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    GENE:

    BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)

    i
    Other names: BCAR4, Breast Cancer Anti-Estrogen Resistance 4, BCAR4, Breast Cancer Anti-Estrogen Resistance 4 (Non-Protein Coding), Breast Cancer Antiestrogen Resistance 4 Protein, HCG1814062, Isoform CRA_a, NONHSAG018621.2, HSALNG0109621
    22d
    Innovations in Oncology Diagnostics: Genetic Research and Liquid Biopsy as Tools of Personalised Medicine. (PubMed, Asian Pac J Cancer Prev)
    The analysis of material obtained from the biological fluids of oncology patients enabled disease prognosis, risk assessment of progression, and the determination of optimal approaches to personalised therapy, ultimately improving treatment efficacy. The collected data may serve as a foundation for clinically valuable laboratory studies and practical research.
    Review • Journal • Liquid biopsy
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    EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • CCNE1 (Cyclin E1) • MUC1 (Mucin 1) • MIR21 (MicroRNA 21) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • MIR181A1 (MicroRNA 181a-1)
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    TP53 mutation • KRAS mutation • EGFR mutation • PIK3CA mutation • EGFR amplification • PTEN mutation
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    gefitinib
    10ms
    Long noncoding RNA BCAR4 regulates osteosarcoma progression by targeting microRNA-1260a. (PubMed, Bull Cancer)
    This study proposes a potential therapeutic approach for treating osteosarcoma by targeting the BCAR4/miR-1260a axis. These insights shed light on the intricate regulatory network underlying osteosarcoma pathogenesis and offer promising avenues for developing targeted therapies against this aggressive cancer.
    Journal
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    BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
    over1year
    Exploring the interplay of natural products and long non-coding RNAs in colorectal cancer: pathogenesis, diagnosis, and overcoming drug resistance. (PubMed, Naunyn Schmiedebergs Arch Pharmacol)
    This review article aims to provide a comprehensive analysis of the current knowledge regarding the effectiveness of natural anti-cancer agents in CRC treatment. Additionally, it offers an in-depth evaluation of lncRNAs in CRC, their role in the disease's progression, and their potential applications in its management.
    Review • Journal
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    HOTAIR (HOX Transcript Antisense RNA) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • GAS5 (Growth Arrest Specific 5)
    over1year
    Oncogenic fusion of CD63-BCAR4 contributes cancer stem cell-like properties via ALDH1 activity. (PubMed, Mol Carcinog)
    Moreover, DEAB, an ALDH1A1 inhibitor, reduced the migration activity induced by CD63-BCAR4 as well as the sphere-forming activity. Our findings suggest that CD63-BCAR4 fusion induces CSC-like properties by upregulating ALDH1A1, which contributes to its metastatic features.
    Journal • Cancer stem
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    SOX2 • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • NANOG (Nanog Homeobox)
    almost2years
    BCAR4 facilitates trastuzumab resistance and EMT in breast cancer via sponging miR-665 and interacting with YAP1. (PubMed, FASEB J)
    Reciprocally, YAP1 could occupy the BCAR4 promoter to enhance its transcription, suggesting that there exists a positive feedback regulation between YAP1 and BCAR4. Targeting the BCAR4/miR-665/YAP1 axis may provide a novel insight of therapeutic approaches for TR in BC.
    Journal
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    YAP1 (Yes associated protein 1) • TGFB1 (Transforming Growth Factor Beta 1) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
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    Herceptin (trastuzumab) • DA 3111 (trastuzumab biosimilar)
    almost2years
    BCAR4 Expression as a Predictive Biomarker for Endocrine Therapy Resistance in Breast Cancer. (PubMed, Clin Breast Cancer)
    This study expands on previous findings by demonstrating that BCAR4 expression is associated with resistance to newer therapies. The identification of patients with intrinsic resistance to hormone therapy is crucial to avoid ineffective treatment strategies. These findings contribute to our understanding of endocrine therapy resistance in breast cancer and could potentially guide the development of more effective treatment strategies.
    Journal
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    ER (Estrogen receptor) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
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    ER positive
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    Prosigna™ Breast Cancer Prognostic Gene Signature Assay
    almost3years
    ROS1 as a possible prognostic biomarker of cervical adenocarcinoma: An exploratory analysis with next-generation sequencing. (PubMed, Gynecol Oncol)
    The current exploratory analysis suggests that ROS1 gene alteration may be a prognostic biomarker in cervical adenocarcinoma in Japanese patients.
    Journal • Next-generation sequencing
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    EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ARID1A (AT-rich interaction domain 1A) • SMAD4 (SMAD family member 4) • PD-L2 (Programmed Cell Death 1 Ligand 2) • EP300 (E1A binding protein p300) • TGFBR2 (Transforming Growth Factor Beta Receptor 2) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
    3years
    LncRNA BCAR4 promotes oxaliplatin resistance in colorectal cancer by modulating miR-484-3p/RAB5C expression. (PubMed, Chemotherapy)
    Knockdown of BCAR4 reduced tumor size and enhanced cell sensitivity to oxaliplatin in vivo. Conclusion The results suggested that BCAR4/miR-483-3p/RAB5C axis has the potential to be explored as a novel therapeutic target for CRC treatment.
    Journal
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    BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • MIR484 (MicroRNA 484) • MIR483 (MicroRNA 483)
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    oxaliplatin
    3years
    LncRNA BCAR4 promotes migration, invasion, and chemo-resistance by inhibiting miR-644a in breast cancer. (PubMed, J Exp Clin Cancer Res)
    Our findings provide insights into the oncogenic role of BCAR4 and implicate BCAR4 as a potential diagnostic biomarker and a promising therapeutic agent to suppress metastasis and inhibit chemo-resistance of breast cancer.
    Journal
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    ABCB1 (ATP Binding Cassette Subfamily B Member 1) • CCR7 (Chemokine (C-C motif) receptor 7) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • MIR644A (MicroRNA 644a)
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    ABCB1 expression
    over3years
    Pan-Cancer Analysis Reveals Recurrent BCAR4 Gene Fusions across Solid Tumors. (PubMed, Mol Cancer Res)
    We show that the minimum common region to all gene fusions harbors an open reading frame that is necessary to drive proliferation. BCAR4 gene fusions represent an underappreciated class of gene fusions that may have biological and clinical implications across solid tumors.
    Journal • Pan tumor
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    BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
    over3years
    Expression pattern of non-coding RNAs in non-functioning pituitary adenoma. (PubMed, Front Oncol)
    GnRH signaling pathway, Tight junction, Gap junction, Melanogenesis, DNA replication, Nucleotide excision repair, Mismatch repair and N-Glycan biosynthesis have been among dysregulated pathways in NFPAs. Taken together, our study has revealed differential expression of several genes and signaling pathways in this type of tumors.
    Journal
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    MALAT1 (Metastasis associated lung adenocarcinoma transcript 1) • NUTM2B (NUT Family Member 2B) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4)
    over3years
    Oncogenic fusion of BCAR4 activates EGFR signaling and is sensitive to dual inhibition of EGFR/HER2. (PubMed, Front Mol Biosci)
    Library screening revealed that erlotinib, canertinib, and lapatinib demonstrated inhibitory effects on cell migration. In addition, canertinib treatment restored E-cadherin expression and reduced the expression of epithelial-mesenchymal transition regulatory factors such as Slug and Snail. Taken together, these results suggest that EGFR/HER2 inhibitors are potential therapeutic options for BCAR4 fusion-harboring lung cancer patients, even in the absence of EGFR mutations.
    Journal
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    CDH1 (Cadherin 1) • BCAR4 (Breast Cancer Anti-Estrogen Resistance 4) • SNAI2 (Snail Family Transcriptional Repressor 2)
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    CDH1 expression • BCAR4 overexpression
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    erlotinib • lapatinib • canertinib (CI-1033)