Evidence map›Paper›PMID 27141064›Full record

ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2016

The molecular pathology of ovarian serous borderline tumors.

A Malpica, K-K Wong

Open access · bronzeAbstract read
In one paragraph

Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Molecular changes driving low-grade serous ovarian cancer and implications for treatment.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. KRAS mutation in primary ovarian serous borderline tumors correlates with tumor recurrence.Virchows Archiv : an international journal of pathology · 2023
    Article
  14. Article
  15. Article
  16. CD133 Act as an Essential Marker in Ovarian Carcinogenesis.Asian Pacific journal of cancer prevention : APJCP · 2021
    Article
  17. Article
  18. Article
  19. TargetingCancers · 2021
    Review
  20. Comprehensive genomic profiling reveals ubiquitous KRAS mutations and frequent PIK3CA mutations in ovarian seromucinous borderline tumor.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    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

2 authors at 2 institutions in 1 country.

A MalpicaDepartment of Pathology amalpica@mdanderson.org.
K-K WongDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA.
Anderson University - South Carolina · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular studies in ovarian serous borderline tumors (OSBTs) have been used to understand different aspects of this neoplasm. (i) Pathogenesis, Kras and Braf mutations represent very early events in the tumorigenesis of OSBT as both are detected in serous cystadenomas associated with OSBTs. In contrast, serous cystadenomas without OSBTs do not show Kras or Braf mutations. In OSBTs, Kras mutations range from 17% to 39.5%, while Braf mutations range from 23% to 48%. The former is comparable with the range of Kras mutations in ovarian low-grade serous carcinomas (OLGSCa), 19%-54.5%. In contrast, Braf mutations in OLGSCa range from 0% to 33%. Serous cystadenomas appear to progress to OSBT due to a Braf mutation, but this mutation is rarely involved in the progression to OLGSCa. OSBTs with Braf mutation are associated with cellular senescence and up-regulation of tumor suppressor genes. In contrast, OSBTs without a Braf mutation may progress to OLGSCa due to Kras mutation or some other genetic alterations. (ii) The relationship between OSBTs and the extraovarian disease, a monoclonal versus mutifocal origin? This is still matter of debate as studies using different techniques have failed to settle this controversy. (iii) Biological behavior, Braf mutations appear to have a protective role against the progression of OSBT to OLGSCa, while Kras mutations are commonly seen in cases of OSBT that recurred as LGSCa. Nevertheless, LGSCa as a recurrence of an OSBT can originate from OSBTs with or without detectable Kras mutations. Also, it appears to be an association between Kras G12v mutation and a more aggressive phenotype of OSBT that recurred as LGSCa. (iv) Actionable targets, currently there are limited data. It has been reported that cancer cell lines with Kras G12v mutation are more sensitive to selumetinib than cell lines with wild-type Kras.

Indexed as

Antineoplastic AgentsCell Transformation, NeoplasticCystadenocarcinoma, SerousFemaleGenes, rasHumansMolecular Targeted TherapyMutationOvarian NeoplasmsPathology, MolecularProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Antineoplastic AgentsBRAF protein, humanKRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BrafimplantsKrasovaryserous borderline tumorserous tumor of low malignant potential

Identifiers

PMID27141064
PMCPMC4852276
OpenAlexW2344152332

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.