Evidence map›Paper›PMID 22161225›Full record

ReviewPathology oncology research : POR2012

Modern trends into the epidemiology and screening of ovarian cancer. Genetic substrate of the sporadic form.

Maria Koutsaki, Apostolos Zaravinos, Demetrios A Spandidos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pathology oncology research : POR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
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

3 authors.

Maria KoutsakiLaboratory of Virology, Medical School, University of Crete, 71110, Heraklion, Crete, Greece.
Apostolos Zaravinos
Demetrios A Spandidos

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer (OC) is a heterogeneous disease, including a broad spectrum of histological subtypes and demonstrating diverse biological behavior. Epithelial-derived ovarian malignant tumours constitute the predominant and most lethal form of the disease. Age, genetic predisposition, gynecological and reproductive factors and environmental factors are the main risk factors that increase the risk for acquiring OC. Vaginal examination, ultrasonography and measurement of blood serum levels of tumour markers, especially CA125 constitute the first-line screening modalities for OC, whereas second-line testing involves more accurate imaging techniques such as color Doppler ultrasound of the lesion or/and a CT scan. Sex steroid hormone pathway genes, cell cycle genes, DNA repair genes, oncogenes and onco-suppressor genes have been associated with a genetic susceptibility to sporadic OC. In the present review we focus on the major oncogenes and onco-suppressor genes in the sporadic form of the disease. Each tumour subtype is associated with a unique molecular signature, as revealed by current genetic and biomarker profiling studies. Different OC pathways emerge early in the process of carcinogenesis, ultimately leading to clinically different tumour types. As mutations acquired early during tumourigenesis will be present in all later stages, large-scale gene expression profiling using DNA microarray analysis techniques can help to classify ovarian cancers into clinically relevant subtypes.

Indexed as

Genes, Tumor SuppressorGenetic Predisposition to DiseaseOncogenesFemaleHumansOvarian Neoplasms

Identifiers

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.