ArticleCell stem cell2016
Persistent Activation of NF-κB in BRCA1-Deficient Mammary Progenitors Drives Aberrant Proliferation and Accumulation of DNA Damage.
Article in Cell stem cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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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.
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Who cites it
66 citing papers in PubMed, 113 citations in OpenAlex.
- Estrogen-mediated NF-κB blockade enables breast cancer sensitivity to oncolytic VSV virotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Insights from three decades of BRCA1/2 modeling in mice.Nature genetics · 2026Review
- Exploring the impact of hAMSCs secretome on Panc1 cells via TNF-α/NF-κB (p50/p65)/Caspase 3 signaling pathways: AnBiochemistry and biophysics reports · 2026Article
- The role of the intratumoral microbiota in breast cancer metastasis and immune regulation: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Human Cancers Derived from Either Genetic or Lifestyle Factors Are Initiated by Impaired Estrogen Signaling.Cancers · 2025Review
- FRMD8 inhibits tumor metastasis in BRCA1-associated TNBC by negatively regulating tmTNF-α.Cellular & molecular biology letters · 2025Article
- Druggable Molecular Networks inBiology · 2025Review
- Cells-of-Origin of Breast Cancer and Intertumoral Heterogeneity.Advances in experimental medicine and biology · 2025Review
- Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer.Nature genetics · 2024Article
- NF-κB role on tumor proliferation, migration, invasion and immune escape.Cancer gene therapy · 2024Review
- A Mechanism for Apoptotic Effects of a Planar Catechin Analog on Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- Associations ofCancers · 2024Article
- Review
- Beyond the barrier: the immune-inspired pathways of tumor extravasation.Cell communication and signaling : CCS · 2024Review
- Signaling Pathway Alterations Driven by BRCA1 and BRCA2 Germline Mutations are Sufficient to Initiate Breast Tumorigenesis by the PIK3CAH1047R Oncogene.Cancer research communications · 2024Article
- Conditional in vivo deletion of LYN kinase has little effect on a BRCA1 loss-of-function-associated mammary tumour model.Disease models & mechanisms · 2024Article
- A transcriptional response to replication stress selectively expands a subset of Brca2-mutant mammary epithelial cells.Nature communications · 2023Article
- Associations of height, body mass index, and weight gain with breast cancer risk in carriers of a pathogenic variant in BRCA1 or BRCA2: the BRCA1 and BRCA2 Cohort Consortium.Breast cancer research : BCR · 2023Article
- Spontaneous cancer remission after COVID-19: insights from the pandemic and their relevance for cancer treatment.Journal of translational medicine · 2023Review
- Pathways Affected by Falcarinol-Type Polyacetylenes and Implications for Their Anti-Inflammatory Function and Potential in Cancer Chemoprevention.Foods (Basel, Switzerland) · 2023Review
6 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
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Human BRCA1 mutation carriers and BRCA1-deficient mouse mammary glands contain an abnormal population of mammary luminal progenitors that can form 3D colonies in a hormone-independent manner. The intrinsic cellular regulatory defect in these presumptive breast cancer precursors is not known. We have discovered that nuclear factor kappaB (NF-κB) (p52/RelB) is persistently activated in a subset of BRCA1-deficient mammary luminal progenitors. Hormone-independent luminal progenitor colony formation required NF-κB, ataxia telangiectasia-mutated (ATM), and the inhibitor of kappaB kinase, IKKα. Progesterone (P4)-stimulated proliferation resulted in a marked enhancement of DNA damage foci in Brca1(-/-) mouse mammary. In vivo, NF-κB inhibition prevented recovery of Brca1(-/-) hormone-independent colony-forming cells. The majority of human BRCA1(mut/+) mammary glands showed marked lobular expression of nuclear NF-κB. We conclude that the aberrant proliferative capacity of Brca1(-/-) luminal progenitor cells is linked to the replication-associated DNA damage response, where proliferation of mammary progenitors is perpetuated by damage-induced, autologous NF-κB signaling.
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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.