ArticleNature communications2018
Integrated genomics and functional validation identifies malignant cell specific dependencies in triple negative breast cancer.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
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- CenSegNet: a generalist high-throughput deep learning framework for centrosome phenotyping at spatial and single-cell resolution in heterogeneous tissues.Nature communications · 2026Article
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- Tumour specific HORMAD1 expression perturbs mitotic arrest and drives sensitivity to mitotic kinase inhibitors.Nature communications · 2026Article
- An antibody-drug conjugate designed through clone and isotype selection restricts the growth of CSPG4-expressing triple-negative breast cancer.NPJ precision oncology · 2026Article
- An Fc-Engineered Glycomodified Antibody Supports Proinflammatory Activation of Immune Effector Cells and Restricts Progression of Breast Cancer.Cancer research · 2025Article
- Kinesin superfamily proteins in ovarian cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2025Review
- The G protein-coupled receptor GPR89A is a novel potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells.The FEBS journal · 2025Article
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- Targeting Kinesins for Therapeutic Exploitation of Chromosomal Instability in Lung Cancer.Cancers · 2025Review
- Identification of KIFC1 as a putative vulnerability in lung cancers with centrosome amplification.Cancer gene therapy · 2024Article
- Anti-EGFR Antibody-Drug Conjugate Carrying an Inhibitor Targeting CDK Restricts Triple-Negative Breast Cancer Growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Functional exploration of copy number alterations in a Drosophila model of triple-negative breast cancer.Disease models & mechanisms · 2024Article
- Proteogenomic characterization of difficult-to-treat breast cancer with tumor cells enriched through laser microdissection.Breast cancer research : BCR · 2024Article
- Kinesin Family Member C1 (KIFC1/HSET) Underlies Aggressive Disease in Androgen Receptor-Low and Basal-Like Triple-Negative Breast Cancers.International journal of molecular sciences · 2023Article
- Discovery of 2-(3-Benzamidopropanamido)thiazole-5-carboxylate Inhibitors of the Kinesin HSET (KIFC1) and the Development of Cellular Target Engagement Probes.Journal of medicinal chemistry · 2023Article
- Glutathione Programmed Mitochondria Targeted Delivery of Lonidamine for Effective Against Triple Negative Breast Cancer.International journal of nanomedicine · 2023Article
Corrections and comments
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Authors and funding
21 authors at 2 institutions in 2 countries.
Funding
Abstract
Triple negative breast cancers (TNBCs) lack recurrent targetable driver mutations but demonstrate frequent copy number aberrations (CNAs). Here, we describe an integrative genomic and RNAi-based approach that identifies and validates gene addictions in TNBCs. CNAs and gene expression alterations are integrated and genes scored for pre-specified target features revealing 130 candidate genes. We test functional dependence on each of these genes using RNAi in breast cancer and non-malignant cells, validating malignant cell selective dependence upon 37 of 130 genes. Further analysis reveals a cluster of 13 TNBC addiction genes frequently co-upregulated that includes genes regulating cell cycle checkpoints, DNA damage response, and malignant cell selective mitotic genes. We validate the mechanism of addiction to a potential drug target: the mitotic kinesin family member C1 (KIFC1/HSET), essential for successful bipolar division of centrosome-amplified malignant cells and develop a potential selection biomarker to identify patients with tumors exhibiting centrosome amplification.
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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.