Results 81 to 90 of about 198,463 (306)

Mutation or loss of p53 differentially modifies TGFβ action in ovarian cancer.

PLoS ONE, 2014
Ovarian cancer is the most lethal gynecological disease affecting women in the US. The Cancer Genome Atlas Network identified p53 mutations in 96% of high-grade serous ovarian carcinomas, demonstrating its critical role.
Eoghainín Ó hAinmhire, Suzanne M Quartuccio, Whay Cheng, Roshan A Ahmed, Shelby M King, Joanna E Burdette   +5 more
doaj   +1 more source

Small Molecule Multi-Targeted Kinase Inhibitor RGB-286638 Triggers P53-Dependent and -Independent Anti-Multiple Myeloma Activity through Inhibition of Transcriptional CDKs [PDF]

, 2014
Small molecule multi-targeted CDK inhibitors (CDKIs) are of particular interest due to their potent antitumor activity independent of p53 gene alterations. P53 deletion is associated with a very poor prognosis in multiple myeloma (MM). In this regard, we
Anderson, Kenneth C., Cirstea, Diana, Cottini, Francesca, Eda, Homare, Gorgun, Gullu, Hideshima, Teru, Hu, Yiguo, Loferer, Hannes, Mimura, Naoya, Mishima, Yuko, Munshi, Nikhil C., Nemani, Neeharika, Ohguchi, Hiroto, Raje, Noopur, Santo, Loredana, Suzuki, Rikio   +15 more
core   +1 more source

A Cytoplasmic PML Mutant Inhibits p53 Function [PDF]

Cell Cycle, 2006
The promyelocytic leukaemia gene (Pml) is a tumor suppressor identified in acute promyelocytic leukaemia (APL), where it is fused to RAR alpha gene as a result of the chromosomal translocation t(15;17). Pml encodes both nuclear and cytoplasmic isoforms. While nuclear PML has been intensively investigated, cytoplasmic PML proteins are less characterized.
Bellodi, C, Kindle, K, BERNASSOLA, FRANCESCA, Cossarizza, A, Dinsdale, D, MELINO, GENNARO, Heery, D, Salomoni, P.   +7 more
openaire   +5 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

EVALUATING THE THERAPEUTIC EFFICACY OF RESTORING WILD-TYPE P53 ACTIVITY IN P53-MUTANT TUMORS [PDF]

, 2017
The p53 transcription factor is the most frequently altered in human cancers usually via missense mutations that undermine its transcriptional activity. Clinically, TP53 mutations have been shown to be remarkably predictive of refractoriness to treatment,
Larsson, Connie A
core   +1 more source

The C-terminus of p63 contains multiple regulatory elements with different functions [PDF]

, 2010
The transcription factor p63 is expressed as at least six different isoforms, of which two have been assigned critical biological roles within ectodermal development and skin stem cell biology on the one hand and supervision of the genetic stability of ...
Straub, Wesley E., Weber, Tobias Alexander, Schäfer, Birgit, Candi, Eleonora, Durst, Florian, Ou, Horng Der, Rajalingam, Krishnaraj, Melino, Gennaro, Dötsch, Volker   +8 more
core   +1 more source

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

Metabolic Pathways Enhancement Confers Poor Prognosis in p53 Exon Mutant Hepatocellular Carcinoma. [PDF]

, 2020
RNA-Sequencing (RNA-Seq), the most commonly used sequencing application tool, is not only a method for measuring gene expression but also an excellent media to detect important structural variants such as single nucleotide variants (SNVs), insertion ...
Chen, Po-Ming, Chiang, Eugene, Li, Jian-Rong, Liu, Chun-Chi, Tang, Feng-Yao   +4 more
core  

A requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancers. [PDF]

, 2019
Cohesin is a multiprotein ring that is responsible for cohesion of sister chromatids and formation of DNA loops to regulate gene expression. Genomic analyses have identified that the cohesin subunit STAG2 is frequently inactivated by mutations in cancer.
Ashworth, Alan, Goode, Benjamin, Mondal, Gourish, Solomon, David A, Stevers, Meredith   +4 more
core   +2 more sources

Rescuing the function of mutant p53

Nature Reviews Cancer, 2001
One protein--p53--plays nemesis to most cancers by condemning damaged cells to death or quarantining them for repair. But the activity of p53 relies on its intact native conformation, which can be lost following mutation of a single nucleotide. With thousands of such mutations identified in patients, how can a future cancer drug buttress this fragile ...
Bullock, A, Fersht, A
openaire   +2 more sources