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https://www.readbyqxmd.com/read/29156626/surface-plasmon-resonance-sensing-of-biorecognition-interactions-within-the-tumor-suppressor-p53-network
#1
REVIEW
Ilaria Moscetti, Salvatore Cannistraro, Anna Rita Bizzarri
Surface Plasmon Resonance (SPR) is a powerful technique to study the kinetics of biomolecules undergoing biorecognition processes, particularly suited for protein-protein interactions of biomedical interest. The potentiality of SPR was exploited to sense the interactions occurring within the network of the tumor suppressor p53, which is crucial for maintaining genome integrity and whose function is inactivated, mainly by down regulation or by mutation, in the majority of human tumors. This study includes p53 down-regulators, p53 mutants and also the p53 family members, p63 and p73, which could vicariate p53 protective function...
November 20, 2017: Sensors
https://www.readbyqxmd.com/read/29138869/cepharanthine-exhibits-a-potent-anticancer-activity-in-p53-mutated-colorectal-cancer-cells-through-upregulation-of-p21waf1-cip1
#2
Arkornnut Rattanawong, Vilawan Payon, Wacharee Limpanasittikul, Chatikorn Boonkrai, Apiwat Mutirangura, Piyanuch Wonganan
Cepharanthine (CEP), a biscoclurine alkaloid isolated from Stephania cepharantha Hayata, has demonstrated anticancer activity in several different types of cancer cells. Colorectal cancer (CRC) is one of the most common cancers in both men and women. Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5‑fluorouracil, oxaliplatin and irinotecan. Many studies reported that mutation of p53 induced chemoresistance through several mechanisms, including induction of drug efflux, disruption of cell cycle regulation, evasion of apoptosis and upregulation of DNA repair...
November 9, 2017: Oncology Reports
https://www.readbyqxmd.com/read/29137657/p53-aberrations-in-low-grade-endometrioid-carcinoma-of-the-endometrium-with-nodal-metastases-possible-insights-on-pathogenesis-discerned-from-immunohistochemistry
#3
Oluwole Fadare, Vinita Parkash
BACKGROUND: TP53 mutations are rarely identified in low grade endometrioid carcinoma of the endometrium, and their pathogenic significance in such tumors is evidenced by the fact that TP53 aberrations have been associated with reduced recurrence-free survival in this subset of tumors. However, TP53 aberrations may not always represent a driving molecular event in a given endometrial cancer with a mutation. In this case study, the immunophenotype of a distinctive low grade endometrioid adenocarcinoma with an unusual pattern of lymph node metastases is used to explore the possible roles for underlying TP53-related molecular events in its pathogenesis...
November 14, 2017: Diagnostic Pathology
https://www.readbyqxmd.com/read/29135114/expression-and-role-of-p53-in-oral-lichen-planus-patients
#4
Milos Hadzi-Mihailovic, Renata Petrovic, Helene Raybaud, Dragan Stanimirovic, Meltem Ozar Koray
PURPOSE: Oral lichen planus (OLP) is an autoimmune skin and mucosal disorder. The range of malignant transformation in OLP varies between 0.1-3%. p53 is a tumor suppressor protein. Defective p53 could allow abnormal cells to proliferate, resulting in cancer. p53 plays an important role in cell cycle control and apoptosis and loss of p53 function has been demonstrated in about half of all human cancers. The purpose of the study was to investigate the malignant potential of OLP on the basis of p53 expression and to correlate p53 expression with clinical and histopathological features of OLP...
September 2017: Journal of B.U.ON.: Official Journal of the Balkan Union of Oncology
https://www.readbyqxmd.com/read/29133366/lifestyle-and-reproductive-factors-and-ovarian-cancer-risk-by-p53-and-mapk-expression
#5
Holly R Harris, Megan S Rice, Amy L Shafrir, Elizabeth M Poole, Mamta Gupta, Jonathan L Hecht, Kathryn L Terry, Shelley S Tworoger
BACKGROUND: One model of ovarian cancer development model divides tumors into two types. Type I tumors are characterized by KRAS and BRAF mutations, which can activate mitogen-activated protein kinase (MAPK). Type II tumors are characterized by tubal precursor lesions with p53 mutations. We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression. METHODS: Epithelial ovarian cancer cases (n=274) and controls (n=1907) were identified from the Nurses' Health Study (NHS) and NHSII prospective cohorts, and the population-based New England Case-Control study...
November 13, 2017: Cancer Epidemiology, Biomarkers & Prevention
https://www.readbyqxmd.com/read/29131020/androgen-triggers-the-pro-migratory-cxcl12-cxcr4-axis-in-ar-positive-breast-cancer-cell-lines-underlying-mechanism-and-possible-implications-for-the-use-of-aromatase-inhibitors-in-breast-cancer
#6
Kalliopi Azariadis, Fotini Kiagiadaki, Vasiliki Pelekanou, Vasiliki Bempi, Kostas Alexakis, Marilena Kampa, Andreas Tsapis, Elias Castanas, George Notas
BACKGROUND/AIMS: Reports regarding the role of androgen in breast cancer (BC) are conflicting. Some studies suggest that androgen could lead to undesirable responses in the presence of certain BC tumor characteristics. We have shown that androgen induces C-X-C motif chemokine 12 (CXCL12) in BC cell lines. Our aim was to identify the mechanisms regulating the phenotypic effects of androgen-induced CXCL12 on Androgen Receptor (AR) positive BC cell lines. METHODS: We analyzed the expression of CXCL12 and its receptors with qPCR and ELISA and the role of Nuclear Receptor Coactivator 1 (NCOA1) in this effect...
November 3, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29130967/endoplasmic-reticulum-stress-promotes-autophagy-and-apoptosis-and-reduces-chemotherapy-resistance-in-mutant-p53-lung-cancer-cells
#7
Ping-Ping Gan, Yang-Ying Zhou, Mei-Zuo Zhong, Yun Peng, Li Li, Jian-Huang Li
BACKGROUND/AIMS: Lung cancer (LC) continues to be one of the most prevalent cancers around the world. During this study we aimed to investigate the involvement of endoplasmic reticulum stress (ERS) in autophagy, apoptosis, and chemotherapy resistance of mutant p53 LC cells. METHODS: Immunohistochemistry was employed to help determine the p53 mutation status of cancer cells from 92 primary LC patients, who were subsequently assigned to either the mutant p53 (n = 39) or wild-type p53 group (n = 53)...
November 6, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29130509/arfhpv-e7-oncogene-lncrna-hotair-mir-331-3p-and-its-target-nrp2-form-a-negative-feedback-loop-to-regulate-the-apoptosis-in-the-tumorigenesis-in-hpv-positive-cervical-cancer
#8
Min Zhang, Yinghui Song, Furui Zhai
BACKGROUND: The objective of this study was to explore the role of HOTAIR in the development of cervical cancer, as well as its downstream signaling pathway. METHOD: We conducted computational analysis, luciferase assay to explore downstream of HOTAIR and miR-331-3p. Real-time PCR and western-blot were carried out to detect the relationship among E7, HOTAIR, miR-331-3p, NRP2 and P53. Finally, MTT assay and flow cytometry analysis were performed to validate the effect of E7 and miR-331-3p on cell apoptosis and proliferation...
November 11, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29117941/loss-of-uracil-dna-glycosylase-selectively-re-sensitizes-p53-mutant-and-deficient-cells-to-5-fdu
#9
Yan Yan, Yulan Qing, John J Pink, Stanton L Gerson
Thymidylate synthase (TS) inhibitors including fluoropyrimidines [e.g., 5-Fluorouracil (5-FU) and 5-Fluorodeoxyuridine (5-FdU, floxuridine)] and antifolates (e.g., pemetrexed) are widely used against solid tumors. Previously, we reported that shRNA-mediated knockdown (KD) of uracil DNA glycosylase (UDG) sensitized cancer cells to 5-FdU. Since p53 has also been shown as a critical determinant of the sensitivity to TS inhibitors, we further interrogated 5-FdU cytotoxicity after UDG depletion with regard to p53 status...
November 8, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29114996/impaired-p53-cep-1-is-associated-with-lifespan-extension-through-an-age-related-imbalance-in-the-energy-metabolism-of-c-%C3%A2-elegans
#10
Sumino Yanase, Hitoshi Suda, Kayo Yasuda, Naoaki Ishii
In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 mediates the stress response, activates germ line apoptosis and regulates meiotic chromosome segregation. A reduction in its expression, which frequently occurs in mammalian cancer cells, extends lifespan and induces an adaptive response in C. elegans. However, these effects do not involve an increase in oxidative stress resistance. Here, we showed that intermittent exposure to hyperoxia, which induces oxidative stress resistance and lowers the production of ROS derived from mitochondrial respiration in C...
November 8, 2017: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/29107110/nimbolide-reduces-cd44-positive-cell-population-and-induces-mitochondrial-apoptosis-in-pancreatic-cancer-cells
#11
Sandeep Kumar, Joseph R Inigo, Rahul Kumar, Ajay K Chaudhary, Jordan O'Malley, Srimmitha Balachandar, Jianmin Wang, Kristopher Attwood, Neelu Yadav, Steven Hochwald, Xinjiang Wang, Dhyan Chandra
Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive disease and current treatment regimens fail to effectively cure PDAC. Development of resistance to current therapy is one of the key reasons for this outcome. Nimbolide (NL), a triterpenoid obtained from Azadirachta indica, exhibits anticancer properties in various cancer including PDAC cells. However, the underlying mechanism of this anticancer agent in PDAC cells remains undefined. We show that NL exerts a higher level of apoptotic cell death compared to the first-line agent gemcitabine for PDAC, as well as other anticancer agents including sorafenib and curcumin...
October 26, 2017: Cancer Letters
https://www.readbyqxmd.com/read/29100360/the-inhibiting-effect-of-neural-stem-cells-on-proliferation-and-invasion-of-glioma-cells
#12
Jing An, Hanqi Yan, Xingxing Li, Ruolan Tan, Xinlin Chen, Zhichao Zhang, Yingfei Liu, Pengbo Zhang, Haixia Lu, Yong Liu
The invasive and infiltrative nature of tumor cells leads to the poor prognosis of glioma. Currently, novel therapeutic means to eliminate the tumor cells without damaging the normal brain tissue are still strongly demanded. Significant attentions had been paid to stem cell-based therapy and neural stem cell (NSC) had been considered as one of the efficient delivery vehicles for targeting therapeutic genes. However, whether the NSCs could directly affect glioma cells remains to be seen. In this study, both rat and human glioma cells (C6 and U251) were co-cultured with normal rat embryonic NSCs directly or in-directly...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29100333/functional-consequence-of-the-p53-codon-72-polymorphism-in-colorectal-cancer
#13
Venkat R Katkoori, Upender Manne, Lakshmi S Chaturvedi, Marc D Basson, Pam Haan, Daniel Coffey, Harvey L Bumpers
Background: The codon 72 polymorphism in p53 has been implicated in colorectal cancer (CRC) risk, prognosis and CRC health disparities. We examined the functional consequence of this polymorphism in CRC. Experimental Design: Plasmids (pCMV6) that express different phenotypes of p53 [p53 wild type (wt) at codon 72 (R72(wt)), R72(wt) with mutation at codon 273 cysteine (R72(273Cys)), p53 mutation at codon 72 (P72(wt)) and P72(wt) with mutation at codon 273 (P72(273Cys))] were constructed...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29099488/mutant-p53-partners-in-crime
#14
REVIEW
Michael P Kim, Guillermina Lozano
Mutant p53 proteins impart changes in cellular behavior and function through interactions with proteins that alter gene expression. The milieu of intracellular proteins available to interact with mutant p53 is context specific and changes with disease, cell type, and environmental conditions. Varying conformations of mutant p53 largely dictate protein-protein interactions as different point mutations within protein-coding regions greatly alter the extent and array of gain-of-function (GOF) activities. Given such variables, how can knowledge regarding p53 missense mutations be translated into predicting or altering biologic activity for therapy? How may knowledge regarding mutant p53 functions within certain disease contexts be harnessed to blunt or ablate mutant p53 GOF for therapy? In this article, we review known proteins that interact with mutant p53 and result in the activation of genes that contribute to p53 GOF with particular emphasis on context dependency and an evolving appreciation of GOF mechanisms...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29099487/why-are-there-hotspot-mutations-in-the-tp53-gene-in-human-cancers
#15
REVIEW
Evan H Baugh, Hua Ke, Arnold J Levine, Richard A Bonneau, Chang S Chan
The p53 gene contains homozygous mutations in ~50-60% of human cancers. About 90% of these mutations encode missense mutant proteins that span ~190 different codons localized in the DNA-binding domain of the gene and protein. These mutations produce a protein with a reduced capacity to bind to a specific DNA sequence that regulates the p53 transcriptional pathway. Eight of these mutations are localized in codons that account for ~28% of the total p53 mutations and these alleles appear to be selected for preferentially in human cancers of many tissue types...
November 3, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29093665/pi3k-and-inhibitor-of-apoptosis-proteins-modulate-gentamicin-induced-hair-cell-death-in-the-zebrafish-lateral-line
#16
Heather Wiedenhoft, Lauren Hayashi, Allison B Coffin
Inner ear hair cell death leads to sensorineural hearing loss and can be a direct consequence of aminoglycoside antibiotic treatment. Aminoglycosides such as gentamicin are effective therapy for serious Gram-negative bacterial infections such as some forms of meningitis, pneumonia, and sepsis. Aminoglycosides enter hair cells through mechanotransduction channels at the apical end of hair bundles and initiate intrinsic cell death cascades, but the precise cell signaling that leads to hair cell death is incompletely understood...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29091765/low-grade-astrocytoma-mutations-in-idh1-p53-and-atrx-cooperate-to-block-differentiation-of-human-neural-stem-cells-via-repression-of-sox2
#17
Aram S Modrek, Danielle Golub, Themasap Khan, Devin Bready, Jod Prado, Christopher Bowman, Jingjing Deng, Guoan Zhang, Pedro P Rocha, Ramya Raviram, Charalampos Lazaris, James M Stafford, Gary LeRoy, Michael Kader, Joravar Dhaliwal, N Sumru Bayin, Joshua D Frenster, Jonathan Serrano, Luis Chiriboga, Rabaa Baitalmal, Gouri Nanjangud, Andrew S Chi, John G Golfinos, Jing Wang, Matthias A Karajannis, Richard A Bonneau, Danny Reinberg, Aristotelis Tsirigos, David Zagzag, Matija Snuderl, Jane A Skok, Thomas A Neubert, Dimitris G Placantonakis
Low-grade astrocytomas (LGAs) carry neomorphic mutations in isocitrate dehydrogenase (IDH) concurrently with P53 and ATRX loss. To model LGA formation, we introduced R132H IDH1, P53 shRNA, and ATRX shRNA into human neural stem cells (NSCs). These oncogenic hits blocked NSC differentiation, increased invasiveness in vivo, and led to a DNA methylation and transcriptional profile resembling IDH1 mutant human LGAs. The differentiation block was caused by transcriptional silencing of the transcription factor SOX2 secondary to disassociation of its promoter from a putative enhancer...
October 31, 2017: Cell Reports
https://www.readbyqxmd.com/read/29078269/ko-of-5-insp7-kinase-activity-transforms-the-hct116-colon-cancer-cell-line-into-a-hypermetabolic-growth-inhibited-phenotype
#18
Chunfang Gu, Hoai-Nghia Nguyen, Douglas Ganini, Zhaowei Chen, Henning J Jessen, Zhen Gu, Huanchen Wang, Stephen B Shears
The inositol pyrophosphates 5-InsP7 (diphosphoinositol pentakisphosphate) and 1,5-InsP8 (bis-diphosphoinositol tetrakisphosphate) are highly energetic cellular signals interconverted by the diphosphoinositol pentakisphosphate kinases (PPIP5Ks). Here, we used CRISPR to KO PPIP5Ks in the HCT116 colon cancer cell line. This procedure eliminates 1,5-InsP8 and raises 5-InsP7 levels threefold. Expression of p53 and p21 was up-regulated; proliferation and G1/S cell-cycle transition slowed. Thus, PPIP5Ks are potential targets for tumor therapy...
November 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29073933/role-of-tumor-suppressor-p53-and-micro-rna-interplay-in-multiple-myeloma-pathogenesis
#19
REVIEW
Jahangir Abdi, Nasrin Rastgoo, Lihong Li, Wenming Chen, Hong Chang
The molecular mechanisms underlying dysregulated wild type (wt) p53 in multiple myeloma (MM) have been subjects of intense investigation for years. Indeed, correlation of rarely occurring TP53 gene mutations or deletions with adverse clinical outcomes in MM patients is strongly established, while in majority of cases wtp53 seems to be non-functional or dysregulated bearing a high clinical impact. Interestingly, findings from recent investigations show that micro-RNAs (miRNAs) may contribute to suppression of wtp53 in MM, as they are now known to function as key regulatory elements in the p53 network...
October 26, 2017: Journal of Hematology & Oncology
https://www.readbyqxmd.com/read/29073078/ninjurin-1-has-two-opposing-functions-in-tumorigenesis-in-a-p53-dependent-manner
#20
Hee Jung Yang, Jin Zhang, Wensheng Yan, Seong-Jun Cho, Christopher Lucchesi, Mingyi Chen, Eric C Huang, Ariane Scoumanne, Weici Zhang, Xinbin Chen
WT p53 is critical for tumor suppression, whereas mutant p53 promotes tumor progression. Nerve injury-induced protein 1 (Ninj1) is a target of p53 and forms a feedback loop with p53 by repressing p53 mRNA translation. Here, we show that loss of Ninj1 increased mutant p53 expression and, subsequently, enhanced cell growth and migration in cells carrying a mutant p53. In contrast, loss of Ninj1 inhibited cell growth and migration in cells carrying a WT p53. To explore the biological significance of Ninj1, we generated a cohort of Ninj1-deficient mice and found that Ninj1(+/-) mice were prone to systemic inflammation and insulitis, but not to spontaneous tumors...
October 24, 2017: Proceedings of the National Academy of Sciences of the United States of America
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