Results 61 to 70 of about 149 (148)

Exploration of heterogeneity and recurrence signatures in hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
This study leveraged public datasets and integrative bioinformatic analysis to dissect malignant cell heterogeneity between relapsed and primary HCC, focusing on intercellular communication, differentiation status, metabolic activity, and transcriptomic profiles.
Wen‐Jing Wu   +15 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

open access: yesMolecular 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   +17 more
wiley   +1 more source

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

open access: yesMolecular 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   +11 more
wiley   +1 more source

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

open access: yesMolecular 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   +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

open access: yesMolecular 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   +19 more
wiley   +1 more source

Interplay of integrins and selectins in metastasis

open access: yesMolecular Oncology, EarlyView.
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

open access: yesMolecular Oncology, EarlyView.
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

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

open access: yesMolecular 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   +11 more
wiley   +1 more source

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

open access: yesMolecular 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   +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

open access: yesMolecular 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   +17 more
wiley   +1 more source

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