Publications by authors named "Claudia Orru"
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
- 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. !*
Activation of the Keap1/Nrf2 pathway, the most important cell defense signal, triggered to neutralize the harmful effects of electrophilic and oxidative stress, plays a crucial role in cell survival. Therefore, its ability to attenuate acute and chronic liver damage, where oxidative stress represents the key player, is not surprising. On the other hand, while Nrf2 promotes proliferation in cancer cells, its role in non-neoplastic hepatocytes is a matter of debate.
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- 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.
Background & Aims: Dysregulation of the Keap1-Nrf2 pathway has been observed in experimental and human tumors, suggesting possible roles of the pathway in cancer development. Herein, we examined whether Nrf2 (Nfe2l2) activation occurs at early steps of rat hepatocarcinogenesis, to assess critical contributions of Nrf2 to the onset of hepatocellular carcinoma (HCC).
Methods: We used wild-type (WT) and Nrf2 knockout (Nrf2KO) rats treated with a single injection of diethylnitrosamine (DENA) followed by choline-devoid methionine-deficient (CMD) diet.