Results 91 to 100 of about 208,633 (265)
Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source
The cell‐autonomous roles of interferon type 1 vary based on duration and intensity. While acute, robust signaling results in cancer cell cytotoxic effects, sustained, low‐level signaling is associated with tumor‐promoting effects. This review summarizes current research of IFN‐1 in cancer and within the clinical setting, with an emphasis on female ...
Ashlyn Conant +7 more
wiley +1 more source
Checkpoint Inhibitors: Applications for Autoimmunity
To limit excessive T cell-mediated inflammatory responses, the immune system has a milieu of inhibitory receptors, called immune checkpoints. Cancer cells have evolved to seize those inhibitory pathways and to prevent T cell-mediated killing of tumor cells.
Anna S, Tocheva, Adam, Mor
openaire +3 more sources
ADP‐ribosylation: An emerging regulator of the epigenome
ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho +2 more
wiley +1 more source
Pharmacological inhibition of PERK in a DEN‐induced mouse model of liver cancer does not reduce tumor burden but alters cellular stress signaling. Despite blocking PERK activity, downstream stress responses, including CHOP expression, remain active, suggesting compensatory mechanisms within the unfolded protein response that may influence tumor ...
Ada Lerma‐Clavero +5 more
wiley +1 more source
A yeast model of 5‐oxoproline accumulation reveals a general toleration to 5‐oxoproline
Using a yeast model, we show that even high accumulation of 5‐oxoproline causes only mild cellular stress and does not trigger oxidative stress. Instead, cells adapt by activating efflux pumps and diverse protective pathways, suggesting that previously proposed harmful effects of 5‐oxoproline may arise from indirect metabolic imbalances rather than the
Pratiksha Dubey +4 more
wiley +1 more source
Anastasia Gkiala,1 Sotiria Palioura2 1National and Kapodistrian University of Athens School of Medicine, Athens, Greece; 2Athens Vision Eye Institute, Athens, GreeceCorrespondence: Sotiria PaliouraAthens Vision Eye Institute, 328-330 Syngrou Ave ...
Gkiala A, Palioura S
doaj
Aquaporin‐3 and aquaporin‐5 impact the development of pancreatic ductal adenocarcinoma spheroids
Schematic representation of the role of aquaporin‐3 (AQP3) and aquaporin‐5 (AQP5) in pancreatic ductal adenocarcinoma (PDAC). Both proteins are upregulated in PDAC and are associated with tumor progression and metastatic potential. Silencing AQP3 or AQP5 in PDAC spheroids results in decreased diameter, area, and overall growth, underscoring their key ...
Catarina Pimpão +3 more
wiley +1 more source
ATZ‐1 promotes DNA replication efficiency to maintain normal meiotic function
Absence of ATZ‐1 interferes with meiotic DNA replication and cell cycle function via CHK‐1. This causes downstream defects associated with DNA damage and genomic integrity. Taken together, this study suggests that ATZ‐1 influences DNA replication efficiency and cell cycle function to maintain normal meiotic function.
Taylin E. Gourley +5 more
wiley +1 more source
Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley +1 more source

