Evidence map›Paper›PMID 39101773›Full record

ArticleHepatology communications2024

Transcriptomic profiling of intermediate cell carcinoma of the liver.

Byungchan Jang, So Mee Kwon, Jang Hyun Kim, Jung Mo Kim, Taek Chung, Jeong Eun Yoo, Haeryoung Kim, Julien Calderaro, Hyun Goo Woo, Young Nyun Park

Abstract read
In one paragraph

Article in Hepatology communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Byungchan JangDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.ORCID 0009-0006-4328-9504
So Mee KwonDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.ORCID 0000-0001-8017-9650
Jang Hyun KimDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Jung Mo KimAjou Translational Omics Center (ATOC), Research Institute for Innovative Medicine, Ajou University Medical Center, Suwon, Republic of Korea.ORCID 0000-0002-6816-9852
Taek ChungDepartment of Pathology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-7567-0680
Jeong Eun YooDepartment of Pathology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-9990-279
Haeryoung KimDepartment of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-4205-9081
Julien CalderaroDepartment of Pathology, Assistance Publique Hôpitaux de Paris, Groupe Hospitalier Henri Mondor, Créteil, France.ORCID 0000-0002-5370-0807
Hyun Goo WooDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.ORCID 0000-0002-0916-893
Young Nyun ParkDepartment of Pathology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0003-0357-7967

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntermediate cell carcinoma (Int-CA) is a rare and enigmatic primary liver cancer characterized by uniform tumor cells exhibiting mixed features of both HCC and intrahepatic cholangiocarcinoma. Despite the unique pathological features of int-CA, its molecular characteristics remain unclear yet.

methodsRNA sequencing and whole genome sequencing profiling were performed on int-CA tumors and compared with those of HCC and intrahepatic cholangiocarcinoma.

resultsInt-CAs unveiled a distinct and intermediate transcriptomic feature that is strikingly different from both HCC and intrahepatic cholangiocarcinoma. The marked abundance of splicing events leading to intron retention emerged as a signature feature of int-CA, along with a prominent expression of Notch signaling. Further exploration revealed that METTL16 was suppressed within int-CA, showing a DNA copy number-dependent transcriptional deregulation. Notably, experimental investigations confirmed that METTL16 suppression facilitated invasive tumor characteristics through the activation of the Notch signaling cascade.

conclusionsOur results provide a molecular landscape of int-CA featured by METTL16 suppression and frequent intron retention events, which may play pivotal roles in the acquisition of the aggressive phenotype of Int-CA.

Indexed as

Carcinoma, HepatocellularCholangiocarcinomaGene Expression ProfilingLiver NeoplasmsBile Duct NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansMaleMethyltransferasesMiddle AgedSignal TransductionTranscriptomeMethyltransferases

Identifiers

PMID39101773
PMCPMC11299988

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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.