Results 61 to 70 of about 285,764 (313)

ESR1 methylation and ESR1 mutations in circulating tumor cells (CTCs) and paired plasma‐cfDNA of advanced breast cancer patients: A feasibility proof‐of‐concept study

open access: yesMolecular Oncology, EarlyView.
Circulating tumor cells (CTCs) and plasma cell‐free DNA (cfDNA) were analyzed to detect ESR1 mutations and methylation in patients with advanced breast cancer. CTC‐derived DNA showed higher sensitivity for mutation detection and revealed complementary genetic and epigenetic alterations, highlighting the added value of CTC analysis for understanding ...
Dimitra Stergiopoulou   +12 more
wiley   +1 more source

The impact of public basic research on industrial innovation: Evidence from the pharmaceutical industry [PDF]

open access: yes
While most economists believe that public scientific research fuels industry innovation and economic growth, systematic evidence supporting this relationship is surprisingly limited. In a recent study, Acemoglu and Linn (2004) identified market size as a
Toole, Andrew A.
core  

Política farmacéutica saludable Healthy pharmaceutical policy

open access: yesSalud Pública de México, 2008
Hoy en día, la industria farmacéutica se encuentra en una transición profunda. La globalización y el avance tecnológico representan las principales presiones de cambio para un mercado mundial de medicamentos donde a este tipo de industria le resulta cada
Eduardo González Pier
doaj  

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

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

Advancements and future prospective of DNA barcodes in the herbal drug industry. [PDF]

open access: yesFront Pharmacol, 2022
Mahima K   +5 more
europepmc   +1 more source

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

A Breath of Fresh Air? Firm types, scale, scope and selection effects in drug development [PDF]

open access: yes
This paper measures differences in the innovation performance of different types of firms in the pharmaceutical industry. We compare the innovation performance of incumbent firms with entrants, controlling for differences in the scale and scope of ...
Gambardella, Alfonso   +3 more
core   +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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