Results 151 to 160 of about 409,184 (262)

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

The PI3Kδ inhibitor roginolisib (IOA‐244) preserves T‐cell function and activity

open access: yesMolecular Oncology, EarlyView.
Identification of novel PI3K inhibitors with limited immune‐related adverse effects is highly sought after. We found that roginolisib and idelalisib inhibit chronic lymphocytic leukemia (CLL) cells and Treg suppressive functions to similar extents, but roginolisib affects cytotoxic T‐cell function and promotion of pro‐inflammatory T helper subsets to a
Elise Solli   +7 more
wiley   +1 more source

Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer

open access: yesMolecular Oncology, EarlyView.
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta   +10 more
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin

open access: yesMolecular Oncology, EarlyView.
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon   +4 more
wiley   +1 more source

RaMBat: Accurate identification of medulloblastoma subtypes from diverse data sources with severe batch effects

open access: yesMolecular Oncology, EarlyView.
To integrate multiple transcriptomics data with severe batch effects for identifying MB subtypes, we developed a novel and accurate computational method named RaMBat, which leveraged subtype‐specific gene expression ranking information instead of absolute gene expression levels to address batch effects of diverse data sources.
Mengtao Sun, Jieqiong Wang, Shibiao Wan
wiley   +1 more source

RIPK4 function interferes with melanoma cell adhesion and metastasis

open access: yesMolecular Oncology, EarlyView.
RIPK4 promotes melanoma growth and spread. RIPK4 levels increase as skin lesions progress to melanoma. CRISPR/Cas9‐mediated deletion of RIPK4 causes melanoma cells to form less compact spheroids, reduces their migratory and invasive abilities and limits tumour growth and dissemination in mouse models.
Norbert Wronski   +9 more
wiley   +1 more source

COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells

open access: yesMolecular Oncology, EarlyView.
This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Konstantinos S. Papadakos   +6 more
wiley   +1 more source

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