SUSD4

Last update 08 May 2025

Basic Info

Synonyms

FLJ10052, SUSD4, sushi domain containing 4

+ [1]

Introduction

Acts as a complement inhibitor by disrupting the formation of the classical C3 convertase. Isoform 3 inhibits the classical complement pathway, while membrane-bound isoform 1 inhibits deposition of C3b via both the classical and alternative complement pathways.

100 Clinical Results associated with SUSD4

100 Translational Medicine associated with SUSD4

0 Patents (Medical) associated with SUSD4

Literatures (Medical) associated with SUSD4

01 Mar 2025·JCO Precision Oncology

Comprehensive Molecular and Genomic Analysis of NCI-MATCH Subprotocol Y: Capivasertib in Patients With an AKT1 E17K –Mutated Tumor

Article

Author: Gross, Jacob ; Bu, Xiangning ; Wang, Victoria ; McShane, Lisa M. ; Harris, Lyndsay N. ; Maican, Cayden ; McCourt, Carolyn K. ; Guan, Ping ; Lahey, Matthew T. ; O'Dwyer, Peter J. ; Patton, David ; Kalinsky, Kevin

PURPOSE NCI-MATCH (EAY131) is a precision medicine trial using genomic testing to allocate patients with advanced malignancies to targeted treatments. Arm Y evaluated capivasertib, a pan AKT inhibitor, in patients with an AKT1 E17K –mutated tumor. Here, we report on the translational objectives of the study, a molecular and genomic analysis of specimens to identify potential biomarkers of response or resistance to capivasertib. METHODS Eligible patients had AKT1 E17K –mutated metastatic tumors that progressed with standard treatment and received capivasertib 480 mg orally twice daily for 4 days on and 3 days off weekly in 28-day cycles. The primary end point was objective response rate (ORR). We performed whole-exome sequencing, RNA sequencing, and gene set and pathway enrichment analysis on 25 pretreatment tissue samples and evaluated findings in responders (complete response [CR], n = 0, and partial response, n = 9) and nonresponders (stable disease, n = 13, and progressive disease, n = 3). RESULTS The ORR was 28.6% (10 of 35) in the reported primary trial and 36% (9 of 25) in this translational cohort. Mutations in the TP53 gene were more frequent in responders, whereas the PI3K/AKT/mTOR pathway genes TYRO3 , SYNJ1 , and CDIPT were significantly altered in nonresponders. DNA repair, p53, E2F, and Wnt-beta catenin pathways were enriched in the responder group. Unsupervised clustering of gene expression identified five genes, ANKRD30A , SUSD4 , TTC6 , POTEJ , and POTEI , that were significantly higher in responders and lower in nonresponders. In addition, EGFR expression was significantly increased in nonresponders. CONCLUSION In patients with AKT1 E17K –mutated tumors, capivasertib achieved a clinically significant ORR. TP53 mutations appear to be associated with response, whereas certain additional PI3K/AKT/mTOR pathway mutations and EGFR overexpression appear to be associated with nonresponse to capivasertib. Further investigation of predictive biomarkers is warranted.

01 Apr 2021·Cancer Biotherapy and RadiopharmaceuticalsQ4 · MEDICINE

Analysis of the Role and Regulation Mechanism of hsa-miR-147b in Lung Squamous Cell Carcinoma Based on The Cancer Genome Atlas Database

Q4 · MEDICINE

Article

Author: Ke, Di ; Xiao, Xue ; Guo, Qiang ; Fan, Teng-Yang

Objective: This study aimed to explore the role and regulatory mechanism of hsa-miR-147b in lung squamous cell carcinoma (LUSC) through The Cancer Genome Atlas (TCGA) database. Methods: The expression and clinical value of miR-147b in LUSC were analyzed in the TCGA database. The target genes of miR-147b were screened via miRWalk 2.0 and verified in TCGA database. Gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed to analyzed the differential target genes of miR-147b. Kaplan-Meier survival analysis and Cox regression were used to screen the prognosis-related target genes. Results: The expression of miR-147b in LUSC tissues increased, and was associated with poor prognosis, gender, and stage of LUSC patients. The area under the curve (AUC) of miR-147b was 0.8478 by the receiver-operating characteristic curve. There were 428 differentially expressed genes of miR-147b that played a critical role in drug transport, DNA binding, calcium signaling pathway, and Ras signaling pathway through GO and KEGG. PTGIS, SUSD4, ARC, HTR2C, SHISA9, and PLA2G4D were independent risk factors for poor prognosis in LUSC patients. LUSC patients in the high-risk group had a higher risk of death. The time-dependent AUC was 0.673. Conclusions: MiR-147b might be a potential molecular marker for poor prognosis in patients with LUSC.

01 Mar 2021·Taiwanese Journal of Obstetrics and Gynecology

Molecular cytogenetic characterization of a de novo chromosome 1q41-q42.11 microdeletion of paternal origin in a 15-year-old boy with mental retardation, developmental delay, autism and congenital heart defects

Author: Chen, Shin-Wen ; Chern, Schu-Rern ; Wu, Fang-Tzu ; Chen, Chih-Ping ; Wu, Peih-Shan ; Wang, Wayseen

OBJECTIVEWe present molecular cytogenetic characterization of a de novo chromosome 1q41-q42.11 microdeletion of paternal origin in a mentally retarded child of a family requesting for genetic counseling of the future pregnancy.CASE REPORTA 43-year-old, gravida 1, para 1, woman, who had a 15-year-old son with mental retardation, planned to have another normal child and requested for genetic counseling of the future pregnancy. Her husband was 48 years old. The 15-year-old boy had a body height of 148 cm (<3rd centile) and a body weight of 40 Kg (<35th centile). He had facial dysmorphism, mental retardation, scoliosis, abnormal gaits, tetralogy of Fallot, pulmonary stenosis and autism but did not have any history of epilepsy. Cytogenetic analysis of the boy and the parents revealed normal karyotypes. Array comparative genomic hybridization (aCGH) analysis of the family revealed a de novo 2.028-Mb 1q41-q42.11 microdeletion, or arr 1q41q42.11 (222,571,596-224,599,234) × 1.0 [GRCh37 (hg19)], encompassing 13 Online Mendelian Inheritance in Man (OMIM) genes including DISP1, SUSD4, FBXO28, TP53BP2 and WDR26 in the child. Quantitative fluorescent polymerase chain reaction analysis confirmed a paternal origin of the deletion. Fluorescence in situ hybridization analysis confirmed a 1q41 deletion.CONCLUSIONGenetic counseling of the parents who have a previous child with mental retardation and who wish to have another normal child in the future pregnancy should include genetic studies, and aCGH is useful under such a circumstance.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

SUSD4

Basic Info

Related

Analysis