Cristina Andreani

ORCID: 0000-0003-3245-670X
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About
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Research Areas
  • Phagocytosis and Immune Regulation
  • PI3K/AKT/mTOR signaling in cancer
  • Monoclonal and Polyclonal Antibodies Research
  • Immunotherapy and Immune Responses
  • vaccines and immunoinformatics approaches
  • Renal and related cancers
  • Protein Degradation and Inhibitors
  • Renal cell carcinoma treatment
  • RNA modifications and cancer
  • Cancer, Lipids, and Metabolism
  • Ferroptosis and cancer prognosis
  • Pancreatic and Hepatic Oncology Research
  • Ubiquitin and proteasome pathways
  • Sirtuins and Resveratrol in Medicine
  • Glycosylation and Glycoproteins Research
  • RNA Interference and Gene Delivery
  • Mitochondrial Function and Pathology
  • Advanced biosensing and bioanalysis techniques
  • Cancer, Hypoxia, and Metabolism
  • Metal complexes synthesis and properties
  • Biochemical effects in animals
  • HER2/EGFR in Cancer Research
  • Cancer-related Molecular Pathways
  • PARP inhibition in cancer therapy
  • Coenzyme Q10 studies and effects

University of Cincinnati Medical Center
2021-2024

Università di Camerino
2013-2023

University of Cincinnati
2019

The University of Texas Southwestern Medical Center
2017

Southwestern Medical Center
2017

Università Cattolica del Sacro Cuore
1987

Abstract Mutant KRAS (KM), the most common oncogene in lung cancer (LC), regulates fatty acid (FA) metabolism. However, role of FA LC tumorigenesis is still not sufficiently characterized. Here, we show that KMLC has a specific lipid profile, with high triacylglycerides and phosphatidylcholines (PC). We demonstrate FASN, rate-limiting enzyme synthesis, while being dispensable EGFR-mutant or wild-type LC, required for viability cells. Integrating lipidomic, transcriptomic functional analyses,...

10.1038/s41467-022-31963-4 article EN cc-by Nature Communications 2022-07-26

Available treatment for obesity and type 2 diabetes mellitus (T2DM) is suboptimal. Thus, identifying novel molecular target(s) exerting protective effects against these metabolic imbalances of enormous medical significance. Sirt6 loss- gain-of-function studies have generated confounding data regarding the role this sirtuin on energy glucose homeostasis, leaving unclear whether activation or inhibition SIRT6 may be beneficial and/or T2DM.To address issues, we developed studied a mouse model...

10.1016/j.molmet.2015.09.003 article EN cc-by-nc-nd Molecular Metabolism 2015-09-25

The phytoestrogen resveratrol has been reported to possess cancer chemo-preventive activity on the basis of its effects tumor cell lines and xenograft or carcinogen-inducible in vivo models.Here we investigated spontaneous mammary carcinogenesis using Δ16HER2 mice as HER2+/ERα+ breast model.Instead inhibiting growth, treatment (0.0001% drinking water; daily intake 4μg/mouse) shortened latency enhanced multiplicity mice.This tumor-promoting effect was associated with up-regulation...

10.18632/aging.101175 article EN cc-by Aging 2017-02-26

The advent of trastuzumab has significantly improved the prognosis HER2-positive (HER2+) breast cancer patients; nevertheless, drug resistance limits its clinical benefit. Anti-HER2 active immunotherapy represents an attractive alternative strategy, but effective immunization needs to overcome patient's immune tolerance against self-HER2. Phage display technology, taking advantage phage intrinsic immunogenicity, permits one generate vaccines able break self-antigens. In this study, we...

10.3390/cancers14164054 article EN Cancers 2022-08-22

The histone deacetylase sirtuin 6 (SIRT6) has been endowed with anti-cancer capabilities in many tumor types. Here, we investigate the impact of SIRT6-overexpression (SIRT6-OE) Delta16HER2 mice, which are a bona fide model HER2-positive breast cancer. After an initial delay onset, SIRT6-OE induces more aggressive phenotype tumors promoting formation higher number foci and metastases than controls. This is associated cancer stem cell (CSC)-like features dormancy, low senescence oxidative DNA...

10.1038/s41598-023-49199-7 article EN cc-by Scientific Reports 2023-12-12

Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such dysfunctions usually associated with structural functional alterations of mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, premature aging high degree oxidative stress, was used to investigate whether combined intervention mild physical exercise ubiquinol supplementation able improve mitochondrial function preserve health during aging. 5-month-old SAMP8 mice,...

10.1155/2018/8936251 article EN cc-by Oxidative Medicine and Cellular Longevity 2018-01-01

Abstract Δ16HER2 is a splice variant of HER2 and defined as the transforming isoform in HER2-positive breast cancer. It has been shown that promotes cancer aggressiveness drug resistance. In present work, we used silico modeling to identify structural differences between wild-type proteins. We then developed DNA vaccines specifically against showed these immunotherapies hampered carcinogenesis transplantable model. However, failed elicit immune protection transgenic mice because tolerogenic...

10.1158/2326-6066.cir-18-0179 article EN Cancer Immunology Research 2018-10-16

Ferroptosis has emerged as a new type of programmed cell death that can be harnessed for cancer therapy. The concept ferroptosis was the first time proposed in early 2000s, an iron-dependent mode regulated caused by unrestricted lipid peroxidation (LPO) and subsequent plasma membrane rupture. Since discovery characterization ferroptosis, wealth research improved our understanding main pathways regulating this process, leading to both repurposing development small molecules. However, is still...

10.3389/fonc.2022.923915 article EN cc-by Frontiers in Oncology 2022-07-15

Abstract Intrinsic resistance to targeted therapeutics in PTEN-deficient glioblastoma (GBM) is mediated by redundant signaling networks that sustain critical metabolic functions. Here, we demonstrate coordinated inhibition of the ribosomal protein S6 kinase 1 (S6K1) and receptor tyrosine AXL using LY-2584702 BMS-777607 can overcome network redundancy reduce GBM tumor growth. This combination S6K1 suppressed glucose flux pyrimidine biosynthesis. Genetic inactivation studies map indicated both...

10.1158/2767-9764.crc-23-0631 article EN cc-by Cancer Research Communications 2024-08-01
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