Mutations and deletions of ARID1A in breast tumors.

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.

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.

Who cites it

39 citing papers in PubMed, 51 citations in OpenAlex.

1. Comprehensive Molecular Characterization of Polymorphous Adenocarcinoma, Cribriform Subtype: Identifying Novel Fusions and Fusion Partners.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2023
   Article
2. The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023
   Review
3. ARID1A in cancer: Friend or foe?Frontiers in oncology · 2023
   Review
4. Endometriosis Stem Cells as a Possible Main Target for Carcinogenesis of Endometriosis-Associated Ovarian Cancer (EAOC).Cancers · 2022
   Review
5. Roles of ARID1A variations in colorectal cancer: a collaborative review.Molecular medicine (Cambridge, Mass.) · 2022
   Review
6. Downregulation of ARID1A is correlated with poor prognosis in non-small cell lung cancer.Translational cancer research · 2020
   Article
7. ARID1A/BAF250a is significantly overexpressed in primary invasive breast cancer.Translational cancer research · 2020
   Article
8. Precision medicine and actionable alterations in lung cancer: A single institution experience.PloS one · 2020
   Article
9. Genomic analyses of flow-sorted Hodgkin Reed-Sternberg cells reveal complementary mechanisms of immune evasion.Blood advances · 2019
   Article
10. Circulating miRNAs as Biomarkers for Endometriosis and Endometriosis-Related Ovarian Cancer-An Overview.Journal of clinical medicine · 2019
    Review
11. Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities.Expert review of anticancer therapy · 2019
    Review
12. Prognostic and Predictive Epigenetic Biomarkers in Oncology.Molecular diagnosis & therapy · 2019
    Review
13. ARID1A and CEBPα cooperatively inhibit UCA1 transcription in breast cancer.Oncogene · 2018
    Article
14. Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017
    Review
15. Pediatric Anaplastic Embryonal Rhabdomyosarcoma: Targeted Therapy Guided by Genetic Analysis and a Patient-Derived Xenograft Study.Frontiers in oncology · 2017
    Article
16. Genomic and proteomic characterization of ARID1A chromatin remodeller in ampullary tumors.American journal of cancer research · 2017
    Article
17. The Chromatin Remodeling Component Arid1a Is a Suppressor of Spontaneous Mammary Tumors in Mice.Genetics · 2016
    Article
18. ARID1A gene mutation in ovarian and endometrial cancers (Review).Oncology reports · 2016
    Review
19. Loss of Tumor Suppressor ARID1A Protein Expression Correlates with Poor Prognosis in Patients with Primary Breast Cancer.Journal of breast cancer · 2015
    Article
20. Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.Seminars in cancer biology · 2015
    Review

Corrections and comments

• Comment on
  An integrated genomic approach identifies ARID1A as a candidate tumor-suppressor gene in breast cancer.2012

Authors and funding

8 authors at 1 institution in 2 countries.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

Indexed as