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Biology subjects

Roman, M.

Publications and source records attributed to Roman, M..

4 recordsLinked to original sources

A microscopy-based readout to assess tumour-specific viability in neuroblastoma co-cultures and short-term cultured patient samples

High-risk neuroblastoma patients face poor survival despite intensive treatment. Drug testing using patient-derived models can support therapy prioritization for precision medicine and drug development. Models incorporating tumour microenvironmental components, such as co-cultures and short-term cultured patient samples containing substantial non-malignant cell fractions, could better recapitulate microenvironment-dependent drug responses. However, conventional viability assays measure the combined signal from all viable cells in a well and therefore cannot determine tumour-specific drug responses. Here, we establish a microscopy-based readout to quantify cell-type-specific viability in two complementary settings: neuroblastoma-PBMC co-cultures and freshly dissociated patient tumour samples. In the co-cultures, PBMCs were pre-labelled with a cell-tracking dye, and Calcein staining was used to independently quantify the viability of tumour cells and PBMCs in the same well. The Calcein-based viability readout correlated strongly with conventional CellTiter-Glo measurements and was compatible with automated high-throughput drug screening. The imaging workflow enabled identification of compounds with differential efficacy in co-culture versus monoculture and distinguished tumour-specific effects from PBMC toxicity. The microscopy-based viability readout was further adapted to short-term cultured patient samples. Neuroblastoma tumour cells were distinguished from the non-malignant cells using a combination of tumour-specific surface markers NCAM, L1CAM and B7H3. This enabled determination of tumour fractions and measurement of tumour-specific drug responses. Tumour fractions varied substantially between patient samples, highlighting the importance of tumour-specific viability measurements. Together, the microscopy-based viability readout for co-cultures and patient samples enables scalable assessment of tumour-specific drug responses.

Cancer Biology↗

An Effective Metal Nanoparticle-Based Drug Delivery System for an In Vitro Model of Non Small Cell Lung Cancer

This study presents the development and spectroscopic characterization of an erlotinib-functionalized gold nanoparticle (erlotinib:AuNP) nanosystem designed for targeted delivery to metastatic non-small cell lung cancer H1299 cells. Initial MTS assays demonstrated that free erlotinib induced a concentration-dependent reduction in cell viability, while 0.1 {micro}M erlotinib exhibited negligible cytotoxicity and was therefore selected for nanosystem fabrication. AuNPs alone showed minimal toxicity toward H1299 cells over the investigated concentration range. Following conjugation of erlotinib with AuNPs, the resulting nanosystems reduced cell viability to approximately 60%, indicating enhanced biological activity of the drug after nanoparticle-assisted delivery. Fluorescence microscopy confirmed the intracellular internalization of the nanosystems in H1299 cells, with nanoparticle aggregates predominantly localized in the perinuclear and perimitochondrial regions. Three-dimensional Raman spectroscopy (3D RS) mapping further verified the intracellular localization of the conjugates through characteristic Raman signatures of erlotinib:AuNPs. Importantly, 3D RS enabled detection of nanosystems at concentrations below the sensitivity limit of fluorescence imaging, demonstrating superior analytical performance for intracellular nanosystem tracking. Atomic force microscopy-infrared (AFM-IR) spectroscopy coupled with principal component analysis (PCA) demonstrated substantial biochemical modifications induced by the erlotinib:AuNP nanosystems, including enhanced lipid-related spectral features and significant alterations in protein secondary structure, particularly the increased contribution of unordered and antiparallel {beta}-turn conformations. The obtained results demonstrate that combining plasmonic nanocarriers with advanced vibrational spectroscopy enables highly sensitive monitoring of intracellular drug delivery and nanosystem-induced biochemical responses in cancer cells.

biophysics↗

Humanized CAR T cells targeting p95HER2

Redirection of T lymphocytes against tumor-associated or tumor-specific antigens, via bispecifc T cells engagers (BiTEs) or chimeric antigen receptors (CARs), is a successful therapeutic strategy against certain hematologic malignancies. In contrast, so far it has failed against solid tumors. Given the scarcity of tumor-specific antigens, the vast majority of BiTEs and CAR Ts developed to date have been directed against tumor-associated antigens. These are expressed in some normal tissues and, as a consequence, frequent and serious side effects caused by on-target off-tumor activity have limited the use of BiTEs and CARs in the clinic. P95HER2 is a fragment of the tyrosine kinase receptor HER2 expressed in more than 30% of HER2-amplified tumors. It has been previoulsy shown that p95HER2 is a tumor-specific antigen. Here we present the generation of CARs targeting p95HER2. p95HER2 CAR T cells show remarkable activity against p95HER2-expressing cells in vitro and in vivo. Further, they are also effective against lung and brain metastasis. These tumor-specific CAR T cells could be used in the near future to deliver additional anti-tumor therapies in a safe manner.

cancer biology↗

Metabolic effects of aripiprazole and olanzapine multiple-dose treatment in healthy volunteers. Association with pharmacogenetics.

BackgroundAripiprazole and olanzapine are atypical antipsychotics. Both drugs can induce metabolic changes, however, the metabolic side effects produced by aripiprazole are more benign. ObjectivesTo evaluate if aripiprazole and olanzapine alter prolactin levels, lipid and glucose metabolism and hepatic, hematological, thyroid and renal function. MethodsTwenty-four healthy volunteers received 5 daily oral doses of 10 mg aripiprazole and 5 mg olanzapine in a crossover randomized clinical trial and were genotyped for 51 polymorphisms in 17 genes by qPCR. Drug plasma concentrations were measured by LC-MS. The biochemical and hematological analyses were performed by enzymatic methods. ResultsOlanzapine induced hyperprolactinemia but not aripiprazole. DRD3 Ser/Gly and ABCB1 rs10280101, rs12720067 and rs11983225 polymorphisms and CYP3A phenotype had an impact on plasma prolactin levels. C-peptide concentrations were higher after aripiprazole administration and were influenced by COMT rs4680 and rs13306278 polymorphisms. Olanzapine and the UGT1A1 rs887829 polymorphism were associated with elevated glucose levels. CYP3A poor metabolizers had increased insulin levels. Triglyceride concentrations were decreased due to olanzapine and aripiprazole treatment and were variable based on CYP3A phenotypes and the APOC3 rs4520 genotype. Cholesterol levels were also decreased and depended on HTR2A rs6314 polymorphism. All hepatic enzymes, platelet and albumin levels and prothrombin time were altered during both treatments. Additionally, olanzapine reduced the leucocyte count, aripiprazole increased free T4 and both decreased uric acid concentrations. ConclusionsShort term treatment with aripiprazole and olanzapine had a significant influence on the metabolic parameters. However, it seems that aripiprazole provokes less severe metabolic changes.

pharmacology and toxicology↗