Evidence map›Paper›PMID 28319069›Full record

ArticleOncogene2017

The branched-chain amino acid transaminase 1 sustains growth of antiestrogen-resistant and ERα-negative breast cancer.

V Thewes, R Simon, M Hlevnjak, M Schlotter, P Schroeter, K Schmidt, Y Wu, T Anzeneder, W Wang, P Windisch and 17 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

27 authors at 8 institutions in 3 countries.

V ThewesDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
R SimonInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M HlevnjakDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
M SchlotterDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
P SchroeterDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
K SchmidtDivision of Inherited Metabolic Diseases, University Children's Hospital, Heidelberg, Germany.
Y WuDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
T AnzenederPATH Foundation Biobank-Patients' Tumor Bank of Hope, Munich, Germany.
W WangDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
P WindischDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
M KirchgäßnerDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
N MellingInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
N KneiselDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
R BüttnerInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
U DeuschlePhenex Pharmaceuticals AG, Heidelberg, Germany.
H P SinnInstitute of Pathology, University of Heidelberg, Heidelberg, Germany.
A SchneeweissGynecologic Oncology, National Center for Tumor Diseases, University of Heidelberg, Heidelberg, Germany.
S HeckDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
S KaulfussBayer Pharma AG, Berlin, Germany.
H Hess-StumppBayer Pharma AG, Berlin, Germany.
J G OkunDivision of Inherited Metabolic Diseases, University Children's Hospital, Heidelberg, Germany.
G SauterInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
A E LykkesfeldtBreast Cancer Group, Danish Cancer Society Research Center, Copenhagen, Denmark.
M ZapatkaDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0001-8287-5967
B RadlwimmerDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-4553-7800
P LichterDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
M TönjesDivision of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
German Cancer Research Center · DEHeidelberg University · DEUniversität Hamburg · DEBayer (Germany) · DEDanish Cancer Society · DKHope Foundation · USPhenex Pharmaceuticals (Germany) · DEUniversity Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antiestrogen-resistant and triple-negative breast tumors pose a serious clinical challenge because of limited treatment options. We assessed global gene expression changes in antiestrogen-sensitive compared with antiestrogen-resistant (two tamoxifen resistant and two fulvestrant resistant) MCF-7 breast cancer cell lines. The branched-chain amino acid transaminase 1 (BCAT1), which catalyzes the first step in the breakdown of branched-chain amino acids, was among the most upregulated transcripts in antiestrogen-resistant cells. Elevated BCAT1 expression was confirmed in relapsed tamoxifen-resistant breast tumor specimens. High intratumoral BCAT1 levels were associated with a reduced relapse-free survival in adjuvant tamoxifen-treated patients and overall survival in unselected patients. On a tissue microarray (n=1421), BCAT1 expression was detectable in 58% of unselected primary breast carcinomas and linked to a higher Ki-67 proliferation index, as well as histological grade. Interestingly, BCAT1 was predominantly expressed in estrogen receptor-α-negative/human epidermal growth factor receptor-2-positive (ERα-negative/HER-2-positive) and triple-negative breast cancers in independent patient cohorts. The inverse relationship between BCAT1 and ERα was corroborated in various breast cancer cell lines and pharmacological long-term depletion of ERα induced BCAT1 expression in vitro. Mechanistically, BCAT1 indirectly controlled expression of the cell cycle inhibitor p27

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmEstrogen AntagonistsEstrogen Receptor alphaFemaleGene Expression ProfilingHeterograftsHumansMCF-7 CellsMiceMice, Inbred BALB CTamoxifenBCAT1 protein, humanESR1 protein, humanEstrogen AntagonistsEstrogen Receptor alphaTamoxifenTransaminases

Identifiers

PMID28319069
OpenAlexW2601915028

What OpenQuestion holds

Textmetadata
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.