Ask about this productRelated genes to: CNAP1 antibody
- Gene:
- NCAPD2 NIH gene
- Name:
- non-SMC condensin I complex subunit D2
- Previous symbol:
- -
- Synonyms:
- CNAP1, hCAP-D2, CAP-D2, KIAA0159
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-04
- Date modifiied:
- 2015-11-12
Related products to: CNAP1 antibody
Related articles to: CNAP1 antibody
- Pediatric gliomas, comprising both low-grade (LGGs) and high-grade gliomas (HGGs), exhibit significant molecular and clinical heterogeneity. While LGGs generally have a favorable prognosis, HGGs are associated with poor long-term survival despite aggressive treatment. Advances in molecular profiling have enabled targeted therapies, but treatment resistance and tumor heterogeneity remain major challenges. The integration of artificial intelligence (AI) and transcriptomic data holds promise for refining prognostic models and guiding personalized treatment strategies, yet its application in pediatric gliomas remains underexplored. - Source: PubMed
Publication date: 2026/03/09
Li GanglongPei FuyuWang Weizhen - Pancreatic ductal adenocarcinoma (PDAC) is the 3 leading cause of cancer mortality in the U.S., where more than 80% of the cases are diagnosed with metastatic PDAC (mPDAC). In this study, Maeda utilized a CRISPR screen in human patient-derived xenografts from primary and lung metastatic tumors and identified the transcription factor KLF5 as an upstream modulator regulating the mPDAC phenotype. Using a combination of biochemical and molecular experiments together with single-cell genome-wide assays, the authors discovered that KLF5 induces epigenetic modifiers including and , which in turn regulate the expression of a distinct gene profiles controlling the biology of mPDAC. Altogether, the authors defined a cascade of events acting as a domino effect triggered by KLF5, modifying the epigenetic landscape in mPDAC to support metastatic growth. - Source: PubMed
Publication date: 2026/02/24
Pena Ruiz Nicole MFernandez-Zapico Martin E - One of the major conundrums of cancer research and treatment is that the metastases that lead to death in most patients do not appear to involve additional driver mutations. Previously, we reported widespread loss of heterochromatin with activation of pro-metastatic genes in the subset of cells of primary pancreatic tumors that gave rise to liver and lung metastases. Here we hypothesized that this change in chromatin could create unique vulnerabilities in distant metastases. Using a CRISPR screen of human patient-derived xenografts from metastases and primary tumors, we identified as essential for metastatic cell proliferation but not primary tumor growth. Further, we found that induced epigenetic modifier genes, including and , which themselves facilitated expression of specific genes driving migration and epithelial-mesenchymal transition, including , , , and . Inhibition of expression of these modifier genes restored heterochromatin in the specific regions that distinguish the primary and metastatic tumors. We backed up this causal chain of evidence with rigorous additional knockdown experiments with the modifier genes, and single cell RNA and chromatin experiments, and we also replicated the main findings in a second set of paired primary and distant metastasis xenograft lines. Finally, expression was strongly associated with patient survival and human PDAC cell plasticity in a dataset of 70 PDAC patients and expression was increased in the majority of lung, liver and peritoneal metastases compared to the matched primary tumor, confirming its importance in PDAC metastasis and mortality. In summary, we have identified a cascade of epigenetic modulators, modifiers and mediators that maintains the widespread heterochromatin loss supporting metastatic cell proliferation in human pancreatic cancer (see Graphical Abstract). - Source: PubMed
Publication date: 2026/02/10
Maeda MasahiroSherman KennaZhou WeiqiangCheng JiaqiNihongaki YutaIdrizi AdrianTryggvadottir RakelCamacho OscarShang XingboMin JiminKoldobskiy Michael AMaitra AnirbanLevchenko AndreSlusher Barbara SJi HongkaiFeinberg Andrew P - Lung adenocarcinoma (LUAD) is one of the leading causes of cancer-related deaths worldwide. While NCAPD2 has been implicated in promoting tumorigenesis across various cancer types, its specific role in LUAD remains underexplored. This study aims to elucidate the molecular mechanisms by which NCAPD2 contributes to LUAD progression, with a focus on its involvement in the AKTMDM2/E2F1 positive feedback loop. - Source: PubMed
Publication date: 2025/11/30
Wu YunLi XiaoqinLin YuchenChen YanXin NingHong DaWei JunminLi HongruGuo TailinLin FanChen YushengLin Ying - Panitumumab shows limited clinical benefit in colorectal cancer (CRC), and reliable predictive biomarkers to guide patient selection remain lacking. To address this gap, we investigated molecular determinants of therapeutic response using tumor samples from patients with primary and metastatic CRC. By integrating PIMS-based metastatic classification, NPOT interaction profiling and quantitative proteomics, this study aimed to identify response-associated pathways and potential prognostic biomarkers that could support improved stratification for panitumumab therapy. - Source: PubMed
Quartier AngeliqueSanin Ahmed YNagelschmitz JuliaSchneider JustineShi WenjieWartmann ThomasDölling MaximilianStelter FrederikeAndric MihailoCroner Roland SEftekhari PierreKahlert Ulf D