosis. Eight concentrations of Al‑Malt were prepared and used for treating the human neuroblastoma cell line, SH‑SY5Y. Subsequent to treatment with Al‑Malt for 3 days, cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured...
August 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28521631/immunohistochemical-profile-of-myc-protein-in-pediatric-small-round-blue-cell-tumors
#11
Karen M Chisholm, Chandra Krishnan, Amy Heerema-McKenney, Yasodha Natkunam
Deregulation of MYC oncoprotein in cancers can result from multiple oncogenic mechanisms. Although MYC translocations define Burkitt lymphoma and MYC protein expression is a poor prognostic factor in undifferentiated neuroblastomas, the distribution of MYC protein (c-MYC) across other pediatric small round blue cell tumors (SRBCT) has not been well characterized. We undertook this study to assess MYC protein expression in a large cohort of pediatric lymphomas, sarcomas, and other SRBCT. Tissue microarrays containing 302 SRBCT were successfully evaluated by immunohistochemistry using anti-MYC clone Y69, with nuclear positivity scored as 0%, 1%-25%, 26%-50%, 51%-75%, or 76%-100%...
June 2017: Pediatric and Developmental Pathology
https://www.readbyqxmd.com/read/28394338/parp-inhibitors-enhance-replication-stress-and-cause-mitotic-catastrophe-in-mycn-dependent-neuroblastoma
#12
V Colicchia, M Petroni, G Guarguaglini, F Sardina, M Sahún-Roncero, M Carbonari, B Ricci, C Heil, C Capalbo, F Belardinilli, A Coppa, G Peruzzi, I Screpanti, P Lavia, A Gulino, G Giannini
High-risk and MYCN-amplified neuroblastomas are among the most aggressive pediatric tumors. Despite intense multimodality therapies, about 50% of these patients succumb to their disease, making the search for effective therapies an absolute priority. Due to the important functions of poly (ADP-ribose) polymerases, PARP inhibitors have entered the clinical settings for cancer treatment and are being exploited in a variety of preclinical studies and clinical trials. PARP inhibitors based combination schemes have also been tested in neuroblastoma preclinical models with encouraging results...
August 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28246384/a-c-myc-regulated-stem-cell-like-signature-in-high-risk-neuroblastoma-a-systematic-discovery-target-neuroblastoma-esc-like-signature
#13
Xinan Holly Yang, Fangming Tang, Jisu Shin, John M Cunningham
c-Myc dysregulation is hypothesized to account for the 'stemness' - self-renewal and pluripotency - shared between embryonic stem cells (ESCs) and adult aggressive tumours. High-risk neuroblastoma (HR-NB) is the most frequent, aggressive, extracranial solid tumour in childhood. Using HR-NB as a platform, we performed a network analysis of transcriptome data and presented a c-Myc subnetwork enriched for genes previously reported as ESC-like cancer signatures. A subsequent drug-gene interaction analysis identified a pharmacogenomic agent that preferentially interacted with this HR-NB-specific, ESC-like signature...
March 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28245597/myc-in-regulating-immunity-metabolism-and-beyond
#14
REVIEW
J N Rashida Gnanaprakasam, Ruoning Wang
Myelocytomatosis oncogene (MYC) family members, including cellular MYC (c-Myc), neuroblastoma derived MYC (MYCN), and lung carcinoma derived MYC (MYCL), have all been implicated as key oncogenic drivers in a broad range of human cancers. Beyond cancer, MYC plays an important role in other physiological and pathological processes, namely immunity and immunological diseases. MYC largely functions as a transcription factor that promotes the expression of numerous target genes to coordinate death, proliferation, and metabolism at the cellular, tissue, and organismal levels...
February 25, 2017: Genes
https://www.readbyqxmd.com/read/28209620/the-histone-methyltransferase-dot1l-promotes-neuroblastoma-by-regulating-gene-transcription
#15
Matthew Wong, Andrew E L Tee, Giorgio Milazzo, Jessica L Bell, Rebecca C Poulos, Bernard Atmadibrata, Yuting Sun, Duohui Jing, Nicholas Ho, Dora Ling, Pei Yan Liu, Xu Dong Zhang, Stefan Hüttelmaier, Jason W H Wong, Jenny Wang, Patsie Polly, Giovanni Perini, Christopher J Scarlett, Tao Liu
Myc oncoproteins exert tumorigenic effects by regulating expression of target oncogenes. Histone H3 lysine 79 (H3K79) methylation at Myc-responsive elements of target gene promoters is a strict prerequisite for Myc-induced transcriptional activation, and DOT1L is the only known histone methyltransferase that catalyzes H3K79 methylation. Here, we show that N-Myc upregulates DOT1L mRNA and protein expression by binding to the DOT1L gene promoter. shRNA-mediated depletion of DOT1L reduced mRNA and protein expression of N-Myc target genes ODC1 and E2F2 DOT1L bound to the Myc Box II domain of N-Myc protein, and knockdown of DOT1L reduced histone H3K79 methylation and N-Myc protein binding at the ODC1 and E2F2 gene promoters and reduced neuroblastoma cell proliferation...
May 1, 2017: Cancer Research
https://www.readbyqxmd.com/read/28179207/down-regulation-of-c-terminal-binding-protein-2-ctbp2-inhibits-proliferation-migration-and-invasion-of-human-shsy5y-cells-in-vitro
#16
Jiang Nan, Sun Guan, Xu Jin, Zhu Jian, Fu Linshan, Guo Jun
Neuroblastoma is the most common extracranial solid tumor in children and is responsible for ∼15% of pediatric cancer deaths. CtBP2 is a member of the CtBP family of proteins that functions as a transcription regulator and has been demonstrated to interact with the C-terminus of the adenoviral E1A oncoprotein. In this study, the expression of CtBP2 in the human neuroblastoma cell line SHSY5Y was down-regulated using lentiviral-mediated RNA interference. Down-regulation of CtBP2 inhibited the expression of c-myc, MMP2, and MMP9 proteins...
April 24, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/27919448/fx11-inhibits-aerobic-glycolysis-and-growth-of-neuroblastoma-cells
#17
Eric J Rellinger, Brian T Craig, Alexandra L Alvarez, Haley L Dusek, Kwang W Kim, Jingbo Qiao, Dai H Chung
BACKGROUND: The MYC family of proteins promotes neuroblastoma tumorigenesis at least in part through the induction of aerobic glycolysis by promoting the transcription of key glycolytic enzymes, such as LDHA. FX11 is a selective inhibitor of LDHA that has demonstrated preclinical efficacy in adult cancers. Herein, we hypothesized that FX11 would inhibit aerobic glycolysis and block growth of neuroblastoma cells. METHODS: We surveyed 3 MYCN-single copy and 5 MYCN-amplified neuroblastoma cell lines to correlate C-MYC/N-MYC protein levels with LDHA expression...
March 2017: Surgery
https://www.readbyqxmd.com/read/27832522/combined-treatments-with-a-retinoid-receptor-agonist-and-epigenetic-modulators-in-human-neuroblastoma-cells
#18
Viviane Rösner Almeida, Igor Araujo Vieira, Marienela Buendia, André Tesainer Brunetto, Lauro J Gregianin, Algemir Lunardi Brunetto, Fábio Klamt, Caroline Brunetto de Farias, Ana Lucia Abujamra, Patrícia Luciana da Costa Lopez, Rafael Roesler
Neuroblastoma (NB) is the most common extracranial solid childhood tumor accounting for around 15% of pediatric cancer deaths and most probably originates from a failure in the development of embryonic neural crest cells. Retinoids can inhibit the proliferation and stimulate differentiation of NB cells. In addition, epigenetic events involving changes in chromatin structure and DNA methylation can mediate the effects of retinoids; hence, the scope of this study is to investigate the use of retinoids and epigenetic drugs in NB cell lines...
December 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/27764804/a-combined-gene-expression-and-functional-study-reveals-the-crosstalk-between-n-myc-and-differentiation-inducing-micrornas-in-neuroblastoma-cells
#19
Zhenze Zhao, Xiuye Ma, Spencer D Shelton, Derek C Sung, Monica Li, Daniel Hernandez, Maggie Zhang, Michael D Losiewicz, Yidong Chen, Alexander Pertsemlidis, Xiaojie Yu, Yuanhang Liu, Liqin Du
MYCN amplification is the most common genetic alteration in neuroblastoma and plays a critical role in neuroblastoma tumorigenesis. MYCN regulates neuroblastoma cell differentiation, which is one of the mechanisms underlying its oncogenic function. We recently identified a group of differentiation-inducing microRNAs. Given the demonstrated inter-regulation between MYCN and microRNAs, we speculated that MYCN and the differentiation-inducing microRNAs might form an interaction network to control the differentiation of neuroblastoma cells...
November 29, 2016: Oncotarget
https://www.readbyqxmd.com/read/27626059/n-myc-expression-enhances-the-oncolytic-effects-of-vesicular-stomatitis-virus-in-human-neuroblastoma-cells
#20
Juan C Corredor, Nicole Redding, Karen Bloté, Stephen M Robbins, Donna L Senger, John C Bell, Paul Beaudry
N-myc oncogene amplification is associated but not present in all cases of high-risk neuroblastoma (NB). Since oncogene expression could often modulate sensitivity to oncolytic viruses, we wanted to examine if N-myc expression status would determine virotherapy efficacy to high-risk NB. We showed that induction of exogenous N-myc in a non-N-myc-amplified cell line background (TET-21N) increased susceptibility to oncolytic vesicular stomatitis virus (mutant VSVΔM51) and alleviated the type I IFN-induced antiviral state...
2016: Molecular Therapy Oncolytics
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