ReviewHepatology forum2026
Role of insulin-like growth factor/receptor signaling in hepatocellular carcinoma.
Review in Hepatology forum, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Acromegaly and Metabolic Dysfunction-Associated Steatotic Liver Disease: Clinical and Therapeutic Implications.Current obesity reports · 2026Review
- A Single‑Center Retrospective Cohort Study: Impact of Glycemic Control on First‑Line TKI Plus PD‑1 Inhibitors versus TKI Alone in Intermediate‑to‑advanced Unresectable Hepatocellular Carcinoma(HCC) with Type 2 Diabetes Mellitus (T2DM).Journal of hepatocellular carcinoma · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most common and deadly forms of liver cancer worldwide. Recent research suggests that the insulin-like growth factor (IGF) system, including insulin-like growth factor-1, insulin-like growth factor-2, and their receptors, may play a critical role in the pathogenesis and progression of HCC. However, the precise mechanisms through which IGFs contribute to HCC development remain unclear. The objective of this review is to explore the association between IGF signaling and HCC, with a focus on understanding the molecular pathways through which the IGF axis influences the pathophysiology of HCC. The review also examines the potential of utilizing the IGF pathway as a therapeutic target for HCC. IGF-1R overexpression, elevated IGF-2 levels, and decreased IGF-1 levels are seen in HCC and are linked to a poor prognosis. The IGF-1R signaling pathway leads to activation of PI3K/AKT/mTOR and RAS/RAF/MEK/ERK, which increases cell growth and proliferation and inhibits apoptosis, resulting in HCC. Also, in diabetic conditions, low levels of IGF-1 contribute to a higher risk of HCC due to hyperinsulinemia, chronic inflammation, and diseases like non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH).
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.