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    GENE:

    SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)

    i
    Other names: SPINK2, Serine Peptidase Inhibitor Kazal Type 2, HUSI-II, Serine Protease Inhibitor Kazal-Type 2, Epididymis Tissue Protein Li 172, Acrosin-Trypsin Inhibitor, Serine Peptidase Inhibitor, Kazal Type 2 (Acrosin-Trypsin Inhibitor), Serine Protease Inhibitor, Kazal Type 2 (Acrosin-Trypsin Inhibitor), SPGF29
    1year
    Single-cell transcriptomics reveals heterogeneity and prognostic markers of myeloid precursor cells in acute myeloid leukemia. (PubMed, Front Immunol)
    This study provides a new approach to AML prognostic assessment and reveals the role of key genes in AML. These genes may become new biomarkers and therapeutic targets that can help improve prognostic prediction and personalized treatment of AML.
    Journal
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    CD34 (CD34 molecule) • IRF8 (Interferon Regulatory Factor 8) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • ARHGAP5 (Rho GTPase Activating Protein 5) • SPATS2L (Spermatogenesis Associated Serine Rich 2 Like)
    over1year
    Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications. (PubMed, J Transl Med)
    This thorough examination of AML biology significantly deepens our grasp of the disease and presents pivotal information that could guide the creation of innovative treatment strategies for AML patients.
    Journal
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    CD74 (CD74 Molecule) • CD34 (CD34 molecule) • LGALS1 (Galectin 1) • MIF (Macrophage Migration Inhibitory Factor) • CD52 (CD52 Molecule) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • FABP5 (Fatty Acid Binding Protein 5) • S100A4 (S100 calcium binding protein A4)
    over1year
    Methylation and transcriptome analyses construct a prognostic model and reveal the suppressor role of VMO1 in lung adenocarcinoma. (PubMed, Cell Signal)
    In summary, our experiments constructed a prognostic model with high capacity for risk prediction in LUAD patients. VMO1 had a malignant suppressor role in LUAD cells. The correlation between risk score and TME might elucidate a potential mechanism of oncogenesis and provide an avenue for further therapeutic targets.
    Journal • IO biomarker
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    SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)
    almost2years
    RARRES1 inhibits hepatocellular carcinoma progression and increases its sensitivity to lenvatinib through interaction with SPINK2. (PubMed, Biol Direct)
    Our findings highlighted that RARRES1 can inhibit HCC progression and regulate HCC sensitivity to lenvatinib by interacting SPINK2, representing a new tumor suppressor RARRES1/SPINK2 axis in HCC that modulates sensitivity to lenvatinib.
    Journal
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    SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)
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    SPINK2 overexpression
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    Lenvima (lenvatinib)
    over2years
    Identification of Acute Myeloid Leukemia Cell Surface Therapeutic Targets Using Single Cell RNA Sequencing Supported By Surface Proteomics (ASH 2023)
    After quality control, we profiled and characterized 103 690 high quality cells (mean of 5185 cells/sample). We trained a Random Forest classifier to annotate cells in a two step process, first identifying plasma cells based on a restricted list of genes abundantly expressed in these cells and subsequently assigning the remaining cells to one of 33 cell types. We performed a five-fold cross validation of the model and subsequently determined the accuracy of our classifier to be 92% on the test subset of the HCA data.
    IO biomarker
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • KMT2A (Lysine Methyltransferase 2A) • CD123 (Interleukin 3 Receptor Subunit Alpha) • CD33 (CD33 Molecule) • CD34 (CD34 molecule) • IL3RA (Interleukin 3 Receptor Subunit Alpha) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • TNFRSF10B (TNF Receptor Superfamily Member 10b) • FAM30A (Family With Sequence Similarity 30 Member A)
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    FLT3-ITD mutation • DNMT3A mutation • MLL rearrangement
    over2years
    Temporary serine protease inhibition and the role of SPINK2 in human bone marrow. (PubMed, iScience)
    Analysis of putative target proteases for SPINK2 revealed the expression of PRSS2 and PRSS57 in HSPCs. Our combined results suggest that SPINK2 and its target serine proteases might play a role in the intercellular communication within the hematopoietic stem cell niche.
    Journal
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    CD34 (CD34 molecule) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)
    over2years
    Upregulation of SPINK2 in acute myeloid leukemia. (PubMed, Adv Lab Med)
    Our results suggest that SPINK2 serves an important role in AML development. Further studies are needed to evaluate SPINK2 expression in AML patients with t(8.21) and investigate to clarify its prognostic value in various subgroups of AML.
    Review • Journal
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    SPINK2 (Serine Peptidase Inhibitor Kazal Type 2)
    over2years
    SPINK2 Protein Expression Is an Independent Adverse Prognostic Marker in AML and Is Potentially Implicated in the Regulation of Ferroptosis and Immune Response. (PubMed, Int J Mol Sci)
    SPINK2 regulated the expression of certain P53 targets and ferroptosis-related genes, including SLC7A11 and STEAP3, and affected cystine uptake, intracellular iron levels and sensitivity to erastin, a specific ferroptosis inducer...Additionally, we identified a potential small-molecule inhibitor of SPINK2, which requires further characterization. In summary, high SPINK2 protein expression was a potent adverse prognostic marker in AML and might represent a druggable target.
    Journal
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    TP53 (Tumor protein P53) • NPM1 (Nucleophosmin 1) • ALCAM (Activated Leukocyte Cell Adhesion Molecule) • SLC7A11 (Solute Carrier Family 7 Member 11) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • STEAP3 (STEAP3 Metalloreductase)
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    NPM1 mutation • TP53 expression
    almost3years
    Investigation of distinct gene expression profile patterns that can improve the classification of intermediate-risk prognosis in AML patients. (PubMed, Front Genet)
    CD109, CPNE3, DDIT4, and INPP4B provided novel targets for better intermediate-risk stratification. This could enhance treatment strategies for this group, which constitutes the majority of adult AML patients.
    Journal • Gene Expression Profile
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    INPP4B (Inositol polyphosphate-4-phosphatase type II B) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • DDIT4 (DNA Damage Inducible Transcript 4)
    over3years
    Multiomic Single-Cell Sequencing of Mixed Phenotypic Acute Leukemia (MPAL) Reveals Complex Immunophenotypic, Transcriptional, and Genetic Heterogeneity (ASH 2022)
    Despite this heterogeneity, in half our cohort, we identified a recurrent gene expression signature associated with immature immunophenotype, which correlated with genetic drivers of immunophenotype in some cases. Future multiomic studies are needed to completely subtype MPAL and elucidate the impact of these subtypes on treatment outcomes.
    FLT3 (Fms-related tyrosine kinase 3) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • PAX5 (Paired Box 5) • CD33 (CD33 Molecule) • CD34 (CD34 molecule) • S100A8 (S100 Calcium Binding Protein A8) • CD14 (CD14 Molecule) • ITGAM (Integrin, alpha M) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • UHRF1 (Ubiquitin Like With PHD And Ring Finger Domains 1) • NDUFA2 (NADH:Ubiquinone Oxidoreductase Subunit A2) • SOX4 (SRY-Box Transcription Factor 4)
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    TP53 mutation • KIT expression • CD14 expression • S100A8 expression
    over3years
    Progenitor Sub-Populations in Treatment Resistant T-ALL (ASH 2022)
    As T-ALL thus far is solely defined by bulk-sample immuno-phenotype, we propose the prospective identification of BMP-like sub-populations and use of non-conventional cytotoxic agents for upfront-risk-stratification and targeted therapy to be realized in high-risk T-ALL. JX & CC, as well as DTT & KT, contributed equally to the work.
    Clinical • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • NOTCH1 (Notch 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • CD123 (Interleukin 3 Receptor Subunit Alpha) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • CD33 (CD33 Molecule) • CD44 (CD44 Molecule) • CD34 (CD34 molecule) • IL7R (Interleukin 7 Receptor) • LGALS1 (Galectin 1) • HOXA9 (Homeobox A9) • NUP214 (Nucleoporin 214) • FLI1 (Fli-1 Proto-Oncogene ETS Transcription Factor) • MEIS1 (Meis Homeobox 1) • MME (Membrane Metalloendopeptidase) • SPI1 (Spi-1 Proto-Oncogene) • ITGA4 (Integrin, alpha 4) • IGKC (Immunoglobulin Kappa Constant) • MEF2C (Myocyte Enhancer Factor 2C) • SPINK2 (Serine Peptidase Inhibitor Kazal Type 2) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor) • S100A4 (S100 calcium binding protein A4)
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    NOTCH1 mutation