Results 151 to 160 of about 11,944 (302)

Computing Subgroups by Exhibition in Finite Solvable Groups

open access: yes, 2008
We present practical algorithms to compute subgroups such as Hall systems, system normalizers, F-normalizers and F-covering subgroups in finite solvable groups.
Bettina Eick, Charles R. B. Wright
core  

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

Broken ergodicity in driven one-dimensional particle systems with short-range interaction

open access: yes, 2006
We present a one-dimensional nonequilibrium model for a driven di usive system which has local interactions and slow nonconservative reaction kinetics.
Schütz, G. M., Rákos, Attila Gábor
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

Interpretation of a General Model for Inventive Problems, the Generalized System of Contradictions [PDF]

open access: yes, 2009
Organised by: Cranfield UniversityDesign of technical systems implies either optimisation or inventive problems resolution. Resolution tools and methods exist for each kind of problems.
Dubois, S., De Guio, R., Rasovska, I.
core  

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

First-order product-type systems of difference equations solvable in closed form

open access: yesElectronic Journal of Differential Equations, 2015
We show that the first-order system of difference equations $$ z_{n+1}=\alpha z_n^aw_n^b,\quad w_{n+1}=\beta z_n^cw_n^d,\quad n\in\mathbb{N}_0, $$ where $a,b,c,d\in\mathbb{Z}$, $\alpha,\beta \in\mathbb{C}\setminus\{0\}$, $z_0, w_0\in\mathbb{C ...
Stevo Stevic
doaj  

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

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