Publications by authors named "M E Burlone"

The determinants of hepatitis C virus (HCV) viral load remain incompletely understood and may differ in females, who are relatively protected from the consequences of HCV infection during their reproductive years. We aimed to evaluate how age affects the relationship between sex and viral load. = 922 patients (males = 497, median age 62 years), all naïve to direct antiviral agents, were studied.

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Introduction: Hepatocellular carcinoma (HCC) presents a formidable challenge in oncology, demanding innovative treatment approaches. Both adjuvant and neoadjuvant therapies, thanks to the introduction of immunotherapy, have emerged as promising strategies in the management of HCC, aiming to reduce the risk of relapse and ultimately to improve survival.

Areas Covered: This review considers current evidence, ongoing clinical trials, and future strategies to elucidate the evolving landscape of neoadjuvant and adjuvant treatments in HCC.

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Article Synopsis
  • The study investigates the impact of hepatic functional reserve and tumor progression on overall survival in patients with hepatocellular carcinoma (HCC) undergoing combination immunotherapy with atezolizumab and bevacizumab.
  • Out of 571 patients analyzed, a significant portion developed tumor progression, while a smaller group experienced hepatic decompensation, both of which greatly affected survival outcomes.
  • Key predictors of poor survival included hepatic decompensation, advanced tumor progression, and specific baseline liver function metrics, with effective antiviral treatment showing potential protective effects against decompensation in patients with viral causes of HCC.
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Metabolic dysfunction-associated steatohepatitis (MASH) is the replacement term for what used to be called nonalcoholic steatohepatitis (NASH). It is characterized by inflammation and injury of the liver in the presence of cardiometabolic risk factors and may eventually result in the development of hepatocellular carcinoma (HCC), the most common form of primary liver cancer. Several pathogenic mechanisms are involved in the transition from MASH to HCC, encompassing metabolic injury, inflammation, immune dysregulation and fibrosis.

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Systemic treatment for advanced hepatocellular carcinoma (HCC) has been revolutionized over the last few years following the approval of immune checkpoint inhibitors (ICI). Despite the promising survival extension seen with ICI combination regimens, responses are not universally seen and the optimal partner for programmed cell death 1 pathway inhibitors remains to be identified. Even fewer encouraging results have been demonstrated with ICI used for monotherapy.

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