Results 31 to 40 of about 1,791,803 (246)

Targeting the MDM2‐MDM4 interaction interface reveals an otherwise therapeutically active wild‐type p53 in colorectal cancer

Molecular Oncology, EarlyView.
This study investigates an alternative approach to reactivating the oncosuppressor p53 in cancer. A short peptide targeting the association of the two p53 inhibitors, MDM2 and MDM4, induces an otherwise therapeutically active p53 with unique features that promote cell death and potentially reduce toxicity towards proliferating nontumor cells.
Sonia Valentini, Giada Mele, Marika Attili, Maria Rita Assenza, Fulvio Saccoccia, Francesca Sardina, Cinzia Rinaldo, Roberto Massari, Nicola Tirelli, Alfredo Pontecorvi, Fabiola Moretti   +10 more
wiley   +1 more source

Thermal proteome profiling and proteome analysis using high‐definition mass spectrometry demonstrate modulation of cholesterol biosynthesis by next‐generation galeterone analog VNPP433‐3β in castration‐resistant prostate cancer

Molecular Oncology, EarlyView.
Elevated level of cholesterol is positively correlated to prostate cancer development and disease severity. Cholesterol‐lowering drugs, such as statins, are demonstrated to inhibit prostate cancer. VNPP433‐3β interrupts multiple signaling and metabolic pathways, including cholesterol biosynthesis, AR‐mediated transcription of several oncogenes, mRNA 5′
Retheesh S. Thankan, Elizabeth Thomas, Mehari M. Weldemariam, Puranik Purushottamachar, Weiliang Huang, Maureen A. Kane, Yuji Zhang, Nicholas Ambulos, Bi‐Dar Wang, David Weber, Vincent C. O. Njar   +10 more
wiley   +1 more source

The atypical KRASQ22K mutation directs TGF‐β response towards partial epithelial‐to‐mesenchymal transition in patient‐derived colorectal cancer tumoroids

Molecular Oncology, EarlyView.
TGF‐β has a complex role in cancer, exhibiting both tumor‐suppressive and tumor‐promoting properties. Using a series of differentiated tumoroids, derived from different stages and mutational background of colorectal cancer patients, we replicate this duality of TGF‐β in vitro. Notably, the atypical but highly aggressive KRASQ22K mutation rendered early‐
Theresia Mair, Philip König, Milena Mijović, Jessica Kalla, Anil Baskan, Loan Tran, Kristina Draganić, Pedro Morata Saldaña, Carlos Uziel Pérez Malla, Janette Pfneissl, Andreas Tiefenbacher, Julijan Kabiljo, Velina S. Atanasova, Lisa Wozelka‐Oltjan, Leonhard Müllauer, Michael Bergmann, Raheleh Sheibani‐Tezerji, Gerda Egger   +17 more
wiley   +1 more source

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

Targeting the AKT/mTOR pathway attenuates the metastatic potential of colorectal carcinoma circulating tumor cells in a murine xenotransplantation model

Molecular Oncology, EarlyView.
Dual targeting of AKT and mTOR using MK2206 and RAD001 reduces tumor burden in an intracardiac colon cancer circulating tumor cell xenotransplantation model. Analysis of AKT isoform‐specific knockdowns in CTC‐MCC‐41 reveals differentially regulated proteins and phospho‐proteins by liquid chromatography coupled mass spectrometry. Circulating tumor cells
Daniel J. Smit, Thais Pereira‐Veiga, Helena Brauer, Michael Horn, Paula Nissen, Thomas Mair, Bente Siebels, Hannah Voß, Ruimeng Zhuang, Marie‐Therese Haider, Desiree Loreth, Margarita Iskhakova, Bele Lindemann, Julian Kött, Laure Cayrefourcq, Jasmin Wellbrock, Hartmut Schlüter, Klaus Pantel, Catherine Alix‐Panabières, Manfred Jücker   +19 more
wiley   +1 more source

Ubiquitination of transcription factors in cancer: unveiling therapeutic potential

Molecular Oncology, EarlyView.
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley   +1 more source

Viral and nonviral delivery systems for gene delivery

Advanced Biomedical Research, 2012
Gene therapy is the process of introducing foreign genomic materials into host cells to elicit a therapeutic benefit. Although initially the main focus of gene therapy was on special genetic disorders, now diverse diseases with different patterns of inheritance and acquired diseases are targets of gene therapy.
Talebi Maedeh, Nouri Nayerossadat, Palizban Abas Ali   +2 more
openaire   +4 more sources

Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?

Molecular Oncology, EarlyView.
Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley   +1 more source

Scheduled delivery [PDF]

Nature Reviews Cancer, 2012
Data from patients with non-small-cell lung cancer (NSCLC) indicate that angiogenesis inhibitors may not increase the delivery of chemotherapy.
openaire   +3 more sources

Loss of proton‐sensing GPR4 reduces tumor progression in mouse models of colon cancer

Molecular Oncology, EarlyView.
G protein‐coupled receptor 4 (GPR4) is a pH‐sensing receptor activated by acidic pH. GPR4 expression is increased in patients with inflammatory bowel disease who are at high risk of developing colorectal cancer. In mouse models, loss of GPR4 attenuated tumor progression. This correlated with increased IL2 and natural killer cell activity.
Leonie Perren, Moana Busch, Pedro A. Ruiz, Ermanno Malagola, Valeria Baumeler, Federica Foti, Adelina Gross, Tobias Grütter, Hendrik Edel, Cordelia Schuler, Kristina Handler, Glenn De Lange, Isabelle C. Arnold, Cheryl de Vallière, Klaus Seuwen, Martin Hausmann, Gerhard Rogler   +16 more
wiley   +1 more source