Results 101 to 110 of about 1,025,832 (207)
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+17 more
wiley +1 more source
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+11 more
wiley +1 more source
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+19 more
wiley +1 more source
Interplay of integrins and selectins in metastasis
Here we review the role of integrins and their interplay with selectins in metastasis. The efficacy of integrin‐targeted therapies may be reduced in tumors where metastasis relies heavily on selectins. In certain tumors, integrins and selectins exhibit a synergistic interaction during intraperitoneal dissemination.
Diana Maltseva+2 more
wiley +1 more source
Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry
Elevated expression of transcriptional regulator inhibitor of DNA binding 1 (ID1) promoted cancer cell‐mediated vasculogenic mimicry (VM) through regulation of pro‐angiogenic and pro‐cancerous genes (e.g. VE‐cadherin (CDH5), TIE2, MMP9, DKK1). Higher ID1 expression also increased metastases to the lung and the liver.
Emma J. Thompson+11 more
wiley +1 more source
Keratins: Markers of cell differentiation or regulators of cell differentiation?
Deepak Kanojia, Milind M. Vaidya
openaire +3 more sources
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+14 more
wiley +1 more source
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+17 more
wiley +1 more source
Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
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
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
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