CK20 Mouse-Mono
- Known as:
- CK20 Mouse-Mono
- Catalog number:
- 413491F
- Product Quantity:
- 6 ml
- Category:
- -
- Supplier:
- Nichereion
- Gene target:
- CK20 Mouse-Mono
Related genes to: CK20 Mouse-Mono
- Gene:
- KRT20 NIH gene
- Name:
- keratin 20
- Previous symbol:
- -
- Synonyms:
- CK20, K20, MGC35423
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-04
- Date modifiied:
- 2016-03-09
Related products to: CK20 Mouse-Mono
Related articles to: CK20 Mouse-Mono
- The somatic mutation (SM) profile of normal colon tissue in colorectal carcinoma (CRC) patients is not well-known. We examined (a) SMs in resected normal colonic tissue adjacent to tumors from non-metastatic CRC patients, (b) identified potentially malignant mutations, and (c) their functional effects and utility for precision medicine. Surgically resected fresh paired tumor and adjacent normal colon tissues from 61 patients were used as sources of tissue DNA. Whole blood (WB) DNA was used as a germline reference. Next-generation sequencing using a custom hybridization capture panel was performed on each. Differential gene expression was assessed and stratified by mutation status in normal tissue. Compared to WB DNA, similar numbers of SMs were detected in tumor and adjacent normal colon tissue. Of all SMs found in adjacent tissue, more than 23% of those same mutations were also detected in the matched tumor. Of the 61 patients, 57 (93.4%) had at least one potentially malignant non-synonymous SM in their normal tissue. The most frequently involved genes were (67% of the patients), (64%), (49%), (41%), (41%), (39%), (39%), (38%), and (38%). The use of WB as a germline reference was important, as using only adjacent normal tissue as a reference caused false negatives for mutations shared between tumor and normal tissue. Mutation status in normal tissue was associated with differential gene expressions in matched tumors. mutations were associated with more marked down-regulation of , , , , and , and more marked up-regulation of , , and , the latter two suggesting the folate pathway as a potential therapeutic target. For the first time, we document a comprehensive SM profile of normal colon tissue adjacent to tumors in CRC patients and observe its functional effect on differential gene expression in matched tumor tissue to identify potential therapeutic applications in precision medicine. - Source: PubMed
Publication date: 2026/09/18
Jasmine FarzanaVasiljevs DaniilAlmazan ArmandoAhsan HabibulKibriya Muhammad G - Eosinophilic solid and cystic renal cell carcinoma (ESC-RCC) is a recently recognized eosinophilic renal neoplasm characterized by distinctive morphologic, immunophenotypic, and molecular features, including frequent TSC/mTOR pathway alterations. Recently, L1 cell adhesion molecule (L1CAM) has gained increasing recognition as a diagnostically and biologically relevant marker in selected eosinophilic renal neoplasms; however, its expression profile in ESC-RCC has not been systematically investigated. We aimed to evaluate L1CAM expression in a multicenter cohort of ESC-RCCs and correlate the findings with clinicopathologic and immunophenotypic features. A retrospective multicenter cohort of 11 ESC-RCCs was collected. Clinicopathologic and immunophenotypic findings were recorded. Immunohistochemistry for L1CAM was performed on representative whole tissue sections and semi-quantitatively scored based on the percentage of positive tumor cells. The cohort included 9 female and 2 male patients with a median age of 50 years (range, 39-79). L1CAM expression was identified in 7 of 11 tumors (63.6%), including 5 cases with diffuse membranous (3+) staining and 2 cases with intermediate (2+) staining; no tumor showed only focal (1+) expression. All tumors showed the characteristic morphology of ESC-RCC and expressed KRT20, irrespective of L1CAM status. Among tumors evaluated with additional markers, SDHB expression was retained in all 6 tested tumors and GATA3 was negative in all 5 tested tumors. Molecular testing was not performed in this cohort. Follow-up was available for all 11 patients (median, 10 months), with all patients alive without disease at last follow-up. Our findings expand the known immunophenotypic spectrum of ESC-RCC by demonstrating L1CAM expression in a substantial subset of tumors. However, because L1CAM expression is neither sensitive nor specific for ESC-RCC, positive or negative staining does not support or exclude the diagnosis and does not currently justify routine use of L1CAM in the diagnostic evaluation of morphologically suspected ESC-RCC. - Source: PubMed
Publication date: 2026/09/10
Kabul SelvaYaprak Bayrak BusraOzbek BusraOzsagir ElifYıldırım Nazif AlperenOzturk EceJafarzadeh HamedBiltekin BurcuBuyukgok MelekSungu NuranOktay MuratCoban GanimeKosemehmetoglu KemalAcosta Andres MCheng LiangAkgul Mahmut - Obesity is a major risk factor for colorectal cancer (CRC), promoting tumor initiation through chronic inflammation and metabolic dysregulation. Cancer stem cells (CSCs) drive CRC progression through Notch1, Wnt/β-catenin (Wnt), and PI3K/mTOR (mTOR) signaling. Omega-3 polyunsaturated fatty acids (EPA and DHA) and epigallocatechin-3-gallate (EGCG) may modulate these pathways. This study investigated the effects of obesogenic-like stimuli on CSC-related CRC signaling and the preventive potential of EPA:DHA-EGCG in patient-derived organoids (PDOs) from normal mucosa (NM) of non-obese (non-OB) patients. CD133 and CD44 expression was evaluated in tumor tissues and matched NM from obese (OB) and non-OB CRC patients. PDOs derived from NM of non-OB patients were exposed to an adipocyte-conditioned medium reproducing an obesogenic adipokine profile, with or without EPA:DHA (1:1) plus EGCG (EDE). Viability, morphology, and molecular markers of stemness, differentiation, and CRC-related pathways were assessed. OB CRC tissues exhibited a CSC change from CD133-high/CD44-low to CD44-high/CD133-low compared with non-OB CRC. In PDOs, OB-EDE recapitulated this CD44-high/CD133-low phenotype, increasing organoid viability and size while maintaining KRT20 comparable to control (CTRL). HES1 was significantly upregulated, consistent with modulation of Notch1 signaling. OB-EDE downregulated Wnt target genes and increased the mTOR downstream effector p-S6R. OB + EDE exerted marker- and pathway-specific effects, maintaining PROM1 at CTRL levels, reducing CD44 and HES1, and increasing KRT20, while LGR5 remained suppressed. Compared with OB-EDE, OB + EDE further reduced the expression of Wnt target genes and reduced p-S6R to CTRL, whereas p-mTOR/mTOR was not significantly affected. Overall, obesogenic-like stimuli were associated with a CD44-high stem-like phenotype accompanied by coordinated changes in Notch1, Wnt and mTOR signaling. EDE exerted differential effects on these molecular alterations, supporting its potential as a complementary bioactive strategy in obesity-associated CRC. Pharmacological inhibition using DAPT provided preliminary functional support for a contribution of Notch1 signaling to the maintenance of this obesogenic phenotype. - Source: PubMed
Publication date: 2026/09/02
Calafato GiuliaBernardi AliceAlquati ChiaraCuicchi DajanaButtitta FrancescoDi Paola Floriana JessicaPierantoni ChiaraCeccarelli ClaudioPariali MilenaPiazzi GiuliaRicciardiello Luigi - Colorectal cancer (CRC) remains one of the most prevalent and lethal malignancies worldwide. Adiponectin, a hormone secreted by adipose tissue, has been increasingly recognized for its pleiotropic effects in several malignancies. In particular, an inverse association between circulating adiponectin levels and CRC incidence supports a potential protective role for adiponectin and its receptors (AdipoR1, AdipoR2). The aim of this study was to investigate the effects of adiponectin on Caco-2 cells, a human CRC cell line, by examining intestinal epithelial differentiation using AdipoRon (AR), a synthetic adiponectin receptor agonist. The effects of AR on Caco-2 cells were assessed by evaluating dome formation and the expression of key molecular markers involved in intestinal epithelial differentiation, including KLF-4, DPPIV, SI, and KRT20, at both transcriptional levels using qRT-PCR and at protein levels using immunofluorescence and Western blot analysis. In addition, mitochondrial reactive oxygen species (ROS) production was assessed using MitoSOX™ Red. Our findings showed that AR administration was associated with a dose-dependent increase in AdipoR1 and AdipoR2 expression as well as with dome formation in Caco-2 cells. Furthermore, AR administration reduced Ki-67 expression with no changes in cell cycle and an increase in the differentiation markers DPPIV and SI, while KRT20 remained unchanged. Finally, AR decreased mitochondrial ROS levels during differentiation. Our findings provide new evidence that AR contributes to intestinal epithelial differentiation and may represent a potential therapy for colorectal cancer. AdipoRon may contribute to the regulation of intestinal epithelial differentiation and may contribute to restoring epithelial homeostasis in tumor cells. Further research is needed to clarify the underlying mechanisms and assess the translational relevance of adiponectin-based therapies. - Source: PubMed
Publication date: 2026/07/28
Mallardo MartaMemon FurqanD'Auria LudovicaPagliaro RaffaellaDaniele AuroraNigro Ersilia - Consensus molecular classes of urothelial carcinoma (UC) include basal/squamous (Ba/Sq), luminal papillary, luminal nonspecified, luminal unstable, stroma-rich, and neuroendocrine-like. We aimed to determine the consensus molecular classifications of micropapillary (MP), plasmacytoid (PC), and sarcomatoid (SM) subtypes of bladder UC and characterize their spatial transcriptomic profiles. - Source: PubMed
Publication date: 2026/08/25
Zhao TingNawrocki ColeXiong LinjieNieman Linda TSaylor Philip JBlute Michael LMiyamoto David TTing David TDahl Douglas MWu Chin-Lee