Results 81 to 90 of about 1,169,770 (361)

Inhibition of focal adhesion kinase overcomes resistance of mantle cell lymphoma to ibrutinib in the bone marrow microenvironment

open access: yesHaematologica, 2018
Mantle cell lymphoma and other lymphoma subtypes often spread to the bone marrow, and stromal interactions mediated by focal adhesion kinase frequently enhance survival and drug resistance of the lymphoma cells. To study the role of focal adhesion kinase
Martina Rudelius   +7 more
doaj   +1 more source

BMP antagonist CHRDL2 enhances the cancer stem‐cell phenotype and increases chemotherapy resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Overexpression of CHRDL2 in colon cancer cells makes them more stem‐like and resistant to chemo‐ and radiotherapy. CHRDL2‐high cells have upregulation of the WNT pathway, genes involved in the DNA damage response (DDR) pathway and epithelial‐to‐mesenchymal transition (EMT). This leads to quicker repair of damaged DNA and more cell migration.
Eloise Clarkson, Annabelle Lewis
wiley   +1 more source

Vascular Endothelial Growth Factor Expression of Intercellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1 (VCAM-1), and E-selectin through Nuclear Factor-κB Activation in Endothelial Cells*

open access: yesJournal of Biological Chemistry, 2001
Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion ...
Injune Kim   +5 more
semanticscholar   +1 more source

EMT‐associated bias in the Parsortix® system observed with pancreatic cancer cell lines

open access: yesMolecular Oncology, EarlyView.
The Parsortix® system was tested for CTC enrichment using pancreatic cancer cell lines with different EMT phenotypes. Spike‐in experiments showed lower recovery of mesenchymal‐like cells. This was confirmed with an EMT‐inducible breast cancer cell line.
Nele Vandenbussche   +8 more
wiley   +1 more source

Integrative miRNOMe profiling reveals the miR‐195‐5p–CHEK1 axis and its impact on luminal breast cancer outcomes

open access: yesMolecular Oncology, EarlyView.
In luminal (ER+) breast carcinoma (BC), miRNA profiling identified miR‐195‐5p as a key regulator of proliferation that targets CHEK1, CDC25A, and CCNE1. High CHEK1 expression correlates with worse relapse‐free survival after chemotherapy, especially in patients with luminal A subtype.
Veronika Boušková   +14 more
wiley   +1 more source

Anti-Epithelial Cell Adhesion Molecule Antibodies and the Detection of Circulating Normal-Like Breast Tumor Cells

open access: yesJournal of the National Cancer Institute, 2009
Identification of specific subtypes of circulating tumor cells in peripheral blood of cancer patients can provide information about the biology of metastasis and improve patient management.
A. Sieuwerts   +9 more
semanticscholar   +1 more source

Association of high‐dose radioactive iodine therapy with PPM1D‐mutated clonal hematopoiesis in older individuals

open access: yesMolecular Oncology, EarlyView.
In thyroid cancer patients, high‐dose (≥7.4 GBq) radioactive iodine therapy (RAIT) was associated with a higher prevalence of clonal hematopoiesis (variant allele frequency >2%) in individuals aged ≥50 years (OR = 2.44). In silico analyses showed that truncating PPM1D mutations conferred a selective advantage under these conditions.
Jaeryuk Kim   +11 more
wiley   +1 more source

Chimeric diphtheria toxin–CCL8 cytotoxic peptide for breast cancer management

open access: yesMolecular Oncology, EarlyView.
DTCCL8 is a recombinant fusion toxin that targets cancer cells expressing chemokine receptors. By combining diphtheria toxin with CCL8, DTCCL8 binds to multiple receptors on tumor cells and induces selective cytotoxicity. This strategy enables receptor‐mediated targeting of cancer and may support the development of chemokine‐guided therapeutics ...
Bernardo Chavez   +5 more
wiley   +1 more source

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