Evidence map›Paper›PMID 37884500›Full record

ReviewOncogenesis2023

Molecular mechanisms in colitis-associated colorectal cancer.

Royce W Zhou, Noam Harpaz, Steven H Itzkowitz, Ramon E Parsons

Open access · goldAbstract readReview
In one paragraph

Review in Oncogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
19.9field-weighted citation impact, top 1% of its field
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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Observational
  6. Article
  7. Article
  8. Article
  9. 5-FU chemotherapy induces functional CD7Science China. Life sciences · 2026
    Article
  10. Pathophysiology of colitis-associated colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  11. Article
  12. Article
  13. Harnessing the microbiome for cancer therapy.Nature reviews. Microbiology · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

20 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Royce W ZhouThe Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Noam HarpazThe Dr. Henry D. Janowitz Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Steven H ItzkowitzThe Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. steven.itzkowitz@mountsinai.org.
Ramon E ParsonsThe Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ramon.parsons@mssm.edu.
Icahn School of Medicine at Mount Sinai · USUniversity of California, San Francisco · US

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
PTEN and CancerR35CA220491 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PARSONS, RAMON E · 2017 to 2023
$6.8M
(PQ9) Developing EZH2 Degraders for Treating Triple-Negative Breast CancerR01CA230854 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI JIN, JIAN, PARSONS, RAMON E · 2018 to 2022
$1.5M
Functional analyses of super-enhancer dysregulation in colorectal carcinoma patient samples.F30CA243207 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHOU, ROYCE · 2019 to 2022
$190k
NCI NIH HHS F30 CA243207NCI NIH HHS P30 CA196521NCI NIH HHS R01 CA230854NCI NIH HHS R35 CA220491
6 · The paper itself

Abstract

Sustained chronic inflammation of the large intestine leads to tissue damage and repair, which is associated with an increased incidence of colitis-associated colorectal cancer (CAC). The genetic makeup of CAC is somewhat similar to sporadic colorectal carcinoma (sCRC), but there are differences in the sequence and timing of alterations in the carcinogenesis process. Several models have been developed to explain the development of CAC, particularly the "field cancerization" model, which proposes that chronic inflammation accelerates mutagenesis and selects for the clonal expansion of phenotypically normal, pro-tumorigenic cells. In contrast, the "Big Bang" model posits that tumorigenic clones with multiple driver gene mutations emerge spontaneously. The details of CAC tumorigenesis-and how they differ from sCRC-are not yet fully understood. In this Review, we discuss recent genetic, epigenetic, and environmental findings related to CAC pathogenesis in the past five years, with a focus on unbiased, high-resolution genetic profiling of non-dysplastic field cancerization in the context of inflammatory bowel disease (IBD).

Identifiers

PMID37884500
PMCPMC10603140
OpenAlexW4387965670

What OpenQuestion holds

Textmetadata
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.