about
Discovery and validation of an INflammatory PROtein-driven GAstric cancer Signature (INPROGAS) using antibody microarray-based oncoproteomicsBRCA1 haploinsufficiency cell-autonomously activates RANKL expression and generates denosumab-responsive breast cancer-initiating cells.An improved axillary staging system using the OSNA assay does not modify the therapeutic management of breast cancer patients.Interferon/STAT1 and neuregulin signaling pathways are exploratory biomarkers of cetuximab (Erbitux®) efficacy in KRAS wild-type squamous carcinomas: a pathway-based analysis of whole human-genome microarray data from cetuximab-adapted tumor cell-liCirculating fatty acid synthase: an exploratory biomarker to predict efficacy of the dual HER1/HER2 tyrosine kinase inhibitor lapatinibMetformin and the ATM DNA damage response (DDR): accelerating the onset of stress-induced senescence to boost protection against cancerCytokeratin 5/6 fingerprinting in HER2-positive tumors identifies a poor prognosis and trastuzumab-resistant basal-HER2 subtype of breast cancer.Metformin: multi-faceted protection against cancer.Metformin-induced preferential killing of breast cancer initiating CD44+CD24-/low cells is sufficient to overcome primary resistance to trastuzumab in HER2+ human breast cancer xenografts.Metabolomic fingerprint reveals that metformin impairs one-carbon metabolism in a manner similar to the antifolate class of chemotherapy drugs.Epithelial-to-mesenchymal transition (EMT) confers primary resistance to trastuzumab (Herceptin).Metformin limits the tumourigenicity of iPS cells without affecting their pluripotency.Cancer stem cell-driven efficacy of trastuzumab (Herceptin): towards a reclassification of clinically HER2-positive breast carcinomas.Anti-protozoal and anti-bacterial antibiotics that inhibit protein synthesis kill cancer subtypes enriched for stem cell-like properties.Autophagy-related gene 12 (ATG12) is a novel determinant of primary resistance to HER2-targeted therapies: utility of transcriptome analysis of the autophagy interactome to guide breast cancer treatment.Repositioning chloroquine and metformin to eliminate cancer stem cell traits in pre-malignant lesions.Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivoThe anti-malarial chloroquine overcomes primary resistance and restores sensitivity to trastuzumab in HER2-positive breast cancerDietary restriction-resistant human tumors harboring the PIK3CA-activating mutation H1047R are sensitive to metforminMetformin and cancer: Quo vadis et cui bono?Metformin and cancer: doses, mechanisms and the dandelion and hormetic phenomena.Activation of AMP-activated protein kinase (AMPK) provides a metabolic barrier to reprogramming somatic cells into stem cells.IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations.Silibinin meglumine, a water-soluble form of milk thistle silymarin, is an orally active anti-cancer agent that impedes the epithelial-to-mesenchymal transition (EMT) in EGFR-mutant non-small-cell lung carcinoma cells.Acquired resistance to metformin in breast cancer cells triggers transcriptome reprogramming toward a degradome-related metastatic stem-like profile.Metformin rescues cell surface major histocompatibility complex class I (MHC-I) deficiency caused by oncogenic transformation.Autophagy positively regulates the CD44(+) CD24(-/low) breast cancer stem-like phenotype.Micro(mi)RNA expression profile of breast cancer epithelial cells treated with the anti-diabetic drug metformin: induction of the tumor suppressor miRNA let-7a and suppression of the TGFβ-induced oncomiR miRNA-181a.Evolution of the predictive markers amphiregulin and epiregulin mRNAs during long-term cetuximab treatment of KRAS wild-type tumor cells.The anti-diabetic drug metformin suppresses the metastasis-associated protein CD24 in MDA-MB-468 triple-negative breast cancer cells.Stem cell property epithelial-to-mesenchymal transition is a core transcriptional network for predicting cetuximab (Erbitux™) efficacy in KRAS wild-type tumor cells.Metformin regulates breast cancer stem cell ontogeny by transcriptional regulation of the epithelial-mesenchymal transition (EMT) status.Lapatinib, a dual HER1/HER2 tyrosine kinase inhibitor, augments basal cleavage of HER2 extracellular domain (ECD) to inhibit HER2-driven cancer cell growth.Dynamic emergence of the mesenchymal CD44(pos)CD24(neg/low) phenotype in HER2-gene amplified breast cancer cells with de novo resistance to trastuzumab (Herceptin).The anti-diabetic drug metformin suppresses self-renewal and proliferation of trastuzumab-resistant tumor-initiating breast cancer stem cells.The Warburg effect version 2.0: metabolic reprogramming of cancer stem cells.Stem cell-like ALDH(bright) cellular states in EGFR-mutant non-small cell lung cancer: a novel mechanism of acquired resistance to erlotinib targetable with the natural polyphenol silibinin.Synthetic lethal interaction of cetuximab with MEK1/2 inhibition in NRAS-mutant metastatic colorectal cancer.Metformin inhibits RANKL and sensitizes cancer stem cells to denosumab.If mammalian target of metformin indirectly is mammalian target of rapamycin, then the insulin-like growth factor-1 receptor axis will audit the efficacy of metformin in cancer clinical trials.
P50
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P50
name
Begoña Martin-Castillo
@ast
Begoña Martin-Castillo
@en
Begoña Martin-Castillo
@nl
type
label
Begoña Martin-Castillo
@ast
Begoña Martin-Castillo
@en
Begoña Martin-Castillo
@nl
prefLabel
Begoña Martin-Castillo
@ast
Begoña Martin-Castillo
@en
Begoña Martin-Castillo
@nl