Results 121 to 130 of about 439,570 (294)
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla +9 more
wiley +1 more source
Targeted therapy was evaluated in SHH medulloblastoma using neuroepithelial stem cell (NES) and tumor‐derived NES‐like (tNES) models in 2D monolayers and 3D spheroids. PI3K, AKT, and CDK4/6 inhibitors had minimal effects in NES but markedly reduced viability and growth and induced apoptosis in tNES cells, revealing distinct therapeutic vulnerabilities.
Monika Lukoseviciute +4 more
wiley +1 more source
Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni +11 more
wiley +1 more source
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau +8 more
wiley +1 more source
NKCC1: A key regulator of glioblastoma progression
Glioblastoma (GBM) progression is driven by disrupted chloride cotransporter homeostasis. NKCC1 is highly expressed in stem‐like, astrocytic, and progenitor cells, correlating with earlier recurrence, while overall survival remains unaffected. NKCC1 serves as a prognostic marker and potential therapeutic target, linking chloride transporter imbalance ...
Anja Thomsen +5 more
wiley +1 more source
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen +9 more
wiley +1 more source
Molecular cancer prevention: Intercepting disease
Oncological practice must evolve, from treating established tumours to proactive cancer interception before clinical manifestation. This will require mechanistic insight into tumour initiation, validated biomarkers of early disease development and redesigned clinical trials, enabling cancer interception to become a core pillar of oncology with the ...
Charlotte Grieco +2 more
wiley +1 more source
Where creativity comes from: the social spaces of embodied minds [PDF]
This paper explores creative design, social interaction and perception. It proposes that creativity at a social level is not a result of many individuals trying to be creative at a personal level, but occurs naturally in the social interaction between ...
Hanna, S
core
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Overview of molecular signatures of senescence and associated resources: pros and cons
Cells can enter a stress response state termed cellular senescence that is involved in various diseases and aging. Detecting these cells is challenging due to the lack of universal biomarkers. This review presents the current state of senescence identification, from biomarkers to molecular signatures, compares tools and approaches, and highlights ...
Orestis A. Ntintas +6 more
wiley +1 more source

