Results 81 to 90 of about 905,362 (332)

The effects of two combined methods of P53 expression and preoperative serum CEA detection on the prognosis of colorectal cancer

Frontiers in Oncology
AimTo explore the effects of two combined methods—P53 expression and preoperative serum carcinoembryonic antigen (S-CEA) detection—on the prognosis of colorectal cancer (CRC).MethodsTwo classified combinations of tissue P53 and S-CEA were utilized ...
Guojun Tong, Guojun Tong, Yanyan Wang, Hai Qian, Zhenhua Tan, Yan Shen, Hui Li   +6 more
doaj   +1 more source

Exon 1 disruption alters tissue-specific expression of mouse p53 and results in selective development of B cell lymphomas.

PLoS ONE, 2012
p53 is a tumor suppressor gene mutated in >50% of human cancers, while p53 deficiency in mice results in cancers and accelerated mortality. Thymic T cell lymphoma is the most common malignancy in p53-deficient mice, making it difficult to study the role ...
Y Jeffrey Chiang, Michael J Difilippantonio, Lino Tessarollo, Herbert C Morse, Richard J Hodes   +4 more
doaj   +1 more source

p53 inhibits CRISPR–Cas9 engineering in human pluripotent stem cells

Nature Medicine, 2018
CRISPR/Cas9 has revolutionized our ability to engineer genomes and conduct genome-wide screens in human cells1–3. Whereas some cell types are amenable to genome engineering, genomes of human pluripotent stem cells (hPSCs) have been difficult to engineer,
Robert J Ihry, Kathleen A. Worringer, M. Salick, Elizabeth Frias, Daniel J. Ho, Kraig M. Theriault, Sravya Kommineni, Julie T. Chen, M. Sondey, Chaoyang Ye, Ranjit Randhawa, Tripti Kulkarni, Zinger Yang, Gregory McAllister, Carsten Russ, John Reece-Hoyes, W. Forrester, G. Hoffman, R. Dolmetsch, A. Kaykas   +19 more
semanticscholar   +1 more source

Active regulator of SIRT1 is required for cancer cell survival but not for SIRT1 activity [PDF]

, 2013
The NAD+-dependent deacetylase SIRT1 is involved in diverse cellular processes, and has also been linked with multiple disease states. Among these, SIRT1 expression negatively correlates with cancer survival in both laboratory and clinical studies ...
Chen GL, Pattison D, Wang H, Yoshida M
core   +1 more source

The neural crest‐associated gene ERRFI1 is involved in melanoma progression and resistance toward targeted therapy

Molecular Oncology, EarlyView.
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang, Qian Sun, Daniel Novak, Lei Zhu, Juliane Poelchen, Tamara Steinfass, Yiman Wang, Viktor Umansky, Jochen Utikal   +8 more
wiley   +1 more source

The antagonism between MCT-1 and p53 affects the tumorigenic outcomes

Molecular Cancer, 2010
Background MCT-1 oncoprotein accelerates p53 protein degradation via a proteosome pathway. Synergistic promotion of the xenograft tumorigenicity has been demonstrated in circumstance of p53 loss alongside MCT-1 overexpression.
Lin Tai-Du, Choy ChikOn, Wu Meng-Hsun, Shih Hung-Ju, Kasiappan Ravi, Chen Linyi, Hsu Hsin-Ling   +6 more
doaj   +1 more source

Mdm2 Is Required for Survival and Growth of p53-Deficient Cancer Cells. [PDF]

, 2017
p53 deletion prevents the embryonic lethality of normal tissues lacking Mdm2, suggesting that cells can survive without Mdm2 if p53 is also absent.
Adams, Clare M., Eischen, Christine M., Feeley, Kyle P, Mitra, Ramkrishna   +3 more
core   +1 more source

Synthetic Lethality of Chk1 Inhibition Combined with p53 and/or p21 Loss During a DNA Damage Response in Normal and Tumor Cells [PDF]

, 2013
Cell cycle checkpoints ensure genome integrity and are frequently compromised in human cancers. A therapeutic strategy being explored takes advantage of checkpoint defects in p53-deficient tumors in order to sensitize them to DNA-damaging agents by ...
A Besson, A Eastman, A Goga, A Goloudina, A Z Munir, AA Levesque, AA Levesque, AJ Fikaris, AN Tse, AT Ferguson, B Xu, C Tapia, CJ Sherr, CS Sorensen, CX Ma, EA Kohn, EA Kohn, F Bunz, FI Raynaud, H Piwnica-Worms, H Zhao, I Hassepass, J Bartkova, J Falck, K Shimuta, L S White, LL Parker, MH Lam, MV Cespedes, O Gilad, O Wang, OA Sedelnikova, PM Fracasso, R Di Micco, R Rodriguez, RP Perez, RT Bunch, S Origanti, S-r Cai, SD Zabludoff, T Abbas, T Waldman, WR Taylor, Y Luo   +43 more
core   +2 more sources

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

Molecular Oncology, EarlyView.
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir, Lukasz Arcimowicz, Lucia Martinkova, Vaclav Hrabal, Filip Zavadil Kokas, Tomas Henek, Martina Kucerikova, Ondrej Bonczek, Pavlina Zatloukalova, Lenka Hernychova, Philip J. Coates, Borivoj Vojtesek, David P. Lane   +12 more
wiley   +1 more source

Phenotype specific analyses reveal distinct regulatory mechanism for chronically activated p53.

PLoS Genetics, 2015
The downstream functions of the DNA binding tumor suppressor p53 vary depending on the cellular context, and persistent p53 activation has recently been implicated in tumor suppression and senescence.
Kristina Kirschner, Shamith A Samarajiwa, Jonathan M Cairns, Suraj Menon, Pedro A Pérez-Mancera, Kosuke Tomimatsu, Camino Bermejo-Rodriguez, Yoko Ito, Tamir Chandra, Masako Narita, Scott K Lyons, Andy G Lynch, Hiroshi Kimura, Tetsuya Ohbayashi, Simon Tavaré, Masashi Narita   +15 more
doaj   +1 more source