ArticleMolecular oncology2020
NOTCH and DNA repair pathways are more frequently targeted by genomic alterations in inflammatory than in non-inflammatory breast cancers.
Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Exome sequencing reveals new insights into the germline landscape of inflammatory breast cancer among Tunisian patients.Journal of translational medicine · 2025Article
- Clinicogenomic Characterization of Inflammatory Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Inflammatory breast cancer, best practice in the community setting.NPJ breast cancer · 2025Review
- Genomic and transcriptomic analyses identify distinctive features of triple-negative inflammatory breast cancer.NPJ precision oncology · 2024Article
- A Subpopulation of Luminal Progenitors Secretes Pleiotrophin to Promote Angiogenesis and Metastasis in Inflammatory Breast Cancer.Cancer research · 2024Article
- Mutational landscape of inflammatory breast cancer.Journal of translational medicine · 2024Article
- Comparison of the genomic alterations present in tumor samples from patients with metastatic inflammatory versus non-inflammatory breast cancer reveals AURKA as a potential treatment target.Breast (Edinburgh, Scotland) · 2023Article
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- Investigation of Molecular Features Involved in Clinical Responses and Survival in Advanced Endometrial Carcinoma Treated by Hormone Therapy.Journal of personalized medicine · 2022Article
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- Genetic Variants and Tumor Immune Microenvironment: Clues for Targeted Therapies in Inflammatory Breast Cancer (IBC).International journal of molecular sciences · 2021Article
- Whole-exome sequencing identifies somatic mutations and intratumor heterogeneity in inflammatory breast cancer.NPJ breast cancer · 2021Article
- Immune landscape of inflammatory breast cancer suggests vulnerability to immune checkpoint inhibitors.Oncoimmunology · 2021Article
- New Treatment Strategies for the Inflammatory Breast Cancer.Current treatment options in oncology · 2021Review
- Immune phenotype of patients with stage IV metastatic inflammatory breast cancer.Breast cancer research : BCR · 2020Observational
- Inflammatory Breast Cancer: Clinical Implications of Genomic Alterations and Mutational Profiling.Cancers · 2020Article
- Genomic landscape of inflammatory breast cancer identifies potential actionable genetic alterations.Oncoscience · 2020Article
- Breast Cancer: A Molecularly Heterogenous Disease Needing Subtype-Specific Treatments.Medical sciences (Basel, Switzerland) · 2020Review
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Authors and funding
20 authors at 5 institutions in 3 countries.
Funding
Abstract
Inflammatory breast cancer (IBC) is the most pro-metastatic form of breast cancer. Better understanding of its pathophysiology and identification of actionable genetic alterations (AGAs) are crucial to improve systemic treatment. We aimed to define the DNA profiles of IBC vs noninflammatory breast cancer (non-IBC) clinical samples in terms of copy number alterations (CNAs), mutations, and AGAs. We applied targeted next-generation sequencing (tNGS) and array-comparative genomic hybridization (aCGH) to 57 IBC and 50 non-IBC samples and pooled these data with four public datasets profiled using NGS and aCGH, leading to a total of 101 IBC and 2351 non-IBC untreated primary tumors. The respective percentages of each molecular subtype [hormone receptor-positive (HR+)/HER2-, HER2+, and triple-negative] were 68%, 15%, and 17% in non-IBC vs 25%, 35%, and 40% in IBC. The comparisons were adjusted for both the molecular subtypes and the American Joint Committee on Cancer (AJCC) stage. The 10 most frequently altered genes in IBCs were TP53 (63%), HER2/ERBB2 (30%), MYC (27%), PIK3CA (21%), BRCA2 (14%), CCND1 (13%), GATA3 (13%), NOTCH1 (12%), FGFR1 (11%), and ARID1A (10%). The tumor mutational burden was higher in IBC than in non-IBC. We identified 96 genes with an alteration frequency (p < 5% and q < 20%) different between IBC and non-IBC, independently from the molecular subtypes and AJCC stage; 95 were more frequently altered in IBC, including TP53, genes involved in the DNA repair (BRCA2) and NOTCH pathways, and one (PIK3CA) was more frequently altered in non-IBC. Ninety-seven percent of IBCs displayed at least one AGA. This percentage was higher than in non-IBC (87%), notably for drugs targeting DNA repair, NOTCH signaling, and CDK4/6, whose pathways were more frequently altered (DNA repair) or activated (NOTCH and CDK4/6) in IBC than in non-IBC. The genomic landscape of IBC is different from that of non-IBC. Enriched AGAs in IBC may explain its aggressiveness and provide clinically relevant targets.
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