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    GENE:

    MYO18A (Myosin XVIIIA)

    i
    Other names: MYO18A, Molecule Associated With JAK3 N-Terminus, Surfactant Protein Receptor SP-R210, Myosin Containing A PDZ Domain, Unconventional Myosin-XVIIIa, MYSPDZ, MAJN, SP-A Receptor Subunit SP-R210 AlphaS, Myosin Containing PDZ Domain, Myosin 18A, SPR210, MYO18A, CD245
    Associations

    News

    Trials
    2ms
    Unveiling Novel Genetic Mutations and Prognostic Indicators in Breast Carcinoma: An Analysis of The Cancer Genome Atlas (TCGA) Data. (PubMed, Cureus)
    Conclusion The TCGA-BRCA cohort analysis emphasizes a potential interplay of metabolic genes like NDUFS1, TRPM4, ARMCX5, SLCO6A1, and epigenetic axis genes like SETDB1 and USP37 in the oncogenesis and prognosis of breast carcinomas. These observations could open potential avenues for exploring novel therapeutics in aggressive breast carcinomas.
    Journal • BRCA Biomarker
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    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA (Breast cancer early onset) • SETDB1 (SET Domain Bifurcated Histone Lysine Methyltransferase 1) • MYO18A (Myosin XVIIIA) • NDUFS1 (NADH:Ubiquinone Oxidoreductase Core Subunit S1)
    3ms
    Descriptive transcriptomic profiling differentiates oral leukoplakia from proliferative verrucous leukoplakia and reveals distinct molecular signatures. (PubMed, Med Oral Patol Oral Cir Bucal)
    Our findings emphasize the intricate transcriptomic profiles in oral leukoplakia and proliferative verrucous leukoplakia development, laying the groundwork for future studies to enhance clinical management and patient outcomes in oral oncology. Syndecan 3 gene polymorphisms may represent a key point in proliferative verrucous leukoplakia differential diagnosis and prognostic prediction.
    Journal
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    ATF7IP (Activating Transcription Factor 7 Interacting Protein) • MIR1246 (MicroRNA 1246) • MIR135B (MicroRNA 135b) • MYO18A (Myosin XVIIIA)
    9ms
    Molecular genetic analysis of pulmonary benign metastasizing leiomyoma and intravenous leiomyomatosis: a comparative study using whole exome sequencing. (PubMed, Discov Oncol)
    BML and IVL exhibit distinct gene mutations in tumor development, with certain shared mutations.
    Journal
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    ABCC2 (ATP Binding Cassette Subfamily C Member 2) • KCNJ12 (Potassium Inwardly Rectifying Channel Subfamily J Member 12) • LRP10 (LDL Receptor Related Protein 10) • DUSP1 (Dual Specificity Phosphatase 1) • MYO18A (Myosin XVIIIA) • RASA1 (RAS P21 Protein Activator 1) • TCIRG1 (T Cell Immune Regulator 1, ATPase H+ Transporting V0 Subunit A3) • ALOX15B (Arachidonate 15-Lipoxygenase Type B)
    12ms
    Golgicide A induces pyroptosis of lung cancer stem cells by regulating dTGN formation via GOLPH3/MYO18A complex. (PubMed, Stem Cell Res Ther)
    GCA induced pyroptosis by promoting the interaction between GOLPH3 and MYO18A, resulting in dTGN formation in lung CSCs. Our findings provide a novel molecular insight into the anti-cancer activities of GCA in lung CSCs.
    Journal
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    NLRP3 (NLR Family Pyrin Domain Containing 3) • MYO18A (Myosin XVIIIA)
    over1year
    Novel genetic alterations in liver cancer distinguish distinct clinical outcomes and combination immunotherapy responses. (PubMed, Front Pharmacol)
    Comprehensive genomic profiling deciphered distinct molecular characterizations underlying VI, location of onset, recurrence, and survival time in liver cancer. The identification of novel genetic predictors of response to anti-PD-1 plus bevacizumab in HCC facilitated the development of an evidence-based approach to therapy.
    Clinical data • Journal • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • RB1 (RB Transcriptional Corepressor 1) • BAP1 (BRCA1 Associated Protein 1) • KMT2D (Lysine Methyltransferase 2D) • MSH2 (MutS Homolog 2) • KMT2C (Lysine Methyltransferase 2C) • FAT1 (FAT atypical cadherin 1) • NOTCH3 (Notch Receptor 3) • FAT3 (FAT Atypical Cadherin 3) • ZFHX3 (Zinc Finger Homeobox 3) • KDM5D (Lysine Demethylase 5D) • PDE4DIP (Phosphodiesterase 4D Interacting Protein) • LATS1 (Large Tumor Suppressor Kinase 1) • PDE3A (Phosphodiesterase 3A) • SYNE1 (Spectrin Repeat Containing Nuclear Envelope Protein 1) • MYO18A (Myosin XVIIIA) • PTPRZ1 (Protein Tyrosine Phosphatase Receptor Type Z1)
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    Avastin (bevacizumab)
    2years
    3D matrix adhesion feedback controls nuclear force coupling to drive invasive cell migration. (PubMed, Cell Rep)
    The recruitment of NM2A to adhesions creates a non-muscle myosin isoform gradient, which extends from the protrusion to the nucleus. We postulate that this gradient facilitates coupling of cell-matrix interactions at the protrusive cell front with nuclear movement, enabling effective invasive migration and front-rear cell polarity.
    Journal
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    MYO18A (Myosin XVIIIA)
    over2years
    Proteomic and yeast 2-hybrid screens to identify PTEN binding partners. (PubMed, Adv Biol Regul)
    We also performed yeast two-hybrid screens which identify the previously recognised PTEN binding partner MSP58 in addition to the nuclear import export receptor TNPO3. These experiments identify several novel candidate binding partners of PTEN and provide further data addressing the set of proteins that interact with this important tumour suppressor.
    Journal
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    PTEN (Phosphatase and tensin homolog) • MMP1 (Matrix metallopeptidase 1) • MYO18A (Myosin XVIIIA)
    over2years
    Golgi Signaling Proteins GOLPH3, MYO18A, PITPNC1 and RAB1B: Implications in Prognosis and Survival Outcomes of AML Patients. (PubMed, Biomarkers)
    This study aims to explore the association between signaling proteins and the diagnosis, prognosis, and survival of AML patients. GOLPH3, MYO18A, PITPNC1, and RAB1B maybe promising diagnostic and prognostic biomarkers in AML patients.
    Journal
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    MYO18A (Myosin XVIIIA)
    almost4years
    Microfluidics-based library preparation strategies for targeted high-throughput sequencing and RNA sequencing in hematological malignancies in clinical samples (AACR 2022)
    It confirms the diagnosis of Phi-like ALL and thus offers a therapeutic target for these patients.Conclusion Microfluidics-based library prep using Juno offers a cost-effective strategy and straightforward workflows for both targeted HTS and RNA sequencing. We validated its use for hematological malignancy evaluation in routine practice.
    Clinical
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    TP53 (Tumor protein P53) • FGFR1 (Fibroblast growth factor receptor 1) • DNMT3A (DNA methyltransferase 1) • JAK2 (Janus kinase 2) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • PDGFRB (Platelet Derived Growth Factor Receptor Beta) • TET2 (Tet Methylcytosine Dioxygenase 2) • ETV6 (ETS Variant Transcription Factor 6) • CRLF2 (Cytokine Receptor Like Factor 2) • SRSF2 (Serine and arginine rich splicing factor 2) • PAX5 (Paired Box 5) • AFF1 (AF4/FMR2 Family Member 1) • TCF3 (Transcription Factor 3) • P2RY8 (P2Y Receptor Family Member 8) • PBX1 (PBX Homeobox 1) • EBF1 (EBF Transcription Factor 1) • MYO18A (Myosin XVIIIA)
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    TP53 mutation • ASXL1 mutation • TET2 mutation • SF3B1 mutation • SRSF2 mutation • FGFR1 fusion
    4years
    RNA Sequencing of Primary Cutaneous and Breast-Implant Associated Anaplastic Large Cell Lymphomas Reveals Infrequent Fusion Transcripts and Upregulation of PI3K/AKT Signaling via Neurotrophin Pathway Genes. (PubMed, Cancers (Basel))
    One of the two BI-ALCL samples showed a complex karyotype, raising the possibility that genomic instability may be responsible for intra-chromosomal fusions in BI-ALCL. Moreover, transcriptional analysis revealed similar upregulation of the PI3K/Akt pathway, associated with enrichment in the expression of neurotrophin signaling genes, which was more conspicuous in BI-ALCL, as well as differences, i.e., over-expression of genes involved in the RNA polymerase II transcription program in BI-ALCL and of the RNA splicing/processing program in cALCL.
    Journal
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    ALK (Anaplastic lymphoma kinase) • NPM1 (Nucleophosmin 1) • NF1 (Neurofibromin 1) • TYK2 (Tyrosine Kinase 2) • TP63 (Tumor protein 63) • MYO18A (Myosin XVIIIA)
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    ALK positive • ALK negative
    over4years
    The Smad4-MYO18A-PP1A complex regulates β-catenin phosphorylation and pemigatinib resistance by inhibiting PAK1 in cholangiocarcinoma. (PubMed, Cell Death Differ)
    The Smad4-MYO18A-PP1A complex dephosphorylates PAK1-T423 and thus inhibits β-catenin-S675 phosphorylation and its intranuclear localization. Smad4 suppresses CCA proliferation, migration, invasion, and sensitivity to Pemigatinib by governing the phosphorylation and intracellular localization of β-catenin.
    Journal
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    SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • MYO18A (Myosin XVIIIA)
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    Pemazyre (pemigatinib)