Results 51 to 60 of about 3,217,144 (212)

Effective therapeutic targeting of CTNNB1‐mutant hepatoblastoma with WNTinib

Molecular Oncology, EarlyView.
WNTinib, a Wnt/CTNNB1 inhibitor, was tested in hepatoblastoma (HB) experimental models. It delayed tumor growth and improved survival in CTNNB1‐mutant in vivo models. In organoids, WNTinib outperformed cisplatin and showed enhanced efficacy in combination therapy, supporting its potential as a targeted treatment for CTNNB1‐mutated HB.
Ugne Balaseviciute, Júlia Huguet‐Pradell, Jordi Abril‐Fornaguera, Albert Gris‐Oliver, Alex Rialdi, Elisa Fernández‐Martínez, Carla Montironi, Vanessa Del Pozo, Peter Houghton, Laura Zanatto, Agavni Mesropian, Ieva Keraite, Swan Thung, Carolina Armengol, Pau Sancho‐Bru, Ernesto Guccione, Roser Pinyol, Josep M. Llovet   +17 more
wiley   +1 more source

Thanks to reviewers

Perspectives on Medical Education, 2016
None
None
doaj   +1 more source

LINC01116, a hypoxia‐lncRNA marker of pathological lymphangiogenesis and poor prognosis in lung adenocarcinoma

Molecular Oncology, EarlyView.
The LINC01116 long noncoding RNA is induced by hypoxia and associated with poor prognosis and high recurrence rates in two cohorts of lung adenocarcinoma patients. Here, we demonstrate that besides its expression in cancer cells, LINC01116 is markedly expressed in lymphatic endothelial cells of the tumor stroma in which it participates in hypoxia ...
Marine Gautier‐Isola, Rafael Lopes Goncalves, Marin Truchi, Caroline Lacoux, Célia Scribe, Hugo Cadis, Laetitia Guardini, Sophie Bekisz, Marius Ilié, Paul Hofman, Georges Vassaux, Bernard Mari, Roger Rezzonico   +12 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source

Crucial parameters for precise copy number variation detection in formalin‐fixed paraffin‐embedded solid cancer samples

Molecular Oncology, EarlyView.
This study shows that copy number variations (CNVs) can be reliably detected in formalin‐fixed paraffin‐embedded (FFPE) solid cancer samples using ultra‐low‐pass whole‐genome sequencing, provided that key (pre)‐analytical parameters are optimized.
Hanne Goris, Vasiliki Siozopoulou, Léon C van Kempen, Anne Sieben, Ella Roelant, Stig Hellemans, Elyne Backx, Laure Sorber, Koen De Winne, Senada Koljenović, Karen Zwaenepoel   +10 more
wiley   +1 more source

Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer

Molecular Oncology, EarlyView.
Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity.
Carolin Salmon, Rui P. L. Neves, Nikolas H. Stoecklein, Sven‐Thorsten Liffers, Jens Siveke, Jan D. Kuhlmann, Pauline Wimberger, Paul Buderath, Rainer Kimmig, Sabine Kasimir‐Bauer   +9 more
wiley   +1 more source

Tumor mutational burden as a determinant of metastatic dissemination patterns

Molecular Oncology, EarlyView.
This study performed a comprehensive analysis of genomic data to elucidate whether metastasis in certain organs share genetic characteristics regardless of cancer type. No robust mutational patterns were identified across different metastatic locations and cancer types.
Eduardo Candeal, Andrea Moreno‐Manuel, Miguel Salvadó‐Pertierra, Cristina Santos‐Vivas, Rebeca Sanz‐Pamplona   +4 more
wiley   +1 more source

The PI3Kδ inhibitor roginolisib (IOA‐244) preserves T‐cell function and activity

Molecular Oncology, EarlyView.
Identification of novel PI3K inhibitors with limited immune‐related adverse effects is highly sought after. We found that roginolisib and idelalisib inhibit chronic lymphocytic leukemia (CLL) cells and Treg suppressive functions to similar extents, but roginolisib affects cytotoxic T‐cell function and promotion of pro‐inflammatory T helper subsets to a
Elise Solli, Alessio Bevilacqua, Mathias Wenes, Denis Migliorini, Lars van der Veen, Sigrid S Skånland, Giusy Di Conza, Kjetil Taskén   +7 more
wiley   +1 more source

Targeting p38α in cancer: challenges, opportunities, and emerging strategies

Molecular Oncology, EarlyView.
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley   +1 more source

Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer

Molecular Oncology, EarlyView.
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta, Yang Song, Madeleine Ndahayo, Anirudh Saxena, Theresa Guo, Dylan Z. Kelley, Jessica Gore, Andrew Hennigan, Alexa Anderson, John C. Papadimitriou, Daria A. Gaykalova   +10 more
wiley   +1 more source