Results 71 to 80 of about 25,789 (213)

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

DELINEATION OF BOUNDARY CONTOURS OF MINERAL RAW MATERIALS WITHIN THE DEPOSIT SPACE CONSIDERING THE QUALITY

Rudarsko-geološko-naftni Zbornik, 1990
On the basis of performed explorations, in the phase of deposit preparation and development for exploitation the obtained results regarding the raw material quality were transfered to the surface.
Ivan Tomašić
doaj  

Attitudes toward Redistributive Policy: An Introduction

Societies, 2019
We provide an overview of the field of preferences for redistribution research, including divergent terminological and theoretical approaches. We review the different uses of public attitudes, policy preferences and public opinion.
Liza G. Steele, Nate Breznau
doaj   +1 more source

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

Molecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak, Iva Staniczková Zambo, Matěj Přikryl, Peter Múdry, Danica Zapletalová, Jarmila Navrátilová, Jiří Navrátil, Jan Šmarda, Liudmyla Drobot, Petr Beneš, Lucia Knopfová   +10 more
wiley   +1 more source

Longitudinal circulating tumor DNA profiling in patients with advanced endometrial cancer using an off‐the‐shelf targeted NGS panel

Molecular Oncology, EarlyView.
Intratumour heterogeneity complicates precision management of advanced endometrial cancer. Circulating tumor DNA (ctDNA) offers a minimally invasive strategy to capture tumor evolution and therapeutic resistance. Here, we compare tumor‐agnostic NGS with tumor‐informed ddPCR, outlining their relative sensitivity, concordance, and clinical implications ...
Carlos Casas‐Arozamena, Karin Teien Lande, Eva Diaz, Ana Vilar, Juan Cueva, Efigenia Arias, Victoria Sampayo, Alicia Abalo, Nerea González, Eva Colás, Antonio Gil‐Moreno, Miguel Abal, Gema Moreno‐Bueno, Therese Sørlie, Kristina Lindemann, Laura Muinelo‐Romay   +15 more
wiley   +1 more source

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

Molecular 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, Athina Markou, Eleonora Nicolo, Mara S Serafini, Qiang Zhang, Youbin Zhang, Lorenzo Gerratana, Andrew A. Davis, Huiping Liu, William J Gradishar, Carolina Reduzzi, Massimo Cristofanilli, Evi Lianidou   +12 more
wiley   +1 more source

Interpreting the effects of DNA polymerase variants at the structural level

Molecular Oncology, EarlyView.
Using MAVISp and molecular dynamics simulations, we analyzed over 60 000 missense variants in POLE and POLD1 from ClinVar, COSMIC, cBioPortal, and saturation mutagenesis. Identified mechanistic indicators, including stability, binding, and long‐range, enable structural interpretation, providing ACMG‐like evidence for possible reclassification of VUS ...
Matteo Arnaudi, Karolina Krzesińska, Ludovica Beltrame, Pablo Sánchez‐Izquierdo Besora, Matteo Tiberti, Mef Nilbert, Anna Rohlin, Elena Papaleo   +7 more
wiley   +1 more source

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

Molecular 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, Koji Ando, Hirofumi Hasuda, Koshi Mimori, Elizabeth C. Unan, Siddhartha Pulukuri, Aahana Tiku, Allison Berger, Eiji Oki, Ajit Bharti, Tomoharu Yoshizumi   +10 more
wiley   +1 more source

DNA methylation and expression of MAPRE3 affect overall survival of early‐stage non‐small cell lung cancer patients

Molecular Oncology, EarlyView.
Both cg12821679MAPRE3 methylation and MAPRE3 expression are significantly associated with overall survival (OS) of non‐small cell lung cancer. Meanwhile, MAPRE3 expression significantly modified the effect of smoking cessation on OS. Smoking cessation benefits OS merely for patients with high MAPRE3 expression.
Chao Chen, Jiancheng Cheng, Ruili Hou, Xiaoyuan Zheng, Li Su, Maria Moksnes Bjaanæs, Anna Karlsson, Maria Planck, Johan Staaf, Åslaug Helland, Manel Esteller, David C. Christiani, Feng Chen, Xiaofei Cao, Ruyang Zhang   +14 more
wiley   +1 more source

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

Molecular 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, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source