keyword
MENU ▼
Read by QxMD icon Read
search

P53 mutation

keyword
https://www.readbyqxmd.com/read/29031038/isocitrate-dehydrogenase-mutations-are-better-prognostic-marker-than-o6-methylguanine-dna-methyltransferase-promoter-methylation-in-glioblastomas-a-retrospective-single-centre-molecular-genetics-study-of-gliomas
#1
M Houdova Megova, J Drábek, Z Dwight, R Trojanec, V Koudeláková, J Vrbková, O Kalita, S Mlcochova, M Rabcanova, M Hajdúch
BACKGROUND: Mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) are a promising prognostic biomarker of gliomas. The purpose of our study was to examine the clinical prognostic properties of IDH1/2 mutations in a glioma patient cohort from the Czech Republic using an improved platform for simple and reliable IDH genotyping. MATERIAL AND METHODS: We retrospectively analyzed a group of 145 glioma patients by testing for the three most frequent IDH mutations, IDH1 R132H, IDH1 R132C, and IDH2 R172K, through the competitive amplification of differentially melting amplicons (CADMA) polymerase chain reaction (PCR)...
2017: Klinická Onkologie: Casopis Ceské a Slovenské Onkologické Spolecnosti
https://www.readbyqxmd.com/read/29029019/combined-loss-of-eaf2-and-p53-induces-prostate-carcinogenesis-in-male-mice
#2
Yao Wang, Laura E Pascal, Mingming Zhong, Junkui Ai, Dan Wang, Yifeng Jing, Jan Pilch, Qiong Song, Lora H Rigatti, Lara E Graham, Joel B Nelson, Anil V Parwani, Zhou Wang
Mutations in the p53 tumor suppressor are frequent in patients with castration-resistant prostate cancer but less so in patients with localized disease, and Li-Fraumeni patients with germline p53 mutations do not have an increased incidence of prostate cancer, suggesting that additional molecular and/or genetic changes are required for p53 to promote prostate carcinogenesis. EAF2 is a tumor suppressor that is frequently down-regulated in advanced prostate cancer. Previous studies have suggested that p53 binds to EAF2, providing a potential mechanism for their functional interactions...
September 27, 2017: Endocrinology
https://www.readbyqxmd.com/read/29026176/primary-astrocytic-tumours-and-paired-recurrences-have-similar-biological-features-in-idh1-tp53-and-tertp-mutation-and-mgmt-atrx-loss
#3
Xia Li, Jie Wei, Yixiong Liu, Peifeng Li, Linni Fan, Yingmei Wang, Mingyang Li, Danhui Zhao, Zhou Yu, Jing Ye, Ying Guo, Qingguo Yan, Shuangping Guo, Zhe Wang
Astrocytic tumours are the most common type of primary malignant brain tumour. Most astrocytic tumours will recur at some point after surgery. Currently, the combination of radiotherapy and chemotherapy does not prevent the recurrence of astrocytic tumours. In this study, we investigated the consistency in isocitrate dehydrogenase 1 (IDH1), tumour protein p53 (TP53) and telomerase reverse transcriptase promoter (TERTp) mutations during astrocytic tumour recurrence. We also evaluated the protein loss of O-6-methylguanine-DNA methyltransferase (MGMT) and alpha-thalassemia/mental retardation, X-linked (ATRX) during disease recurrence...
October 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29022915/wild-type-and-mutant-p53-differentially-modulate-mir-124-iaspp-feedback-following-pohotodynamic-therapy-in-human-colon-cancer-cell-line
#4
Kuijie Liu, Weidong Chen, Sanlin Lei, Li Xiong, Hua Zhao, Dong Liang, Zhendong Lei, Nanjiang Zhou, Hongliang Yao, Ying Liang
Colorectal cancer (CRC) is a most common digestive system malignant tumor. p53 mutation has essential role in cancers and is frequently observed in CRC and presents a huge challenge. p53 mutation has been reported to attenuate the inhibitory effect of photofrin-based photodynamic therapy (PDT). p53 mutation-induced gain of function brings up the dysfunction of carcinogenic factors, including miRNAs. Our research found that PDT suppressed CRC cell viability, reduced the tumor size and prolonged the survival time, all of which could be attenuated by p53 mutation or deletion...
October 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/29021240/integrative-genome-analysis-of-somatic-p53-mutant-osteosarcomas-identifies-ets2-dependent-regulation-of-small-nucleolar-rnas-by-mutant-p53-protein
#5
Rasoul Pourebrahim, Yun Zhang, Bin Liu, Ruli Gao, Shunbin Xiong, Patrick P Lin, Mark J McArthur, Michael C Ostrowski, Guillermina Lozano
TP53 is the most frequently mutated gene in human cancer. Many mutant p53 proteins exert oncogenic gain-of-function (GOF) properties that contribute to metastasis, but the mechanisms mediating these functions remain poorly defined in vivo. To elucidate how mutant p53 GOF drives metastasis, we developed a traceable somatic osteosarcoma mouse model that is initiated with either a single p53 mutation (p53R172H) or p53 loss in osteoblasts. Our study confirmed that p53 mutant mice developed osteosarcomas with increased metastasis as compared with p53-null mice...
October 11, 2017: Genes & Development
https://www.readbyqxmd.com/read/29020632/activation-of-the-p53-transcriptional-program-sensitizes-cancer-cells-to-cdk7-inhibitors
#6
Sampada Kalan, Ramon Amat, Miriam Merzel Schachter, Nicholas Kwiatkowski, Brian J Abraham, Yanke Liang, Tinghu Zhang, Calla M Olson, Stéphane Larochelle, Richard A Young, Nathanael S Gray, Robert P Fisher
Cdk7, the CDK-activating kinase and transcription factor IIH component, is a target of inhibitors that kill cancer cells by exploiting tumor-specific transcriptional dependencies. However, whereas selective inhibition of analog-sensitive (AS) Cdk7 in colon cancer-derived cells arrests division and disrupts transcription, it does not by itself trigger apoptosis efficiently. Here, we show that p53 activation by 5-fluorouracil or nutlin-3 synergizes with a reversible Cdk7(as) inhibitor to induce cell death. Synthetic lethality was recapitulated with covalent inhibitors of wild-type Cdk7, THZ1, or the more selective YKL-1-116...
October 10, 2017: Cell Reports
https://www.readbyqxmd.com/read/29017057/a-p53-super-tumor-suppressor-reveals-a-tumor-suppressive-p53-ptpn14-yap-axis-in-pancreatic-cancer
#7
Stephano S Mello, Liz J Valente, Nitin Raj, Jose A Seoane, Brittany M Flowers, Jacob McClendon, Kathryn T Bieging-Rolett, Jonghyeob Lee, Danton Ivanochko, Margaret M Kozak, Daniel T Chang, Teri A Longacre, Albert C Koong, Cheryl H Arrowsmith, Seung K Kim, Hannes Vogel, Laura D Wood, Ralph H Hruban, Christina Curtis, Laura D Attardi
The p53 transcription factor is a critical barrier to pancreatic cancer progression. To unravel mechanisms of p53-mediated tumor suppression, which have remained elusive, we analyzed pancreatic cancer development in mice expressing p53 transcriptional activation domain (TAD) mutants. Surprisingly, the p53(53,54) TAD2 mutant behaves as a "super-tumor suppressor," with an enhanced capacity to both suppress pancreatic cancer and transactivate select p53 target genes, including Ptpn14. Ptpn14 encodes a negative regulator of the Yap oncoprotein and is necessary and sufficient for pancreatic cancer suppression, like p53...
October 9, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28993836/natural-and-unnatural-small-molecules-as-pharmacological-chaperones-and-inhibitors-in-cancer
#8
Isabel Betancor-Fernández, David J Timson, Eduardo Salido, Angel L Pey
Mutations causing single amino acid exchanges can dramatically affect protein stability and function, leading to disease. In this chapter, we will focus on several representative cases in which such mutations affect protein stability and function leading to cancer. Mutations in BRAF and p53 have been extensively characterized as paradigms of loss-of-function/gain-of-function mechanisms found in a remarkably large fraction of tumours. Loss of RB1 is strongly associated with cancer progression, although the molecular mechanisms by which missense mutations affect protein function and stability are not well known...
October 10, 2017: Handbook of Experimental Pharmacology
https://www.readbyqxmd.com/read/28993478/the-effect-of-mutant-p53-proteins-on-glycolysis-and-mitochondrial-metabolism
#9
Matilda Eriksson, Gorbatchev Ambroise, Amanda Tomie Ouchida, Andre Lima Queiroz, Dominique Smith, Alfredo Gimenez-Cassina, Marcin P Iwanicki, Patricia A Muller, Erik Norberg, Helin Vakifahmetoglu-Norberg
TP53 is one of the most commonly mutated genes in human cancers. Unlike other tumor suppressors that are frequently deleted or acquire loss-of-function mutations, the majority of TP53 mutations in tumors are missense substitutions, which lead to the expression of full-length mutant proteins that accumulate in cancer cells and may confer unique gain-of-function (GOF) activities to promote tumorigenic events. Recently, mutant p53 proteins have been shown to mediate metabolic changes as a novel GOF to promote tumor development...
October 9, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28987347/association-study-of-apoptosis-gene-polymorphisms-in-mitochondrial-diabetes-a-potential-role-in-the-pathogenicity-of-md
#10
Mouna Tabebi, Bodour Khabou, Hanen Boukadi, Mariam Ben Hamad, Bochra Ben Rhouma, Slim Tounsi, Abdellatif Maalej, Hassen Kamoun, Leila Keskes-Ammar, Mohamed Abid, Mouna Mnif, Faiza Fakhfakh
Mitochondrial diabetes (MD) is a heterogeneous disorder characterized by a chronic hyperglycemia and is maternally transmitted. Syndromic MD is a subgroup of MD including diabetic microangiopathy and macroangiopathy, in addition to extrapancreatic disorder. MD is caused by genetic mutations and deletions affecting mitochondrial DNA. This mitochondrial damage initiates apoptosis. In this study, we hypothesized that functional polymorphisms in genes involved in apoptotic pathway could be associated with the development of apoptosis in MD disease and increased its risk...
October 4, 2017: Gene
https://www.readbyqxmd.com/read/28985945/multi-walled-carbon-nanotube-induced-genotoxic-inflammatory-and-pro-fibrotic-responses-in-mice-investigating-the-mechanisms-of-pulmonary-carcinogenesis
#11
Luna Rahman, Nicklas Raun Jacobsen, Syed Abdul Aziz, Dongmei Wu, Andrew Williams, Carole L Yauk, Paul White, Hakan Wallin, Ulla Vogel, Sabina Halappanavar
The International Agency for Research on Cancer has classified one type of multi-walled carbon nanotubes (MWCNTs) as possibly carcinogenic to humans. However, the underlying mechanisms of MWCNT- induced carcinogenicity are not known. In this study, the genotoxic, mutagenic, inflammatory, and fibrotic potential of MWCNTs were investigated. Muta™Mouse adult females were exposed to 36±6 or 109±18μg/mouse of Mitsui-7, or 26±2 or 78±5μg/mouse of NM-401, once a week for four consecutive weeks via intratracheal instillations, alongside vehicle-treated controls...
November 2017: Mutation Research
https://www.readbyqxmd.com/read/28984774/a-case-report-of-tongue-metastasis-from-lung-squamous-cell-carcinoma-and-literature-review
#12
REVIEW
Xiaolong Cheng, Zhenli Hu, Yipin Han, Chong Bai
RATIONALE: Tongue metastasis from lung cancer is extremely rare, and the prognosis of these patients is rather poor. PATIENT CONCERS: A 56-year-old man was found a 4-cm cavity lesion in the left upper lobe, which was initially misdiagnosed as tuberculosis. DIAGNOSES: A case of lung squamous cell carcinoma that metastasized to the base of a patient's tongue. INTERVATIONS: We send the biopsy of the lung and the tongue lesions for gene sequencing...
October 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28981088/hsf4-regulates-lens-fiber-cell-differentiation-by-activating-p53-and-its-downstream-regulators
#13
Meng Gao, Yuwen Huang, Ling Wang, Mi Huang, Fei Liu, Shengjie Liao, Shanshan Yu, Zhaojing Lu, Shanshan Han, Xuebin Hu, Zhen Qu, Xiliang Liu, Tinsae Assefa Yimer, Lifang Yang, Zhaohui Tang, David Wan-Cheng Li, Mugen Liu
Cataract refers to opacities of the lens that impede the passage of light. Mutations in heat shock transcription factor 4 (HSF4) have been associated with cataract; however, the mechanisms regarding how mutations in HSF4 cause cataract are still obscure. In this study, we generated an hsf4 knockout zebrafish model using TALEN technology. The mutant zebrafish developed an early-onset cataract with multiple developmental defects in lens. The epithelial cells of the lens were overproliferated, resulting in the overabundance of lens fiber cells in hsf4(null) zebrafish lens...
October 5, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28980932/estimating-the-modulatory-effect-of-cadmium-chloride-on-the-genotoxicity-and-mutagenicity-of-silver-nanoparticles-in-mice
#14
H R H Mohamed
Silver (Ag) nanoparticles (nano-Ag) are widely used because of their distinctive antimicrobial properties, but this widespread use increases Ag release into the environment along with many other pollutants such as heavy metals. Therefore, this study was undertaken to study the modulatory effect of cadmium chloride (CdCl2) on the genotoxicity and mutagenicity of nano-Ag in mice liver, kidney and brain tissues. Co-injections of CdCl2 (1.5 mg/kg) with nano-Ag (20, 41, or 82 mg/kg) resulted in significant elevations in both single and double DNA strand breaks that triggered higher apoptotic DNA damage, as revealed by the more fragmented appearance of genomic DNA and the significant increase in apoptotic fractions...
September 30, 2017: Cellular and Molecular Biology
https://www.readbyqxmd.com/read/28979810/enhancing-chemotherapy-sensitivity-by-targeting-pcg-via-the-atm-p53-pathway
#15
Shu-Bin Gao, Kang-Li Li, Huan Qiu, Ling-Yu Zhu, Chang-Bao Pan, Yue Zhao, Shu-Hua Wei, Shu Shi, Guang-Hui Jin, Li-Xiang Xue
Histone modification and chromatin remodeling are important events in response to DNA damage, and Polycomb group (PcG) proteins, catalyzing H3K27 methylation, are involved. However, the biological function and mechanism of PcG in DNA damage are not fully understood. Additionally, downstream effectors in hepatocellular carcinoma (HCC) remain unclear. The present study investigated the biological and mechanistic roles of PcG in the DNA damage response induced by chemotherapeutic drugs in HCC. It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/28979716/epigenetics-of-gastroenteropancreatic-neuroendocrine-tumors-a-clinicopathologic-perspective
#16
REVIEW
Brendan M Finnerty, Katherine D Gray, Maureen D Moore, Rasa Zarnegar, Thomas J Fahey Iii
Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are a heterogeneous group of rare tumors whose site-specific tumor incidence and clinical behavior vary widely. Genetic alterations associated with familial inherited syndromes have been well defined; however, the genetic profile of sporadic tumors is less clear as their tumorigenesis does not appear to be controlled by classic oncogenes such as P53, RB, or KRAS. Even within GEP-NETs, there are no common oncogenic drivers; for example, DAXX/ATRX mutations are strongly implicated in the tumorigenesis of pancreatic but not small bowel NETs...
September 15, 2017: World Journal of Gastrointestinal Oncology
https://www.readbyqxmd.com/read/28978265/modulation-of-interaction-of-mutant-tp53-and-wild-type-brca1-by-alkaloids-a-computational-approach-towards-targeting-protein-protein-interaction-as-a-futuristic-therapeutic-intervention-strategy-for-breast-cancer-impediment
#17
Sameeksha Tiwari, Manika Awasthi, Swati Singh, Veda P Pandey, Upendra N Dwivedi
Protein-protein interactions (PPI) are a new emerging class of novel therapeutic targets. In order to probe these interactions, computational tools provide a convenient and quick method towards the development of therapeutics. Keeping this in view the present study was initiated to analyze interaction of tumour suppressor protein p53 (TP53) and breast cancer associated protein (BRCA1) as promising target against breast cancer. Using computational approaches such as protein-protein docking, hot spot analyses, molecular docking and molecular dynamics simulation (MDS), stepwise analyses of the interactions of the wild type and mutant TP53 with that of wild type BRCA1 and their modulation by alkaloids were done...
October 5, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28977491/p53-controls-expression-of-the-dna-deaminase-apobec3b-to-limit-its-potential-mutagenic-activity-in-cancer-cells
#18
Manikandan Periyasamy, Anup K Singh, Carolina Gemma, Christian Kranjec, Raed Farzan, Damien A Leach, Naveenan Navaratnam, Hajnalka L Pálinkás, Beata G Vértessy, Tim R Fenton, John Doorbar, Frances Fuller-Pace, David W Meek, R Charles Coombes, Laki Buluwela, Simak Ali
Cancer genome sequencing has implicated the cytosine deaminase activity of apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) genes as an important source of mutations in diverse cancers, with APOBEC3B (A3B) expression especially correlated with such cancer mutations. To better understand the processes directing A3B over-expression in cancer, and possible therapeutic avenues for targeting A3B, we have investigated the regulation of A3B gene expression. Here, we show that A3B expression is inversely related to p53 status in different cancer types and demonstrate that this is due to a direct and pivotal role for p53 in repressing A3B expression...
August 16, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28976134/tumor-protein-53-mutations-mapping-to-its-tertiary-structure-with-in-silico-prediction-of-neoepitopic-vaccine-candidates-in-bone-tumors
#19
Hamid Nawaz Tipu, Abdul Rehman Arshad
Mapping of tp 53 mutations in bone cancers present in COSMIC database to its secondary and tertiary structure with in silico prediction of newly formed HLA binding epitopes as candidates for synthetic peptide vaccine. Mutations in bone cancers present in COSMIC database were listed and manually induced in wt p53 FASTA sequence. Wt p53 secondary structure was predicted. Template identified and tertiary structure of wt p53 was modelled in Cn3D followed by individual mutations mapping onto this model. HLA class I binding affinity was determined for mutated sequences to determine any newly binding peptide sequences...
September 2017: Journal of Experimental Therapeutics & Oncology
https://www.readbyqxmd.com/read/28976121/strategies-used-in-the-clinical-trials-of-gene-therapy-for-cancer
#20
Thekkuttuparambil Ananthanarayanan Ajith
Advances in understanding and manipulating genes have set the stage for scientists to alter a person's genetic material to prevent or treat diseases. Over the past decade, somatic gene therapy has been increasingly applied in clinical trials where the genetic material (DNA and RNA) introduced into a person's cell. Mutation and inactivation of the tumor suppressor genes are the unified concept of the development of tumor in humans. Therefore, researchers have discovered potential of gene therapies in the treatment of cancer...
September 2017: Journal of Experimental Therapeutics & Oncology
keyword
keyword
35360
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"