Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera were examined for the presence of antibody against E7 protein of human papillomavirus type 16 (HPV-16) by Western blot analysis using the bacterially derived unfused protein. The occurrence rates of anti-E7 antibody against HPV-16 were 14.1% (10/71) in cervical cancer patients, 0% (0/48) in cervical intraepithelial neoplasia patients, and 0% (0/41) in female non-malignant patients. Three patients (one with endometrial cancer, one with breast cancer, and one male patient with colon polyp) out of 115 patients with tumors in organs other than the cervix, had antibody against E7 protein of HPV-16. The serum antibody, once positive, could be detected for a long time after surgical removal of the cancers in all cases that could be followed up. HPV-16 DNA could be detected in 50% (13/26) of cervical cancer patients. Sixty-nine percent (9/13) of patients with HPV-16 DNA in cancers had the antibody and all the patients with stages II, III, and IV cervical cancer (8/8) harboring HPV-16 DNA showed the presence of the antibody against E7 protein of HPV-16. In contrast, only 20% (1/5) of cervical cancer patients with stage Ia or Ib harboring HPV-16 DNA showed positive for the anti-E7 antibody in sera. These findings suggest that the presence of anti-E7 antibody in serum depends on the staging of cervical cancer and extent of HPV infection.
 ...
PMID:Serum antibody against unfused recombinant E7 protein of human papillomavirus type 16 in cervical cancer patients. 773 6

We studied the expressions of aberrant epidermal growth factor receptor (EGFR) gene or erbB-2, which is highly homologous to EGFR gene, and erbA or estrogen receptor (ER) gene, which is highly homologous to erbA, as a preliminary study, to know which oncogene expressions are associated with the development of endometrial cancers. ErbB-2 mRNA lacked only extracellular domain (EX), suggesting the lack of downregulation of erbB-2 expression by a ligand, which led to regulated tyrosine kinase activity. Mutated DNA binding domain of ER mRNA were found in 3 of the 13 cases, suggesting the promotion disorder of estrogen-inducible proteins in these 3 endometrial cancers. The behavior of aberrant erbB-2 and ER gene co-expressions is considered of similar to that of erbA and erbB co-expressions in the chicken introduced by the avian erythroblastosis virus, which leads to the development of erythroblastosis in the chick, and seems to be associated with the development of endometrial cancer.
 ...
PMID:Preliminary study of oncogene expressions in endometrial cancers. Aberrant estrogen receptor gene and erbB-2 expressions. 774 15

Seventy-three patients with endometrial carcinoma have been retrospectively evaluated in this paper. Stage, grade, depth of myometrial invasion, flow cytometric DNA ploidy and ERB-B2 oncogene expression by immunohistochemical method have been analyzed on paraffin embedded tissue. Results showed the existence of a significant correlation between stage and grade of neoplasia and between DNA ploidy and course of disease; it has been observed that patients with aneuploid tumor tend to have a shorter time before relapse of disease. No significant correlation between depth of myometrial invasion and survival was found. Besides, it has been shown that tumours with ERB-B2 oncogene hyperexpression seem to have a more aggressive evolution.
 ...
PMID:Role of DNA ploidy and ERB-B2 oncogene expression in the prognosis of endometrial carcinoma. 774 37

The endometrial expression of the gene encoding porcine uteroferrin (UF), during pregnancy is presumed to be mediated by cis-regulatory regions distinct from those that confer its limited expression to other mammalian tissues and cell types. In the present study, chimeric DNA constructs of native and progressive 5' deleted promoter regions fused to the promoter chloramphenicol acetyl-transferase reporter gene were transiently transfected in the human endometrial carcinoma cell line ECC-1 to examine their ability to direct UF promoter activity. The region between -1935 and -831 bp contained negatively acting elements which drastically reduced basal promoter activity. In contrast, the region between -831 and -484 bp contributed significantly to high level basal activity. Gel retardation and footprinting assays identified factor-binding sites between -1601 and -484 bp for human endometrial nuclear proteins. One binding site corresponds to a heptamer motif (TGCTAGA) present twice within the -1601 to -831 bp region and previously shown to bind an 80 kDa porcine endometrial protein. This heptamer bound an 80 kDa nuclear protein from human ECC-1 and human Ishikawa endometrial cells and a 92 kDa protein from human placental JEG-3 cells. The other binding region within -831 to -484 bp contained GC-rich sequences, which bind human Sp1. The protected GC-rich sequence (GC-Box 1) between -768 and -749 bp also binds a 24 kDa M(r) protein. Nuclear proteins of molecular weight 40-60 kDa and distinct from Sp1, Sp2 and Sp3 bound a second GC-rich sequence (GC-Box 3) between -628 and -616 bp. These studies demonstrate that multiple elements within the UF gene promoter bind nuclear proteins which are similarly expressed in other endometrial cells and suggest that common transactivating factors may functionally mediate expression of endometrial-associated genes.
 ...
PMID:Multiple upstream promoter elements of the gene for the pregnancy-associated tartrate-resistant acid phosphatase, uteroferrin bind human endometrial nuclear proteins. 775 40

Nucleolar organizer regions (NORs) are loops of DNA that transcribe to ribosomal RNA. They can be visualized as intranuclear black dots by histochemical staining with a colloid silver solution. We applied this method to 78 sections of endometrial tissue obtained either from curettage or from hysterectomy specimens. The histological diagnoses were as follows: normal proliferative (N = 9) or secretory (N = 5) endometrium, simple hyperplasia (N = 10), complex hyperplasia (N = 18), atypical hyperplasia (N = 8), and adenocarcinoma (N = 28). Mean silver-stained NOR (AgNOR) counts per cell were 3.2 (standard error of the mean [SEM], 0.2) in normal proliferative and 2.7 (SEM, 0.2) in normal secretory epithelium, and increased to 4.1 (SEM, 0.3) in simple hyperplasia, to 5.4 (SEM, 0.4) in complex hyperplasia, to 8.1 (SEM, 0.7) in atypical hyperplasia, and finally to 10.0 (SEM, 0.5) in endometrial carcinoma. The differences were significant (one-factor analysis of variance [ANOVA], P < .001). A slight increase but no significant difference was seen between the mean AgNOR counts in endometrial carcinomas of different histological grades. Our study suggests that AgNOR counts are reliable markers of endometrial proliferation and allow a clear distinction between benign, premalignant, and malignant epithelial changes. Our AgNOR findings in endometrial hyperplasia support the concept of various degrees of hyperplasia that can be differentiated on morphological grounds.
 ...
PMID:Nucleolar organizer regions as markers of endometrial proliferation: a study of normal, hyperplastic, and neoplastic tissue. 777 98

Estra-1,3,5 (10)-triene-3,17-diol (17 beta)-, 3-[bis(2-chloroethyl) carbamate] (Estramustine EM) was tested for its anticancer effect on human endometrial cancer cell lines: Ishikawa and its estrogen (E) independent sub-clone EIIL (Estrogen Independent Ishikawa Line). The results showed: (1) EM inhibited growth of both cell lines in a dose dependent manner giving ID50 for Ishikawa as 12 microM and for EIIL as 65 microM. (2) The addition of EM to the culture medium caused cell detachment and death associated with a breakdown of DNA to approximately 90 base pair fragments. (3) Reverse transcription-polymerase chain reaction to examine expressions of c-erbB-2, nidogen and fas showed that EM completely abolished fas expression and resulted in a 40% decrease in nidogen expression in Ishikawa but not in EIIL. No change was seen in c-erbB-2 expression. The present data indicate that the E component of EM does not stimulate the growth of Ishikawa or EIIL. Since the growth of both cell lines was inhibited but apparently in an E receptor (ER) dependent manner, EM may be of value in an adjuvant therapy for endometrial cancer, especially an ER positive one.
 ...
PMID:[Estramustine phosphate, estrogen conjugated with nitrogen mustard inhibits the growth of endometrial cancer cells in vitro]. 777 15

The natural history and biological behavior of cystic glandular hyperplasia (CGH), which has been considered to be a precursor of endometrial carcinoma, still remain unclear. The present prospective study included 52 patients with CGH, who were followed up for 6 months to 5 years with occasional curettage, surgical procedures or hormonal therapy. The lesion disappeared in 35 cases (67.3%), persisted in 12 cases (23.1%) and became more serious in 5 cases (9.6%). Of these 5 cases, one case was found to have endometrial carcinoma during her follow-up. Nuclear DNA analysis was performed by Flow cytometry in 8 CGH cases. Eighty four point nine % of the cells from these 8 cases were in G0+1 phase, 8.3% in S phase and 7.4% in G2 + M phase. The proliferation index for CGH was 15.7%. Proliferative and mitotic activities of CGH were found to be similar to those of adenomatous hyperplasia, and the levels of these activities were between those of normal endometrium and atypical hyperplasia.G1.
 ...
PMID:[Characteristic of cystic glandular hyperplasia as a precursor of endometrial carcinoma]. 784 42

The presence of human papillomavirus (HPV) type 16 and 18 transcripts was determined by reverse transcription/polymerase chain reaction (PCR) in ovarian and endometrial carcinoma tissue. HPV-16 DNA sequences were detected in 50.0% (9/18) of the ovarian carcinomas and in 44.4% (8/18) of endometrial carcinomas. HPV-18 DNA sequences were found in 16.7% (3/18) of both the ovarian and endometrial carcinomas. Using RNA-PCR analysis, we found 3 out of 9 (33.3%) of the HPV-16 DNA-positive and 1 in 3 (33.3%) of the HPV-18 DNA-positive ovarian carcinomas were transcriptionally active, contrary to the HPV-16 DNA-positive or HPV-18 DNA-positive endometrial carcinomas. The results suggest that HPV RNA may be detected in ovarian carcinomas though its biological significance remains to be elucidated. HPV RNA is not demonstrable in endometrial carcinoma using the current primer sets. Further investigations are necessary for a final conclusion.
 ...
PMID:Detection of human papillomavirus RNA in ovarian and endometrial carcinomas by reverse transcription/polymerase chain reaction. 785 15

The authors previously reported a significant frequency of activating point mutations in codon 12 and 13 of the K-ras gene in endometrial carcinoma and endometrial atypical hyperplasia from Osaka, Japan. They also showed that alterations of the p53 gene are found frequently in those tumors. This study was designed to reveal possible demographic differences in the prevalence of K-ras and p53 mutations in endometrial carcinoma. Tumor-enriched areas of paraffin-embedded histologic sections obtained through the Colorado Central Cancer Registry were isolated and extracted for DNA. Fragments amplified by polymerase chain reaction (PCR) were screened for transforming mutations in codon 12, 13, or 59-63 of K-ras by direct sequencing. Of 38 endometrial adenocarcinomas that were analyzed, K-ras activation was detected in 4 cases (11%), three in codon 12 (a single case with a GGT-->AGT transition, a single case with a GGT-->GAT transition, and a single case with a GGT-->TGT transversion) and one in codon 13 (a GGC-->GAC mutation). The prevalence of K-ras mutations was significantly lower in endometrial carcinomas from Colorado (4 of 38, 11%) than in those from Osaka, Japan (17 of 57, 31%; P = .02). Mutations in exons 5-8 of p53 were screened by PCR-SSCP analysis, and subsequently confirmed by direct sequencing. Mutations in the p53 gene were detected in 5 of 38 endometrial carcinomas from Colorado (13%), including a single base substitution mutation in 3 cases (60%) and a deletion mutation in 2 cases (40%). Mutations in the p53 gene were significantly more frequently found in G3 cancers (3 of 7, 43%) than G1-G2 cancers combined (2 of 31, 6%; P = .025). Although the prevalence of p53 mutations in endometrial carcinomas from Colorado was not significantly different compared to that from Osaka, Japan (9 of 40, 23%), a G:C-->A:T transition at a CpG site, which was the most common base substitution mutation among Japanese, was not included in any tumors from Colorado. A rare polymorphism in codon 213 (CGA-->CGG) was observed in three cases. These observations may indicate that genetic or environmental factors may significantly influence the pathway of endometrial carcinogenesis.
 ...
PMID:Alteration of the p53 tumor suppressor gene and activation of c-K-ras-2 protooncogene in endometrial adenocarcinoma from Colorado. 785 67

Mutations of the Ki-ras oncogene in endometrial carcinoma have been reported in Japan, but the prevalence and clinical significance of such mutations in the United States remains unclear. DNA extracted from paraffin sections of 112 carcinomas of the endometrium was amplified by the polymerase chain reaction with mismatched primers that generated a BstNI recognition site with the wild-type codon 12. Loss of this recognition site indicating Ki-ras codon 12 mutations was observed in 13 tumors (11.6%), including 11 endometrioid carcinomas, one undifferentiated carcinoma, and one carcinosarcoma. None of 17 papillary serous-clear cell carcinomas contained Ki-ras codon 12 mutations. These mutations were confirmed and characterized by direct sequencing. We found no evidence of correlation of the presence of Ki-ras mutations with stage, grade, depth of invasion, or clinical outcome. Our results indicate that Ki-ras oncogene mutations in carcinoma of the endometrium may be less prevalent in the United States than in Japan.
 ...
PMID:Mutations of the Ki-ras oncogene in carcinoma of the endometrium. 785 26


<< Previous 1 2 3 4 5 6 7 8 9 10