Results 51 to 60 of about 81,406 (283)

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

Molecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni, Antonella Palmese, Stefano Scalera, Laura Cipriani, Davide Mascolo, Patrizia Vici, Teresa Arcuri, Lorena Filomeno, Eriseld Krasniqi, Giovanni Blandino, Giulia Bon, Marcello Maugeri‐Saccà   +11 more
wiley   +1 more source

Age-related mutational signature negatively associated with immune activity and survival outcome in triple-negative breast cancer

OncoImmunology, 2020
Triple-negative breast cancer (TNBC) is characterized by broad genomic and transcriptional heterogeneity and results in a worse prognosis than other breast cancer types.
Hao Chen, Wei Chong, Xiaorong Yang, Yuan Zhang, Shaowei Sang, Xiangchun Li, Ming Lu   +6 more
doaj   +1 more source

Phase I dose-escalation trial of the oral AKT inhibitor uprosertib in combination with the oral MEK1/MEK2 inhibitor trametinib in patients with solid tumors. [PDF]

, 2020
PurposeThis study aimed to determine the safety, tolerability, and recommended phase II doses of trametinib plus uprosertib (GSK2141795) in patients with solid tumors likely to be sensitive to MEK and/or AKT inhibition.MethodsThis was a phase I, open ...
Becerra, Carlos, D'Amelio, Anthony M, Ellis, Catherine, Gauvin, Jennifer, Gonzalez, Rene, Heist, Rebecca S, Ibrahim, Nageatte, Kalyana-Sundaram, Shanker, Kleha, Joseph F, Kurzrock, Razelle, Leonowens, Cathrine, Means-Powell, Julie, Tan, Antoinette R, Tolcher, Anthony W, Valero, Vincente, Wang, Chenxi, Werner, Theresa L, Yan, Li   +17 more
core  

Blockade of insulin-like growth factors increases efficacy of paclitaxel in metastatic breast cancer. [PDF]

, 2017
Breast cancer remains the leading cause of cancer death in women owing to metastasis and the development of resistance to established therapies. Macrophages are the most abundant immune cells in the breast tumor microenvironment and can both inhibit and ...
A Fantozzi, A Sica, Ainhoa Mielgo, Almudena Santos, B Ruffell, B Weigelt, BA Pulaski, BP Schneider, BZ Qian, C Marquette, Carlos Figueiredo, CD Mills, CJ Aslakson, CT Guy, CX Ma, D Ohlund, Dean Hammond, DF Quail, DF Quail, DG DeNardo, DH Fagan, DL Dexter, EA Rakha, EM Fox, EY Lin, F Klemm, Fiona Campbell, HA Wahba, JB Wyckoff, JE Maglione, JFR Robertson, JL Gooch, K Friedbichler, KA Lodhia, KM Bussard, KR Bauer, L Bingle, L Ireland, Lesley G. Ellies, Lucy Ireland, M Augsten, M Guha, M Pollak, MC Schmid, Michael Schmid, MJ Campbell, OC Olson, PJ Murray, RD Leek, RL Jones, RL Siegel, S Massarweh, SA Davie, SK Denduluri, SM Farabaugh, SR Nielsen, T Shree, TD Schmittgen, Thomas Bogenrieder, Ulrike Weyer-Czernilofsky, V Bronte, WJ Gradishar, XHF Zhang, Y Mao, YH Lu, YH Zhang, YW Wan   +66 more
core   +2 more sources

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

Molecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen, Kristiane Søreng, Chiara Veroni, Laura Trachsel‐Moncho, Nagham Asp, Robin Gaupset, Lars Gustav Lyckander, Helene Knævelsrud, Lars Eftang, Anne Simonsen   +9 more
wiley   +1 more source

Targeting TNBC: core–shell polycationic polyurea dendrimers with inherent anticancer activity

FEBS Open Bio, EarlyView.
Core–shell polycationic PURE dendrimers were tested in TNBC‐derived tumor models. Both formulations selectively targeted TNBC and effectively reduced tumor volume. PUREG4‐OEI48 suppressed tumor growth without detectable toxicity, whereas PUREG4‐OCEI24, despite showing efficacy, induced hepatic toxicity.
Adriana Cruz, Bruna Abreu, Cindy Mendes, Catarina Freitas‐Dias, Filipe Gonçalves, Fernanda Silva, José Ramalho, Saudade André, Vasco D. B. Bonifácio, Jacinta Serpa   +9 more
wiley   +1 more source

Concomitant activation of GLI1 and Notch1 contributes to racial disparity of human triple negative breast cancer progression

eLife, 2021
Mortality from triple negative breast cancer (TNBC) is significantly higher in African American (AA) women compared to White American (WA) women emphasizing ethnicity as a major risk factor; however, the molecular determinants that drive aggressive ...
Sumit Siddharth, Sheetal Parida, Nethaji Muniraj, Shawn Hercules, David Lim, Arumugam Nagalingam, Chenguang Wang, Balazs Gyorffy, Juliet M Daniel, Dipali Sharma   +9 more
doaj   +1 more source

RORγ is a targetable master regulator of cholesterol biosynthesis in a cancer subtype. [PDF]

, 2019
Tumor subtype-specific metabolic reprogrammers could serve as targets of therapeutic intervention. Here we show that triple-negative breast cancer (TNBC) exhibits a hyper-activated cholesterol-biosynthesis program that is strongly linked to nuclear ...
Bold, Richard J, Borowsky, Alexander D, Cai, Demin, Chen, Hong-Wu, Chen, Xinbin, Evans, Ronald M, Fiehn, Oliver, Gao, Bei, Huang, Zenghong, Jiang, Yuqian, Kung, Hsing-Jien, Lam, Kit S, Lara, Primo N, Li, Jian Jian, Li, Jin, To, Ka-Fai, Wang, Junjian, Wu, Feng, Xu, Jianzhen, Zhao, Ruqian, Zou, Hongye, Zou, June X   +21 more
core  

Bursts of Chromosome Changes Drive TNBC [PDF]

Cancer Discovery, 2016
Abstract A recent study suggests that complex genomic rearrangements in triple-negative breast cancer cells occur through a “Big Bang” model—early, short bursts of copy number aberrations, rather than progressive accumulation over time.
openaire   +2 more sources

Common Signatures of Altered Gene Regulation and Invasiveness of Different Breast Cancer Cell Lines after Matrix Interface Crossing

Advanced Healthcare Materials, EarlyView.
Interface transmigration reprograms triple‐negative breast cancer cells, triggering a shared switch toward more aggressive and invasive phenotypes. Using a collagen I interface model, this study identifies shared transcriptional changes involving proliferation, chromatin remodeling, and DNA repair pathways.
Cornelia Clemens, Hannah Trampert, Nataliia Kotsiuba, Tilo Pompe   +3 more
wiley   +1 more source