Oxaliplatin is the first-choice chemotherapy method for patients with advanced colon cancer. However, its resistance leads to treatment failure for many patients. In our experiments, we aim to elucidate the associations among TRIM29 protein, mutant P53, and the resistance of colon cancer cells to oxaliplatin. HCT116 and HT-29 cells were cultured and transfected with plasmids pIRES2-ZsGreen1-TRIM29-flag. Western blot and real-time qRT-PCR were utilized to examine the protein and mRNA expressions of TRIM29 and other related markers, respectively. MTT assay was utilized to determine the cell growth rate and generate the inhibition curve. Continuous culture in low-concentration oxaliplatin was conducted to construct oxaliplatin-resistant cell lines. The coimmunoprecipitation method and immunofluorescence detection were used to examine the interaction between TRIM29 and mutant P53 protein in HT29 cells. We successfully transfected pIRES2-ZsGreen1-TRIM29-flag into HCT116 and HT29 cells, which were utilized inTRIM29 may increase the sensitivity of HT29 to oxaliplatin by blocking the transcriptional function of mutant P53, which inhibits the transcription function of its downstream gene such as MDR1. Changes in BUN have been proposed as a risk factor for complications in acute pancreatitis (AP). Our study aimed to compare changes in BUN versus the Bedside Index for Severity in Acute Pancreatitis (BISAP) score and the Acute Physiology and Chronic Health Evaluation-II score (APACHE-II), as well as other laboratory tests such as haematocrit and its variations over 24 h and C-reactive protein, in order to determine the most accurate test for predicting mortality and severity outcomes in AP. Clinical data of 410 AP patients, prospectively enrolled for study at our institution, were analyzed. We define AP according to Atlanta classification (AC) 2012. The laboratory test's predictive accuracy was measured using area-under-the-curve receiver-operating characteristics (AUC) analysis and sensitivity and specificity tests. Rise in BUN was the only score related to mortality on the multivariate analysis ( =0.000, OR 12.7; CI 95% 4.2-16.6). On the comparative analysis of AUC, the rise in BUN was an accurate test in predicting mortality (AUC 0.842) and persisting multiorgan failure (AUC 0.828), similar to the BISAP score (AUC 0.836 and 0.850) and APACHE-II (AUC 0.756 and 0.741). The BISAP score outperformed both APACHE-II and rise in BUN at 24 hours in predicting severe AP (AUC 0.873 vs. 0.761 and 0.756, respectively). Rise in BUN at 24 hours is a quick and reliable test in predicting mortality and persisting multiorgan failure in AP patients.Rise in BUN at 24 hours is a quick and reliable test in predicting mortality and persisting multiorgan failure in AP patients. Hepatocellular carcinoma (HCC) is a malignant tumor with great variation in prognosis among individuals. Changes in metabolism influence disease progression and clinical outcomes. Tubacin in vivo The objective of this study was to determine the overall survival (OS) risk of HCC patients from a metabolic perspective. The model was constructed using the least absolute shrinkage and selection operator (LASSO) COX regression based on The Cancer Genome Atlas (TCGA, n=342) dataset. The International Cancer Genome Consortium (ICGC, n=232), GSE14520 (n=242) datasets, and a clinical cohort (n=64) were then used to assess the prognostic value of the signature. A 10 metabolic gene-based signature was constructed and verified as a robust and independent prognostic classifier in public and real-world validation cohorts. Meanwhile, the signature enabled the identification of HCC molecular subtypes, yielding an AUC value of 0.678 [95% CI 0.592-0.763]. Besides, the signature was associated with metabolic processes like glycolysis, supported by a clear correlation between the risk score and expression of rate-limiting enzymes. Furthermore, high-risk tumor was likely to have a high tumor infiltration status of immunosuppressive cells, as well as elevated expression of some immune checkpoint molecules. For final clinical translation, a nomogram integrating the signature and tumor stage was established, and showed improved predictive accuracy of 3- and 5-year OS and brought more net benefit to patients. We developed a prognostic signature based on 10 metabolic genes, which has proven to be an independent and reliable prognostic predictor for HCC and reflects the metabolic and immune characteristics of tumors.We developed a prognostic signature based on 10 metabolic genes, which has proven to be an independent and reliable prognostic predictor for HCC and reflects the metabolic and immune characteristics of tumors.The systemic treatment of advanced hepatocellular carcinoma (HCC) has significantly changed over the last years, with the introduction of two new standard-of-care first-line treatments (lenvatinib and the combination of atezolizumab and bevacizumab) and the success of several new agents in second line. In particular, after the approval of regorafenib, ramucirumab and cabozantinib, the landscape of second-line treatment has become notably complex, providing a serious challenge in clinical practice. In this review, we focus on cabozantinib, a multikinase inhibitor which was proven effective in improving overall and progression-free survival of patients previously treated with sorafenib in the randomized Phase III CELESTIAL trial. CELESTIAL is the only phase III study to have included patients in the third-line setting and cabozantinib efficacy was confirmed in several post hoc analyses, irrespective of alpha-fetoprotein levels, albumin-bilirubin score, age, and duration of previous sorafenib treatment. The safety profile of cabozantinib in the CELESTIAL trial was comparable with other multikinase inhibitors used for HCC and the most frequent grade ≥3 adverse events were diarrhea, palmar-plantar erythrodysesthesia, fatigue, hypertension, and aspartate aminotransferase increase. Tolerability did not differ between younger and older patients and quality of life was significantly improved compared to placebo during the treatment. In this review, we also make a particular mention to the use of cabozantinib in populations which are normally excluded from clinical trials, such as older patients and Child-Pugh B patients. Finally, we present the new treatment strategies in which cabozantinib is being tested, most notably the combination of cabozantinib and atezolizumab in the first-line setting in the phase III COSMIC-312 trial and the use of cabozantinib after progression on immune-checkpoint inhibitors.