Evidence map›Paper›PMID 39835087›Full record

ReviewCureus2024

Association of Chronic Hepatitis B With Colorectal Cancer and Its Dual Impact on Colorectal Liver Metastasis: A Narrative Review.

Avneet Kaur, Gibran A Azeez, Mounika Thirunagari, Nazeefa Fatima, Abhinav Anand, Aadi R Palvia, Ann Kashmer Yu

Abstract readReview
In one paragraph

Review in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Comparative urinary metabolomics reveals unique and shared pathways in COVID-19 and liver diseases.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Avneet KaurInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Gibran A AzeezInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Mounika ThirunagariInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Nazeefa FatimaInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Abhinav AnandInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Aadi R PalviaInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Ann Kashmer YuInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viral hepatitis B is infamous for being contracted in young adulthood and adolescence, as high-risk behaviors like unprotected sexual intercourse and intravenous drug abuse are common. Most infections caused by the hepatitis B virus (HBV) are cleared without any long-term sequelae, but some may persist and cause chronic hepatitis B (CHB). This chronicity may produce a state of prolonged inflammation and significantly increase the risk of developing colorectal adenomas (CRA) and colorectal carcinomas (CRC). The aim of this review is to deep-dive into the mechanisms by which CHB may predispose a patient to develop CRA and, more grimly, CRC. It also focuses on studying the influence of CHB on colorectal cancer liver metastases (CRLM). We conducted a comprehensive literature search using databases like PubMed and Google Scholar, focusing on studies that investigate the role of HBV in colorectal carcinogenesis and CRLM rates in patients suffering from CHB. Chronic inflammation, viral protein interactions with tumor suppressor genes, alteration of cellular pathways such as wingless-related integration site (Wnt) signaling, and extrahepatic accumulation of hepatitis B surface antigen (HBsAg) were the key mechanisms identified. Quite peculiarly, CHB, which is thought to increase the risk for CRA, seemed to protect against CRLM probably due to its sclerosing effect on the liver parenchyma and due to certain immune-mediated mechanisms that suppress tumor growth. Nonetheless, high viral count or the presence of hepatitis B envelope antigen (HBeAg) was found to increase the risk for CRLM, potentially due to increased angiogenesis in the liver. These findings provide convincing evidence that enhanced colonoscopic screening and stronger management protocols for patients suffering from it have the potential to reduce the risk of developing CRC and CRLM.

Indexed as

adenoma carcinoma sequencechronic hepatitis bcolorectal adenomacolorectal cancercolorectal liver metastasishepatitis b virusscreening colonoscopytumor suppressor gene (tp53) mutation

Identifiers

PMID39835087
PMCPMC11743875

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.