Evidence map›Paper›PMID 32226926›Full record

ArticleCancer drug resistance (Alhambra, Calif.)2020

Lipid metabolic reprogramming as an emerging mechanism of resistance to kinase inhibitors in breast cancer.

William W Feng, Manabu Kurokawa

Open access · diamondAbstract read
In one paragraph

Article in Cancer drug resistance (Alhambra, Calif.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Metabolic hallmarks of trastuzumab resistance.Expert opinion on therapeutic targets · 2025
    Review
  7. Article
  8. Article
  9. HER2-Positive Breast Cancer Treatment and Resistance.Advances in experimental medicine and biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Phytochemicals Target Multiple Metabolic Pathways in Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
  15. Article
  16. Article
  17. Journal of traditional and complementary medicine · 2023
    Article
  18. Characterization of Lipid Alterations by OncogenicOmics : a journal of integrative biology · 2023
    Article
  19. Article
  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

2 authors at 2 institutions in 1 country.

William W FengDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.
Manabu KurokawaDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.
Dartmouth College · USKent State University · US

Funding

Molecular mechanisms of chemoresistance in breast cancerR00CA140948 · NCI · DARTMOUTH COLLEGE · PI KUROKAWA, MANABU · 2012 to 2014
$708k
Role of CD36 in Breast TumorsR03CA208384 · NCI · KENT STATE UNIVERSITY · PI KUROKAWA, MANABU · 2017 to 2018
$150k
NCI NIH HHS R00 CA140948NCI NIH HHS R03 CA208384
6 · The paper itself

Abstract

Breast cancer is one of the leading causes of death in women in the United States. In general, patients with breast cancer undergo surgical resection of the tumor and/or receive drug treatment to kill or suppress the growth of cancer cells. In this regard, small molecule kinase inhibitors serve as an important class of drugs used in clinical and research settings. However, the development of resistance to these compounds, in particular HER2 and CDK4/6 inhibitors, often limits durable clinical responses to therapy. Emerging evidence indicates that PI3K/AKT/mTOR pathway hyperactivation is one of the most prominent mechanisms of resistance to many small molecule inhibitors as it bypasses upstream growth factor receptor inhibition. Importantly, the PI3K/AKT/mTOR pathway also plays a pertinent role in regulating various aspects of cancer metabolism. Recent studies from our lab and others have demonstrated that altered lipid metabolism mediates the development of acquired drug resistance to HER2-targeted therapies in breast cancer, raising an interesting link between reprogrammed kinase signaling and lipid metabolism. It appears that, upon development of resistance to HER2 inhibitors, breast cancer cells rewire lipid metabolism to somehow circumvent the inhibition of kinase signaling. Here, we review various mechanisms of resistance observed for kinase inhibitors and discuss lipid metabolism as a potential therapeutic target to overcome acquired drug resistance.

Indexed as

Drug resistanceHER2lipid metabolismsmall molecule inhibitortyrosine kinase

Identifiers

PMID32226926
PMCPMC7100881
OpenAlexW2998382082

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.