Results 101 to 110 of about 332,161 (328)

Combining antibody conjugates with cytotoxic and immune‐stimulating payloads maximizes anti‐cancer activity

open access: yesMolecular Oncology, EarlyView.
Methods to improve antibody–drug conjugate (ADC) treatment durability in cancer therapy are needed. We utilized ADCs and immune‐stimulating antibody conjugates (ISACs), which are made from two non‐competitive antibodies, to enhance the entry of toxic payloads into cancer cells and deliver immunostimulatory agents into immune cells.
Tiexin Wang   +3 more
wiley   +1 more source

Xist and Tsix transcription dynamics is regulated by the X-to-autosome ratio and semistable transcriptional states [PDF]

open access: yes, 2016
In female mammals, X chromosome inactivation (XCI) is a key process in the control of gene dosage compensation between Xlinked genes and autosomes.
Berge, D. (Derk) ten   +7 more
core   +1 more source

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

open access: yesMolecular 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   +8 more
wiley   +1 more source

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

open access: yesMolecular 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   +10 more
wiley   +1 more source

Selection of X-chromosome Inactivation Model

open access: yesCancer Informatics, 2017
To address the complexity of the X-chromosome inactivation (XCI) process, we previously developed a unified approach for the association test for X-chromosomal single-nucleotide polymorphisms (SNPs) and the disease of interest, accounting for different ...
Jian Wang, Rajesh Talluri, Sanjay Shete
doaj   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin

open access: yesMolecular Oncology, EarlyView.
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon   +4 more
wiley   +1 more source

Dosage compensation in the process of inactivation/reactivation during both germ cell development and early embryogenesis in mouse

open access: yesScientific Reports, 2017
Ohno proposed that dosage compensation in mammals evolved as a two-step mechanism involving X-inactivation and X-upregulation. While X-inactivation is well characterized, it remains to further analysis whether upregulation of the single activated X ...
Xiaoyong Li   +7 more
doaj   +1 more source

Overexpression of CDT1 inhibits cell cycle progression at S phase by interacting with the mini‐chromosome maintenance complex and causes DNA damage

open access: yesFEBS Open Bio, EarlyView.
CDT1 is an essential protein for DNA replication licensing that loads the MCM complex, the eukaryotic replicative DNA helicase, onto replication origins. Overexpression of CDT1 induces cell cycle arrest at the S phase. Here we showed CDT1 inhibits the progression of replication forks by interacting with the MCM complex, leading to the stalling and ...
Takashi Tsuyama   +7 more
wiley   +1 more source

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