Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-nine ovarian serous and mucinous borderline tumors, 36 stage I carcinomas and 39 stage II-IV carcinomas were studied for p53 protein accumulation with monoclonal antibody PAb1801.p53 protein was expressed in 14% of borderline tumors, 36% of stage I carcinomas, and 64% of higher stage carcinomas. All immunopositive carcinomas accumulated p53 protein in the primary tumor, and 95% of them showed concordance in staining among different tissue blocks. A difference in frequency of p53 protein accumulation between stage I and higher stage serous carcinomas was not statistically significant. p53 positivity was associated with microinvasion, microcarcinoma and coexistent carcinoma in mucinous borderline tumors (P = .025). An association between p53 protein expression and poor tumor differentiation in Stage I carcinomas as statistically significant (P = .03). p53 positivity was observed in a poorly differentiated endometrioid carcinoma as well as in adjacent benign endometriotic tissue. These results suggest that p53 abnormalities may be early events in ovarian cancer, possibly contributing to malignant transformation of some borderline tumors, endometriosis and other carcinoma precursors.
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PMID:p53 expression in ovarian borderline tumors and stage I carcinomas. 794 35

No activating mutations in codons 12, 13 and 61 of ras genes nor inactivating mutations in exons 5-9 of the p53 tumor suppressor gene were detected by polymerase chain reaction and single-strand conformation polymorphism methods in either eutopic or ectopic endometrium from 10 women with severe endometriosis.
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PMID:Analysis of p53 and ras gene mutations in endometriosis. 795 33

Endometriosis is a very common gynecological condition in which tissue similar to endometrium proliferates at sites outside the uterine cavity, most commonly the ovary. Although it generally remains a benign condition, malignant transformation has been documented. and it is commonly found in association with endometrioid subtype ovarian cancer. Tumor suppressor genes are commonly altered in ovarian cancers, and the development of endometriosis may involve mutations in the same class of genes. We have investigated this possibility by examining DNA from 40 cases of endometriosis for clonal status, alterations in TP53 and RASK, and allelic losses at candidate ovarian tumor suppressor loci on chromosome arms 6q, 9p, l1q, 17p, l7q, and 22q. The majority of endometriotic cysts were monoclonal, but interestingly, 8 of 10 normal endometrial glands were also monoclonal, demonstrating that both are able to develop from a single progenitor cell. No mutations were detected in TP53 or RASK. Loss of heterozygosity (LOH) was detected on chromosomes 9p (18%), 1lq (18%), and 22q (15%). In total, 11 of 40 (28%) cases demonstrated LOH at one or more of these loci. This study, which is the first to report LOH in endometriosis, supports the notion that tumor suppressor gene inactivation may play a role in the development of at least a subset of cases.
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PMID:Microsatellite analysis of endometriosis reveals loss of heterozygosity at candidate ovarian tumor suppressor gene loci. 875 23

We studied the expression of oncogenes and tumor-suppressor genes in human endometriosis in a retrospective pilot study. Sixteen patients with histologically verified pelvic endometriosis at the university-based tertiary care referral center were studied. Immunohistochemical determination of c-myc, c-erb-B2, nm23 and p53 expression in archival, paraffin-embedded pathological samples were used from patients operated upon for pelvic endometriosis. c-myc was expressed in 8/15 cases (53.3%). nm23 was expressed in 7/16 cases (43.7%). c-erb-B2 and p53 reactivity was undetectable in the samples studied. The c-myc oncogene and nm23 are overexpressed in many cases of endometriosis, and may play a still undefined role in its pathogenesis. Immuno-histochemistry is a useful tool for the study of oncogenic activation in this disease.
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PMID:c-myc, c-erb-B2, nm23 and p53 expression in human endometriosis. 945 91

Endometriosis is a common gynecological disease in which tissue similar to the endometrium proliferates at sites outside the uterine cavity. Malignant transformation of endometriosis to endometrioid and clear cell ovarian carcinomas has been documented in histological studies, but no molecular genetic evidence exists to support that endometriosis is the clonal precursor of such malignancies. We examined 14 cases of endometriosis synchronous with ovarian cancer for loss of heterozygosity on 12 chromosome arms, X chromosome inactivation, and TP53 mutation to determine whether they shared genetic alterations. In all four of the cases where the carcinoma had arisen within endometriosis and in five of the seven cases where the carcinoma was adjacent to the endometriosis, common genetic lesions were detected, consistent with a common lineage. A TP53 mutation was also detected in one case of endometriosis adjacent to carcinoma. These findings support the numerous histological observations that endometrioid and clear cell ovarian carcinomas may arise through malignant transformation of endometriotic lesions.
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PMID:Allelotyping of endometriosis with adjacent ovarian carcinoma reveals evidence of a common lineage. 956 87

A case of a yolk sac tumor (YST) with an ovarian endometrioid adenocarcinoma arising from endometriosis in a postmenopausal woman is described. Clinically, the case showed an aggressive course and did not respond to chemotherapy; the patient died of her disease 6 months after the operation. Histologically, the tumor consisted predominantly of an endometrioid adenocarcinoma, but it also showed microscopic features characteristic of YST. The tumor also contained benign endometriotic lesions with direct transition to the endometrioid adenocarcinoma. Immunohistochemical study revealed that not only the YST, but also the endometrioid adenocarcinoma was partly positive for alpha-fetoprotein. There was an inverse relationship between the endometriosis and the endometrioid adenocarcinoma in terms of the expression of sex steroid receptors and p53: adenocarcinoma cells were positive for p53 but negative for sex steroid receptors, whereas endometriotic epithelial cells were positive for sex steroid receptors but negative for p53.
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PMID:Ovarian yolk sac tumor with endometrioid carcinoma arising from endometriosis in a postmenopausal woman, with special reference to expression of alpha-fetoprotein, sex steroid receptors, and p53. 974 Jul 9

In a series of studies, we have hypothesised that endometriotic proliferation is, in part, precipitated by mutations in oncogenes or deletions in tumor suppressor genes that have been shown to be important steps in the transformation from a benign to a malignant epithelium. We reported previously that we could find no mutations in the TP53 and RASK genes in cases of endometriosis. However, having shown that endometriotic deposits were monoclonal, we showed loss of heterozygosity on chromosomes 9p (18%), 11q (18%), and 22q (15%) - in total 28% of endometriotic lesions showed loss of heterozygosity at one or more sites [1]. We could not demonstrate any loss of heterozygosity in normal endometrium. We examined adjacent endometriosis, atypical endometriosis, and endometrioid carcinoma of the ovary and showed common genetic alterations that are consistent with a common lineage. These common alterations were not seen in lesions that were distant from each other [2]. In endometrioid tumors, we reported an increased frequency of mutations in the PTEN/MMAC tumor suppressor genes that was not seen in clear cell or serous carcinoma, suggesting distinct developmental pathways for these tumors [3].
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PMID:Molecular genetic defects in endometriosis. 1109 61

A 43 year old woman who underwent a hysterectomy and bilateral salpingo-oophorectomy for secondary dysmenorrhoea was found to have bilateral ovarian endometriosis. During the following four years she developed a series of tumour-like vaginal masses, which were locally excised, a pelvic mass causing acute large bowel obstruction, which necessitated an emergency Hartmann's procedure, and a further pelvic mass causing hydronephrosis with a non-functioning kidney. Pathological examination of all the resected specimens showed endometriosis with abundant stromal and glandular elements. Immunoreactivity for p53 protein was detected within endometriotic foci from the initial oophorectomy as well as the latest resection specimens. Immunostaining for p53 may help identify potentially aggressive cases of endometriosis for proactive treatment.
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PMID:An unusually aggressive case of endometriosis showing p53 expression. 1132 41

It has been reported that cases of ovarian endometriosis those with epithelial cytological atypia have potential for malignant transformation. This study was planned to determine the incidence of atypical endometriosis and its cytological criteria, to evaluate the malignant potential of atypical endometriosis via immunohistochemical methods (p53). In this study we evaluated 140 samples obtained from 120 cases of ovarian endometriosis and 10 ovarian endometrioid carcinomas that have been previously diagnosed histopathologically. We re-evaluated endometriosis cases with respect to their epithelial and stromal features, existence of acute or chronic inflammatory cells in endometriotic epithelium or stroma and other accompanying histological findings. We observed atypia in 7 (5.8%) cases; reactive atypia in 37 (30.8%) cases, no atypia in 76 (63.4%) cases. We evaluated immunohistochemical p53 expression in 7 atypical cases, 37 reactive atypical cases, and in 10 of those without atypia and in 10 endometrioid carcinoma cases. We noted no staining in cases with atypia, reactive atypia and without atypia while 3 cases of endometrioid carcinoma had positive staining for p53. We concluded that prominent nucleolus and angulation of nuclear contour could be added to criteria of atypia that were mentioned before in the literature. In our study, even though p53 expression could not be shown with immunohistochemical methods in atypical endometriotic cases; it can not be determined that atypical endometriosis lesions are not premalignant. Still, endometriosis cases should be evaluated carefully by the pathologist for foci of cytological atypia and it should be kept in mind that malignant transformation might occur in these atypical endometriosis cases.
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PMID:Atypical epithelial changes and mutant p53 gene expression in ovarian endometriosis. 1134 18

p21, an important regulator of the cell cycle, acts as a mediator of the growth-suppressing and -promoting functions of p53. We aimed to investigate the association between codon 31 polymorphisms of p21 gene and endometriosis. Women were divided into two groups: endometriosis (n = 102) and nonendometriosis (n = 119). The gene polymorphism for p21 codon 31 involved a base change from AGC to AGA and amino acid changes from serine (Ser) to arginine (Arg). Polymorphisms (Ser homozygotes, heterozygotes, Arg homozygotes) between both groups were detected and compared. Associations between the endometriosis and polymorphisms were evaluated. The results revealed that the distributions of different p21 polymorphisms in both groups were nonsignificantly different. The proportions of Ser homozygote/heterozygote/Arg homozygote in endometriosis and nonendometriois populations were 26.5/48.0/25.5% and 17.6/50.4/31.9%, respectively. We concluded the noncorrelation between the endometriosis and the p21 codon 31 polymorphism. p21 gene codon 31 arginine/serine polymorphism is not a useful marker for prediction of endometriosis susceptibility.
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PMID:p21 gene codon 31 arginine/serine polymorphism: non-association with endometriosis. 1143


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