Results 101 to 110 of about 2,511 (267)
Resolvable group divisible designs with block size four and general index
In this paper, we investigate the existence of resolvable group divisible designs (RGDDs) with block size four, group-type hn and general index λ. The necessary conditions for the existence of such a design are n≥4, hn≡0(mod4) and λh(n−1)≡0(mod3).
Ge, Gennian, Sun, Xianwei
core +1 more source
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
An analogue of group divisible designs for Moore graphs
AbstractWe study graphs whose adjacency matrix S of order n satisfies the equation S + S2 = J − K + kI, where J is a matrix of order n of all 1's, K is the direct sum on nl matrices of order l of all 1's, and I is the identity matrix. Moore graphs are the only solutions to the equation in the case l = 1 for which K = I.
openaire +2 more sources
On uniform partial group divisible designs with block size three.
Group divisible designs (GDDs) play a crucial role in the development of combinatorial design theory. We know that GDDs require that each pair of points in distinct groups occurs in exactly $\lambda$ blocks.
Zhang, Luchan
core
Divisible designs from twisted dual numbers
The generalized chain geometry over the local ring $K(\epsilon;\sigma)$ of twisted dual numbers, where $K$ is a finite field, is interpreted as a divisible design obtained from an imprimitive group action.
Zanella, Corrado +2 more
core +1 more source
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
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
Many patients with urothelial cancer do not benefit from treatment with pembrolizumab, while at risk of severe side effects. Changes in the levels of circulating tumor DNA early during treatment, measured by a simple and affordable assay that can be easily implemented in the clinic, can be used as a prognostic tool to identify these patients.
Youssra Salhi +14 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
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
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

