Results 91 to 100 of about 646,683 (270)

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

Molecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak, Karolina Pytlak, Sandra Jaworowska, Bogusz Kulawiak, Piotr Bednarczyk   +4 more
wiley   +1 more source

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

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

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

Molecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller, Susanne Ebner, Carmen Haselrieder, Julia K. Günther, Astrid Drasche, Sophie Strich, Chiara Volani, Andrea Medici, Aleksandar Nikolajevic, Alex Deltedesco, Johannes E. Sigmund, Michael J. Blumer, Martin Hermann, Johanna Vanacker, Gerald Brandacher, Eduard Stefan, Omar Torres‐Quesada, Jakob Troppmair   +17 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

Loss of MECP2 Leads to Activation of P53 and Neuronal Senescence. [PDF]

, 2018
To determine the role for mutations of MECP2 in Rett syndrome, we generated isogenic lines of human induced pluripotent stem cells, neural progenitor cells, and neurons from patient fibroblasts with and without MECP2 expression in an attempt to ...
Allen, Denise, Chronis, Contantinos, Cinkornpumin, Jessica, Fu, Kai, Germanguz, Igal, Korsakova, Elena, Kuoy, Edward, Langerman, Justin, Lee, Peiyee, Lowry, William E, Ohashi, Minori, Park, Jenny C, Pellegrini, Matteo, Plath, Kathrin, Salas, Carlos, Tran, Stephen, Vargas, Benni S, Xiao, Xinshu   +17 more
core   +2 more sources

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

Molecular Oncology, EarlyView.
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon, Peter T. Gallagher, Orly I. Richter, Neermala Poudel Neupane, Amy C. Mandigo, Jennifer J. McCann, Emanuela Dylgjeri, Irina Vasilevskaya, Christopher McNair, Channing J. Paller, Wm. Kevin Kelly, Karen E. Knudsen, Matthew J. Schiewer, Ayesha A. Shafi   +13 more
wiley   +1 more source

p32 is a negative regulator of p53 tetramerization and transactivation

Molecular Oncology, 2019
p53 is a sequence‐specific transcription factor, and proper regulation of p53 transcriptional activity is critical for orchestrating different tumor‐suppressive mechanisms.
Nikhil Baban Ghate, Jinman Kim, Yonghwan Shin, Alan Situ, Tobias S. Ulmer, Woojin An   +5 more
doaj   +1 more source

Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer

Molecular Oncology, EarlyView.
Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity.
Carolin Salmon, Rui P. L. Neves, Nikolas H. Stoecklein, Sven‐Thorsten Liffers, Jens Siveke, Jan D. Kuhlmann, Pauline Wimberger, Paul Buderath, Rainer Kimmig, Sabine Kasimir‐Bauer   +9 more
wiley   +1 more source