Evidence map›Paper›PMID 21336636›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2011

Pathology of hereditary breast cancer.

Petra van der Groep, Elsken van der Wall, Paul J van Diest

Abstract readReview
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 3 pooled it
–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

73 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. FASLG T844C polymorphism and susceptibility to breast cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Association between vitamin D receptor poly(A) polymorphism and breast cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Significant association between Nijmegen breakage syndrome 1 657del5 polymorphism and breast cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  4. Review
  5. Article
  6. Molecular Basis of Breast Tumor Heterogeneity.Advances in experimental medicine and biology · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Potential of Anti-inflammatory Molecules in the Chemoprevention of Breast Cancer.Recent advances in inflammation & allergy drug discovery · 2022
    Review
  16. Article
  17. Article
  18. Current oncology (Toronto, Ont.) · 2021
    Article
  19. Article
  20. Review

13 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

3 authors.

Petra van der GroepDepartment of Pathology, University Medical Center Utrecht, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands.
Elsken van der Wall
Paul J van Diest

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHereditary breast cancer runs in families where several members in different generations are affected. Most of these breast cancers are caused by mutations in the high penetrance genes BRCA1 and BRCA2 accounting for about 5% of all breast cancers. Other genes that include CHEK2, PTEN, TP53, ATM, STK11/LKB1, CDH1, NBS1, RAD50, BRIP1 and PALB2 have been described to be high or moderate penetrance breast cancer susceptibility genes, all contributing to the hereditary breast cancer spectrum. However, in still a part of familial hereditary breast cancers no relationship to any of these breast cancer susceptibility genes can be found. Research on new susceptibility genes is therefore ongoing.

designIn this review we will describe the function of the today known high or moderate penetrance breast cancer susceptibility genes and the consequences of their mutated status. Furthermore, we will focus on the histology, the immunophenotype and genotype of breast cancers caused by mutations in BRCA1 and BRCA2 genes and the other high or moderate penetrance breast cancer susceptibility genes. Finally, an overview of the clinical implications of hereditary breast cancer patients will be provided.

conclusionThis information leads to a better understanding of the morphological, immunohistochemical and molecular characteristics of different types of hereditary breast cancers. Further, these characteristics offer clues for diagnosis and new therapeutic approaches.

Indexed as

BRCA1 ProteinBRCA2 ProteinBreast NeoplasmsFamily HealthFemaleGene FrequencyGenetic Predisposition to DiseaseHumansMutationBRCA1 ProteinBRCA2 Protein

Identifiers

PMID21336636
PMCPMC3063560

What OpenQuestion holds

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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.