Evidence map›Paper›PMID 15111296›Full record

ReviewThe American journal of pathology2004

Ovarian tumorigenesis: a proposed model based on morphological and molecular genetic analysis.

Ie-Ming Shih, Robert J Kurman

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03860805 (SALpingectomy for STERilization), which is not on this map. Cited by 502 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
502citing papers in PubMed, 2 pooled it
43.6field-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.

NCT03860805 naactive not recruitingnot on this mapstarted 2019, after this paper: background citation

SALpingectomy for STERilization (SALSTER); a Randomized Trial

TypeinterventionalSponsorGöteborg UniversityRan2019 to 2050Enrolled900ConditionsSterilization Tubal, Salpingectomy, Laparoscopy, Ovarian ReserveArmsLaparoscopic tubal ligation, Laparoscopic bilateral salpingectomy
3 · Its place in the literature

Who cites it

502 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,195 citations in OpenAlex.

  1. Pooled it
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  18. Aspirin-induced acetylation of APE1/Ref-1 enhances RAGE binding and promotes apoptosis in ovarian cancer cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  19. Cellular origins of mucinous ovarian carcinoma.The Journal of pathology · 2025
    Review
  20. Article

442 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

2 authors at 2 institutions in 1 country.

Ie-Ming ShihDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. shihie@yahoo.com
Robert J Kurman
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of ovarian carcinoma, the most lethal gynecological malignancy, is unknown because of the lack of a tumor progression model. Based on a review of recent clinicopathological and molecular studies, we propose a model for their development. In this model, surface epithelial tumors are divided into two broad categories designated type I and type II tumors that correspond to two main pathways of tumorigenesis. Type I tumors tend to be low-grade neoplasms that arise in a stepwise manner from borderline tumors whereas type II tumors are high-grade neoplasms for which morphologically recognizable precursor lesions have not been identified, so-called de novo development. As serous tumors are the most common surface epithelial tumors, low-grade serous carcinoma is the prototypic type I tumor and high-grade serous carcinoma is the prototypic type II tumor. In addition to low-grade serous carcinomas, type I tumors are composed of mucinous carcinomas, endometrioid carcinomas, malignant Brenner tumors, and clear cell carcinomas. Type I tumors are associated with distinct molecular changes that are rarely found in type II tumors, such as BRAF and KRAS mutations for serous tumors, KRAS mutations for mucinous tumors, and beta-catenin and PTEN mutations and microsatellite instability for endometrioid tumors. Type II tumors include high-grade serous carcinoma, malignant mixed mesodermal tumors (carcinosarcoma), and undifferentiated carcinoma. There are very limited data on the molecular alterations associated with type II tumors except frequent p53 mutations in high-grade serous carcinomas and malignant mixed mesodermal tumors (carcinosarcomas). This model of carcinogenesis reconciles the relationship of borderline tumors to invasive carcinoma and provides a morphological and molecular framework for studies aimed at elucidating the pathogenesis of ovarian cancer.

Indexed as

CarcinomaDisease ProgressionFemaleHumansMicrosatellite RepeatsModels, BiologicalModels, GeneticMutationOvarian Neoplasms

Identifiers

PMID15111296
PMCPMC1615664
OpenAlexW1961928411

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.