Results 141 to 150 of about 15,644,828 (310)
Synthetic DNA Synthesis and Assembly: Putting the Synthetic in Synthetic Biology.
Cold Spring Harbor Perspectives in Biology, 2017 R. Hughes, A. Ellington
semanticscholar +1 more source
Molecular 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
Molecular 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
Cancer Stem Cells and Molecular Biology Test in Colorectal Cancer: Therapeutic Implications
Acta Medica Indonesiana, 2018 Colorectal cancer (CRC) is the third most frequent cancer in males, the second in females, and is the second leading cause of cancer related death worldwide.
Rustam Effendi-YS
doaj
Methylation Biology of a Blood-Based MDS Risk Stratification Test
, 2023 Alvin Shi +6 more
openalex +1 more source
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Molecular Oncology, EarlyView.Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley +1 more source
Molecular 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