Results 141 to 150 of about 4,238,851 (307)

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

Molecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou, Niki Tzenaki, Anna Tsapara, Maria Tzardi, Evangelia A. Papakonstanti   +4 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

Profiling neoadjuvant therapy response in rectal cancer using meta‐analysis of publicly available transcriptomic RNA‐seq datasets

Molecular Oncology, EarlyView.
This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic, Rafael Stroggilos, Mladen Marinkovic, Ana Djuric, Suzana Stojanovic‐Rundic, Radmila Jankovic, Sergi Castellvi‐Bel, Remond J.A. Fijneman, Antonia Vlahou, Jerome Zoidakis, Milena Cavic   +10 more
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

Molecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad, Silvio Carlo Ermanno Tosatto, Emanuela Leonardi   +2 more
wiley   +1 more source

Extracellular matrix remodeling and immune reprogramming drive residual tumor progression of liver cancer after incomplete microwave ablation

Molecular Oncology, EarlyView.
Incomplete microwave ablation (iMWA) of liver cancer triggers a biphasic progression in residual tumors. At Day 3, the microenvironment is characterized by acute inflammatory responses and extracellular matrix (ECM) remodeling. By Day 14, a profound shift occurs toward oncogenic signal transduction and immunosuppression, marked by macrophage ...
Yu Liu, Yubei He, Nikolaus Berndt, Michael Mülleder, Kathrin Textoris‐Taube, Jing Guo, Matthias Stechele, Justus Ramtke, Shraga Nahum Goldberg, Lynn Jeanette Savic   +9 more
wiley   +1 more source

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

Molecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso, Md Shohel Ul Islam, Rosa M Xicola, Raj Ramesar, Xavier Llor, Sinclair Steele   +5 more
wiley   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

Molecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim, Aurelie Genoux, Nadiia Zubchuk, Haoyang Zheng, Perla Salameh, Theo Ziegelmeyer, Fabien Dalonneau, Margot Rouchette, Christiane Oddou, Simona Miron, Helene Polveche, Adiilah Mamode Cassim, Carmen Garrido, Eleni Nikolakaki, Didier Auboeuf, Tao Jia, Sophie Zinn‐Justin, Beatrice Eymin   +17 more
wiley   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

Molecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim, Alvin Kunyao Guo, Yoko Itahana, Srinivasaraghavan Kannan, Valerie Goh, Mingmin Ong, Terina Yan Wen Tay, Weiying Ye, Sabhashina Radha Krishnan, Jun Nishiyama, Chandra S Verma, Koji Itahana   +11 more
wiley   +1 more source

Receptors: Binding Assays

, 2014
Leysen, Josee E., Langlois, Xavier, Heylen, Lieve, Lammertsma, Adriaan A.   +3 more
openaire   +4 more sources

Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer

Molecular Oncology, EarlyView.
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba, Mark Shacker, Timothy P. Fleming, Michael A. Smith, Ross M. Bremner, Narendra V. Sankpal   +5 more
wiley   +1 more source