0000000000931184

AUTHOR

Pablo Minguez

showing 2 related works from this author

Controlled Ovarian Stimulation Induces a Functional Genomic Delay of the Endometrium with Potential Clinical Implications

2008

Context: Controlled ovarian stimulation induces morphological, biochemical, and functional genomic modifications of the human endometrium during the window of implantation. Objective: Our objective was to compare the gene expression profile of the human endometrium in natural vs. controlled ovarian stimulation cycles throughout the early-mid secretory transition using microarray technology. Method: Microarray data from 49 endometrial biopsies obtained from LH+1 to LH+9 (n = 25) in natural cycles and from human chorionic gonadotropin (hCG) +1 to hCG+9 in controlled ovarian stimulation cycles (n = 24) were analyzed using different methods, such as clustering, profiling of biological processes…

medicine.medical_specialtyendocrine systemEndocrinology Diabetes and Metabolismmedia_common.quotation_subjectClinical BiochemistryStimulationLuteal PhaseBiologyEndometriumChorionic GonadotropinBiochemistryHuman chorionic gonadotropinEndometriumEndocrinologyOvulation InductionReference ValuesInternal medicinemedicineHumansMenstrual CycleMenstrual cycleOligonucleotide Array Sequence Analysismedia_commonRegulation of gene expressionGlutathione PeroxidaseGenome HumanReverse Transcriptase Polymerase Chain ReactionMicroarray analysis techniquesurogenital systemBiochemistry (medical)Luteinizing HormoneInsulin-Like Growth Factor Binding ProteinsGene expression profilingInsulin-Like Growth Factor Binding Protein 3Endocrinologymedicine.anatomical_structureGene Expression RegulationGene chip analysisRNAFemaleAlgorithms
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Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
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