Evidence map›Paper›PMID 41675331›Full record

ReviewTranslational gastroenterology and hepatology2026

Mechanistic insights into hepatic metastasis of pancreatic cancer: molecular perspectives.

Hanwen Yang, Yangkai Fu, Bo Zhang, Simeng Lei, Zhili Ji

Abstract readReview
In one paragraph

Review in Translational gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Hanwen Yang *Department of Hepatobiliary Surgery, Beijing Organ Transplant Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0001-7904-1654
Yangkai Fu *Department of Hepatobiliary Surgery, Beijing Organ Transplant Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0002-4683-6220
Bo ZhangDepartment of Hepatobiliary Surgery, Beijing Organ Transplant Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0009-0003-2474-6237
Simeng LeiDepartment of Hepatobiliary Surgery, Beijing Organ Transplant Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0009-0008-4739-0348
Zhili JiDepartment of Hepatobiliary Surgery, Beijing Organ Transplant Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0009-0007-6642-6652

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PC) is characterized by its aggressive nature and delayed diagnosis, with hepatic metastasis significantly worsening patient prognosis. Recent studies have unveiled multi-layered molecular mechanisms underlying liver metastasis (LM), offering novel perspectives for clinical intervention. Firstly, dysregulation of key genes critically influences metastatic progression. Secondly, metabolic reprogramming fuels metastatic processes, suggesting metabolic targeting as a potential strategy. Additionally, the tumor microenvironment (TME) plays a pivotal role: cancer-associated fibroblasts (CAFs) remodel the niche via extracellular matrix (ECM) and growth factor secretion, while neutrophil extracellular traps (NETs) foster pre-metastatic niches through high-mobility group box 1 (HMGB1) signaling. Immune suppression is further exacerbated by dysfunctional effector T cells and immunosuppressive cells, though targeting insulin-like growth factor I receptor (IGF-IR) or programmed cell death protein 1 (PD-1) may reverse immune tolerance. Key signaling pathways, including aberrant signal transducers and activators of transcription (STAT) family activation, Yes-associated protein (YAP)/transcriptional coactivator (TAZ)-mediated mechanotransduction, and dysregulated phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) pathways, are intricately linked to metastasis. Epithelial-mesenchymal transition (EMT), a central mechanism, is regulated by p21-activated kinase 2 (PAK2)/transforming growth factor (TGF)-β and sex determining region Y-box 2 (SOX2)/Slug pathways, with combined targeting of metabolism and EMT offering therapeutic promise. Future research should focus on elucidating the spatiotemporal dynamics of these mechanisms and integrating immunotherapy with molecular targeting to improve outcomes for PC patients with hepatic metastasis. This review aims to provide a reference for the mechanism research and therapeutic intervention of hepatic metastasis of pancreatic cancer (HMPC).

Indexed as

hepatic metastasisimmune microenvironmentPancreatic cancer (PC)

Identifiers

PMID41675331
PMCPMC12887293

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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.