Results 101 to 110 of about 1,205,260 (264)

Engineered extracellular vesicles enriched with the miR‐214/199a cluster enhance the efficacy of chemotherapy in ovarian cancer

Molecular Oncology, EarlyView.
Loss of the miR‐214/199a cluster is associated with recurrence in ovarian cancer. Engineered small extracellular vesicles (m214‐sEVs) elevate miR‐214‐3p/miR‐199a‐5p in tumor cells, suppress β‐catenin, TLR4, and YKT6 signaling, reprogram tumor‐derived sEV cargo, reduce chemoresistance and migration, and enhance carboplatin efficacy and survival in ...
Weida Wang, Ayesha Alvero, Yi Qin, Mingjin Wang, Alexandra Fox, Yanfeng Li, Michael Millman, Amy Kemper, Gil Mor, Xian Shuang Liu, Michael Chopp, Zheng Gang Zhang, Yi Zhang   +12 more
wiley   +1 more source

Keratin 19 as a prognostic marker and contributing factor of metastasis and chemoresistance in high‐grade serous ovarian cancer

Molecular Oncology, EarlyView.
Keratin 19 (KRT19) is overexpressed in high‐grade serous ovarian cancer with high levels of Kallikrein‐related peptidases (KLK) 4–7 and is associated with poor survival. In vivo analyses demonstrate that elevated KRT19 increases peritoneal tumour burden.
Sophia Bielesch, Isabel Vogel, Sina Nokodian, Johanna Moeller, Antonia Blechschmidt, Vicky Hecht, Vanessa Kuentzel, Katharina Thiedig, Melissa Schwab, Oliver Schilling, Holger Bronger, Marion Kiechle, Viktor Magdolen, Tobias Dreyer   +13 more
wiley   +1 more source

Establishment of a humanized patient‐derived xenograft mouse model of high‐grade serous ovarian cancer for preclinical evaluation of combination immunotherapy

Molecular Oncology, EarlyView.
We have established a humanized orthotopic patient‐derived xenograft (Hu‐oPDX) mouse model of high‐grade serous ovarian cancer (HGSOC) that recapitulates human tumor–immune interactions. Using combined anti‐PD‐L1/anti‐CD73 immunotherapy, we demonstrate the model's improved biological relevance and enhanced translational value for preclinical ...
Luka Tandaric, Line Bjørge, Martine Rott Lode, Cecilie Fredvik Torkildsen, Pia Aehnlich, Rammah Elnour, Daniela Elena Costea, Lars Andreas Akslen, Liv Cecilie Vestrheim Thomsen, Emmet McCormack, Katrin Kleinmanns   +10 more
wiley   +1 more source

Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation

Molecular Oncology, EarlyView.
Pancreatic sensory neurons innervating healthy and PDAC tissue were retrogradely labeled and profiled by single‐cell RNA sequencing. Tumor‐associated innervation showed a dominant neurofilament‐positive subtype, altered mitochondrial gene signatures, and reduced non‐peptidergic neurons.
Elena Genova, Michele Montrone, Uday Rangaswamy, Francesco Diversi, Irene Schiavo, Denise Ferrarini, Roberta Di Florio, Irene Longo, Michele Coscia, Nicola Zamboni, Giorgia Demontis, Lisa Veghini, Vincenzo Corbo, Remo Sanges, Paul Heppenstall   +14 more
wiley   +1 more source

Differential expression of cancer‐related genes supports prediction of poor response to first‐line treatments in T‐ALL pediatric patients with high minimal residual disease

Molecular Oncology, EarlyView.
In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera, Laura Vela‐Martín, Pablo Fernández‐Navarro, José Luis López‐Lorenzo, Javier Cornago, Pilar Llamas, Eduardo Pérez‐Gómez, José Luis Marín‐Rubio, Manuel Fresno, Javier Santos, José Fernández‐Piqueras, María Villa‐Morales   +11 more
wiley   +1 more source

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

Molecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh, Nitzan Medina‐Itzhaki, Milena Chekov, Eden Gal‐Swisa, Roba Gabesh‐Wahabi, Inbar Savyon, Inna Naroditsky, Hilary A. Kenny, Basem Fares, Lina Korsensky, Einav Girsh, Liron Berger, Ruth Perets   +12 more
wiley   +1 more source

Prolegomena to any future e-publishing model [PDF]

, 1999
Considers why, after nearly twenty years of development, the electronic publishing model has not replaced the paper based model for academic journals. Gives three insights that attempt to explain this: the first is the ‘means-end’ confusion of commercial publishers, the second is the failure to realise it is the purpose not the form that is important ...
openaire   +1 more source

ANALYZING THE IMPACT OF E-PUBLISHING ON LIBRARIES

The advent of e-publishing has dramatically transformed the landscape of libraries worldwide. This paper examines the multifaceted impact of e-publishing on libraries, exploring both the challenges and opportunities it presents. By analyzing changes in acquisition strategies, access models, user behavior, and the role of librarians, this study provides
Abdumuminova, Gulchekhrakhon, Sindarov, Jurabek, Ahmadjanov, Azizbek, Hafizov, Shukrullo   +3 more
openaire   +2 more sources

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

Molecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan, Veronika M Metzler, Simone de Brot, Corinne L Woodcock, Anna E Harris, Jennifer Lothion‐Roy, Emeli M Nilsson, Atara Ntekim, Michael S Toss, Jenny L Persson, Francesca Khani, Brian D Robinson, Lorraine J Gudas, Emad Rakha, David M Heery, Catrin S Rutland, Nigel P Mongan   +16 more
wiley   +1 more source

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