PIK3C2B

更新于：2025-05-07

基本信息

别名

C2-PI3K、Phosphatidylinositol 4-phosphate 3-kinase C2 domain-containing subunit beta、phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta

+ [7]

简介

Phosphorylates PtdIns and PtdIns4P with a preference for PtdIns (PubMed:10805725, PubMed:11533253, PubMed:9830063). Does not phosphorylate PtdIns(4,5)P2 (PubMed:9830063). May be involved in EGF and PDGF signaling cascades (PubMed:10805725).

关联

100 项与 PIK3C2B 相关的临床结果

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100 项与 PIK3C2B 相关的转化医学

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0 项与 PIK3C2B 相关的专利（医药）

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106

项与 PIK3C2B 相关的文献（医药）

2025-05-01·The Prostate

Transcriptome‐Wide Association Study Identified Novel Blood Tissue Gene Biomarkers for Prostate Cancer Risk

Article

作者: Zhong, Hua ; Yu, Jie ; Liu, Yanhui ; Liu, Jiawen ; Wang, Liang ; Wu, Lang ; Zhang, Zichen ; Zhu, Jingjing ; Deng, Youping ; Sun, Yanfa ; Nakamura, Akira ; Zeng, Guanghua ; Wang, Fubo ; Lin, Xin ; Zhou, Dan ; Wu, Chong

ABSTRACTObjectiveA number of susceptibility genes in prostate tissue have been identified to be associated with prostate cancer (PCa) risk. However, the reported genes based on assessing prostate tissue could not fully explain PCa genetic susceptibility. It is believed that genes functioning in the immune system may fill in the gap of some missing heritability.MethodsTo study potential susceptibility genes acting in such pathways, we performed a transcriptome‐wide association study (TWAS) of 79,194 PCa cases and 61,112 control of European ancestry by using three sets of gene expression prediction models of blood tissue.ResultsA total of 470 genes were associated at false discovery rates‐corrected p‐value < 0.05, of which 51 were implicated as likely causal genes based on fine‐mapping analysis. Compared with previous literature, 133 novel genes were reported for the first time. Of the identified genes, five (CREB3L4, GSTP1, MAPK3, NKX3‐1, and PIK3C2B) were enriched in a PCa signaling pathway, and 128 genes were enriched in five PCa categories. Importantly, 13 genes (SCP2, LMNA, ZNF148, H2AFV, TACC1, FLII, SUPT4H1, CD300LF, MYO9B, COX6B1, CTSA, EP300, and TSPO) showed consistent effect directions for the measured levels in circulating immune cells between PCa cases and controls, and 14 genes (SLC39A1, ZBTB7B, TRIM59, NCEH1, N4BP2, TAGAP, TACC1, TRAF1, AIP, SECTM1, C18orf54, ZNF793, YIF1B, and TSPO) showed consistency for levels in blood exosomes between PCa patients and controls.ConclusionThe identified blood‐based candidate susceptibility genes provide further insights into the genetic basis of PCa risk.

2025-04-01·Modern Pathology

Molecular Diversity of Embryonic-Type Neuroectodermal Tumors Arising From Testicular Germ Cell Tumors

Article

作者: Zong, Yang ; Drakaki, Alexandra ; Lin, Douglas I ; Zhang, Liying ; Ye, Huihui ; Huang, Rongrong ; Bitar, Mireille

Embryonic-type neuroectodermal tumors (ENTs) arising from testicular germ cell tumors (GCTs) are a relatively common type of somatic transformation in GCTs with poor prognosis and limited therapeutic options, particularly when patients develop disease recurrence or metastasis. Knowledge of key events driving this transformation is limited to the paucity of comprehensive genomic data. We performed a retrospective database search in a Clinical Laboratory Improvement Amendments- and College of American Pathologists-certified laboratory for testicular GCT-derived ENTs that had previously undergone next-generation sequencing-based comprehensive genomic profiling during the course of clinical care. Clinicopathological and genomic data were centrally rereviewed. Here, we report the molecular features of 10 ENTs of testicular GCT origin. All tumors harbored gain of chromosome 12p, often with KRAS, CCND2, and KMD5A coamplification, supporting a germ cell origin. The tumors were microsatellite-stable and exhibited a low tumor mutational burden. Three tumors (30%) exhibited MYCN or MYC amplification with co-occurring inactivation of the p53 pathway via either TP53 mutations or MDM2 amplification in 2 tumors. Three additional tumors (30%) had activation of the PI3K pathway via PIK3CA and PIK3CG mutations or PIK3C2B amplification; 1 tumor with co-occurring CDK4 amplification. Gene rearrangements were detected in 3 tumors (30%), with novel BRD4::MAU2 and BCOR::CLIP2 fusions as well as an internal truncating ATRX rearrangement, respectively. In summary, ENTs arising from GCTs are molecularly heterogeneous; however, a large fraction of testicular ENTs could be stratified by 2 distinct sets of genetic alterations, including MYCN/MYC amplification with concurrent suppression of the p53 pathway, and activation of the PI3K pathway with co-occurring CDK4 amplification. Moreover, the novel gene fusions identified in a subset of testicular GCT-derived ENTs overlap with molecularly defined tumors of embryonic-type neuroectodermal features in the central nervous system, indicating the potential common driving events for tumorigenesis from different anatomical sites.

2025-01-01·Oral Diseases

Proliferative verrucous and homogeneous Leukoplakias exhibit differential methylation patterns

Article

作者: Bagan, José ; Bagán, Leticia ; Herreros‐Pomares, Alejandro ; Proaño, Alex ; Hervás, David

AbstractObjectiveProliferative verrucous leukoplakia (PVL) is considered a clinically distinct entity from other oral leucoplakias (OLs) due to its clinical presentation and evolution. However, molecular differences between them remain unclear. We aimed to determine whether there are methylation differences between PVL and other forms of OLs.Materials and MethodsOral biopsies from 12 patients with PVL, eight patients with homogeneous leucoplakia (HL), and 10 healthy individuals were obtained for a genome‐wide DNA methylation analysis via the Infinium EPIC Platform.ResultsA total of 1815 differentially methylated CpGs were found between PVL and HL, with a prominent state of hypermethylation in HL patients. CpGs covered 813 genes with distinct roles, including cell adhesion, extracellular matrix organization, and cell and synaptic signaling. 43% of these genes had been previously described in cancer and associated with prognosis. We developed a multinomial logistic regression model able to differentiate HL, PVL, and control samples. The model had a cross‐validated estimate of 73% and included differentially methylated cancer‐related genes between the pathological conditions and the healthy donors, including ADNP, BRCA2, CDK13, GNB1, NIN, NUMB, PIK3C2B, PTK2, SHISA4, THSD7B, WWP1, and ZNF292. It also included CpGs covering differentially methylated genes in HL (MEN1 and TNRC6B) and PVL (ACOXL, ADH1B, CAMTA1, CBFA2T3, CPXM2, LRFN2, SORCS2, and SPN).ConclusionsPVL and HL present differential methylation patterns that could be linked to their differential clinical behavior. Our findings show the potential of methylation markers and suggest novel diagnostic biomarkers.

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