ReviewBiomolecules2017
MYC-Driven Pathways in Breast Cancer Subtypes.
Review in Biomolecules, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled 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.
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
120 citing papers in PubMed, 1 synthesis or guideline pooled it, 248 citations in OpenAlex.
- Pooled it
- Biomarkers of response to neoadjuvant palbociclib plus anastrozole in endocrine-resistant estrogen receptor-positive/HER2-negative breast cancer: a phase 2 trial.Nature communications · 2026Trial
- Article
- Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism.World journal of stem cells · 2026Article
- Amino acids metabolism: a potential target for cancer treatment.Molecular cancer · 2025Review
- SMART 2.0 Statistical Metabolomics Analysis: An R Tool 2.0.Analytical chemistry · 2025Article
- Endocrine disruption to metastasis: How phthalates promote breast carcinogenesis.Ecotoxicology and environmental safety · 2025Review
- BMI-dependent prognostic role of EEF1G in breast cancer: A 15-year follow-up of the Guangzhou Breast Cancer Cohort Study.Cancer medicine · 2025Article
- Article
- Targeting miR-32-5p suppresses c-MYC-driven proliferation and induces apoptosis in MCF-7 breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Unveiling Epigenetic Regulatory Elements Associated with Breast Cancer Development.International journal of molecular sciences · 2025Article
- Twenty-five years of WWOX insight in cancer: a treasure trove of knowledge.Functional & integrative genomics · 2025Review
- c-Myc knockdown restores tamoxifen sensitivity in triple-negative breast cancer by reactivating the expression of ERα: the central role of miR-152 and miR-148a.Breast cancer (Tokyo, Japan) · 2025Article
- Active Substances from the Micro-Immunotherapy Medicine 2LC1International journal of molecular sciences · 2025Article
- A single-cell network approach to decode metabolic regulation in gynecologic and breast cancers.NPJ systems biology and applications · 2025Article
- Blocking interplay between TERT and c-Myc: a new therapeutic strategy forInternational journal of biological sciences · 2025Article
- Integrating Network Pharmacology andCombinatorial chemistry & high throughput screening · 2025Article
- Article
- CDK9 inhibition inhibits multiple oncogenic transcriptional and epigenetic pathways in prostate cancer.British journal of cancer · 2024Article
- Autophagy-related lncRNAs and exosomal lncRNAs in colorectal cancer: focusing on lncRNA-targeted strategies.Cancer cell international · 2024Review
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor MYC (MYC proto-oncogene, bHLH transcription factor) is an essential signaling hub in multiple cellular processes that sustain growth of many types of cancers. MYC regulates expression of RNA, both protein and non-coding, that control central metabolic pathways, cell death, proliferation, differentiation, stress pathways, and mechanisms of drug resistance. Activation of MYC has been widely reported in breast cancer progression. Breast cancer is a complex heterogeneous disease and treatment options are primarily guided by histological and biochemical evaluations of the tumors. Based on biochemical markers, three main breast cancer categories are ER+ (estrogen receptor alpha positive), HER2+ (human epidermal growth factor receptor 2 positive), and TNBC (triple-negative breast cancer; estrogen receptor negative, progesterone receptor negative, HER2 negative). MYC is elevated in TNBC compared with other cancer subtypes. Interestingly, MYC-driven pathways are further elevated in aggressive breast cancer cells and tumors that display drug resistant phenotype. Identification of MYC target genes is essential in isolating signaling pathways that drive tumor development. In this review, we address the role of MYC in the three major breast cancer subtypes and highlight the most promising leads to target MYC functions.
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.