Results 161 to 170 of about 7,450,685 (340)

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

ShcD adaptor protein drives invasion of triple negative breast cancer cells by aberrant activation of EGFR signaling

Molecular Oncology, EarlyView.
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau, Hayley S. Smith, Begüm Alural, Claire E. Martin, Laura A. New, Manali Tilak, Sara L. Banerjee, Hannah N. Robeson, Nicolas Bisson, Anne‐Claude Gingras, Jasmin Lalonde, Nina Jones   +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

Assessment of Glenohumeral Internal Rotation Deficit and Scapula Upward Rotation Differency Within Hungarian NB2Handball Players

Studia Universitatis Babeş-Bolyai: Educatio Artis Gymnasticae
The aim of our cross-sectional study was to assess the rotational range of motion of the shoulder joint and the scapula movement of Hungarian NBII handball players, to find out how many athletes may be affected by a rotational range of motion deficit ...
Máté PINTÉR, Iuliana BOROS-BALINT, Márta HOCK, Melinda JÁROMI, Alexandra MAKAI, Eleonóra LEIDECKER   +5 more
doaj   +1 more source

Weighted Least-Squares PARSIM [PDF]

arXiv
Subspace identification methods (SIMs) have proven very powerful for estimating linear state-space models. To overcome the deficiencies of classical SIMs, a significant number of algorithms has appeared over the last two decades, where most of them involve a common intermediate step, that is to estimate the range space of the extended observability ...
arxiv  

The principal component analysis (PCA) score scatter plot (A) and partial least square-discriminate analysis (PLS-DA) score scatter plot (B) represent significant differences of metabolites between the wild-type (WT) and the cir1 mutant (cir1Δ).

, 2012
Choi Jung Nam, Kim Jeongmi, Jiyoung Kim, Hee Jung Won, Lee Choong Hwan   +4 more
openalex   +1 more source

MET and NF2 alterations confer primary and early resistance to first‐line alectinib treatment in ALK‐positive non‐small‐cell lung cancer

Molecular Oncology, EarlyView.
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu, Ning Ding, Xiaobo Xu, Yedan Chen, Yong Zhang, Jingwen Liu, Jiebai Zhou, Hairong Bao, Donghui Zhang, Yijun Song, Yang Shao, Yuanlin Song   +11 more
wiley   +1 more source

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation

Molecular Oncology, EarlyView.
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani, Gilgi Friedlander, Gili Perry, Nora Balint‐Lahat, Shlomit Gilad, Dana Morzaev‐Sulzbach, Anjana Shenoy, Noa Bossel Ben‐Moshe, Anya Pavlovsky, Rinat Bernstein‐Molho, Eytan Domany, Iris Barshack, Tamar Geiger, Bella Kaufman, Einav Nili Gal‐Yam   +14 more
wiley   +1 more source

Tonic signaling of the B‐cell antigen‐specific receptor is a common functional hallmark in chronic lymphocytic leukemia cell phosphoproteomes at early disease stages

Molecular Oncology, EarlyView.
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez, Pablo Juanes‐Velasco, Marina L. García‐Vaquero, Conrad Droste, Alicia Landeira‐Viñuela, Miguel Alcoceba, Helena Fidalgo‐Gómez, Sara Misiego‐Herrero, Almudena Navarro‐Bailón, Mónica Baile, José M. Bastida, Jose Manuel Sanchez‐Santos, Rafael Góngora, Julia Almeida, Marcos Gonzalez‐Diaz, Alberto Orfao, Javier De Las Rivas, Manuel Fuentes   +17 more
wiley   +1 more source

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

Molecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen, Chung‐Teng Wang, Jia‐Ming Chang, Ai‐Li Shiau, Gia‐Shing Shieh, Yau‐Lin Tseng, Yi‐Ting Yen, Tang‐Hsiu Huang, Li‐Hsin Cheng, Yu‐Chih Wu, Chao‐Liang Wu, Bing‐Hua Su, Pensee Wu   +12 more
wiley   +1 more source