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    GENE:

    INPP5D (Inositol Polyphosphate-5-Phosphatase D)

    i
    Other names: INPP5D, Inositol Polyphosphate-5-Phosphatase D, SH2 Domain-Containing Inositol 5'-Phosphatase 1, Hp51CN, SHIP1, SHIP, Phosphatidylinositol 3,4,5-Trisphosphate 5-Phosphatase 1, Phosphatidylinositol 4,5-Bisphosphate 5-Phosphatase, Inositol Polyphosphate-5-Phosphatase, 145kDa, Inositol Polyphosphate-5-Phosphatase, 145kD, P150Ship, SIP-145, SHIP-1, Signaling Inositol Polyphosphate 5 Phosphatase SIP-145, Signaling Inositol Polyphosphate Phosphatase SHIP II, Inositol Polyphosphate-5-Phosphatase Of 145 KDa, SH2 Domain-Containing Inositol Phosphatase 1
    3ms
    INPP5D/SHIP1 is a dual regulator of endo-lysosome function and selective phagocytosis in human microglia. (PubMed, bioRxiv)
    Together, these results identify SHIP1 as a regulator of endo-lysosomal function and selective phagocytosis of lipid-rich substrates in microglia. These findings have important implications for therapeutic hypotheses that target SHIP1 for treatment of AD, autoimmune diseases, and cancer.
    Journal
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    INPP5D (Inositol Polyphosphate-5-Phosphatase D) • NLRP3 (NLR Family Pyrin Domain Containing 3)
    4ms
    Human Papilloma Virus Does Not Fully Inactivate p53 Cellular Activity in HNSCC. (PubMed, Head Neck)
    Together, our findings challenge the prevailing view that p53 is completely inactivated in HPV+ HNSCC and reveal tumor suppressive, p53-driven mechanisms that persist in these tumors. These insights highlight a potential role for TP53-based stratification in guiding treatment decisions and suggest new therapeutic vulnerabilities in HPV+ HNSCC.
    Journal
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    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • INPP5D (Inositol Polyphosphate-5-Phosphatase D)
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    TP53 mutation • TP53 wild-type
    5ms
    Human Papilloma Virus does not fully inactivate p53 cellular activity in HNSCC. (PubMed, bioRxiv)
    Together, our findings challenge the prevailing view that p53 is completely inactivated in HPV+ HNSCC and reveal tumor suppressive, p53-driven mechanisms that persist in these tumors. These insights highlight a potential role for TP53 -based stratification in guiding treatment decisions and suggest new therapeutic vulnerabilities in HPV+ HNSCC.
    Journal
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    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • INPP5D (Inositol Polyphosphate-5-Phosphatase D)
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    TP53 mutation • TP53 wild-type
    9ms
    Integrative Immune Signature of Complementary Circulating and Tumoral Biomarkers Maximizes the Predictive Power of Adjuvant Immunotherapeutic Benefits in High-Risk Melanoma. (PubMed, Clin Cancer Res)
    Integrating candidate blood and tumor immune-related biomarkers generated a baseline signature that maximizes the prediction of immunotherapeutic benefits in reference to the compartmental biomarker signatures.
    Journal • IO biomarker
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    CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CTLA4 (Cytotoxic T-Lymphocyte Associated Protein 4) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • CD33 (CD33 Molecule) • IDO1 (Indoleamine 2,3-dioxygenase 1) • CXCL9 (Chemokine (C-X-C motif) ligand 9) • CXCL11 (C-X-C Motif Chemokine Ligand 11) • CCL3 (C-C Motif Chemokine Ligand 3) • CXCR3 (C-X-C Motif Chemokine Receptor 3) • IGKC (Immunoglobulin Kappa Constant) • INPP5D (Inositol Polyphosphate-5-Phosphatase D)
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    Yervoy (ipilimumab)
    10ms
    GDC-0084 With Radiation Therapy for People With PIK3CA-Mutated Solid Tumor Brain Metastases or Leptomeningeal Metastases (clinicaltrials.gov)
    P1, N=21, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
    Trial completion date • Trial primary completion date
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    PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • PIK3R1 (Phosphoinositide-3-Kinase Regulatory Subunit 1) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) • INPP4B (Inositol polyphosphate-4-phosphatase type II B) • AKT2 (V-akt murine thymoma viral oncogene homolog 2) • INPP5D (Inositol Polyphosphate-5-Phosphatase D) • PIK3C3 (Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3) • PIK3R2 (Phosphoinositide-3-Kinase Regulatory Subunit 2 ) • PIK3R3 (Phosphoinositide-3-Kinase Regulatory Subunit 3)
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    paxalisib (GDC-0084)
    over1year
    Integrative analysis of single-nucleus RNA sequencing and Mendelian randomization to explore novel risk genes for Alzheimer's disease. (PubMed, Medicine (Baltimore))
    Except for the CACNA2D3 gene, the other 6 genes showed increased expression levels in the macrophages, particularly EPB41L2 and SSH2. Our findings highlight the potential of specific genetic markers identified through integrative analysis of sn-RNA-Seq and MR in guiding the diagnosis and therapeutic strategies for Alzheimer's disease.
    Journal
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    INPP5D (Inositol Polyphosphate-5-Phosphatase D) • SSH2 (Slingshot Protein Phosphatase 2)
    over1year
    Expression and clinical significance of PIKFYVE gene in hepatocellular carcinoma analyzed based on TCGA database and experimental validation (PubMed, Zhonghua Gan Zang Bing Za Zhi)
    The immunohistochemistry staining results showed that the expression of PIKFYVE in HCC tissues was significantly higher than that of nontumorous tissues (P<0.05), and there was a negative correlation with the degree of differentiation. PIKFYVE, as an independent risk factor for HCC, is expected to be developed as a clinical diagnostic biomarker for HCC, which will provide a reference for new drugs for the treatment of HCC.
    Journal
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    PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • PIK3R1 (Phosphoinositide-3-Kinase Regulatory Subunit 1) • INPP4B (Inositol polyphosphate-4-phosphatase type II B) • INPP5D (Inositol Polyphosphate-5-Phosphatase D) • PRKCA (Protein Kinase C Alpha) • PLCB4 (Phospholipase C Beta 4)
    over1year
    Potentially functional variants of INPP5D and EXOSC3 in immunity B cell-related genes are associated with non-small cell lung cancer survival. (PubMed, Front Immunol)
    Expression quantitative trait loci (eQTL) analysis suggested that the INPP5D rs6782875 T allele was significantly correlated with elevated INPP5D mRNA expression levels in normal lung tissues and whole blood samples, while the EXOSC3 rs3208406 G allele was significantly correlated with increased EXOSC3 mRNA expression levels in normal lung tissues. Our data indicated that genetic variants in these immunity B cell-related genes may predict NSCLC survival possibly by influencing the gene expression.
    Journal
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    INPP5D (Inositol Polyphosphate-5-Phosphatase D)
    over1year
    Ikaros sets the threshold for negative B-cell selection by regulation of the signaling strength of the AKT pathway. (PubMed, Cell Commun Signal)
    Conversely, hyperactivation of a single AKT isoform is sufficient to induce negative selection by increased oxidative stress. In summary, our study demonstrates the regulatory function of Ikaros on SHIP1 expression in B-ALL and highlights the relevance of sustained SHIP1 expression to prevent cells with hyperactivated PI3K/AKT/mTOR signaling from undergoing negative selection.
    Journal
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    RUNX1 (RUNX Family Transcription Factor 1) • ETV6 (ETS Variant Transcription Factor 6) • IKZF1 (IKAROS Family Zinc Finger 1) • PAX5 (Paired Box 5) • INPP5D (Inositol Polyphosphate-5-Phosphatase D)
    almost2years
    Molecular targets of glucocorticoids that elucidate their therapeutic efficacy in aggressive lymphomas. (PubMed, Cancer Cell)
    CSK inhibition attenuates the constitutive BCR signaling of lymphomas by hyperactivating Src-family kinases, triggering their ubiquitination and degradation. With the knowledge that glucocorticoids disable oncogenic BCR signaling, they can now be deployed rationally to treat BCR-dependent aggressive lymphomas and used to construct mechanistically sound combination regimens with inhibitors of BTK, PI3 kinase, BCL2, and CSK.
    Journal
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    BCL2 (B-cell CLL/lymphoma 2) • INPP5D (Inositol Polyphosphate-5-Phosphatase D) • KLHL14 (Kelch like family member 14) • DDIT4 (DNA Damage Inducible Transcript 4) • LAPTM5 (Lysosomal Protein Transmembrane 5)
    almost2years
    GDC-0084 With Radiation Therapy for People With PIK3CA-Mutated Solid Tumor Brain Metastases or Leptomeningeal Metastases (clinicaltrials.gov)
    P1, N=21, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Recruiting --> Active, not recruiting | N=36 --> 21
    Enrollment closed • Enrollment change
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    PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • PIK3R1 (Phosphoinositide-3-Kinase Regulatory Subunit 1) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) • INPP4B (Inositol polyphosphate-4-phosphatase type II B) • AKT2 (V-akt murine thymoma viral oncogene homolog 2) • INPP5D (Inositol Polyphosphate-5-Phosphatase D) • PIK3C3 (Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3) • PIK3R2 (Phosphoinositide-3-Kinase Regulatory Subunit 2 ) • PIK3R3 (Phosphoinositide-3-Kinase Regulatory Subunit 3)
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    paxalisib (GDC-0084)
    2years
    Concomitant double-fusion of PLEKHA7-ALK and INPP5D-ALK reveals favorable alectinib sensitivity in lung adenocarcinoma: a case report and literature review. (PubMed, Discov Oncol)
    The prescription of alectinib revealed potent efficacy and resulted in an increase in the survival rate. This case presented two uncommon and concomitant ALK fusion partners in NSCLC; more importantly, the INPP5D-ALK subtype has not been reported, therefore this study broadens the spectrum of ALK double-fusion variants and provides insight into the use of ALK inhibitors for the treatment of NSCLC in patients with double ALK fusions.
    Review • Journal
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    ALK (Anaplastic lymphoma kinase) • INPP5D (Inositol Polyphosphate-5-Phosphatase D)
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    ALK fusion
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    Alecensa (alectinib)