Mouse cytokeratin 18(CK-18)

Efficacy of Arg-1, Hep Par-1, and CK19 expressions in diagnosing pup types of primary hepatocellular carcinoma and excluding metastases.

Many conflicts arise when immunohistochemistry is used for hepatocellular carcinoma (HCC), and some of these conflicts arise from the biliary portion within the tumor itself or from liver metastases. The aim of this study is to investigate the expression of Arg-1, HepPar-1 and CK-19 in primary HCC subtypes, as well as to study some metastatic cases to find a distinct immunohistochemical panel to use in characterizing these entities. ….
MATERIALS AND METHODS: A paraffin block including 62 cases of primary HCC and 18 cases diagnosed as metastatic tumors were submitted to this study using a liver arginase antibody (ab125134 Cambridge, USA, polyclonal antibody, 3.75 μg/ml). ). ), HepPar-1 (mouse OCH1E5 polyclonal antibody; 1:600; DAKO, CA, USA) and CK19 anti-cytokeratin 19 antibody (ab15463, rabbit polyclonal antibody; 1:100; Cambridge, USA). )). The intensity of immunofluorescence staining was scored (0 to 3+). Nuclear and visceral staining with Arg-1 and cytoplasmic staining for HepPar-1 and CK 19 have been reported.
RESULTS: The histopathological phenotypes were mainly trabecular (24, 38.7%) and pseudotumor (N = 14, 22.5%), with mixed hepatocellular carcinoma present in one case (1.6%). Positivity for arginase-1 was in 55 cases (88.7%) versus 46 (74.19%) and 8 (12.9%) for HepPAr.1%-1 and CK 19, respectively. Expression intensity was marked in good and medium differentiation for both Arg-1 and HepPar-1 and poorly differentiated for CK 19. The cases of metastatic cancer revealed 2 positive for Arg-1 (11.1%), 4 cases (22.2. 2 (%) are positive for HepPar-1, and 13 cases (72.2%) are positive for CK 19.
Arg-1 and HepPar-1 are emphatic in the diagnosis of primary HCC in most cases, either separately or together, but the priority of selection is more skewed towards Arg-1. Arg-1 and HepPar-1 positive with negative expressions of CK 19 give further support to the diagnosis of primary HCC while the opposite supports the diagnosis of tumor of biliary origin or hepatic metastasis.

SIX1 regulates aberrant endometrial cell differentiation and genetic latency after exposure to developmental estrogenic chemicals.

Early exposure to estrogenic chemicals may increase the risk of cancer, possibly by disrupting normal patterns of cell differentiation. Newborn female mice undergo synthetic diethylstilbestrol (DES) changes in uterine granulomas and neoplasia in adulthood. Abnormal endometrial glands express the oncofetal sine oculis homeobox 1 (SIX1) protein and contain cells with basal (cytokeratin [CK] 14+/18-) and poorly differentiated (CK14+/18+) properties, and strongly associate SIX1 with differentiation. Anomalies and cancer. Here we tested whether SIX1 expression is required for abnormal endometrial differentiation and carcinogenesis using Pgr-cre to generate six conditional knockout mice (Six1d/d). Interestingly, 6-day/day mice treated with corn oil (CO) develop focal adenomatous dysplasia and features of carcinoma in situ compared to wild-type Six1 (Six1 +/+) mice. In addition, 6-day/day mice newly exposed to DES had a 42% higher incidence rate of endometrial carcinomas compared to DES Six1 +/+ mice. Whereas DES Six1d/d mice had 10 times more CK14+/18- basal cells within the uterine horns compared with DES Six1+/+ mice, the appearance of CK14+/18+ remained a hallmark of neoplastic lesions. These results indicate that SIX1 is required for normal endometrial epithelial differentiation, CK14+/18+ cells function as a cancer progenitor group, and SIX1 delays DES-induced endometrial carcinogenesis by promoting the initial differentiation of CK14+/18+ cells. In human endometrial biopsies, 35% of malignancies showed CK14+/18+ expression, which was positively correlated with tumor stage and grade and was not present in normal endometriosis. IMPLICATIONS: Aberrant epithelial differentiation is an essential feature in both the DES mouse model of endometrial carcinoma and human endometrial carcinoma. The association of CK14+/18+ cells with human endometrial cancer provides a new biomarker for cancer and could lead to new therapeutic strategies.

The antiapoptotic effects of recombinant human hepatocyte growth factor on hepatocytes have been associated with suppression of intrahepatic hemorrhage.

Hepatocyte growth factor (HGF) is an endogenously expressed bioactive substance that has a strong anti-apoptotic effect. In this study, we biochemically and histologically characterized the effects of rh-HGF on in vitro human hepatocyte injury and mouse acute liver failure (ALF) models, both of which were induced by antibody-mediated Fas signaling. rh-HGF inhibited intracellular caspase-3/7 activation and cytokeratin 18 (CK-18) fragment release in both models. Histologically, rh-HGF dramatically suppressed parenchymal damage and intrahepatic hemorrhage. Among the laboratory parameters, prothrombin time (PT) was strongly preserved by rh-HGF, and PT was well correlated with the degree of intrahepatic hemorrhage. These results showed that the anti-apoptotic effect of rh-HGF on hepatocytes coincided strikingly with the suppression of intrahepatic hemorrhage. PT was considered to be the best parameter that correlated with the intrahepatic hemorrhages associated with hepatocellular damage. The action of rh-HGF might derive not only from its anti-apoptosis effects on liver parenchymal cells but also from its stabilization of structural and vasculature integrity.

Mouse cytokeratin 18(CK-18)

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Mouse cytokeratin 18-M65(CK-18-M65)

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Mouse Cytokeratin 18-M30(CK 18-M30)

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Cytokeratin 18 / CK-18 (KRT18) Antibody

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Sweat gland organoids contribute to cutaneous wound healing and sweat gland regeneration.

Sweat glands perform a vital thermoregulatory function in mammals. Like other skin components, they originate from epidermal progenitors. However, they have low regenerative potential in response to injury. We have established a sweat gland culture and expansion method using 3D organoids cultures. The epithelial cells derived from sweat glands in dermis of adult mouse paw pads were embedded into Matrigel and formed sweat gland organoids (SGOs). These organoids maintained remarkable stem cell features and demonstrated differentiation capacity to give rise to either sweat gland cells (SGCs) or epidermal cells. Moreover, the bipotent SGO-derived cells could be induced into stratified epidermis structures at the air-liquid interface culture in a medium tailored for skin epidermal cells in vitro. The SGCs embedded in Matrigel tailored for sweat glands formed epithelial organoids, which expressed sweat-gland-specific markers, such as cytokeratin (CK) 18 and CK19, aquaporin (AQP) 5 and αATP. More importantly, they had potential of regeneration of epidermis and sweat gland when they were transplanted into the mouse back wound and claw pad with sweat gland injury, respectively. In summary, we established and optimized culture conditions for effective generation of mouse SGOs. These cells are candidates to restore impaired sweat gland tissue as well as to improve cutaneous skin regeneration.

inhibition in vivo results in mammary tumor regression and reduced mammary tumorsphere-forming activity in vitro.

activation has been recently implicated in human breast cancers, associated with a poor prognosis, and tumor-initiating cells are hypothesized to mediate resistance to treatment and disease relapse. To address the role of NOTCH1 in mammary gland development, transformation, and mammary tumor-initiating cell activity, we developed a doxycycline-regulated mouse model of NOTCH1-mediated mammary transformation.

Mammary gland development was analyzed by using whole-mount analysis and by flow cytometry in nulliparous transgenic mice maintained in the presence/absence of doxycycline (or intracellular NOTCH1). Mammary tumors were examined histologically and immunophenotyped by staining with antibodies followed by flow cytometry. Tumors were transplanted into mammary fat pads under limiting dilution conditions, and tumor-initiating cell frequency was calculated. Mammary tumor cells were also plated in vitro in a tumorsphere assay in the presence/absence of doxycycline. RNA was isolated from mammary tumor cell lines cultured in the presence/absence of doxycycline and used for gene-expression profiling with Affymetrix mouse arrays. NOTCH1-regulated genes were identified and validated by using quantitative real-time polymerase chain reaction (PCR). Mammary tumor-bearing mice were treated with doxycycline to suppress NOTCH1 expression, and disease recurrence was monitored.

Similar to published studies, we show that constitutive expression of human intracellular NOTCH1 in the developing mouse mammary gland inhibits side branching and promotes luminal cell fate. These mice develop mammary adenocarcinomas that express cytokeratin (CK) 8/18. In vivo limiting-dilution analyses revealed that these mammary tumors exhibit functional heterogeneity and harbor a rare (1/2,978) mammary tumor-initiating cell population. With this dox-regulated NOTCH1 mammary tumor model, we demonstrate that NOTCH1 inhibition results in mammary tumor regression in vivo and prevents disease recurrence in four of six tumors tested. Consistent with the in vivo data, NOTCH1 inhibition reduces mammary tumorsphere activity in vitro. We also identify the embryonic stem cell transcript

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