Abstract IA37: Prevention of Hepatocellular Carcinoma (HCC) with antiviral therapy
Notice bibliographique
Résumé
Abstract On a world-wide basis, chronic viral hepatitis accounts for nearly 75% of all cases of HCC. One of the important implications of this is that HCC may be more readily preventable either by vaccination or with anti-viral therapy. Antiviral therapy against hepatitis B has largely evolved away from using alpha interferon to nucleoside analogues. Lamivudine is the nucleoside analogue agent that has been best studied in preventing HCC. In a large prospective, randomized placebo-controlled trial of lamivudine therapy in patients with advanced liver disease associated with HBV infection, 3.9% of patients receiving lamivudine developed HCC compared to 7.4% on placebo (p=0.047) (1). More recently entecavir and tenofovir have become widely used as the main antiviral agents to control HBV infection. Both agents appear to be very effective in controlling HBV infection but data on their ability to reduce the risk of HCC are controversial. At least two meta-analyses have been done of the anti-cancer benefits of antiviral therapy. Chronic HCV infection appears to be associated with about 30% of HCCs worldwide but in some regions including Europe and the United States it is the leading underlying cause of HCC. The evidence is substantial that effective treatment of hepatitis C can reduce the risk of HCC. The HALT-C Trial was a large randomized controlled trial carried out at multiple sites within the United States, enrolling more than 1,000 patients and randomized patients with HCV infection and advanced fibrosis (bridging hepatic fibrosis or cirrhosis) to receive long-term maintenance therapy with a low dose of peginterferon alfa or to remain untreated for a period of 4 years (2). The initial report from this study showed that antiviral therapy did not reduce the rate of either hepatic decompensation or HCC but an analysis of liver related outcomes after 7 to 8 years of follow up among patients who did not respond to therapy colleagues found that patients who achieved viral cure had significantly lower rates of hepatic decompensation, liver transplantation, or HCC than patients with remained non-responders to interferon (3). This was confirmed in other large cohort studies from several countries in Europe and Canada and meta-analyses. In summary, antiviral treatment for viral hepatitis appears to have benefits in decreasing the risk of HCC in chronically infected patients. This benefit is most pronounced in patients with chronic hepatitis C and advanced hepatic fibrosis or cirrhosis in patients achieving viral clearance and seems much more marginal in patients with chronic hepatitis B where antiviral therapy usually results in viral suppression rather than elimination. References 1. Liaw YF, Sung JJ, Chow WC et al. Lamivudine for patients with chronic hepatitis B and advanced liver disease. N Engl J Med 2004; 351:1521-31. 2. Di Bisceglie AM, Shiffman ML, Everson GT et al for the HALT-C Trial Investigators. Prolonged Therapy of Advanced Chronic Hepatitis C with Low-Dose Peginterferon. N Engl J Med 2008;359:2429-41. 3. Morgan TR, Ghany MG, Kim HY et al and the HALT-C Trial Group. Outcome of Sustained Virological Responders with Histologically Advanced Chronic Hepatitis C. Hepatology 2010;52:833-44. Citation Format: Adrian M. Di Bisceglie. Prevention of Hepatocellular Carcinoma (HCC) with antiviral therapy [abstract]. In: Proceedings of the AACR International Conference: New Frontiers in Cancer Research; 2017 Jan 18-22; Cape Town, South Africa. Philadelphia (PA): AACR; Cancer Res 2017;77(22 Suppl):Abstract nr IA37.
Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.
Comment cette classification a été obtenuedéplier
Prédiction machine sur la base complète
Imitation des enseignantsNi prévalence calibrée, ni vérité terrain. Validation humaine à venir. Le volet Gemma est une étiquette directe du modèle pour chaque travail de la base, lue sur la notice réduite au titre. Le volet Codex est un classifieur appris des 10 348 étiquettes directes de Codex et calibré sur les taux pondérés de l'échantillon; les champs sans appui suffisant ne portent aucun appel Codex. Le mode candidate est l'union des deux volets; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont pas des étiquettes humaines.
Scores du classifieur distillé par catégorie (deux têtes)
| Catégorie | Codex | Gemma |
|---|---|---|
| Métarecherche | 0,001 | 0,002 |
| Méta-épidémiologie (sens strict) | 0,001 | 0,000 |
| Méta-épidémiologie (sens large) | 0,001 | 0,002 |
| Bibliométrie | 0,001 | 0,001 |
| Études des sciences et des technologies | 0,000 | 0,000 |
| Communication savante | 0,001 | 0,000 |
| Science ouverte | 0,000 | 0,000 |
| Intégrité de la recherche | 0,001 | 0,001 |
| Charge utile insuffisante (le modèle a refusé de juger) | 0,017 | 0,002 |
Scores machine (provisoires)
Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.
Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.
score_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découleClassification
machine, non validéePrédiction automatique; un appel candidat d’une seule source (Gemma direct ou Codex distillé), pas un consensus.
Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».