Results 211 to 220 of about 18,512,812 (309)

Hotspot propensity across mutational processes

open access: yes, 2022
Arnedo-Pac C   +3 more
europepmc   +1 more source

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation

open access: yesMolecular Oncology, EarlyView.
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani   +14 more
wiley   +1 more source

A novel splice-acceptor site mutation (IVS13-2A>T) of polycystic kidney disease 1 (PKD1) gene resulting in an RNA processing defect with a 74-nucleotide deletion in exon 14 of the mRNA transcript [PDF]

open access: gold, 2000
Anna Thongnoppakhun   +5 more
openalex   +1 more source

Tonic signaling of the B‐cell antigen‐specific receptor is a common functional hallmark in chronic lymphocytic leukemia cell phosphoproteomes at early disease stages

open access: yesMolecular Oncology, EarlyView.
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez   +17 more
wiley   +1 more source

Ubiquitination of transcription factors in cancer: unveiling therapeutic potential

open access: yesMolecular Oncology, EarlyView.
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley   +1 more source

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

open access: yesMolecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen   +12 more
wiley   +1 more source

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