Zkscan1 antibody - C-terminal region (ARP33524_P050)
- Known as:
- Zkscan1 (anti-) - C-terminal region (ARP33524_P050)
- Catalog number:
- arp33524_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Zkscan1 antibody - C-terminal region (ARP33524_P050)
Related genes to: Zkscan1 antibody - C-terminal region (ARP33524_P050)
- Gene:
- ZKSCAN1 NIH gene
- Name:
- zinc finger with KRAB and SCAN domains 1
- Previous symbol:
- ZNF139, ZNF36
- Synonyms:
- KOX18, PHZ-37, ZSCAN33
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-30
- Date modifiied:
- 2016-10-05
Related products to: Zkscan1 antibody - C-terminal region (ARP33524_P050)
Related articles to: Zkscan1 antibody - C-terminal region (ARP33524_P050)
- Characterizing the typical clinical, morphologic, and molecular findings of distinct subtypes of Spitz neoplasms may help facilitate diagnosis and management of these cases. Approximately 1%-2% of Spitz neoplasms have a MET fusion driver. However, there is minimal data in the current literature regarding this specific subtype of Spitz neoplasm. Most cases in our series (9/10) were diagnosed as atypical Spitz tumors, whereas 1 case was diagnosed as a Spitz nevus. We found 3 characteristic morphologic patterns, the first consisted of either expansile nests of spindle shaped spitzoid melanocytes with plexiform arrangement in the dermis forming a large nodular lesion or thin chords and fascicles of spindle shaped spitzoid melanocytes with a tightly interwoven plexiform pattern in the dermis forming a plaque-like architecture. The second pattern consisted of sheets of epithelioid melanocytes with spitzoid cytology, and the third pattern consisted of a both epithelioid and spindle shaped cytology with plexiform arrangement in the dermis as seen in various subtypes of Spitz neoplasms. Compared to a cohort of 81 control Spitz neoplasms, MET fusions were more likely to have spindle cytology and a plexiform growth pattern in the dermis. The most common fusion pattern was ZKSCAN1 (4/10). Copy number gains of the fusion gene were frequent, seen in 61% of cases. None of our cases had a TERT promoter mutation or homozygous deletions of CDKN2A . All of our patients had an uneventful clinical course with no evidence of recurrence after reexcision with average follow-up time of 35 months. - Source: PubMed
Publication date: 2025/09/26
Jeyakumar Julia EdwinAddo Afua KonaduBeydoun Haya MaryOlivares ShantelDittmann DavidDos Santos Lucas SantanaVolek MichaelJennings LawrenceBridges AlinaFinelt NikaLowe LoriBusam Klaus JGerami Pedram - Congenital Spitz nevi have been rarely reported, and the diagnoses were usually based on the histopathological and immunohistochemical findings. We describe a case of a congenital Spitz tumor in which the molecular studies demonstrated a ZKSCAN1::MET fusion. No other somatic mutations and/or copy number variations outside of the MET gene were identified. Activating MET kinase rearrangements were previously reported only in a few cases of atypical Spitz tumors and spitzoid melanomas. Specifically, the ZKSCAN1::MET fusion was previously described in a single case of spitzoid melanoma demonstrating an uneventful course. Altogether, the histopathological, immunohistochemical, and molecular studies in our case supported a diagnosis of a congenital Spitz melanocytoma. This underscores the value of molecular analyses in Spitz tumors. - Source: PubMed
Publication date: 2025/07/15
Feldman TzahZaaroura HibaAbaya Hanaa HajZohar YanivBergman Reuven - Intrahepatic cholangiocarcinoma (ICC) is the second most prevalent liver cancer after hepatocellular carcinoma and is characterized by high malignancy and poor prognosis. Gemcitabine combined with cisplatin is the standard first-line therapy for metastatic or unresectable ICC. The combination of immunotherapy and targeted therapy represents a promising new direction for ICC treatment. Common genetic mutations in ICC include those in TP53, FGFR2, IDH1/2, and KRAS. MET alterations such as fusions and amplifications are rare in ICC. However, limited research has been conducted on the efficacy of specific MET inhibitors. We present two cases: the first with refractory ICC treated with a combination of immunotherapy and targeted therapy, harboring a ZKSCAN1-MET fusion and the second with a metastatic ICC with MET amplification. Both patients demonstrated a significant clinical response to crizotinib, a MET-specific tyrosine kinase inhibitor. - Source: PubMed
Publication date: 2025/06/14
Wu Jian-HuiFan Yu-ZeSun JingDuan Xue-Zhang - Idiopathic pulmonary fibrosis (IPF) is a complex and heterogeneous disease. Given this, we reasoned that differences in genetic profiles may be associated with unique clinical and radiologic features. Computational image analysis, sometimes referred to as radiomics, provides objective, quantitative assessments of radiologic features in subjects with pulmonary fibrosis. To determine if the genetic risk profile of patients with IPF identifies unique computational imaging phenotypes. Participants with IPF were included in this study if they had genotype data and computed tomography (CT) scans of the chest available for computational image analysis. The extent of lung fibrosis and the likelihood of a usual interstitial pneumonia (UIP) pattern were scored automatically using two separate, previously validated deep learning techniques for CT analysis. UIP pattern was also classified visually by radiologists according to established criteria. Among 329 participants with IPF, and were independently associated with the deep learning-based UIP score. None of the common variants were associated with fibrosis extent by computational imaging. We did not find an association between or and visually assessed UIP pattern. Select genetic variants are associated with computer-based classification of UIP on CT in this IPF cohort. Analysis of radiologic features using deep learning may enhance our ability to identify important genotype-phenotype associations in fibrotic lung diseases. - Source: PubMed
Blumhagen Rachel ZHumphries Stephen MPeljto Anna LLynch David ACardwell JonathanBang Tami JTeague Shawn DSigakis ChristopherWalts Avram DPuthenvedu DeepaWolters Paul JBlackwell Timothy SKropski Jonathan ABrown Kevin KSchwarz Marvin IYang Ivana VSteele Mark PSchwartz David ALee Joyce S - Connectome studies have shown how Alzheimer's disease (AD) disrupts functional and structural connectivity among brain regions. But the molecular basis of such disruptions is less studied, with most genomic/transcriptomic studies performing within-brain-region analyses. To inspect how AD rewires the correlation structure among genes in different brain regions, we performed an Inter-brain-region Differential Correlation (Inter-DC) analysis of RNA-seq data from Mount Sinai Brain Bank on four brain regions (frontal pole, superior temporal gyrus, parahippocampal gyrus and inferior frontal gyrus, comprising 264 AD and 372 control human post-mortem samples). An Inter-DC network was assembled from all pairs of genes across two brain regions that gained (or lost) correlation strength in the AD group relative to controls at FDR 1%. The differentially correlated (DC) genes in this network complemented known differentially expressed genes in AD, and likely reflects cell-intrinsic changes since we adjusted for cell compositional effects. Each brain region used a distinctive set of DC genes when coupling with other regions, with parahippocampal gyrus showing the most rewiring, consistent with its known vulnerability to AD. The Inter-DC network revealed master dysregulation hubs in AD (at genes ZKSCAN1, SLC5A3, RCC1, IL17RB, PLK4, etc.), inter-region gene modules enriched for known AD pathways (synaptic signaling, endocytosis, etc.), and candidate signaling molecules that could mediate region-region communication. The Inter-DC network generated in this study is a valuable resource of gene pairs, pathways and signaling molecules whose inter-brain-region functional coupling is disrupted in AD, thereby offering a new perspective of AD etiology. - Source: PubMed
Publication date: 2024/05/09
Mitra SangaBp KailashC R SrivatsanSaikumar Naga VenkataPhilip PhilgeNarayanan Manikandan