Reanalysis of our UV study of p53-mutant mouse embryonic fibroblasts revealed an intriguing orchestration of massive transcriptome responses. However, close scrutiny of the data uncovered an affected mRNA/rRNA ratio, effectively inhibiting valid data analysis. UV-dose range-finding showed low-dose UV specific- and high-dose stress-related responses, which represent a plea for UV dose range-finding in experimental design.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023578 | PMC |
| http://dx.doi.org/10.4161/trns.1.3.13487 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Small-molecule MMRi36 induces apoptosis in p53-mutant lymphomas by targeting MDM2/MDM4/XIAP for degradation.
Front Oncol
December 2024
Department of Pharmacology and Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States.
Rituximab combined with systemic chemotherapy significantly improves the rate of complete response in B-cell lymphomas. However, acquired rituximab resistance develops in most patients leading to relapse. The mechanisms underlying rituximab resistance are not well-understood.
View Article and Find Full Text PDFMolecular Mechanisms of Synergistic Effect of PRIMA-1 and Oxaliplatin in Colorectal Cancer With Different p53 Status.
Cancer Med
January 2025
Department of Gastroenterology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, People's Republic of China.
Article Synopsis
- The study investigates combining PRIMA-1 with oxaliplatin (L-OHP) to enhance treatment efficacy for colorectal cancer (CRC) while addressing the drug's toxicity and resistance issues.
- The results show that the combination therapy significantly improves cancer cell death and reduces cell migration and colony formation, regardless of p53 mutation status.
- RNA-seq analysis reveals different cellular responses to the treatments based on p53 status, and in vivo studies confirm that the combination therapy enhances effectiveness and reduces toxicity compared to PRIMA-1 alone.
Outcomes of relapsed/refractory acute myeloid leukemia (AML) are poor, and strategies to improve outcomes are urgently needed. One important factor promoting relapse and chemoresistance is the ability of AML cells to thrive in vivo within an intrinsically hypoxic bone marrow microenvironment. Here we show that human AML cells exhibit enhanced autophagy, specifically mitophagy (i.
View Article and Find Full Text PDFSynergistic effects of MK-1775 and gemcitabine on cytotoxicity in non-small cell lung cancer.
Heliyon
November 2024
Division of Hematology-Oncology, Department of Internal Medicine, Chang Gung Memorial Hospital at Linkou, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Background: Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality. Chemotherapy is crucial in NSCLC treatment, and targeting Wee1 kinase, a key regulator of the G2/M cell cycle checkpoint, may enhance the efficacy of cytotoxic agents. This study investigates the potential of the Wee1 inhibitor MK-1775 in combination with gemcitabine and pemetrexed to enhance cytotoxicity in NSCLC cell lines.
View Article and Find Full Text PDFSelective metabolic regulations by p53 mutant variants in pancreatic cancer.
J Exp Clin Cancer Res
November 2024
Chair for Systems Toxicology, Department of Biology, University of Konstanz, Konstanz, Germany.
Background: Approximately half of all human cancers harbour mutations in the p53 gene, leading to the generation of neomorphic p53 mutant proteins. These mutants can exert gain-of-function (GOF) effects, potentially promoting tumour progression. However, the clinical significance of p53 GOF mutations, as well as the selectivity of individual variants, remains controversial and unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!