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Results for “Cellular differentiation”

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At least 685 records · Page 38Linked to original sources

PubMed2003

c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signaling.

The c-Jun N-terminal kinase (JNK) branch of the mitogen-activated protein kinase (MAPK) signaling pathway regulates cellular differentiation, stress responsiveness and apoptosis in multicellular eukaryotic organisms. Here we investigated the functional importance of JNK signaling in regulating differentiated cellular growth in the post-mitotic myocardium. JNK1/2 gene-targeted mice and transgenic mice expressing dominant negative JNK1/2 were determined to have enhanced myocardial growth following stress stimulation or with normal aging. A mechanism underlying this effect was suggested by the observation that JNK directly regulated nuclear factor of activated T-cell (NFAT) activation in culture and in transgenic mice containing an NFAT-dependent luciferase reporter. Moreover, calcineurin Abeta gene targeting abrogated the pro-growth effects associated with JNK inhibition in the heart, while expression of an MKK7-JNK1 fusion protein in the heart partially reduced calcineurin-mediated cardiac hypertrophy. Collectively, these results indicate that JNK signaling antagonizes the differentiated growth response of the myocardium through direct cross-talk with the calcineurin-NFAT pathway. These results also suggest that myocardial JNK activation is primarily dedicated to modulating calcineurin-NFAT signaling in the regulation of differentiated heart growth.

Animals↗

PubMed2002

Toward a theory of intracrine hormone action.

A growing body of evidence indicates that in some cases, peptide hormones can function in the intracellular space. These findings are reviewed. In addition, this laboratory has made proposals regarding the origin, nature and function of intracrines--that is, intracellularly acting peptide hormones that also function in an autocrine, paracrine or endocrine manner. Here, these hypotheses are developed, and potential implications/applications of this point of view are discussed. Possible implications for cellular differentiation, cellular memory and hormonal responsiveness, as well as for the assumption of novel functions by intracellular regulatory proteins are discussed.

Angiotensins↗

PubMedDate not supplied

[Sarcomatoid carcinoma of the larynx].

Sarcomatoid carcinoma of the upper aerodigestive tract is an unusual neoplasm with differential cellular differentiation. Microscopically, sarcomatoid carcinomas have an element of squamous-cell carcinoma and a pleomorphic sarcoma-like component, which may simulate granulation tissue, malignant fibrous histiocytoma, osteosarcoma, or malignant giant-cell tumor of soft tissues.

Aged↗

PubMed2002

Identification and cloning of human polynucleotide phosphorylase, hPNPase old-35, in the context of terminal differentiation and cellular senescence.

Terminal differentiation and cellular senescence display common properties including irreversible growth arrest. To define the molecular and ultimately the biochemical basis of the complex physiological changes associated with terminal differentiation and senescence, an overlapping-pathway screen was used to identify genes displaying coordinated expression as a consequence of both processes. This approach involved screening of a subtracted cDNA library prepared from human melanoma cells induced to terminally differentiate by treatment with fibroblast IFN and mezerein with mRNA derived from senescent human progeria cells. This strategy identified old-35, which encodes an evolutionary conserved gene, human polynucleotide phosphorylase (hPNPase(old-35)), that is regulated predominantly by type I IFNs. The hPNPase(OLD-35) protein localizes in the cytoplasm of human cells and induces RNA degradation in vitro, as does its purified bacterial protein homologue. Ectopic expression of hPNPase(old-35) in human melanoma cells reduces colony formation, confirming inhibitory activity of this RNA-degradation enzyme. Identification of hPNPase(old-35), an IFN-inducible 3'-5' RNA exonuclease, provides additional support for a relationship between IFN action and RNA processing and suggests an important role for this gene in growth control associated with terminal differentiation and cellular senescence.

Amino Acid Sequence↗

PubMed1996

The influence of polarized epithelial (Caco-2) cell differentiation on the cellular binding of phosphodiester and phosphorothioate oligonucleotides.

Cell aging and the degree of cellular differentiation are thought to be important variables governing uptake of oligonucleotides but remain poorly understood. The Caco-2 colon carcinoma cell line has the ability to spontaneously differentiate into enterocytes in vitro and serves as a useful model to further investigate the effect of differentiation on oligonucleotide binding and uptake. In this study, we report that the extent of oligonucleotide association and the expression of cell surface binding proteins are governed by the age and thus the degree of differentiation of Caco-2 epithelial cells in culture. Cellular association (normalized for cell number) of an all phosphodiester (PO), all phosphorothioate (PS), and a phosphodiester oligonucleotide containing two terminal phosphorothioate internucleotide linkages at the 3' end (EC-PO) gradually increased from day 3 to around day 17 of the culture, followed by a plateau, or slight decrease, up to day 21 of the cell aging study. Overall, a threefold to fourfold increase in binding was observed from day 3 to day 17. Oligonucleotide binding was temperature and pH dependent, but the magnitude of the effect was influenced by cell aging and the degree of differentiation. PS oligonucleotides exhibited greater binding (up to threefold) at the basolateral surface compared with the apical surface within the pH range 5-7. These findings could be directly correlated with the expression levels of cell surface oligonucleotide binding proteins during the aging study. A Caco-2 cell surface protein binding complex of around 46 kDa was identified as the major site of binding for both PO and PS oligonucleotides, although the latter also bound to several other proteins, especially at low pH.

Caco-2 Cells↗

PubMed2002

Effects of pulsed electromagnetic field (PEMF) stimulation on bone tissue like formation are dependent on the maturation stages of the osteoblasts.

The effects of pulsed electromagnetic field (PEMF, 15 Hz pulse burst, 7 mT peak) stimulation on bone tissue-like formation on osteoblasts (MC3T3-E1 cell line) in different stages of maturation were assessed to determine whether the PEMF stimulatory effect on bone tissue-like formation was associated with the increase in the number of cells and/or with the enhancement of the cellular differentiation. The cellular proliferation (DNA content), differentiation (alkaline phosphatase activity), and bone tissue-like formation (area of mineralized matrix) were determined at different time points. PEMF treatment of osteoblasts in the active proliferation stage accelerated cellular proliferation, enhanced cellular differentiation, and increased bone tissue-like formation. PEMF treatment of osteoblasts in the differentiation stage enhanced cellular differentiation and increased bone tissue-like formation. PEMF treatment of osteoblasts in the mineralization stage decreased bone tissue-like formation. In conclusion, PEMF had a stimulatory effect on the osteoblasts in the early stages of culture, which increased bone tissue-like formation. This stimulatory effect was most likely associated with enhancement of the cellular differentiation, but not with the increase in the number of cells.

3T3 Cells↗

PubMed2005

Cellular differentiation-induced attenuation of LPS response in HT-29 cells is related to the down-regulation of TLR4 expression.

Intestinal epithelial cells not only present a physical barrier to bacteria but also participate actively in immune and inflammatory responses. The migration of epithelial cells from the crypt base to the surface is accompanied by a cellular differentiation that leads to important morphological and functional changes. It has been reported that the differentiation of colonic epithelial cells is associated with reduced interleukin (IL)-8 responses to IL-1beta. Although toll-like receptor 4 (TLR4) has been previously identified to be an important component of mucosal immunity to lipopolysaccharide (LPS) in the colon, little is known about the regulation of TLR4 in colonic epithelial cells during cellular differentiation. We investigated the effects of differentiation on LPS-induced IL-8 secretion and on the expression of TLR4. Differentiation was induced in colon cancer cell line HT-29 cells by butyrate treatment or by post-confluence culture and assessed by measuring alkaline phosphatase (AP) activity. IL-8 secretion was measured by ELISA, and TLR4 protein and mRNA expressions were followed by Western blot and RT-PCR, respectively. HT-29 cells were found to be dose-dependently responsive to LPS. AP activity increased in HT-29 cells by differentiation induced by treatment with butyrate or post-confluence culture. We found that IL-8 secretion induced by LPS was strongly attenuated in differentiated cells versus undifferentiated cells, and that cellular differentiation also attenuated TLR4 mRNA and protein expressions. Pretreating HT-29 cells with tumor necrosis factor (TNF)-alpha or interferon (INF)-gamma augmented LPS-induced IL-8 secretion and TLR4 expression. These TNF-alpha- or INF-gamma-induced augmentations of LPS response and TLR4 expression were all down-regulated by differentiation. Collectively, we conclude that cellular differentiation attenuates IL-8 secretion induced by LPS in HT-29 cells, and this attenuation is related with the down-regulation of TLR4 expression.

Alkaline Phosphatase↗

PubMed2002

Analysis of human cellular retinol-binding protein II promoter during enterocyte differentiation.

Cellular retinol binding protein II (CRBP II) is a vitamin A-binding protein that is expressed specifically in small intestinal villus absorptive cells. Previous studies have shown that retinoic acid upregulates endogenous human CRBP II gene expression in differentiated Caco-2 cells. To better characterize the regulation of human CRBP II expression, we analyzed the ability of receptor-selective agonists to enhance transcription from the 5'-upstream flanking region of the human CRBP II gene. Stable transfection experiments showed that the proximal 2.8-kb region of the human CRBP II gene is sufficient for retinoic acid inducibility in differentiated Caco-2 cells. However, direct sequence analysis and transient transfection experiments indicate that, unlike the rat CRBP II promoter, the human CRBP II promoter is not a direct retinoid X receptor target. The results indicate that the retinoic acid responsiveness of the human CRBP II promoter is mediated by an indirect mechanism and that this mechanism is associated with enterocyte differentiation.

5' Flanking Region↗

PubMed1991

A role for osteocalcin in osteoclast differentiation.

Specific cellular interactions with components of the extracellular matrix can influence cellular differentiation and development of many tissues. The extracellular matrix of bone is composed of organic constituents and a solid phase of calcium and inorganic phosphate (apatite). When implanted subcutaneously in rats, particles of bone matrix (BPs) recruit progenitors that differentiate into multinucleated cells with osteoclastic features. Because BPs deficient in osteocalcin, a bone matrix protein, were less efficient at promoting osteoclast formation than were normal BPs, we directly examined the influence of osteocalcin on osteoclast differentiation. We evaluated tissue responses to particles of synthetic crystalline apatite alone (Ap), having many of the features of native apatite of mature bone, or to apatite prepared with osteocalcin (Ap/OC), bovine serum albumin (Ap/BSA) or rat bone collagen (Ap/Col). Twelve days after subcutaneous implantation in normal rats, Ap, Ap/BSA, and Ap/Col particles generated a mild foreign body reaction with multinucleated cells in direct contact with the particles; these cells were negative for tartrate-resistant acid phosphatase (TRAP) activity and lacked ruffled borders. In contrast, Ap particles containing approximately 0.1% osteocalcin were partially resorbed and they generated more multinucleated cells that were TRAP-positive, were immunoreactive with an antibody against tartrate-resistant purple acid phosphatase, and displayed ultrastructural features of active osteoclasts including ruffled borders and clear zones. These data support the hypothesis that osteocalcin may function as a matrix signal in the recruitment and differentiation of bone-resorbing cells.

Acid Phosphatase↗

PubMed1999

Differentiation and the cytomorphology of salivary gland tumors with specific reference to oncocytic metaplasia.

OBJECTIVE: The different cell types and many growth patterns found in salivary gland tumors provide ample reason for the diagnostic problems caused by these tumors. To improve criteria for differential diagnosis, the potential range of cytologic features possible in salivary gland tumor cells must be better appreciated. STUDY DESIGN: From our respective pathology archives, normal salivary tissue and salivary gland tumours--other than Warthin's tumor and oncocytoma--with oncocytic differentiation were identified and studied by means of light and electron microscopy. RESULTS: In this article, we cite a number of different salivary gland tumors, including basal cell adenoma, pleomorphic adenoma, myoepithelioma, polymorphous low-grade adenocarcinoma, and mucoepidermoid carcinoma, showing varying degrees of oncocytic differentiation. CONCLUSIONS: Variable cellular differentiation is probably the basis for foci of tumor cells unexpected for a particular salivary gland neoplasm, further compounding differential diagnosis. Illustration of oncocytic differentiation serves 2 purposes. First, it can alert pathologists to this potential in otherwise typical salivary gland tumors; an awareness of this and other possible variations in cellular differential patterns can help prevent misdiagnosis. Second, these particular tumors illustrate the role of the cellular differentiation that is responsible for the range of histologic features within any one subtype of salivary gland tumors.

Cell Differentiation↗

PubMed1997

Tracheobronchial cytology in inhalation injury.

The aim of this study is to establish whether tracheobronchial cytology is useful in the diagnosis of inhalation injury. Twenty patients diagnosed to have inhalation injury by existing clinical criteria and 20 control patients were admitted into the study. Bronchoscopy and brush biopsies were carried out. They were then scored using a Total Cellular Score and Differential Cellular Score. These were compared with clinical and bronchoscopic scores and respiratory outcome. The average Total Cellular Score of the patients with inhalation injury was 497.4 +/- 281.9 and that of the control patients was 1004.2 +/- 88.4. There was a strong correlation between clinical, bronchoscopic, and total cellular scores. The Differential Cellular Score showed a left shift in patients with inhalation injury. This study shows that tracheobronchial cytology is a useful adjunct in diagnosing and assessing the severity of inhalation injury. Furthermore, our results suggest that it may be superior to current methods in predicting respiratory outcome.

Bronchi↗

PubMed1996

mu-Opioid receptor-induced Ca2+ mobilization and astroglial development: morphine inhibits DNA synthesis and stimulates cellular hypertrophy through a Ca(2+)-dependent mechanism.

Morphine, a preferential mu-opioid receptor agonist, alters astroglial development by inhibiting cell proliferation and by promoting cellular differentiation. Although morphine affects cellular differentiation through a Ca(2+)-dependent mechanism, few studies have examined whether Ca2+ mediates the effect of opioids on cell proliferation, or whether a particular Ca2+ signal transduction pathway mediates opioid actions. Moreover, it is uncertain whether one or more opioid receptor types mediates the developmental effects of opioids. To address these questions, the present study examined the role of mu-opioid receptors and Ca2+ mobilization in morphine-induced astrocyte development. Morphine (1 microM) and non-morphine exposed cultures enriched in murine astrocytes were incubated in Ca(2+)-free media supplemented with < 0.005, 0.3, 1.0, or 3.0 mM Ca2+ ([Ca2+]o), or in unmodified media containing Ca2+ ionophore (A23187), nifedipine (1 microM), dantrolene (10 microM), thapsigargin (100 nM), or L-glutamate (100 microM) for 0-72 h. mu-Opioid receptor expression was examined immunocytochemically using specific (MOR1) antibodies. Intracellular Ca2+ ([Ca2+]i) was measured by microfluorometric analysis using fura-2. Astrocyte morphology and bromodeoxyuridine (BrdU) incorporation (DNA synthesis) were assessed in glial fibrillary acidic protein (GFAP) immunoreactive astrocytes. The results showed that morphine inhibited astroglial growth by activating mu-opioid receptors. Astrocytes expressed MOR1 immunoreactivity and morphine's actions were mimicked by the selective mu agonist PL017. In addition, morphine inhibited DNA synthesis by mobilizing [Ca2+]i in developing astroglia. At normal [Ca2+]o, morphine attenuated DNA synthesis by increasing [Ca2+]i; low [Ca2+]o (0.3 mM) blocked this effect, while treatment with Ca2+ ionophore or glutamate mimicked morphine's actions. At extremely low [Ca2+]o (< 0.005 mM), morphine paradoxically increased BrdU incorporation. Although opioids can increase [Ca2+]i in astrocytes through several pathways, not all affect DNA synthesis or cellular morphology. Nifedipine (which blocks L-type Ca2+ channels) did not prevent morphine-induced reductions in BrdU incorporation or cellular differentiation, while thapsigargin (which depletes IP3-sensitive Ca2+ stores) severely affected inhibited DNA synthesis and cellular differentiation-irrespective of morphine treatment. However, dantrolene (an inhibitor of Ca(2+)-dependent Ca2+ release) selectively blocked the effects of morphine. Collectively, the findings suggest that opioids suppress astroglial DNA synthesis and promote cellular hypertrophy by inhibiting Ca(2+)-dependent Ca2+ release from dantrolene-sensitive intracellular stores. This implies a fundamental mechanism by which opioids affect central nervous system maturation.

Animals↗

PubMed2006

Repression of HIP/RPL29 expression induces differentiation in colon cancer cells.

We had previously shown that the expression of heparin/heparan sulfate interacting protein/ribosomal protein L29 (HIP/RPL29) was upregulated in colon cancer tissues. The present study investigated the role of HIP/RPL29 in differentiation in colon cancer cells. Inducing cellular differentiation in HT-29 cells by both sodium butyrate and glucose deprivation resulted in a significant downregulation of HIP/RPL29 expression. The beta-catenin/Tcf-4 pathway is the most important pathway controlling the switch between cellular differentiation and proliferation in intestinal epithelial cells. Inducing differentiation by dominant-negative inhibition of the beta-catenin/Tcf-4 complexes in LS174T cells also resulted in downregulation of HIP/RPL29. To determine whether a lower expression of HIP/RPL29 could induce differentiation in cancer cells, small interfering RNA (siRNA) targeting HIP/RPL29 was transfected into LS174T cells. The resultant knockdown of HIP/RPL29 expression induced cellular differentiation, as shown by the increased expression of two known markers of differentiation in LS174T cells, galectin-4 and mucin-2. In addition, the differentiation process induced by repression of HIP/RPL29 expression was accompanied by the upregulation of p21 and p53. In conclusion, HIP/RPL29 plays a role in the cellular differentiation process in colon cancer cells. The differentiation process is at least partially mediated by the upregulation of p21 and p53 pathways.

Alkaline Phosphatase↗

PubMed2005

The crystal structure of CREG, a secreted glycoprotein involved in cellular growth and differentiation.

The cellular repressor of E1A-stimulated genes (CREG) is a secreted glycoprotein that inhibits proliferation and enhances differentiation of human embryonal carcinoma cells. CREG binds to the cation-independent mannose 6-phosphate (M6P)/insulin-like growth factor II (IGF2) receptor (IGF2R) (M6P/IGF2R), and this receptor has been shown to be required for CREG-induced growth suppression. To better understand CREG function in cellular growth and differentiation, we solved the 3D crystal structure of this protein to 1.9-A resolution. CREG forms a tight homodimeric complex, and CREG monomers display a beta-barrel fold. The three potential glycosylation sites on CREG map to a confined patch opposite the dimer interface. Thus, dimerization of glycosylated CREG likely presents a bivalent ligand for the M6P/IGF2R. Closely related structural homologs of CREG are FMN-binding split-barrel fold proteins that bind flavin mononucleotide. Our structure shows that the putative flavin mononucleotide-binding pocket in CREG is sterically blocked by a loop and several key bulky residues. A mutant of CREG lacking a part of this loop maintained overall structure and dimerization, as well as M6P/IGF2R binding, but lost the growth suppression activity of WT CREG. Thus, analysis of a structure-based mutant of CREG revealed that binding to M6P/IGF2R, while necessary, is not sufficient for CREG-induced growth suppression. These findings indicate that CREG utilizes a known fold for a previously undescribed function [corrected]

Amino Acid Sequence↗

PubMed2005

Differentially expressed cellular genes following HBV: potential targets of anti-HBV drugs?

The aim of the study was to screen for cellular genes that are differentially expressed following hepatitis B virus (HBV) infection, in an attempt to identify potential targets of anti-HBV drugs. An oligonucleotide microarray containing 231 virus-infection-associated genes was prepared. Differential gene expression in HepG2.2.15 cells compared to control with HepG2 cells was analysed by this in-house microarray. The change in gene expression in HepG2.2.15 cells treated by lamivudine on days 4 and 8 after exposure was also studied. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to comfirm the differentially expressed genes induced by HBV and lamivudine. There were 31 upregulated and four downregulated genes in HepG2.2.15 cells compared with the HepG2 control cells. Eleven genes were consistently altered by lamivudine at both time points. Of the 31 genes that were upregulated in HepG2.2.15 cells, there were seven genes which were downregulated by lamivudine. Of the four downregulated genes, there was one gene which was upregulated by lamivudine. Of the differentially expressed genes induced by HBV and lamivudine, the expression of five genes was confirmed by semi-quantitative RT-PCR. These results shed new light on the effects of HBV and lamivudine on cellular gene expression. Differentially expressed genes induced by HBV and lamivudine could potentially become new anti-HBV drug targets in novel therapies.

Antiviral Agents↗

PubMed2004

The PML-RARalpha fusion protein and targeted therapy for acute promyelocytic leukemia.

Acute promyelocytic leukemia (APL) is an unique subtype of acute myeloid leukemia typically carrying a specific reciprocal chromosome translocation t(15;17) leading to the expression of a leukemia-generating fusion protein, PML-RARalpha. Nearly all de novo APL patients undergo disease remission when treated with all trans retinoic acid (ATRA) plus chemotherapy. APL patients that relapse following this type of therapy respond to As2O3 with disease remission once again. The mechanism of action of both ATRA and As2O3 appears to be by inducing granulocytic differentiation and this cellular differentiation seems to depend on PML-RARalpha proteolysis. ATRA treatment results in partial cleavage and complete degradation of PML-RARalpha protein in differentiation sensitive, but not in differentiation resistant APL cells. As2O3 treatment results in only complete degradation of PML-RARalpha protein in both ATRA-sensitive and -resistant APL cells. PML-RARalpha appears to cause leukemia by acting as a transcriptional repressor of RARalpha target genes and by inhibiting activity of transcription factor C/EBPalpha. Therefore, PML-RARalpha proteolysis induced by ATRA and As2O3 may play an important role in overcoming the repressive activity of PML-RARalpha and allowing cellular differentiation to proceed. This review will focus on the status of the PML-RARalpha fusion protein and its relationship to gene and differentiation induction as well as differentiation resistance of APL cells.

Arsenic Trioxide↗

PubMed1995

Inhibition of in vitro myogenic differentiation by cellular transcription factor E2F1.

Terminal differentiation of cultured myocytes requires withdrawal of the cells from the cell cycle. Constitutive overexpression of several oncogenes in myoblasts can inhibit in vitro myogenesis. Here we studied the role of the cellular transcription factor E2F1 on myogenic differentiation. E2F1 expression is irreversibly down-regulated during differentiation of C2C12 myocytes. Furthermore, deregulated E2F1 expression in C2C12 cells prevented myogenic differentiation. This inhibition of myogenesis was associated with the repression of myogenin expression and an elevated cyclin D1 expression. Moreover, E2F1-overexpressing myocytes failed to exit the cell cycle under differentiation conditions. These results are consistent with the notion that E2F1 can function as an oncogene and further suggest that E2F1 down-regulation is required for myogenic differentiation.

Animals↗

PubMed1998

Comparison of estrogen and progesterone receptor, Ki-67, and p53 immunoreactivity in uterine endometrioid carcinoma and endometrioid carcinoma with squamous, mucinous, secretory, and ciliated cell differentiation.

An analysis of 77 uterine endometrioid carcinomas was performed to compare pure endometrioid carcinomas and endometrioid carcinomas with various types of cellular differentiation for the expression of estrogen (ER) and progesterone (PR) receptors, p53, and Ki-67 and to correlate these findings with clinicopathologic features. Forty-three pure endometrioid carcinomas and 34 endometrioid carcinomas displaying additional types of cellular differentiation in at least 10% of the tumor (16 squamous, 11 mucinous, four ciliated cell, and three secretory) were analyzed. In 8 of the 16 tumors with squamous differentiation, the squamous component was histologically benign (low grade), and in eight tumors it was histologically malignant (high grade). In tumors showing various types of cellular differentiation except those with a high-grade squamous component, comparison of the endometrioid glandular component with the squamous, mucinous, secretory, and ciliated cell components showed that ER/PR, Ki-67, and p53 expression were generally higher in the glandular component compared with the various differentiated components. These findings parallel the changes that occur in the endometrium in the secretory phase of the menstrual cycle and, therefore, suggest that the differentiated components have undergone terminal differentiation. In contrast, in endometrioid carcinomas with a high-grade squamous component, Ki-67 and p53 expression were the same in the glandular and squamous components suggesting that squamous epithelium in these tumors represented another pathway of cellular differentiation but not one that was terminally differentiated. Endometrioid carcinomas with a high-grade squamous component had significantly higher grade (P = .002), stage (P < .001), cellular proliferation index (P = .0005), and worse outcome (P = .0009) compared with tumors with the other types of cellular differentiation, including those with a low-grade squamous component and pure low-grade endometrioid carcinomas. In addition, carcinomas with a high-grade squamous component occurred in older women and were more frequently associated with atrophic endometrium and less replacement hormone therapy, but the differences were not statistically significant. In conclusion, endometrioid carcinomas with various types of cellular differentiation can be broadly divided into two groups. Tumors with mucinous, secretory, and ciliated cell differentiation and those with a low-grade squamous component are similar to pure low-grade endometrioid carcinomas in that most have high ER and PR expression, low cellular proliferation indices, low p53 immunoreactivity, and good prognosis. In contrast, endometrioid carcinomas with a high-grade squamous component lack expression of ER and PR, have high cellular proliferation indices, often express p53, and have a prognosis similar to poorly differentiated endometrioid carcinomas.

Adult↗