0000000000181381

AUTHOR

Teresa Lozano

0000-0001-7122-5475

showing 2 related works from this author

FOXP3 Inhibitory Peptide P60 Increases Efficacy of Cytokine-induced Killer Cells Against Renal and Pancreatic Cancer Cells

2019

Background/aim Cytokine-induced killer (CIK) cells are ex vivo expanded major histocompatibility complex (MHC)-unrestricted cytotoxic cells with promising effects against a variety of cancer types. Regulatory T-cells (T-reg) have been shown to reduce the effectiveness of CIK cells against tumor cells. Peptide P60 has been shown to inhibit the immunosuppressive functions of T-regs. This study aimed at examining the effect of p60 on CIK cells efficacy against renal and pancreatic cancer cells. Materials and methods The effect of P60 on CIK cytotoxicity was examined using flow cytometry, WST-8-based cell viability assay and interferon γ (IFNγ) ELISA. Results P60 treatment resulted in a signifi…

Cytotoxicity ImmunologicCancer ResearchFOXP3Cell SurvivalImmunotherapy.KidneyMajor histocompatibility complexT-Lymphocytes RegulatoryInterferon-gamma03 medical and health sciencesCytokine-Induced Killer Cells0302 clinical medicineCytokine-induced killer (CIK) cellCell Line TumorPancreatic cancermedicineHumansCytotoxic T cellViability assayCytotoxicityPancreasCancerCytokine-induced killer cellbiologyChemistryFOXP3Forkhead Transcription FactorsGeneral Medicinemedicine.diseaseCoculture TechniquesKidney NeoplasmsPancreatic NeoplasmsOncologyCell culture030220 oncology & carcinogenesisAdoptive cell transferCancer researchbiology.proteinCytokinesPeptidesAnticancer Research
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Preclinical models for prediction of immunotherapy outcomes and immune evasion mechanisms in genetically heterogeneous multiple myeloma

2023

AbstractThe historical lack of preclinical models reflecting the genetic heterogeneity of multiple myeloma (MM) hampers the advance of therapeutic discoveries. To circumvent this limitation, we screened mice engineered to carry eight MM lesions (NF-κB, KRAS, MYC, TP53, BCL2, cyclin D1, MMSET/NSD2 and c-MAF) combinatorially activated in B lymphocytes following T cell-driven immunization. Fifteen genetically diverse models developed bone marrow (BM) tumors fulfilling MM pathogenesis. Integrative analyses of ∼500 mice and ∼1,000 patients revealed a common MAPK–MYC genetic pathway that accelerated time to progression from precursor states across genetically heterogeneous MM. MYC-dependent time …

multiple myeloma mouse model immune system immunotherapyGeneral MedicineGeneral Biochemistry Genetics and Molecular Biology
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