A5019516085- Bioinformatics and Genomic Networks
- Computational Drug Discovery Methods
- Cancer Genomics and Diagnostics
- Prostate Cancer Treatment and Research
- Growth Hormone and Insulin-like Growth Factors
- Pituitary Gland Disorders and Treatments
- TGF-β signaling in diseases
- Mathematical Biology Tumor Growth
- Pharmacogenetics and Drug Metabolism
- Statistical Methods in Clinical Trials
- Health Systems, Economic Evaluations, Quality of Life
- Pancreatic function and diabetes
- Cancer, Hypoxia, and Metabolism
- Metabolism, Diabetes, and Cancer
- Neurogenesis and neuroplasticity mechanisms
- Protein Tyrosine Phosphatases
- Fibroblast Growth Factor Research
- Cytokine Signaling Pathways and Interactions
- Endoplasmic Reticulum Stress and Disease
- Multiple Myeloma Research and Treatments
- Effects and risks of endocrine disrupting chemicals
- Kruppel-like factors research
- Cancer, Stress, Anesthesia, and Immune Response
- Protein Kinase Regulation and GTPase Signaling
- Milk Quality and Mastitis in Dairy Cows
Columbia University Irving Medical Center
2023-2025
Columbia University
2022-2025
Instituto de Investigaciones en Ciencias de la Salud
2017-2023
Consejo Nacional de Investigaciones Científicas y Técnicas
2017-2023
Universidad Nacional de Córdoba
2017-2023
National University of the Littoral
2015
Abstract Prioritizing treatments for individual patients with cancer remains challenging, and performing coclinical studies using patient-derived models in real time is often unfeasible. To circumvent these challenges, we introduce OncoLoop, a precision medicine framework that predicts drug sensitivity human tumors their preexisting high-fidelity (cognate) model(s) by leveraging perturbation profiles. As proof of concept, applied OncoLoop to prostate genetically engineered mouse (GEMM)...
In somatotroph tumors, over 50% of patients do not respond satisfactorily to the octreotide (OCT) treatment. Stimulation SSTR2 with OCT triggers anti-proliferative signaling pathways mediated by phosphatase SHP2. This can exercise its functions through STAT3, SHP2/STAT3 subcellular localization being crucial for understanding mechanisms action. We investigated expression SHP2 in somatotrophs role on cell proliferation, effects STAT3 phosphorylation, and localization, using vitro a...
Abstract Metastatic prostate cancer, the major cause of cancer lethality, presents as several distinct subtypes. Treatment naïve metastatic often called oligometastatic disease, develops within an androgen-intact context and, given its low frequency in population, remains understudied. The more prevalent type disease arises from castration-resistant (CRPC) a consequence treatment failure response to androgen deprivation therapy (ADT). Both types metastases have eluded curative treatments,...
In this study, we focused on ERβ regulation in the adenohypophysis under different estrogenic milieu, by analyzing whether ER modulates phosphatase and tensin homolog deleted chromosome 10 (PTEN) expression its subcellular localization anterior pituitary glands from Wistar rats GH3 lactosomatotroph cells that over‐expressed ERβ. was regulated a cyclic manner, underwent dynamic changes throughout estrous cycle, with decreased ERβ+ estrus E2 treatment, but increased ovariectomized rats....
The molecular mechanisms underlying the ERα nuclear/cytoplasmic pool that modulates pituitary cell proliferation have been widely described, but it is still not clear how targeted to plasma membrane. aim of this study was analyse palmitoylation and membrane (mERα) pool, their participation in E2-triggered membrane-initiated signalling normal tumour growth. Cell cultures were prepared from anterior pituitaries female Wistar rats GH3 cells, treated with 10 nM oestradiol (E2). basal expression...
In pituitary adenomas, early recurrences and resistance to conventional pharmacotherapies are common, but the mechanisms involved still not understood. The high expression of epidermal growth factor receptor 2 (HER2)/extracellular signal-regulated kinase (ERK1/2) signal observed in human together with low levels antimitogenic transforming beta (TBR2), encouraged us evaluate effect specific HER2 inhibition trastuzumab on experimental tumor cell its antiproliferative response TGFB1....
Serum prolactin levels gradually increase from birth to puberty in both male and female rats, with higher observed since the first days of life. The lactotroph secretion was attributed maturation prolactin-inhibiting prolactin-releasing factors; however, those mechanisms could not fully explain gender differences observed. Prolactin isolated lactotrophs, absence hypothalamic control, also increases during weeks life, suggesting involvement intra-pituitary factors. We postulate that pituitary...
Introduction: Macroautophagy is a lysosome-mediated degradation process that controls the quality of cytoplasmic components and organelles, with its regulation depending on autophagy-related proteins (Atg) Beclin1/Atg6 microtubule-associated protein light chain 3 (LC3/Atg8) being key players in mammalian autophagy. As reports this mechanism field pituitary neuropathology neuroendocrinology are scarce, our study analyzed ultrastructural signs macroautophagy expression Beclin1 LC3 human...
Intracellular communication is essential for the maintenance of anterior pituitary gland plasticity. The aim this study was to evaluate whether GPCR-Gαi modulates basic fibroblast growth factor (FGF2)-induced proliferative activity in normal cell populations. Anterior primary cultures from Wistar female rats were treated with FGF2 (10ng/mL) or somatostatin analog (SSTa, 100nM) alone co-incubated without inhibitors GPCR-Gαi, pertussis toxin (PTX, 500nM), MEK inhibitor (U0126, 100µM) PI3K (LY...
Abstract Octreotide (OCT) is used to inhibit hormone secretion and growth in somatotroph tumors, although a significant percentage of patients are resistant. It has also been tested nonfunctioning (NF) tumors but with poor results, these outcomes having associated SSTR2 levels impaired signaling. We investigated whether OCT inhibitory effects can be improved by TGF‐β1 functioning tumor cells. on proliferation were analyzed the presence WT SSTR2‐overexpressing secreting GH3 silent The...
<div>Abstract<p>Prioritizing treatments for individual patients with cancer remains challenging, and performing coclinical studies using patient-derived models in real time is often unfeasible. To circumvent these challenges, we introduce OncoLoop, a precision medicine framework that predicts drug sensitivity human tumors their preexisting high-fidelity (cognate) model(s) by leveraging perturbation profiles. As proof of concept, applied OncoLoop to prostate genetically engineered...
<p>Detailed Materials and Methods</p>
<p>Detailed Materials and Methods</p>
<div>Abstract<p>Prioritizing treatments for individual patients with cancer remains challenging, and performing coclinical studies using patient-derived models in real time is often unfeasible. To circumvent these challenges, we introduce OncoLoop, a precision medicine framework that predicts drug sensitivity human tumors their preexisting high-fidelity (cognate) model(s) by leveraging perturbation profiles. As proof of concept, applied OncoLoop to prostate genetically engineered...
<p>Figure S1: Genomic alterations in prostate cancer represented the GEMMs (related to Fig. 2). Figure S2: Additional phenotypic analyses of S3: Phenotypic analysis allograft and organoid models S4: transcriptomic 3). S5: Analyses AR activity GEMMS S6: Regulatory sub-networks GEMM clusters S7. MR-match cells lines human PCa Figs. 5). S8. Drug perturbation protein profiles from DU145 5, 6, 7). S9. LNCaP Pharmacotyping patients S10: validation drug candidates Figs S11: 6).</p>
<p>Index of Supplementary Data</p>
<p>Supplementary Table 3: Transcriptomic analyses of the human patient samples A. TCGA Interactome B. SU2C C. Protein activity D. Activity SU2C</p>
<p>Supplementary Table 4: OncoMatch A. TCGA B. SU2C</p>
<p>Supplementary Table 1: Phenotypic analysis of the GEMMs</p>
<p>Supplementary Table 1: Phenotypic analysis of the GEMMs</p>