Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subclinical or latent cases of gluten-sensitive enteropathy (GSE) are difficult to diagnose, and serology-positive, histology-negative (minimal morphologic change) and serology-negative, histology-positive patients have been identified. Both, particularly the histology-negative group, require the correct diagnosis for proper management, especially because the concept of minimal histologic change GSE has escaped attention in standard textbooks. We assessed the numbers and distribution of intraepithelial T cells and their subsets with CD3, CD8, and CD4 immunostaining and examined for crypt hyperplasia with mitotic and Ki-67 proliferative indices with the aim of refining the criteria for the diagnosis of minimal change GSE. Duodenal biopsies from 46 clinically suspected cases of GSE tested for antigliadin, antiendomysium, and antitissue transglutaminase antibodies were divided into four groups: serology-positive, histology-positive (S+H+, n = 20); serology-positive, histology-negative (S+H-, n = 22), representing the minimal morphologic change group; serology-negative, histology-positive (S-H+, n = 4); and serology-negative, histology-negative (S-H-, n = 28), controls with histologically normal duodenal biopsies obtained for unrelated reasons. The numbers of CD3+ and CD8+ intraepithelial T cells (IETCs) were significantly higher in histology-positive biopsies with (mean, 40.3/100 and 39.3/100 enterocytes, respectively) and without positive serology (mean, 33.3/100 and 35/100 enterocytes, respectively) compared with all other groups (S+H-, mean, 26.5/100 and 24.3/100 enterocytes, respectively; S-H-, mean, 23.3/100 and 17.9/100 enterocytes, respectively). Values for Ki-67 index in crypt enterocytes were also significantly different between histology-positive and histology-negative groups (P = 0.000). The distribution of CD3+ and CD8+ IETCs was mostly even along the surface enterocytes in histology-positive cases compared with the controls, which showed an uneven distribution. The 2 parameters that significantly discriminated between minimal morphologic change GSE (S+H-) and controls (S-H-) were Ki-67 index (P = 0.007) and the distribution pattern of CD8+ IETCs (P = 0.049). CD4 IETC counts were generally low, with no significant difference between all groups. The few S-H+ cases seen most likely represented false-negative serology, because the assessed parameters of this group and S+H+ cases were indistinguishable.
Appl Immunohistochem Mol Morphol 2004 Sep
PMID:Immunohistologic parameters in minimal morphologic change duodenal biopsies from patients with clinically suspected gluten-sensitive enteropathy. 1555 31

The progesterone receptor (PR) has two isoforms, A and B, among which PR-B is mainly involved in regulating proliferation of the uterine endometrium. In this study, immunohistochemical analysis was carried out to investigate the correlation of PR-A and -B expressions with cell cycle-regulatory proteins and clinicopathological parameters in endometrial adenocarcinoma. One hundred and forty-one endometrioid adenocarcinomas [76 with well-differentiated (G1), 35 with moderately differentiated (G2) and 30 with poorly differentiated (G3)] were used. Specimens of formalin-fixed and paraffin-embedded tissue were immunohistochemically stained using the high polymer method (HISTOFINE, NICHIREI). The percentage of positive nuclei of tumor cells observed in three high power fields was expressed as a labeling index (LI). PR-B expression significantly occurred more frequently in G1. It was inversely correlated with p53 gene mutation and p53 over expression, and also with clinicopathological variables, including myometrial and lymph-vascular space invasion and the FIGO stage. Patients with negative PR-B had a poorer prognosis than positive cases. PR-A expression was also significantly higher in G1 and was inversely correlated with Ki-67 expression and myometrial invasion, but not with prognosis. PR-A and -B expressions were significantly correlated with biologically malignant potential. Especially, PR-B expression is useful as a prognostic indicator of endometrial adenocarcinoma.
J Steroid Biochem Mol Biol 2004 Oct
PMID:Significance of progesterone receptor-A and -B expressions in endometrial adenocarcinoma. 1555 5

While the study of in vitro regulation of neural stem cell lineage from both embryonic and adult neurospheres is greatly advanced, much less is known about factors acting in situ for neural stem cell lineage in adult brain. We reported that neurotrophin low affinity receptor p75(NTR) is present in the subventricular zone (SVZ) in adult male rats. We then characterized co-distribution of markers associated with precursor cells (nestin and PSA-NCAM) with growth factor receptors (p75(NTR), trkA, EGFr) and proliferation-associated antigens (Ki67 and BrDU-uptake) in adult male rat by immunocytochemistry and confocal laser scan microscopy. Distribution of p75(NTR)-immunoreactivity (IR) was investigated using different mono- and polyclonal antisera. p75(NTR-) is not co-distributed with glial fibrillary acid protein. It was found to be co-distributed with a small number of nestin-IR cells, whereas no coexistence with PSA-NCAM-IR was observed. Conversely, p75(NTR)-IR was present in numerous dividing cells (Ki-67-positive) and co-distributed with EGFr. In order to verify the possible association between p75(NTR) and cell death, we investigated co-distribution of p75(NTR)-IR with nuclear condensation images as visualized by Hoechst 33258 staining. While few images indicating nuclear condensation were observed in the SVZ, no coexistence with p75(NTR) was found. TrkA- and trkB-IR was not found in the SVZ. We also investigated p75(NTR) immunostaining on post-natal day 1 and day 16, because of the dramatic reduction of proliferating cells in SVZ over this time-interval. p75(NTR)-IR was not increased in the early post-natal phase. Thus, p75(NTR) seems to be associated with cell cycle regulation in SVZ in adult rat brain.
J Mol Histol 2004 Nov
PMID:p75(NTR)-immunoreactivity in the subventricular zone of adult male rats: expression by cycling cells. 1560 87

The myelodysplastic syndromes (MDS) are a group of disorders characterized by dysplastic hemopoiesis and an increased risk of leukemic transformation. The process of angiogenesis has been implicated in the pathogenesis and evolution of MDS. In this study the proliferative activity and extent of angiogenesis was examined in bone marrow samples from 54 patients with MDS in relation to clinicopathologic features. Cellular proliferation and microvascular density (MVD) were examined immunohistochemically, using the monoclonal antibody MIB-1 (Ki-67) and an anti-CD34 monoclonal antibody respectively. Serum concentrations of interleukin-6 (IL-6) were measured by ELISA. The results showed that the MIB-1 Labeling Index (MIB-1 LI), MVD and IL-6 increased significantly with advancing severity of disease. Among the MDS-FAB subtypes, MIB-1 LI, MVD and IL-6 were significantly higher in RAEB-t, RAEB and CMML in comparison to RA and RARS (p < 0.0001 in all cases). Similarly, MIB-1 and MVD were increased in patients with score 3 in comparison to scores 0 and 1 in the IPSS system (p < 0.05). All parameters studied were significantly higher in patients versus controls. We conclude that cellular proliferative activity and angiogenesis are associated with disease progression in MDS patients.
J Mol Histol 2004 Nov
PMID:Expression of the proliferation-associated nuclear protein MIB-1 and its relationship with microvascular density in bone marrow biopsies of patients with myelodysplastic syndromes. 1560 99

The etiology of ulcerative colitis (UC) is not known. Recent studies support a primary role of the appendix in the pathogenesis of UC, however phenotypical studies of proliferating cells in the appendix have not been reported. We report phenotypical studies of lymphocytes and of proliferating subpopulations in the appendix of patients with inflammatory bowel disease and of controls. Surgical samples of the appendix were obtained from 5 patients with colon cancer, 5 with acute appendicitis, 12 with UC and 7 with Crohn's disease (CD). Frozen sections were cut from fixed samples, and immunostained with lymphocyte markers and anti-Ki-67 antibodies. The number of Ki-67(+) proliferating cells, CD19, and CD138 cells was significantly higher in the appendix of patients with UC than in controls, patients with acute appendicitis, and patients with CD. Immunohistological double staining revealed significant proliferation of CD3, CD19, and CD138 cells in the appendix of patients with UC. The proportions of Ki-67(+) cells in CD3, CD19, and CD138 cells were significantly higher in both total UC patients and patients in remission-stage UC, than in controls, patients with acute appendicitis, and patients with CD. Lamina propria cells in the appendix of patients with UC showed augmented proliferation with increased numbers of CD19 and CD138 cells. The number of CD3 cells was not significantly increased, but the proportion of proliferating CD3 cells was increased. An increased proportion of Ki-67(+) cells in CD19 and CD138 cells represents proliferation of immature plasma cells in the appendix of patients with UC, and proliferation of such immature plasma cells was seen in both active- and remission-stage UC. Proliferation of immature plasma cells in the appendix of patients with UC suggests a primary role of humoral immune responses in the pathogenesis of UC.
Int J Mol Med 2005 Mar
PMID:Significance of increased proliferation of immature plasma cells in the appendix of patients with ulcerative colitis. 1570 31

Recent studies have suggested that pancreatobiliary reflux occurs not only in patients with pancreaticobiliary maljunction (PBM), but also in patients without PBM and thereby possibly causes biliary tract disease. In this study, we examined prospectively histological findings and genetic analysis in the non-cancerous epithelium of the gallbladder in patients with high biliary amylase levels and a normal pancreaticobiliary junction. Ki-67 L.I of non-cancerous epithelium was 14.4 and 3.5% in the high biliary amylase levels (HBA) group and the low biliary amylase levels (LBA) group, respectively (p<0.01). There was no case showing p53 overexpression regardless of amylase levels of bile. COX-2 expression was detected in the cytoplasm of non-cancerous epithelium in 9 cases in the HBA group and 5 cases in the LBA group. The positive rate of COX-2 overexpression was significantly higher in the HBA group than in the LBA group (p<0.05). COX-2 overexpression cases showed higher Ki-67 L.I than COX-2 non-overexpression cases (21.2 vs. 7.9%, p<0.05). Mutations of the K-ras gene were detected in non-cancerous gallbladder epithelium in 3 cases, only in the HBA group. Patterns of K-ras mutation at codon 12 were GAT in two cases and GTT in one case. Three cases showing COX-2 overexpression also showed K-ras mutation. These three cases showing K-ras mutation had comparatively high cellular proliferative activity (28, 26 and 14%). In conclusion, our data suggest that occult pancreaticobiliary reflux, especially with high biliary amylase levels, represents an important risk factor for the development of gallbladder carcinoma as well as PBM, and it may be possible to detect patients with such high biliary amylase levels by ERCP.
Int J Mol Med 2005 Mar
PMID:Histologic and genetic analysis of the gallbladder in patients with occult pancreatobiliary reflux. 1570 32

Tumors often exhibit deregulation of the cell cycle and overexpression of cyclins and cyclin-dependent kinases (CDKs). Response gene to complement (RGC)-32 is a substrate and regulator of CDC2 and its overexpression induces cell cycle activation. We investigated RGC-32 mRNA and protein expression in tumors with special emphasis in colon carcinoma. By using an expression array technique we found that 19% of tumor tissues showed increased RGC-32 mRNA expression over the levels of corresponding normal tissues. On the other hand, an increased RGC-32 protein was found in 70% of colon adenocarcinoma samples tested. In colon carcinomas, two major patterns of RGC-32 immunoreactivity were seen: staining of malignant epithelial cells only in some tumors and RGC-32 reactivity of both malignant epithelia as well as cells in the interstitium in others. Colonic epithelium obtained from normal individuals was consistently negative for RGC-32 protein. Overexpression of RGC-32 protein was found in other tumors including prostate, bladder, breast, lung, and other digestive tract tumors. RGC-32 expression was present in the same malignant epithelial cells that also expressed the proliferation marker Ki-67. Our data suggest that RGC-32 overexpression might be part of the deregulation of the cell cycle that is required for the growth of tumor cells.
Exp Mol Pathol 2005 Apr
PMID:Overexpression of RGC-32 in colon cancer and other tumors. 1571 36

The estrogen receptor (ER)-beta isoform has been recently identified to be distinct from ERalpha isoform and regulates separate sets of genes, and can exert opposite signaling functions depending on the ligand and response elements. Previous studies of ERbeta have been at the mRNA level and few by immunohistochemistry, and the results are inconsistent. In this study the authors compared expression of ERbeta with those of other prognostic biomarkers by immunohistochemistry on tissue microarray slides, and with morphologic parameters on 147 cases of primary breast cancer. Immunoreactivity of more than 10% of cancer cells was considered to be positive. Associations between categoric variables were analyzed using the chi test, and a P value less than 0.05 was considered to be significant. ERbeta was expressed in benign epithelium and stromal cells, and breast cancer cells in 59% of different histologic types of breast cancer. ERbeta was coexpressed with ERalpha in 45% of cases. There was a statistically significant association between expression of ERbeta and Her-2/neu (P<0.000), cathepsin D (P<0.02), p53 (P<0.03), and PS2 (P<0.002). Ki-67 was almost exclusively expressed in ERbeta-positive cells. No statistically significant association was seen between ERbeta expression and histologic grade, DNA ploidy, or S-phase.
Appl Immunohistochem Mol Morphol 2005 Mar
PMID:Estrogen receptor beta in breast cancer: associations between ERbeta, hormonal receptors, and other prognostic biomarkers. 1572 89

The authors' previous studies revealed that a subset of ductal carcinoma in situ (DCIS) contained focally disrupted myoepithelial (ME) cell layers and basement membrane (BM). As the disruption of these two structures is a prerequisite for tumor invasion, and white blood cells (WBCs) contain digestive enzymes capable of degrading both the BM and damaged host cells, this study was designed to assess the possible roles of WBC in ME cell layer disruptions and tumor invasion. A total of 23 DCIS containing ducts with focally disrupted ME cell layers were selected from 94 such cases identified in the authors' previous studies. Two consecutive sections from each case were double immunostained, one with leukocyte common antigen (LCA) plus smooth muscle actin (SMA) and the other with Ki-67 plus SMA. Ducts lined by at least 50 epithelial cells and distinct ME cell layers were examined. A total of 191 duct cross-sections were found to contain focal ME cell layer disruptions; of these, 186 (97.4%) were with and 5 (2.6%) were without WBC infiltration. Of 207 morphologically similar sections without ME disruptions, 46 (22.2%) were with and 161 (77.8%) were without WBC infiltration. Ki-67-positive cells in ducts with focally disrupted ME cell layers were generally subjacent to ME cell layers, and more than 30 clusters of multiple proliferating cells were seen directly overlying or near focally disrupted ME cell layers. In contrast, Ki-67-positive cells in ducts without ME disruptions were scattered over the entire epithelial compartment. The significantly different frequency of WBC infiltration and clusters of multiple proliferating cells in ducts with and without ME disruptions suggests that WBCs might play important roles in ME disruption and tumor invasion.
Appl Immunohistochem Mol Morphol 2005 Mar
PMID:Mammary ducts with and without focal myoepithelial cell layer disruptions show a different frequency of white blood cell infiltration and growth pattern: implications for tumor progression and invasion. 1572 91

The use of tissue microarrays has become an efficient method for the high-throughput analysis of tissues with molecular markers, yet these studies have not been used to leverage the limited materials present in needle biopsies of human tissues. The use of these biopsy tissues is crucial to study diseases in patients who are treated by nonsurgical methods such as radiation, chemotherapy, or palliative care. The authors present a simple, inexpensive method for using needle biopsy specimens in tissue microarrays. Using this process with prostate cancer specimens, the authors demonstrate that over 150 slides can be produced from a single area of cancer in a needle biopsy and that the length of the core involved by cancer in the needle biopsy determines the number of available tissue microarray slides. The authors also note the optimal number of samples (three) needed from a single patient biopsy to guarantee sufficient material for analysis and perform an immunohistochemical correlation between needle biopsy and surgical resection tissue microarray samples for the quantitative marker Ki-67. This process can be extended to any type of needle biopsy specimen, increasing the number of studies and potential use of these tissues as a practical reality.
Appl Immunohistochem Mol Morphol 2005 Mar
PMID:A simple inexpensive method for the production of tissue microarrays from needle biopsy specimens: examples with prostate cancer. 1572 1


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