Evidence map›Paper›PMID 8460634›Full record

ArticleAmerican journal of human genetics1993

Genetic linkage analysis in familial breast and ovarian cancer: results from 214 families. The Breast Cancer Linkage Consortium.

D F Easton, D T Bishop, D Ford, G P Crockford

Abstract read
In one paragraph

Article in American journal of human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 329 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
329citing papers in PubMed, 3 pooled it
73.6field-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.

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

329 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,253 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Putative linkage signals identified for breast cancer in African American families.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2015
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  13. Approaches and methods to study wildlife cancer.The Journal of animal ecology · 2024
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  19. A new wave of innovations within the DNA damage response.Signal transduction and targeted therapy · 2023
    Review
  20. Article

269 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

4 authors at 2 institutions in 1 country.

D F EastonInstitute of Cancer Research, Section of Epidemiology, Belmont, Surrey, England.
D T Bishop
D Ford
G P Crockford
Cancer Research UK · GBSt James's University Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is known to have an inherited component, consistent in some families with autosomal dominant inheritance; in such families the disease often occurs in association with ovarian cancer. Previous genetic linkage studies have established that in some such families disease occurrence is linked to markers on chromosome 17q. This paper reports the results of a collaborative linkage study involving 214 breast cancer families, including 57 breast-ovarian cancer families; this represents almost all the known families with 17q linkage data. Six markers on 17q, spanning approximately 30 cM, were typed in the families. The aims of the study were to define more precisely the localization of the disease gene, the extent of genetic heterogeneity and the characteristics of linked families and to estimate the penetrance of the 17q gene. Under the assumption of no genetic heterogeneity, the strongest linkage evidence was obtained with D17S588 (maximum LOD score [Zmax] = 21.68 at female recombination fraction [theta f] = .13) and D17S579 (Zmax = 13.02 at theta f = .16). Multipoint linkage analysis allowing for genetic heterogeneity provided evidence that the predisposing gene lies between the markers D17S588 and D17S250, an interval whose genetic length is estimated to be 8.3 cM in males and 18.0 cM in females. This position was supported over other intervals by odds of 66:1. The location of the gene with respect to D17S579 could not be determined unequivocally. Under the genetic model used in the analysis, the best estimate of the proportion of linked breast-ovarian cancer families was 1.0 (lower LOD-1 limit 0.79). In contrast, there was significant evidence of genetic heterogeneity among the families without ovarian cancer, with an estimated 45% being linked. These results suggest that a gene(s) on chromosome 17q accounts for the majority of families in which both early-onset breast cancer and ovarian cancer occur but that other genes predisposing to breast cancer exist. By examining the fit of the linkage data to different penetrance functions, the cumulative risk associated with the 17q gene was estimated to be 59% by age 50 years and 82% by age 70 years. The corresponding estimates for the breast-ovary families were 67% and 76%, and those for the families without ovarian cancer were 49% and 90%; these penetrance functions did not differ significantly from one another.

Indexed as

Chromosomes, Human, Pair 17Proto-OncogenesAdultAgedAged, 80 and overAllelesBase SequenceBreast NeoplasmsChromosome MappingDNA, NeoplasmDNA ProbesFamily HealthFemaleGene ExpressionGene Expression Regulation, NeoplasticGenetic LinkageDNA, NeoplasmDNA ProbesGenetic Markers

Identifiers

PMID8460634
PMCPMC1682082
OpenAlexW2772971838

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.