Evidence map›Paper›PMID 27713419›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2017

Genetic analysis of microglandular adenosis and acinic cell carcinomas of the breast provides evidence for the existence of a low-grade triple-negative breast neoplasia family.

Felipe C Geyer, Samuel H Berman, Caterina Marchiò, Kathleen A Burke, Elena Guerini-Rocco, Salvatore Piscuoglio, Charlotte Ky Ng, Fresia Pareja, Hannah Y Wen, Zoltan Hodi and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  4. Article
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  6. Article
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Molecular pathology in breast disease: diagnostic, prognostic, and therapeutic tools.Virchows Archiv : an international journal of pathology · 2024
    Review
  14. Article
  15. Review
  16. NR4A3 Expression Is Consistently Absent in Acinic Cell Carcinomas of the Breast: A Potential Nosologic Shift.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2023
    Article
  17. Article
  18. Pitfalls in breast pathology.Histopathology · 2023
    Review
  19. Review
  20. Pathogenesis of Triple-Negative Breast Cancer.Annual review of pathology · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

Felipe C GeyerDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Samuel H BermanDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Caterina MarchiòDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Kathleen A BurkeDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Elena Guerini-RoccoDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Salvatore PiscuoglioDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Charlotte Ky NgDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Fresia ParejaDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Hannah Y WenDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Zoltan HodiDepartment of Pathology, Nottingham University, Nottingham, UK.
Stuart J SchnittDepartment of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Emad A RakhaDepartment of Pathology, Nottingham University, Nottingham, UK.
Ian O EllisDepartment of Pathology, Nottingham University, Nottingham, UK.
Larry NortonDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Britta WeigeltDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Jorge S Reis-FilhoDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Memorial Sloan Kettering Cancer Center · USUniversity of Nottingham · GBBeth Israel Deaconess Medical Center · USEuropean Institute of Oncology · ITHospital Israelita Albert Einstein · BR

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Acinic cell carcinoma is an indolent form of invasive breast cancer, whereas microglandular adenosis has been shown to be a neoplastic proliferation. Both entities display a triple-negative phenotype, and may give rise to and display somatic genomic alterations typical of high-grade triple-negative breast cancers. Here we report on a comparison of previously published data on eight carcinoma-associated microglandular adenosis and eight acinic cell carcinomas subjected to targeted massively parallel sequencing targeting all exons of 236 genes recurrently mutated in breast cancer and/or DNA repair-related. Somatic mutations, insertions/ deletions, and copy number alterations were detected using state-of-the-art bioinformatic algorithms. All cases were of triple-negative phenotype. A median of 4.5 (1-13) and 4.0 (1-7) non-synonymous somatic mutations per carcinoma-associated microglandular adenosis and acinic cell carcinoma were identified, respectively. TP53 was the sole highly recurrently mutated gene (75% in microglandular adenosis versus 88% in acinic cell carcinomas), and TP53 mutations were consistently coupled with loss of heterozygosity of the wild-type allele. Additional somatic mutations shared by both groups included those in BRCA1, PIK3CA, and INPP4B. Recurrent (n=2) somatic mutations restricted to microglandular adenosis or acinic cell carcinomas included those affecting PTEN and MED12 or ERBB4, respectively. No significant differences in the repertoire of somatic mutations were detected between microglandular adenosis and acinic cell carcinomas, and between this group of lesions and 77 triple-negative carcinomas from The Cancer Genome Atlas. Microglandular adenosis and acinic cell carcinomas, however, were genetically distinct from estrogen receptor-positive and/or HER2-positive breast cancers from The Cancer Genome Atlas. Our findings support the contention that microglandular adenosis and acinic cell carcinoma are part of the same spectrum of lesions harboring frequent TP53 somatic mutations, and likely represent low-grade forms of triple-negative disease with no/minimal metastatic potential, of which a subset has the potential to progress to high-grade triple-negative breast cancer.

Indexed as

BRCA1 ProteinBreastBreast NeoplasmsCarcinoma, Acinar CellClass I Phosphatidylinositol 3-KinasesFemaleFibrocystic Breast DiseaseGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansMediator ComplexNeoplasm GradingPhosphoric Monoester HydrolasesReceptor, ErbB-4Triple Negative Breast NeoplasmsBRCA1 ProteinBRCA1 protein, humanClass I Phosphatidylinositol 3-KinasesERBB4 protein, humanMED12 protein, humanMediator Complexphosphatidylinositol-3,4-bisphosphate 4-phosphatasePhosphoric Monoester HydrolasesPIK3CA protein, humanReceptor, ErbB-4

Identifiers

PMID27713419
PMCPMC5221420
OpenAlexW2529429444

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.