Evidence map›Paper›PMID 42782195›Full record

ArticleAnimal models and experimental medicine2026

Developing a strain-dependent susceptibility to hepatocellular carcinoma in a murine model based on histopathological evidence and genetic context.

Osayd Zohud, Aysar Nashef, Imad Abu-Elnaaj, Fuad A Iraqi

Abstract read
In one paragraph

Article in Animal models and experimental medicine, 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

4 authors.

Osayd ZohudDepartment of Clinical Microbiology and Immunology, Gray Faculty of Medicine and Health Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Aysar NashefDepartment of Oral and Maxillofacial Surgery, Baruch Padeh Medical Center, Poriya, Israel.
Imad Abu-ElnaajDepartment of Oral and Maxillofacial Surgery, Baruch Padeh Medical Center, Poriya, Israel.
Fuad A IraqiDepartment of Clinical Microbiology and Immunology, Gray Faculty of Medicine and Health Sciences, Tel-Aviv University, Tel-Aviv, Israel.ORCID https://orcid.org/0000-0001-5525-206X

Funding

Department of Oral and Maxillofacial Surgery, Baruch Padeh Medical Center, PoriyaMinistry of the Negev, Galilee, and National ResilienceTel Aviv University
6 · The paper itself

Abstract

Hepatocellular carcinoma is a leading cause of cancer-related mortality worldwide. Smad4, a well-established tumor suppressor within the transforming growth factor-β (TGF-β) signaling pathway, has an oncogenic potential of its heterozygous loss, still poorly defined, especially across genetically diverse backgrounds. The aim was to investigate whether heterozygous loss of Smad4 increases susceptibility to spontaneous liver tumor development in a genetically diverse murine population. We generated 260 F1(C57BL/6J/Smad4

Indexed as

CC micegenetic susceptibilityhepatocellular carcinomaheterozygous Smad4 deletionliver cancermouse modelSmad4systems geneticsTGF‐β signalingtumor modifiers

Identifiers

PMID42782195
PMCPMC13603076

What OpenQuestion holds

Textmetadata
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.