Sandra Cascio

ORCID: 0000-0003-4234-0508
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About
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Research Areas
  • Glycosylation and Glycoproteins Research
  • Genetic factors in colorectal cancer
  • Immune cells in cancer
  • Galectins and Cancer Biology
  • BRCA gene mutations in cancer
  • RNA modifications and cancer
  • Cancer Immunotherapy and Biomarkers
  • Nutrition, Genetics, and Disease
  • Helicobacter pylori-related gastroenterology studies
  • Regulation of Appetite and Obesity
  • Adipose Tissue and Metabolism
  • Cancer-related molecular mechanisms research
  • Cancer, Lipids, and Metabolism
  • Ferroptosis and cancer prognosis
  • Cancer-related Molecular Pathways
  • Growth Hormone and Insulin-like Growth Factors
  • Gastric Cancer Management and Outcomes
  • Cancer, Hypoxia, and Metabolism
  • Cancer Genomics and Diagnostics
  • Cytokine Signaling Pathways and Interactions
  • Estrogen and related hormone effects
  • Monoclonal and Polyclonal Antibodies Research
  • Lung Cancer Treatments and Mutations
  • Cancer and Skin Lesions
  • CRISPR and Genetic Engineering

University of Pittsburgh
2014-2024

Magee-Womens Research Institute
2021-2024

Temple University
2005-2024

UPMC Hillman Cancer Center
2023-2024

Ri.MED
2010-2019

Sidney Kimmel Comprehensive Cancer Center
2011

Johns Hopkins University
2011

University of Palermo
2004-2010

European School of Oncology
2005

Thomas Jefferson University
2004

Abstract Purpose: Recent in vitro studies suggested that the autocrine leptin loop might contribute to breast cancer development by enhancing cell growth and survival. To evaluate whether system could become a target therapy, we examined expression of its receptor (ObR) primary metastatic noncancer mammary epithelium. We also studied leptin/ObR can be induced obesity-related stimuli, such as elevated levels insulin, insulin-like factor-I (IGF-I), estradiol, or hypoxic conditions....

10.1158/1078-0432.ccr-05-1913 article EN Clinical Cancer Research 2006-03-01

MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of different genes, including genes involved in cancer progression. A functional link between hypoxia, a key feature tumor microenvironment, and miRNA has been documented. We investigated whether how miR-20b can vascular endothelial growth factor (VEGF) MCF-7 breast cells under normoxic hypoxia-mimicking conditions (CoCl(2) exposure). Using immunoblotting, ELISA, quantitative real-time PCR, we demonstrated decreased...

10.1002/jcp.22126 article EN Journal of Cellular Physiology 2010-03-15

Abstract Patients with ulcerative colitis have an increased risk of developing colitis-associated colon cancer (CACC). Changes in glycosylation the oncoprotein MUC1 commonly occur chronic inflammation, including colitis, and this abnormally glycosylated promotes development progression. It is not known what causes changes MUC1. Gene expression profiling myeloid cells inflamed malignant tissues showed levels inflammatory macrophage–associated cytokines compared normal tissues. We analyzed...

10.1158/2326-6066.cir-19-0514 article EN Cancer Immunology Research 2019-12-12

Abstract High-grade serous ovarian carcinoma (HGSOC) is a heterogeneous disease, and highstromal/desmoplastic tumor microenvironment (TME) associated with poor outcome. Stromal cell subtypes, including fibroblasts, myofibroblasts, cancer-associated mesenchymal stem cells, establish complex network of paracrine signaling pathways tumor-infiltrating immune cells that drive effector exclusion inhibit the antitumor response. In this work, we integrate single-cell transcriptomics HGSOC TME from...

10.1038/s42003-023-05733-x article EN cc-by Communications Biology 2024-01-05

Previous work has shown that the transcriptional regulator beta-catenin can translocate to nuclei when cells are stimulated with type 1 insulin-like growth factor (IGF-1). We show by immunocoprecipitation and confocal microscopy binds co-localizes insulin receptor substrate-1 (IRS-1), a docking protein for both IGF-1 receptors. IRS-1 is required IGF-1-mediated nuclear translocation of beta-catenin, resulting in activation target genes. facilitated IRS-1. Both recruited cyclin D1 promoter, an...

10.1074/jbc.m504516200 article EN cc-by Journal of Biological Chemistry 2005-06-21

Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates expression leptin, an obesity hormone that has been shown promote cancer progression in autocrine or paracrine way. Using MDA-MB-231 cells, found (a) stimulated leptin mRNA protein expression, was increased activation gene promoter; (b) nuclear accumulation transcription factors...

10.1158/0008-5472.can-08-0642 article EN Cancer Research 2008-06-15

Abstract Both leptin and vascular endothelial growth factor (VEGF) are angiogenic cytokines that upregulated in different types of cancer have been implicated neoplastic progression. Here we investigated the molecular mechanism by which VEGF expression regulated colon epidermal (EGF). In cell line HT‐29, EGF induced binding signal transducer activator transcription 3 (STAT3) to STAT3 consensus motifs within promoters stimulated mRNA protein synthesis. All these effects were significantly...

10.1002/jcp.21843 article EN Journal of Cellular Physiology 2009-06-02

// Sandra Cascio, 1,2 Adam M. Farkas 1 , Rebecca P. Hughey 3 and Olivera J. Finn Department of Immunology, University Pittsburgh School Medicine, Pittsburgh, PA, 15261 2 Fondazione Ri.Med, via Bandiera, Palermo, 90133, Italy Renal-Electrolyte Division, PA 15261. Correspondence: email: Finn, Keywords : MUC1/CIN85 complex, protein-protein interaction, cell migration, invadopodia-like structures, cancer metastasis Received August 8, 2013 Accepted September 5, Published 7, Abstract MUC1 is a...

10.18632/oncotarget.1265 article EN cc-by Oncotarget 2013-09-07

Cross-talk between insulin-like growth factor 1 (IGF-1) and estrogen receptor alpha (ER) regulates gene expression in breast cancer cells, but the underlying mechanisms remain unclear. Here, we studied how 17-beta-estradiol (E2) IGF-1 affect ER transcriptional machinery MCF-7 cells. E2 treatment stimulated loading on response element (ERE) pS2 promoter AP-1 motif cyclin D1 promoter. On ERE, similar amounts of liganded were found at 1-24-h time points, whereas AP-1, binding fluctuated over...

10.1074/jbc.m606244200 article EN cc-by Journal of Biological Chemistry 2006-12-14

We previously reported that CIN85, an 85 KDa protein known to be involved in tumor cell migration and metastasis through its interaction with Cbl, associates MUC1 cells. MUC1/CIN85 complex also regulates invasion of cells vitro. Here, we examined specifically human colon carcinoma tissue microarrays (TMA) by immunohistochemistry for the expression CIN85 their potential role cancer progression metastasis. detected a significant increase both associated advanced stage lymph node further...

10.3390/cancers7010342 article EN cc-by Cancers 2015-02-10

Background: Insulin receptor substrate 1 (IRS-1), a cytoplasmic protein transmitting signals from the insulin and insulin-like growth factor receptors, has been implicated in breast cancer. Previously, it was reported that IRS-1 can be translocated to nucleus modulate oestrogen α (ERα) activity vitro. However, expression of nuclear cancer biopsy specimens never examined. Aims: To assess whether is present non-cancer mammary epithelium, correlates with other markers, especially ERα. Parallel...

10.1136/jcp.2006.039107 article EN Journal of Clinical Pathology 2006-08-01

Tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) play a critical role in resistance to immunotherapy. In this study, we identified epidermal growth factor-like 6 (Egfl6) as new regulator of myeloid cell functions. Our analyses indicated that Egfl6, via binding with β3 integrins activation p38 SYK signaling, acts chemotactic factor for migration promotes their differentiation towards an immunosuppressive state. syngeneic mouse models ovarian cancer (OvCa),...

10.1172/jci175147 article EN cc-by Journal of Clinical Investigation 2024-09-19
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