Evidence map›Paper›PMID 36918928›Full record

ReviewBreast cancer research : BCR2023

RET signaling in breast cancer therapeutic resistance and metastasis.

Geoffrey Pecar, Simeng Liu, Jagmohan Hooda, Jennifer M Atkinson, Steffi Oesterreich, Adrian V Lee

Open access · goldFull text readReview
In one paragraph

Review in Breast cancer research : BCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Guideline
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  16. Precision therapy in metastatic breast cancer: the current landscape of molecular alteration-based therapies.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. The potential of lenvatinib in breast cancer therapy.Medical oncology (Northwood, London, England) · 2024
    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

6 authors at 3 institutions in 2 countries.

Geoffrey PecarWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA.
Simeng LiuWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA.
Jagmohan HoodaWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA.
Jennifer M AtkinsonWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA.
Steffi OesterreichWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA.
Adrian V LeeWomen's Cancer Research Center, UPMC Hillman Cancer Center and Magee-Womens Research Institute, Pittsburgh, PA, USA. leeav@upmc.edu.
Cancer Research Center · USMagee-Womens Research Institute · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
NCI NIH HHS P30 CA047904Susan G. Komen SAC110021Susan G. Komen SAC160073
6 · The paper itself

Abstract

RET, a single-pass receptor tyrosine kinase encoded on human chromosome 10, is well known to the field of developmental biology for its role in the ontogenesis of the central and enteric nervous systems and the kidney. In adults, RET alterations have been characterized as drivers of non-small cell lung cancer and multiple neuroendocrine neoplasms. In breast cancer, RET signaling networks have been shown to influence diverse functions including tumor development, metastasis, and therapeutic resistance. While RET is known to drive the development and progression of multiple solid tumors, therapeutic agents selectively targeting RET are relatively new, though multiple multi-kinase inhibitors have shown promise as RET inhibitors in the past; further, RET has been historically neglected as a potential therapeutic co-target in endocrine-refractory breast cancers despite mounting evidence for a key pathologic role and repeated description of a bi-directional relationship with the estrogen receptor, the principal driver of most breast tumors. Additionally, the recent discovery of RET enrichment in breast cancer brain metastases suggests a role for RET inhibition specific to advanced disease. This review assesses the status of research on RET in breast cancer and evaluates the therapeutic potential of RET-selective kinase inhibitors across major breast cancer subtypes.

Indexed as

Breast NeoplasmsCarcinoma, Non-Small-Cell LungLung NeoplasmsAdultDrug Resistance, NeoplasmFemaleHumansProtein Kinase InhibitorsProto-Oncogene Proteins c-retSignal TransductionProtein Kinase InhibitorsProto-Oncogene Proteins c-retRET protein, humanBreast cancerDrug resistanceGDNFMetastasisRET

Identifiers

PMID36918928
PMCPMC10015789
OpenAlexW4324140946

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read24
identifiers read6
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.