Evidence map›Paper›PMID 16695985›Full record

ArticleClinical molecular pathology1995

Loss of heterozygosity in lobular carcinoma in situ of the breast.

S R Lakhani, N Collins, J P Sloane, M R Stratton

Open access · bronzeAbstract read
In one paragraph

Article in Clinical molecular pathology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 92 citations in OpenAlex.

  1. Lobular carcinoma in situ: diagnostic criteria and molecular correlates.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    Review
  2. Genomic profiling of pleomorphic and florid lobular carcinoma in situ reveals highly recurrent ERBB2 and ERRB3 alterations.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  3. Lobular Carcinoma In Situ.Surgical pathology clinics · 2018
    Review
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Preinvasive breast cancer.Annual review of pathology · 2010
    Review
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Review
  17. Review
  18. Review
  19. Biological features of premalignant disease in the human breast.Journal of mammary gland biology and neoplasia · 2000
    Review
  20. 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

4 authors at 2 institutions in 1 country.

S R LakhaniDepartment of Histopathology, The Royal Marsden NHS Trust, Downs Road, Sutton, Surrey SM2 5PT.
N Collins
J P Sloane
M R Stratton
Royal Marsden NHS Foundation Trust · GBInstitute of Cancer Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims-(1) To investigate whether loss of heterozygosity identified at various loci in invasive breast carcinoma or is present in lobular carcinoma in situ (LCIS). (2) To investigate whether LCIS is a monoclonal (neoplastic) or a polyclonal (hyperplastic) proliferation.Methods-Forty three cases of LCIS (30 with associated invasive carcinoma or in situ ductal carcinoma (DCIS) and 13 cases of pure LCIS) were investigated for loss of heterozygosity on chromosomes 16q, 17q, 17p, and 13q using a microdissection technique, polymorphic DNA markers, and the polymerase chain reaction (PCR).Results-Loss of heterozygosity was detected in both subgroups of LCIS at all the loci examined. There was no significant difference in the frequency of the loss between the group associated with invasive carcinoma and the pure LCIS group. The frequency of loss of heterozygosity ranged from 8% on 17p to 50% on 17q.Conclusions-Because of the nature of the technique employed, our findings show that LCIS is a monoclonal (neoplastic) proliferation rather than a hyperplastic proliferation. The incidence of loss of heterozygosity on 17p (D17S796) is lower than we have observed previously in DCIS, suggesting that LCIS and DCIS are different genetically as well as clinically and morphologically. The similar incidence of loss of heterozygosity on 16q and 17q, however, suggests that DCIS and LCIS may share a common pathway of evolution.

Identifiers

PMID16695985
PMCPMC407928
OpenAlexW2080236745

What OpenQuestion holds

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Registered trials

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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.