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https://www.readbyqxmd.com/read/29470984/ribosome-biogenesis-protein-urb2-regulates-hematopoietic-stem-cells-development-via-p53-pathway-in-zebrafish
#1
Pengcheng Cai, Xiaoyu Mao, Jieqiong Zhao, Lingfei Luo
Ribosome biogenesis is a significant process in cells. Dysfunction in this process will result in the defects of protein synthesis and consequently cause the development of specific diseases called ribosomopathies. Mutations in ribosome biogenesis protein Rps19, Rpl5, or Rpl11 can lead to hematopoietic defects in human, thus triggering the disease Diamond Blackfan anemia. However, the regulatory mechanisms of ribosome biogenesis in hematopoiesis remain incompletely understood. In this study, we describe a zebrafish mutant cq42, which carries a nonsense mutation in the gene that encodes ribosome biogenesis 2 homolog (Urb2)...
February 19, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29464071/activation-of-p53-and-destabilization-of-androgen-receptor-by-combinatorial-inhibition-of-mdm2-and-mdmx-in-prostate-cancer-cells
#2
Harman Chopra, Zara Khan, Jamie Contreras, Herui Wang, Abanob Sedrak, Yan Zhu
Castration-resistant prostate cancer (CRPC) frequently develops after initial standard radiation and androgen deprivation therapy, leaving patients with limited further treatment options. Androgen receptor (AR) is a transcription factor that plays a key role in the initiation and progression of prostate cancer. p53, a major tumor suppressor that is rarely mutated in early-stages of prostate cancer, is often deregulated during prostate cancer progression. Here, we report an unusual co-amplification of MDM2 and MDMX, two crucial negative regulators of p53, in CRPC datasets...
January 19, 2018: Oncotarget
https://www.readbyqxmd.com/read/29463243/anacardic-acid-inhibits-pancreatic-cancer-cell-growth-and-potentiates-chemotherapeutic-effect-by-chmp1a-atm-p53-signaling-pathway
#3
Maiyon Park, Danielle Upton, Melodie Blackmon, Valerie Dixon, Scott Craver, Dawn Neal, Derek Perkins
BACKGROUND: Pancreatic cancer is one of the leading causes of cancer related death and its incidence has risen steadily. Although anticancer drugs have been developed based on the new molecular findings, the drugs have produced unsatisfactory results due to toxicity and resistance. Thus, a complementary therapeutic intervention is urgently needed for pancreatic cancer patients. METHODS: The aim of this study was to assess the potential therapeutic effect of Anacardic acid on pancreatic cancer in vitro and elucidate its underlying mechanisms...
February 20, 2018: BMC Complementary and Alternative Medicine
https://www.readbyqxmd.com/read/29462961/a-phase-i-ii-study-targeting-angiogenesis-using-bevacizumab-combined-with-chemotherapy-and-a-histone-deacetylase-inhibitor-valproic-acid-in-advanced-sarcomas
#4
Varun Monga, Umang Swami, Munir Tanas, Aaron Bossler, Sarah L Mott, Brian J Smith, Mohammed Milhem
Epigenetic events and genetic alterations under the control of the tumor microenvironment potentially mediate tumor induced angiogenesis involved in soft tissue sarcoma (STS) metastasis. Addition of antiangiogenic agent, such as bevacizumab, to standard chemotherapy in treatment of sarcoma has been studied in clinical trials, but most of the findings have not supported its use. We hypothesized the existence of an epigenetically mediated "angiogenic switch", and the tumor microenvironment, prevents bevacizumab from truly blocking angiogenesis...
February 17, 2018: Cancers
https://www.readbyqxmd.com/read/29462690/xpf-plays-an-indispensable-role-in-relieving-silver-nanoparticle-induced-dna-damage-stress-in-human-cells
#5
Dan Wang, Huali Yang, Zheng Zhou, Man Zhao, Runsheng Chen, Simon H Reed
Due to the specific antimicrobial activity of silver nanoparticles (AgNPs), they are widely used in wound dressings, coatings in medical devices and household products. In spite of the well-documented genotoxicity of AgNPs, the molecular mechanisms of relieving AgNP-induced DNA damage stress remain poorly understood. We report here that one of the DNA repair factors, XPF, plays a crucial role in resisting AgNP-induced DNA damage stress in human cells. Following culture with AgNP-containing media, severely decreased colony forming abilities have been observed in XPF mutant and knockdown cells compared with wild type or control cells respectively, demonstrating that XPF is required to resist the AgNP-induced stress...
February 17, 2018: Toxicology Letters
https://www.readbyqxmd.com/read/29454568/the-phenotypic-heterogeneity-of-hereditary-diffuse-gastric-cancer-the-report-of-one-family-with-early-onset-disease
#6
Irene Gullo, Vitor Devezas, Manuela Baptista, Luzia Garrido, Sérgio Castedo, Rui Morais, Xiaogang Wen, Elisabete Rios, Jorge Pinheiro, Inȇs Pinto-Ribeiro, Rui M Ferreira, John Preto, João Santos-Antunes, Margarida Marques, Miquel Campos, Filipe Almeida, Maria do Céu Espinheira, Jorge Amil Dias, Céu Figueiredo, Carla Oliveira, Eunice Trindade, Fátima Carneiro
BACKGROUND AND AIMS: The time-course for the development of clinically significant hereditary diffuse gastric cancer (HDGC) is unpredictable. Little is known about the progression from pre-clinical, indolent lesions to widely invasive, aggressive phenotypes. Gastro-endoscopy often fails to detect early lesions and risk-reducing/prophylactic total gastrectomy (PTG) is the only curative approach. We present a HDGC family with early-onset disease, in which clinical and histological findings provided insight into the understanding of different HDGC phenotypes...
February 15, 2018: Gastrointestinal Endoscopy
https://www.readbyqxmd.com/read/29454261/frequency-of-somatic-tp53-mutations-in-combination-with-known-pathogenic-mutations-in-colon-adenocarcinoma-non-small-cell-lung-carcinoma-and-gliomas-as-identified-by-next-generation-sequencing
#7
Zahra Shajani-Yi, Francine B de Abreu, Jason D Peterson, Gregory J Tsongalis
The tumor suppressor gene TP53 is the most frequently mutated gene in human cancer. It encodes p53, a DNA-binding transcription factor that regulates multiple genes involved in DNA repair, metabolism, cell cycle arrest, apoptosis, and senescence. TP53 is associated with human cancer by mutations that lead to a loss of wild-type p53 function as well as mutations that confer alternate oncogenic functions that enable them to promote invasion, metastasis, proliferation, and cell survival. Identifying the discrete TP53 mutations in tumor cells may help direct therapies that are more effective...
February 13, 2018: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29451912/expression-of-cell-cycle-regulators-and-frequency-of-tp53-mutations-in-high-risk-gastrointestinal-stromal-tumors-prior-to-adjuvant-imatinib-treatment
#8
Michaela Angelika Ihle, Sebastian Huss, Wiebke Jeske, Wolfgang Hartmann, Sabine Merkelbach-Bruse, Hans-Ulrich Schildhaus, Reinhard Büttner, Harri Sihto, Kirsten Sundby Hall, Mikael Eriksson, Peter Reichardt, Heikki Joensuu, Eva Wardelmann
Despite of multitude investigations no reliable prognostic immunohistochemical biomarkers in GIST have been established so far with added value to predict the recurrence risk of high risk GIST besides mitotic count, primary location and size. In this study, we analyzed the prognostic relevance of eight cell cycle and apoptosis modulators and of TP53 mutations for prognosis in GIST with high risk of recurrence prior to adjuvant treatment with imatinib. In total, 400 patients with high risk for GIST recurrence were randomly assigned for adjuvant imatinib either for one or for three years following laparotomy...
2018: PloS One
https://www.readbyqxmd.com/read/29449434/msh6-haploinsufficiency-at-relapse-contributes-to-the-development-of-thiopurine-resistance-in-pediatric-b-lymphoblastic-leukemia
#9
Nikki A Evensen, P Pallavi Madhusoodhan, Julia Meyer, Jason Saliba, Ashfiyah Chowdhury, David J Araten, Jacob Nersting, Teena Bhatla, Tiffaney L Vincent, David Teachey, Stephen P Hunger, Jun Yang, Kjeld Schmiegelow, William L Carroll
Survival of children with relapsed acute lymphoblastic leukemia is poor and understanding mechanisms underlying resistance is essential in developing new therapy. Relapse-specific heterozygous deletions in MSH6, a crucial part of DNA Mismatch Repair, are frequently detected. Our aim was to determine whether MSH6 deletion results in a hypermutator phenotype associated with generation of secondary mutations involved in drug resistance or leads to a failure to initiate apoptosis directly in response to chemotherapeutic agents...
February 15, 2018: Haematologica
https://www.readbyqxmd.com/read/29448085/plk2-loss-commonly-occurs-in-colorectal-carcinomas-but-not-adenomas-relationship-to-mtor-signaling
#10
Elizabeth M Matthew, Zhaohai Yang, Suraj Peri, Mark Andrake, Roland Dunbrack, Eric Ross, Wafik S El-Deiry
Plk2 is a target of p53. Our previous studies demonstrated that with wild-type p53, Plk2 impacts mTOR signaling in the same manner as TSC1, and Plk2-deficient tumors grew larger than control. Other investigators have demonstrated that Plk2 phosphorylates mutant p53 in a positive feedback loop. We investigated Plk2's tumor suppressor functions in relationship to mTOR signaling. Archival specimens from 12 colorectal adenocarcinomas were stained for markers including Plk2, phosphorylated mTOR (serine 2448) and ribosomal S6 (Serine 235/236)...
February 12, 2018: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/29439926/association-of-single-nucleotide-polymorphisms-of-the-mdm4-gene-with-the-susceptibility-to-breast-cancer-in-a-southeast-iranian-population-sample
#11
Mohammad Hashemi, Sara Sanaei, Seyeh Mehdi Hashemi, Ebrahim Eskandari, Gholamreza Bahari
INTRODUCTION: The murine double minute 4 (MDM4) protein is a negative regulator of p53, and its upregulation has been observed in many tumor types. Previous literature suggested that genetic variations in the MDM4 gene are associated with risk of different cancers. The objective of the present study was to examine the effect of 3 common genetic variants of MDM4, rs4245739 A>C, rs11801299 G>A, and rs1380576 C>G, on the risk of breast cancer (BC) in a southeast Iranian population sample...
January 31, 2018: Clinical Breast Cancer
https://www.readbyqxmd.com/read/29435436/osteosarcoma-accelerating-progress-makes-for-a-hopeful-future
#12
REVIEW
Amanda J Saraf, Joelle M Fenger, Ryan D Roberts
Patients who develop osteosarcoma in 2017 receive treatment that remains essentially unchanged since the 1970s. Outcomes likewise remain largely unimproved. Large, collaborative, multinational efforts to improve therapy have evaluated strategies leveraging both cytotoxic intensification and immunomodulatory agents. While these have confirmed our capacity to conduct such trials, results have proved largely disappointing. This has motivated efforts to focus on the basic biology of osteosarcoma, where understanding remains poor but has improved significantly...
2018: Frontiers in Oncology
https://www.readbyqxmd.com/read/29434894/down-expression-of-poly-adp-ribose-polymerase-in-p53-regulated-pancreatic-cancer-cells
#13
Zhenyu Hou, Yunfeng Cui, Huizhi Xing, Xiaoyan Mu
The present study investigated whether poly(ADP-ribose) polymerase (PARP) has an effect on p53-regulated pancreatic cancer. The results of the present study demonstrated that the expression of PARP affects proliferation and apoptosis of pancreatic cancer cells. Olaparib was used to suppress the expression level of PARP-1 in PanC-1 cells. Decreased expression of PARP-1 suppressed cell proliferation and induced apoptosis of PanC-1 cells when compared with controls. Furthermore, decreased expression of PARP-1 resulted in decreased levels of pro-caspase-3 expression, increased caspase-3 activity, suppressed B-cell lymphoma 2 (Bcl-2) protein expression and increased p53 protein expression in PanC-1 cells...
February 2018: Oncology Letters
https://www.readbyqxmd.com/read/29434842/comprehensive-characterization-of-cancer-genes-in-hepatocellular-carcinoma-genomes
#14
Zhihao Zhang, Liping Xu, Changyu Sun
The present study was performed to detect moderate or low-frequency mutated cancer driver genes in hepatocellular carcinoma (HCC), using OncodriveFM and Dendrix. Following this, integrated analyses were conducted on these novel cancer driver genes. A total of 112,980 somatic mutations were retrieved from TCGA and classified into 11 categories based on their function. Driver genes and pathways were predicted by OncodriveFM and Dendrix, followed by differential expression, DNA-methylation, copy number variations and survival analyses...
February 2018: Oncology Letters
https://www.readbyqxmd.com/read/29434792/pine-needle-oil-induces-g2-m-arrest-of-hepg2-cells-by-activating-the-atm-pathway
#15
Bing Qiu, Wei Jiang, Wenliang Qiu, Wenling Mu, Yujing Qin, Yongcui Zhu, Jianying Zhang, Qingyi Wang, Dongjie Liu, Zhangyi Qu
Over the last two decades, inducing DNA damage of cancer cells by natural medicines has become a research hotspot in the field of cancer treatment. Although various natural medicines have anticancer effects, very few studies have been conducted to explore the anti-cancer effect of pine needle oil. In the present study, the role of pine needle oil in inducing G2/M arrest in HepG2 cells was investigated. The data revealed that pine needle oil could induce DNA damage in a dose-dependent manner. In the pine needle oil-treated HepG2 cells, the protein levels of phosphorylated (p)-ataxia-telangiectasia mutated (ATM), γ-H2A histone family, member X, p-p53, p-checkpoint kinase 2 and p-cell division cycle 25C were evidently increased, indicating that pine needle oil facilitated G2/M arrest in HepG2 cells through the ATM pathway...
February 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29434041/polo-like-kinase-4-inhibition-produces-polyploidy-and-apoptotic-death-of-lung-cancers
#16
Masanori Kawakami, Lisa Maria Mustachio, Lin Zheng, Yulong Chen, Jaime Rodriguez-Canales, Barbara Mino, Jonathan M Kurie, Jason Roszik, Pamela Andrea Villalobos, Kelsie L Thu, Jennifer Silvester, David W Cescon, Ignacio I Wistuba, Tak W Mak, Xi Liu, Ethan Dmitrovsky
Polo-like kinase 4 (PLK4) is a serine/threonine kinase regulating centriole duplication. CFI-400945 is a highly selective PLK4 inhibitor that deregulates centriole duplication, causing mitotic defects and death of aneuploid cancers. Prior work was substantially extended by showing CFI-400945 causes polyploidy, growth inhibition, and apoptotic death of murine and human lung cancer cells, despite expression of mutated KRAS or p53. Analysis of DNA content by propidium iodide (PI) staining revealed cells with >4N DNA content (polyploidy) markedly increased after CFI-400945 treatment...
February 6, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29433555/sf3b1-deficiency-impairs-human-erythropoiesis-via-activation-of-p53-pathway-implications-for-understanding-of-ineffective-erythropoiesis-in-mds
#17
Yumin Huang, John Hale, Yaomei Wang, Wei Li, Shijie Zhang, Jieying Zhang, Huizhi Zhao, Xinhua Guo, Jing Liu, Hongxia Yan, Karina Yazdanbakhsh, Gang Huang, Christopher D Hillyer, Narla Mohandas, Lixiang Chen, Ling Sun, Xiuli An
BACKGROUND: SF3B1 is a core component of splicing machinery. Mutations in SF3B1 are frequently found in myelodysplastic syndromes (MDS), particularly in patients with refractory anemia with ringed sideroblasts (RARS), characterized by isolated anemia. SF3B1 mutations have been implicated in the pathophysiology of RARS; however, the physiological function of SF3B1 in erythropoiesis remains unknown. METHODS: shRNA-mediated approach was used to knockdown SF3B1 in human CD34+ cells...
February 12, 2018: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/29429991/p53-isoforms-regulate-premature-aging-in-human-cells
#18
Natalia von Muhlinen, Izumi Horikawa, Fatima Alam, Kazunobu Isogaya, Delphine Lissa, Borek Vojtesek, David P Lane, Curtis C Harris
Cellular senescence is a hallmark of normal aging and aging-related syndromes, including the premature aging disorder Hutchinson-Gilford Progeria Syndrome (HGPS), a rare genetic disorder caused by a single mutation in the LMNA gene that results in the constitutive expression of a truncated splicing mutant of lamin A known as progerin. Progerin accumulation leads to increased cellular stresses including unrepaired DNA damage, activation of the p53 signaling pathway and accelerated senescence. We previously established that the p53 isoforms ∆133p53 and p53β regulate senescence in normal human cells...
February 12, 2018: Oncogene
https://www.readbyqxmd.com/read/29428221/the-inflammatory-microenvironment-that-promotes-gastrointestinal-cancer-development-and-invasion
#19
REVIEW
Kanae Echizen, Hiroko Oshima, Mizuho Nakayama, Masanobu Oshima
Accumulating evidence has indicated that the inflammatory response is important for tumor promotion. However, the mechanisms underlying the induction of the inflammatory response in cancer tissues and how it promotes tumorigenesis remain poorly understood. We constructed several mouse models that develop inflammation-associated gastric and intestinal tumors and examined the in vivo mechanisms of tumorigenesis. Of note, the activation of cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathway and Toll-like receptor (TLR)/MyD88 signaling cooperatively induced the generation of an inflammatory microenvironment, which is required for early-stage tumorigenesis...
February 5, 2018: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29427417/-tp53-haploinsufficiency-rescues-emergency-granulopoiesis-in-fancc-mice
#20
Liping Hu, Weiqi Huang, Ling Bei, Larisa Broglie, Elizabeth A Eklund
Emergency (stress) granulopoiesis is an episodic process for the production of granulocytes in response to infectious challenge. We previously determined that Fanconi C, a component of the Fanconi DNA-repair pathway, is necessary for successful emergency granulopoiesis. Fanconi anemia results from mutation of any gene in this pathway and is characterized by bone marrow failure (BMF) in childhood and clonal progression in adolescence. Although murine Fanconi anemia models exhibit relatively normal steady-state hematopoiesis, FANCC -/-mice are unable to mount an emergency granulopoiesis response...
February 2, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
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