Results 101 to 110 of about 7,287,837 (290)

A context‐dependent modulatory role for eIF6 in acquired resistance to vemurafenib in melanoma

open access: yesFEBS Letters, EarlyView.
Acquired resistance to vemurafenib upregulates the translation factor eIF6 in melanoma cells. Silencing eIF6 in resistant cells reduces proliferation and partially restores drug sensitivity, whereas its overexpression increases sensitivity across melanoma lines regardless of BRAF status, via modulation of mTOR, S6K, and MAPK signaling.
George Kyriakopoulos   +9 more
wiley   +1 more source

The ubiquitin system in normal and infected germinal center B cells

open access: yesFEBS Letters, EarlyView.
The ubiquitin system plays a central role in germinal center (GC) B cells, influencing differentiation to long‐lived memory B cells. Oncogenic gammaherpesviruses gain access to memory B cells by establishing latency in GC B cells. Mapping ubiquitin mechanisms in normal and infected GC B cells will define specific molecular circuits in B cells germane ...
Destiny Davis   +2 more
wiley   +1 more source

Circular RNA expression landscapes in myelodysplastic neoplasms: Associations with mutational signatures and disease progression

open access: yesMolecular Oncology, EarlyView.
In this explorative study, the abundance of circular RNA molecules in bone marrow stem cells was found to be elevated in patients with high‐risk myelodysplastic neoplasms, and to be associated with an increased risk of progression to acute myeloid leukemia.
Eileen Wedge   +17 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

open access: yesMolecular Oncology, EarlyView.
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

Július Barč-Ivan: Collected Dramatic Works. [PDF]

open access: yesSlovenska Literatura, 2002
Dagmar Kročanová Garay
doaj  

A SKETCH FOR THE PORTRAIT OF THE DIALECTOLOGIST PETAR ŠIMUNOVIĆ

open access: yesFluminensia: Journal for Philological Research, 2014
The paper addresses the dialectological work of the academician Petar Šimunović (published works and unpublished manuscripts), primarily his works on the dialects of Central Dalmatian islands and dialects in the Buzet region, as well as his ...
Silvana Vranić
doaj  

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 more
wiley   +1 more source

[Baldwin Locomotive Works, Six-Coupled Locomotive, Stock]

open access: yes
Verso: Negative No. 9227, The Baldwin Locomotive Works, Six-coupled Locomotive, Class 6-38-D, 164, Built for Stock. Construction No.
Baldwin Locomotive Works
core  

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

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