CADM3

Last update 08 May 2025

Basic Info

Synonyms

BIgR, Brain immunoglobulin receptor, CADM3

+ [11]

Introduction

Involved in cell-cell adhesion. Has both calcium-independent homophilic cell-cell adhesion activity and calcium-independent heterophilic cell-cell adhesion activity with IGSF4, NECTIN1 and NECTIN3. Interaction with EPB41L1 may regulate structure or function of cell-cell junctions (By similarity).

100 Clinical Results associated with CADM3

100 Translational Medicine associated with CADM3

0 Patents (Medical) associated with CADM3

Literatures (Medical) associated with CADM3

31 Dec 2024·Epigenetics

Methylation patterns associated with C-reactive protein in racially and ethnically diverse populations

Article

Author: Ye, Ting ; Smith, Jennifer A. ; Xu, Huichun ; Kasela, Silva ; Haessler, Jeff ; Liu, Chunyu ; Rotter, Jerome I. ; Hu, Yao ; Liu, Yongmei ; Ratliff, Scott M. ; Joehanes, Roby ; Matise, Tara ; Zhao, Wei ; Raffield, Laura M. ; Tracy, Russell ; Van den Berg, David ; Lu, Ake ; Benjamin, Emelia J. ; Lapalainien, Tuuli ; Brody, Jennifer A. ; Levy, Daniel ; Haiman, Chris ; North, Kari E. ; Sotoodehnia, Nona ; Kooperberg, Charles ; Cushman, Mary ; Lundin, Jessica I. ; Guo, Xiuqing ; Rich, Stephen S. ; Avery, Christy L. ; Loos, Ruth J.F. ; Kenny, Eimear ; Ammous, Farah ; Carlson, Chris ; Gignoux, Chris ; Bis, Joshua C. ; Peters, Ulrike ; Park, Sungshim L. ; Reiner, Alex

Systemic low-grade inflammation is a feature of chronic disease. C-reactive protein (CRP) is a common biomarker of inflammation and used as an indicator of disease risk; however, the role of inflammation in disease is not completely understood. Methylation is an epigenetic modification in the DNA which plays a pivotal role in gene expression. In this study we evaluated differential DNA methylation patterns associated with blood CRP level to elucidate biological pathways and genetic regulatory mechanisms to improve the understanding of chronic inflammation. The racially and ethnically diverse participants in this study were included as 50% White, 41% Black or African American, 7% Hispanic or Latino/a, and 2% Native Hawaiian, Asian American, American Indian, or Alaska Native (total n = 13,433) individuals. We replicated 113 CpG sites from 87 unique loci, of which five were novel (CADM3, NALCN, NLRC5, ZNF792, and cg03282312), across a discovery set of 1,150 CpG sites associated with CRP level (p < 1.2E-7). The downstream pathways affected by DNA methylation included the identification of IFI16 and IRF7 CpG-gene transcript pairs which contributed to the innate immune response gene enrichment pathway along with NLRC5, NOD2, and AIM2. Gene enrichment analysis also identified the nuclear factor-kappaB transcription pathway. Using two-sample Mendelian randomization (MR) we inferred methylation at three CpG sites as causal for CRP levels using both White and Black or African American MR instrument variables. Overall, we identified novel CpG sites and gene transcripts that could be valuable in understanding the specific cellular processes and pathogenic mechanisms involved in inflammation.

01 Dec 2024·Histopathology

Clinicopathologic and molecular study of superficial CD34‐positive fibroblastic tumours mimicking atypical fibrous histiocytoma (dermatofibroma)

Article

Author: Mertens, Fredrik ; Wakefield, Craig B ; Fletcher, Christopher D M ; Anderson, William J

AimsSuperficial CD34‐positive fibroblastic tumour (SCD34FT) is an uncommon but distinctive low‐grade neoplasm of the skin and subcutis that shows frequent CADM3 expression by immunohistochemistry (IHC). In this study, prompted by an index case resembling ‘atypical fibrous histiocytoma (FH)’ that was positive for CADM3 IHC, we systematically examined a cohort of tumours previously diagnosed as ‘atypical FH’ by applying CADM3 and fluorescence in situ hybridization (FISH) for PRDM10 rearrangement, to investigate the overlap between these tumour types.Methods and ResultsForty cases of atypical FH were retrieved, including CD34‐positive tumours (n = 20) and CD34‐negative tumours (n = 20). All tumours were stained for CADM3. All CADM3‐positive tumours were evaluated by FISH to assess for PRDM10 rearrangement. Eleven CD34‐positive tumours (11/20, 55%) coexpressed CADM3 and were reclassified as SCD34FT. None (0/20) of the CD34‐negative atypical FH were CADM3‐positive. Reclassified SCD34FT (10/11) arose on the lower extremity, with frequent involvement of the thigh (n = 8). Features suggestive of atypical FH were observed in many reclassified cases including variable cellularity, spindled morphology, infiltrative tumour margins, collagen entrapment, epidermal hyperpigmentation, and acanthosis. Variably prominent multinucleate giant cells, including Touton‐like forms, were also present. An informative FISH result was obtained in 10/11 reclassified tumours, with 60% (6/10) demonstrating PRDM10 rearrangement.ConclusionA significant subset of tumours that histologically resemble atypical FH, and are positive for CD34, coexpress CADM3 and harbour PRDM10 rearrangement, supporting their reclassification as SCD34FT. Awareness of this morphologic overlap and the application of CADM3 IHC can aid the distinction between SCD34FT and atypical FH.

28 Oct 2024·Journal of Cancer

Mendelian Randomization Analysis of Non-small Cell Lung Cancer and Five Exposure Factors Based on Pathway Enrichment Analysis

Article

Author: Zhu, Shuqiang ; Zhang, Jieshu ; Zhou, Weijun ; Wu, Jiajun ; Hu, Zhuozheng ; Guo, Zishun ; Zhang, Wenxiong

Background: Increasing knowledge has made it crucial to identify and minimize potential risk factors in order to prevent non-small cell lung cancer (NSCLC). This initiative aims to utilize Mendelian randomization analysis to identify exposure factors that could be causally linked to NSCLC. The results will help create new ways of controlling and preventing NSCLC. Methods: The GEO database's NSCLC data were used to find differentially expressed genes, which were further analyzed for GO and KEGG pathway enrichment. Use pathway enrichment analysis as a guide to screen exposure factors. The exposure variables that are causally associated with NSCLC were screened using a two-sample Mendelian randomization technique. Heterogeneity and pleiotropy analyze were employed to assess the validity of the study's findings. Results: Coronary atherosclerosis, cell adhesion molecule 3 (a molecule that maintains the normal structure and function of the lungs), dipeptidase 1 (one of the major adhesion receptors for neutrophils), thimet oligopeptidase (involved in hydrolyzing a variety of vasoactive signal peptides), and dipeptidyl peptidase 2 (an intracellular protease involved in the cell differentiation process and preventing cell death). The above five exposure factors were discovered to have an inverse relationship with NSCLC. Essentially, this implies that higher levels of these components can decrease the likelihood of developing lung cancer. No heterogeneity or pleiotropy was detected, and the study results were reliable. Conclusion: The study identified five potential exposure variables for NSCLC, laying the groundwork for treatment and prevention strategies and suggesting a new path for future research.

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