Results 91 to 100 of about 198,463 (306)

Mutant p53 Gain-of-Function in Cancer [PDF]

Cold Spring Harbor Perspectives in Biology, 2009
In its wild-type form, p53 is a major tumor suppressor whose function is critical for protection against cancer. Many human tumors carry missense mutations in the TP53 gene, encoding p53. Typically, the affected tumor cells accumulate excessive amounts of the mutant p53 protein.
Oren, M
openaire   +2 more sources

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

Investigating the role of Hedgehog/GLI1 signaling in glioblastoma cell response to temozolomide. [PDF]

, 2018
Resistance to chemotherapy substantially hinders successful glioblastoma (GBM) treatment, contributing to an almost 100% mortality rate. Resistance to the frontline chemotherapy, temozolomide (TMZ), arises from numerous signaling pathways that are ...
Day, Emily S, Gleghorn, Jason P, Ioele, Stephen A, Melamed, Jilian R, Morgan, Joshua T, Sims-Mourtada, Jennifer   +5 more
core   +1 more source

Treating p53 Mutant Aggregation-Associated Cancer [PDF]

Cancers, 2018
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function ...
openaire   +2 more sources

Targeting HAUSP in both p53 wildtype and p53-mutant tumors [PDF]

Cell Cycle, 2018
Inhibition of Mdm2 function is a validated approach to restore p53 activity for cancer therapy; nevertheless, inhibitors of Mdm2 such as Nutlin-3 have certain limitations, suggesting that additional targets in this pathway need to be further elucidated.
Omid, Tavana, Hongbin, Sun, Wei, Gu
openaire   +2 more sources

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

Molecular Oncology, EarlyView.
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee, Byung‐Cheol Han, Gi‐Bang Koo, Jihye Park, Mijin Kwon, Young Bin Park, Jae‐Mun Choi, Seung‐Ho Lee, Sangho Roh   +8 more
wiley   +1 more source

Acetylation halts missense mutant p53 aggregation and rescues tumor suppression in non-small cell lung cancers

iScience, 2023
Summary: TP53 mutations are ubiquitous with tumorigenesis in non-small cell lung cancers (NSCLC). By analyzing the TCGA database, we reported that TP53 missense mutations are correlated with chromosomal instability and tumor mutation burden in NSCLC. The
Daxing Xu, Wei Qian, Zhenkun Yang, Zhenhao Zhang, Ping Sun, Quan Wan, Ying Yin, Yaling Hu, Lingli Gong, Bo Zhang, Xusheng Yang, Zhening Pu, Peihua Lu, Jian Zou   +13 more
doaj   +1 more source

Structural analysis of MDM2 RING separates degradation from regulation of p53 transcription activity [PDF]

, 2017
MDM2–MDMX complexes bind the p53 tumor-suppressor protein, inhibiting p53's transcriptional activity and targeting p53 for proteasomal degradation. Inhibitors that disrupt binding between p53 and MDM2 efficiently activate a p53 response, but their use in
A Plechanovová, A Plechanovová, Andreas K Hock, CS Chen, D Migliorini, D Shi, Danny T Huang, DC Scott, DE Christensen, Dominika Kowalczyk, E Branigan, E Meulmeester, Gary J Sibbet, H Dou, H Dou, H Kawai, H Kawai, I Ray-Coquard, J Momand, J Parant, JC Badciong, JD Oliner, JG Sanchez, JN Pruneda, K Itahana, K Linke, Karen H Vousden, KH Khoo, Koji Nomura, L Buetow, L Buetow, L Huang, LA Tollini, LC Storoni, LK Linares, LT Vassilev, M Andreeff, M Argentini, M Bista, M Kostic, Marta Klejnot, MG Koliopoulos, MHG Kubbutat, ML Choong, MS Dai, MS Dai, MV Poyurovsky, MW Jackson, N Minsky, N Zheng, P Dolezelova, P Emsley, P Roxburgh, PD Adams, PS Brzovic, Q Cheng, Q Cheng, Q Ding, R Honda, R Montes de Oca Luna, R Stad, R Stad, RA Finch, RK Geyer, S Iyappan, S Shangary, S Uldrijan, SN Jones, UM Moll, V Pant, W Kabsch, Y Pan   +71 more
core   +1 more source

Mutant p53 protein expression interferes with p53-independent apoptotic pathways [PDF]

Oncogene, 1998
Loss of normal p53 function was found frequently to interfere with response of cancer cells to conventional anticancer therapies. Since more than half of all human cancers possess p53 mutations, we decided to explore the involvement of mutant p53 in drug induced apoptosis.
R, Li, P D, Sutphin, D, Schwartz, D, Matas, N, Almog, R, Wolkowicz, N, Goldfinger, H, Pei, M, Prokocimer, V, Rotter   +9 more
openaire   +2 more sources

Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer

Molecular Oncology, EarlyView.
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta, Yang Song, Madeleine Ndahayo, Anirudh Saxena, Theresa Guo, Dylan Z. Kelley, Jessica Gore, Andrew Hennigan, Alexa Anderson, John C. Papadimitriou, Daria A. Gaykalova   +10 more
wiley   +1 more source