Evidence map›Paper›PMID 30338425›Full record

ReviewJournal of mammary gland biology and neoplasia2018

The Emerging Roles of Steroid Hormone Receptors in Ductal Carcinoma in Situ (DCIS) of the Breast.

Hugo Villanueva, Sandra Grimm, Sagar Dhamne, Kimal Rajapakshe, Adriana Visbal, Christel M Davis, Erik A Ehli, Sean M Hartig, Cristian Coarfa, Dean P Edwards

Erratum issuedOpen access · hybridAbstract readReview
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Hugo VillanuevaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Sandra GrimmDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Sagar DhamneDepartment of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Kimal RajapaksheDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Adriana VisbalDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Christel M DavisAvera Institute for Human Genetics, 3720 W 69th St, Sioux Falls, SD, 57108, USA.
Erik A EhliAvera Institute for Human Genetics, 3720 W 69th St, Sioux Falls, SD, 57108, USA.
Sean M HartigDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Cristian CoarfaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Dean P EdwardsDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA. deane@bcm.edu.
Baylor College of Medicine · USAvera Health · US

Funding

Research Education and Career Horizons ProgramK12GM084897 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SIFERS, RICHARD NORMAN, SLAUGHTER, GAYLE · 2008 to 2016
$8.3M
METABOLIC IMPACTS OF TYPE II INTERFERON SIGNALS IN OBESITYR01DK114356 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI HARTIG, SEAN · 2017 to 2025
$4.6M
Regulation of SYSTEMIC INSULIN SENSITIVITY by miRNA-30aR03DK105006 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI HARTIG, SEAN · 2016 to 2017
$159k
Cancer Prevention and Research Institute of Texas RP150232NIDDK NIH HHS R01 DK114356NIDDK NIH HHS R03 DK105006NIGMS NIH HHS K12 GM084897NIH HHS R01DK114356NIH HHS R03DK105006
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is a non-obligate precursor to most types of invasive breast cancer (IBC). Although it is estimated only one third of untreated patients with DCIS will progress to IBC, standard of care for treatment is surgery and radiation. This therapeutic approach combined with a lack of reliable biomarker panels to predict DCIS progression is a major clinical problem. DCIS shares the same molecular subtypes as IBC including estrogen receptor (ER) and progesterone receptor (PR) positive luminal subtypes, which encompass the majority (60-70%) of DCIS. Compared to the established roles of ER and PR in luminal IBC, much less is known about the roles and mechanism of action of estrogen (E2) and progesterone (P4) and their cognate receptors in the development and progression of DCIS. This is an underexplored area of research due in part to a paucity of suitable experimental models of ER+/PR + DCIS. This review summarizes information from clinical and observational studies on steroid hormones as breast cancer risk factors and ER and PR as biomarkers in DCIS. Lastly, we discuss emerging experimental models of ER+/PR+ DCIS.

Indexed as

AnimalsAntineoplastic Agents, HormonalBiomarkers, TumorBreastBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingClinical Trials as TopicDisease Models, AnimalDisease ProgressionEstrogensFemaleHumansNeoplasm InvasivenessObservational Studies as TopicPredictive Value of TestsProgesteroneAntineoplastic Agents, HormonalBiomarkers, TumorEstrogensProgesteroneReceptors, EstrogenReceptors, ProgesteroneDuctal carcinoma In SituEstrogen receptorProgesterone receptorSteroid hormones

Identifiers

PMID30338425
PMCPMC6244884
OpenAlexW2896583832

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.