ArticlePloS one2015
Patterns of HER2 Gene Amplification and Response to Anti-HER2 Therapies.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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
36 citing papers in PubMed, 60 citations in OpenAlex.
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- A Study on the Diagnostic and Prognostic Value of Extrachromosomal Circular DNA in Breast Cancer.Genes · 2025Article
- Complex rearrangements fuel ERNature · 2025Article
- Exploring the potential of extrachromosomal DNA as a novel oncogenic driver.Science China. Life sciences · 2025Review
- Depicting Biomarkers for HER2-Inhibitor Resistance: Implication for Therapy in HER2-Positive Breast Cancer.Cancers · 2024Review
- Categorizing Extrachromosomal Circular DNA as Biomarkers in Serum of Cancer.Biomolecules · 2024Review
- Extrachromosomal DNA in cancer.Nature reviews. Cancer · 2024Review
- FISH Diagnostic Assessment ofInternational journal of molecular sciences · 2023Article
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- Article
- Extrachromosomal circular DNA: biogenesis, structure, functions and diseases.Signal transduction and targeted therapy · 2022Review
- Gasdermin B over-expression modulates HER2-targeted therapy resistance by inducing protective autophagy through Rab7 activation.Journal of experimental & clinical cancer research : CR · 2022Article
- Gene regulation on extrachromosomal DNA.Nature structural & molecular biology · 2022Review
- Unravelling the tumour genome: The evolutionary and clinical impacts of structural variants in tumourigenesis.The Journal of pathology · 2022Review
- Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.Cancer cell international · 2022Review
- Targeting HER2-AXL heterodimerization to overcome resistance to HER2 blockade in breast cancer.Science advances · 2022Article
- Article
- Emerging Biomarkers and Targeted Therapies in Feline Mammary Carcinoma.Veterinary sciences · 2021Review
- Predictive significance of HER2 intratumoral heterogeneity, determined by simultaneous gene and protein analysis, for resistance to trastuzumab-based treatments for HER2-positive breast cancer.Virchows Archiv : an international journal of pathology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A chromosomal region that includes the gene encoding HER2, a receptor tyrosine kinase (RTK), is amplified in 20% of breast cancers. Although these tumors tend to respond to drugs directed against HER2, they frequently become resistant and resume their malignant progression. Gene amplification in double minutes (DMs), which are extrachromosomal entities whose number can be dynamically regulated, has been suggested to facilitate the acquisition of resistance to therapies targeting RTKs. Here we show that ~30% of HER2-positive tumors show amplification in DMs. However, these tumors respond to trastuzumab in a similar fashion than those with amplification of the HER2 gene within chromosomes. Furthermore, in different models of resistance to anti-HER2 therapies, the number of DMs containing HER2 is maintained, even when the acquisition of resistance is concomitant with loss of HER2 protein expression. Thus, both clinical and preclinical data show that, despite expectations, loss of HER2 protein expression due to loss of DMs containing HER2 is not a likely mechanism of resistance to anti-HER2 therapies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.