ReviewCancer drug resistance (Alhambra, Calif.)2019
Insights into breast cancer phenotying through molecular omics approaches and therapy response.
Review in Cancer drug resistance (Alhambra, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Plasma Metabolome Signatures to Predict Responsiveness to Neoadjuvant Chemotherapy in Breast Cancer.Cancers · 2024Article
- Medical gas plasma technology: Roadmap on cancer treatment and immunotherapy.Redox biology · 2023Review
- MRGCN: cancer subtyping with multi-reconstruction graph convolutional network using full and partial multi-omics dataset.Bioinformatics (Oxford, England) · 2023Article
- Biomarkers for Early Detection of Cancer: Molecular Aspects.International journal of molecular sciences · 2023Article
- Delineating intra-tumoral heterogeneity and tumor evolution in breast cancer using precision-based approaches.Frontiers in genetics · 2023Review
- Tumor-derived exosomes in the regulation of macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- "Pharmacogenetics of Cancer" -Cancer drug resistance (Alhambra, Calif.) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most common cancer in the world. Despite advances in early detection and understanding of the molecular bases of breast cancer biology, approximately 30% of all patients with early-stage breast cancer have metastatic disease. Breast cancers are comprised of molecularly distinct subtypes that respond differently to pathway-targeted therapies and neoadjuvant systemic therapy. However, no tumor response is observed in some cases and development of resistance is most commonly seen in patients with heterogeneous breast cancer subtype. To offer better treatment with increased efficacy and low toxicity of selecting therapies, new technologies that incorporate clinical and molecular characteristics of intratumoral heterogeneity have been investigated. This short review provides some examples of integrative omics approaches (genome, epigenome, transcriptome, immune profiling) and mathematical/computational analyses that provide mechanistic and clinically relevant insights into underlying differences in breast cancer subtypes and patients'responses to specific therapies.
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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.