Evidence map›Paper›PMID 31420779›Full record

ArticleBreast cancer research and treatment2019

Genomic landscape of ductal carcinoma in situ and association with progression.

Chieh-Yu Lin, Sujay Vennam, Natasha Purington, Eric Lin, Sushama Varma, Summer Han, Manisha Desa, Tina Seto, Nicholas J Wang, Henning Stehr and 3 more

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Multi-omics portrait of ductal carcinoma in situ in young women.Breast cancer research and treatment · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Ductal Carcinoma in Situ: Molecular Changes Accompanying Disease Progression.Journal of mammary gland biology and neoplasia · 2022
    Review
  12. Article
  13. Article
  14. Whole-Exome Sequencing Analysis of the Progression from Non-Low-Grade Ductal CarcinomaClinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Observational
  15. 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

13 authors.

Chieh-Yu LinDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Sujay VennamDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Natasha PuringtonDepartment of Medicine, Quantitative Sciences Unit, Stanford University, Stanford, CA, USA.
Eric LinDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Sushama VarmaDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Summer HanDepartment of Medicine, Quantitative Sciences Unit, Stanford University, Stanford, CA, USA.
Manisha DesaDepartment of Medicine and of Biomedical Data Science, Quantitative Sciences Unit, Stanford University, Stanford, CA, USA.
Tina SetoResearch Information Technology, Stanford University School of Medicine, Stanford, CA, USA.
Nicholas J WangDepartment of Biomedical Engineering, Oregon Health and Science University, Portland, OR, USA.
Henning StehrDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Megan L TroxellDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Allison W KurianDepartments of Medicine and of Health Research and Policy, Stanford University School of Medicine, Stanford, CA, USA.
Robert B WestDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA. rbwest@stanford.edu.ORCID http://orcid.org/0000-0002-8330-8283

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
Stanford Center for Clinical & Translational Education and Research (Spectrum)UL1TR003142 · NCATS · STANFORD UNIVERSITY · PI O'HARA, RUTH M · 2019 to 2023
$45.0M
CALIFORNIA'S PARTICIPATION IN THE NATIONAL CANCER PREVENTION AND CONTRO PROGRAMU58DP000807 · DP · PUBLIC HEALTH INSTITUTE · PI SNIPES, KURT P · 2007 to 2011
$22.5M
Stanford Center for Clinical and Translational Education and Research (SCCTER)UL1UL1RR025744 · NCRR · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2008 to 2011
$22.4M
Genomic and Morphologic Predictor of High-Risk DCISR01CA193694 · NCI · STANFORD UNIVERSITY · PI WEST, ROBERT B · 2016 to 2020
$3.5M
NCATS NIH HHS UL1 TR003142NCCDPHP CDC HHS U58 DP000807NCI NIH HHS HHSN261201000034CNCI NIH HHS HHSN261201000035CNCI NIH HHS HHSN261201000035INCI NIH HHS HHSN261201000140CNCI NIH HHS P30 CA124435NCI NIH HHS R01 CA193694NCRR NIH HHS UL1 RR025744NIH HHS R01CA193694
6 · The paper itself

Abstract

purposeThe detection rate of breast ductal carcinoma in situ (DCIS) has increased significantly, raising the concern that DCIS is overdiagnosed and overtreated. Therefore, there is an unmet clinical need to better predict the risk of progression among DCIS patients. Our hypothesis is that by combining molecular signatures with clinicopathologic features, we can elucidate the biology of breast cancer progression, and risk-stratify patients with DCIS.

methodsTargeted exon sequencing with a custom panel of 223 genes/regions was performed for 125 DCIS cases. Among them, 60 were from cases having concurrent or subsequent invasive breast cancer (IBC) (DCIS + IBC group), and 65 from cases with no IBC development over a median follow-up of 13 years (DCIS-only group). Copy number alterations in chromosome 1q32, 8q24, and 11q13 were analyzed using fluorescence in situ hybridization (FISH). Multivariable logistic regression models were fit to the outcome of DCIS progression to IBC as functions of demographic and clinical features.

resultsWe observed recurrent variants of known IBC-related mutations, and the most commonly mutated genes in DCIS were PIK3CA (34.4%) and TP53 (18.4%). There was an inverse association between PIK3CA kinase domain mutations and progression (Odds Ratio [OR] 10.2, p < 0.05). Copy number variations in 1q32 and 8q24 were associated with progression (OR 9.3 and 46, respectively; both p < 0.05).

conclusionsPIK3CA kinase domain mutations and the absence of copy number gains in DCIS are protective against progression to IBC. These results may guide efforts to distinguish low-risk from high-risk DCIS.

Indexed as

Genome-Wide Association StudyGenomicsAgedAged, 80 and overCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingDNA Copy Number VariationsFemaleGenetic Predisposition to DiseaseHumansIn Situ Hybridization, FluorescenceMiddle AgedNeoplasm MetastasisNeoplasm StagingTumor BurdenBreast cancerCopy number variantDuctal carcinoma in situPIK3CA

Identifiers

PMID31420779
PMCPMC6800639

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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.