Evidence map›Paper›PMID 31744909›Full record

ArticleGut2020

Genomic and transcriptomic profiling of carcinogenesis in patients with familial adenomatous polyposis.

Jingyun Li, Rui Wang, Xin Zhou, Wendong Wang, Shuai Gao, Yunuo Mao, Xinglong Wu, Limei Guo, Haijing Liu, Lu Wen and 2 more

Abstract read
In one paragraph

Article in Gut, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Translational cancer research · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Polyclonal origins of human premalignant colorectal lesions.bioRxiv : the preprint server for biology · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Gastrointestinal Cancer Precursor Conditions and Their Detection.Hematology/oncology clinics of North America · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Identification of driving genes of familial adenomatous polyposis by differential gene expression analysis and weighted gene co-expression network analysis.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024
    Article
  20. Predicting Duodenal Cancer Risk in Patients with Familial Adenomatous Polyposis Using Machine Learning Model.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    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

12 authors.

Jingyun Li *Beijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Rui Wang *Beijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Xin Zhou *Beijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Wendong Wang *Beijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.ORCID 0000-0002-8631-3109
Shuai GaoBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Yunuo MaoBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Xinglong WuBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Limei GuoDepartment of Pathology, School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Peking University, Beijing, China.
Haijing LiuDepartment of Pathology, School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Peking University, Beijing, China.
Lu WenBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China.
Wei FuBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China tangfuchou@pku.edu.cn fuwei@bjmu.edu.cn.
Fuchou TangBeijing Advanced Innovation Center for Genomics, Department of General Surgery, College of Life Sciences, Third Hospital, Peking University, Beijing, China tangfuchou@pku.edu.cn fuwei@bjmu.edu.cn.ORCID 0000-0002-8625-7717

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveFamilial adenomatous polyposis (FAP) is characterised by the development of hundreds to thousands of adenomas at different evolutionary stages in the colon and rectum that will inevitably progress to adenocarcinomas if left untreated. Here, we investigated the genetic alterations and transcriptomic transitions from precancerous adenoma to carcinoma.

designWhole-exome sequencing, whole-genome sequencing and single-cell RNA sequencing were performed on matched adjacent normal tissues, multiregionally sampled adenomas at different stages and carcinomas from six patients with FAP and one patient with

resultsGenomic evolutionary analysis showed that adjacent lesions from the same patient with FAP can originate from the same cancer-primed cell. In addition, the tricarboxylic acid cycle pathway was strongly repressed in adenomas and was then slightly alleviated in carcinomas. Cells from the 'normal' colon epithelium of patients with FAP already showed metabolic reprogramming compared with cells from the normal colon epithelium of patients with sporadic colorectal cancer.

conclusionsThe process described in the previously reported field cancerisation model also occurs in patients with FAP and can contribute to the formation of adjacent lesions in patients with FAP. Reprogramming of carbohydrate metabolism has already occurred at the precancerous adenoma stage. Our study provides an accurate picture of the genomic and transcriptomic landscapes during the initiation and progression of carcinogenesis, especially during the transition from adenoma to carcinoma.

Indexed as

Adenomatous Polyposis ColiCarcinogenesisExome SequencingFemaleGene Expression ProfilingHumansMaleMetabolic Networks and PathwaysPedigreePrecancerous ConditionsSequence Analysis, RNASingle-Cell AnalysisWhole Genome Sequencingcolon carcinogenesiscolorectal adenomasFamilial adenomatous polyposis (FAP)Field cancerizationMUTYH-associated polyposis (MAP)Single-cell transcriptome profilingTumor heterogeneity

Identifiers

PMID31744909
PMCPMC7306982

What OpenQuestion holds

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Registered trials

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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.