Publications by authors named "Elisabetta Puliga"
Article Synopsis
- Gastric cancer is a leading cause of cancer-related deaths, and this study focuses on the role of KRAS mutations in understanding therapeutic responses.
- Researchers utilized over 200 patient-derived xenograft models to analyze different KRAS mutations and established primary cell lines to test their reactions to specific inhibitors.
- Results showed that the rare KRAS A146T mutant had unique characteristics compared to more common mutations, suggesting that tailored treatments targeting these differences could improve therapy effectiveness for gastric cancer patients.
Article Synopsis
- Cancer cells adapt their metabolism to meet energy and growth needs, and this study investigates if similar changes occur in normal liver cells during proliferation.
- The research showed that normal liver cells, when stimulated by lead nitrate, exhibited metabolic traits resembling those of cancer cells, particularly through Nrf2 activation.
- Nrf2 is crucial for these metabolic transformations; however, it did not play a role in metabolic changes when liver proliferation was induced by other methods, highlighting different responses based on the stimuli used.
Article Synopsis
- Despite negative results in broader clinical trials for gastric cancer, PARP inhibitors (PARPi) could still benefit a small group of patients with specific genetic mutations. !* -
- Research using patient-derived xenografts showed that gastric cancer tumors with BRCA2 mutations respond well to olaparib, particularly when combined with oxaliplatin. !* -
- Overall, patients with gastric cancer who have BRCA2 mutations or high homologous recombination deficiency (HRD) scores may find PARP inhibition to be an effective treatment option, making genetic testing advisable for these individuals. !*
Background: Thyroid hormones (THs) inhibit hepatocellular carcinoma (HCC) through different mechanisms. However, whether microRNAs play a role in the antitumorigenic effect of THs remains unknown.
Methods: By next generation sequencing (NGS) we performed a comprehensive comparative miRNomic and transcriptomic analysis of rat hepatic preneoplastic lesions exposed or not to a short-term treatment with triiodothyronine (T3).
Nrf2 Mutation/Activation Is Dispensable for the Development of Chemically Induced Mouse HCC.
Cell Mol Gastroenterol Hepatol
April 2022
Background & Aims: Activation of the kelch-like ECH-associated protein 1 (Keap1)-nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway has been associated with metabolic reprogramming in many tumors, including hepatocellular carcinoma (HCC). However, the contribution of Nrf2 mutations in this process remains elusive. Here, we investigated the occurrence of Nrf2 mutations in distinct models of mouse hepatocarcinogenesis.
View Article and Find Full Text PDFGastric cancer (GC) represents an important contributor to the global burden of cancer, being one of the most common and deadly malignancies worldwide. According to TCGA and ACRG classifications, the microsatellite instable (MSI) group represents a significant subset of GCs and is currently in the limelight of many researches due to its favorable survival outcome in resectable stages compared to microsatellite stable tumors. MSI GCs hypermutated phenotype triggers immunosurveillance, making this molecular subgroup a promising candidate for immune checkpoint inhibitors treatment.
View Article and Find Full Text PDFArticle Synopsis
- Activation of the Nrf2-Keap1 pathway, a key defense against environmental stress, is evident in various human cancers, particularly hepatocellular carcinoma (HCC), suggesting different activation mechanisms during cancer progression.
- In a study using a diethylnitrosamine (DENA) model followed by a specific diet, Nrf2 activation was found at early cancer stages and persisted throughout tumor development.
- The research showed that while mutations triggered early Nrf2 activation, their frequency decreased with tumor progression, indicating a shift to p62 accumulation as the primary mechanism for pathway activation in later stages of hepatocarcinogenesis.
Background & Aims: Only limited therapeutic options are currently available for hepatocellular carcinoma (HCC), making the development of effective alternatives essential. Based on the recent finding that systemic or local hypothyroidism is associated with HCC development in humans and rodents, we investigated whether the thyroid hormone triiodothyronine (T3) could inhibit the progression of HCCs.
Methods: Different rat and mouse models of hepatocarcinogenesis were investigated.
The thyromimetic agent GC-1 induces hepatocyte proliferation via Wnt/β-catenin signaling and may promote regeneration in both acute and chronic liver insufficiencies. However, β-catenin activation due to mutations in CTNNB1 is seen in a subset of hepatocellular carcinomas (HCC). Thus, it is critical to address any effect of GC-1 on HCC growth and development before its use can be advocated to stimulate regeneration in chronic liver diseases.
View Article and Find Full Text PDFAlthough the hepatomitogenic activity of T3 is well established, the wide range of harmful effects exerted by this hormone precludes its use in regenerative therapy. The aim of this study was to investigate whether an agonist of TRβ, KB2115 (Eprotirome), could exert a mitogenic effect in the liver, without most of the adverse T3/TRα-dependent side effects. F-344 rats treated with KB2115 for 1 week displayed a massive increase in bromodeoxyuridine incorporation (from 20% to 40% vs.
View Article and Find Full Text PDFTriiodothyronine (T3) induces hepatocyte proliferation in rodents. Recent work has shown molecular mechanism for T3's mitogenic effect to be through activation of β-catenin signaling. Since systemic side effects of T3 may preclude its clinical use, and hepatocytes mostly express T3 hormone receptor β (TRβ), we investigated if selective TRβ agonists like GC-1 may also have β-catenin-dependent hepatocyte mitogenic effects.
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