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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The current literature on endometrial neoplasia deals with proliferative lesions such as endometrial proliferation in early pregnancy, atypical polypoid adenomyofibromata and their possible relationship to carcinoma, and histological grading of endometrial cancer with emphasis on nuclear grading and subtypes of endometrial cancer including the newly described intestinal and hepatoid types. Recent publications dealing with p53 protein, genetic studies, and nucleolar organizer regions are of interest but have provided no striking new insight into endometrial neoplasia. Angiogenesis has appeared for the first time in the literature in connection with endometrial neoplasia. Tamoxifen continues to occupy an important place in the literature, and endometrial adenosarcoma has been identified recently as one of the myriad of lesions which patients treated with tamoxifen are prone to develop.
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PMID:Endometrial pathology. 909 Apr 83

A case-control study was designed to identify associations between polymorphisms at p53, cytochrome P-450 (CYP1A1) and glutathione-S-transferases and endometrial cancer susceptibility. Among all polymorphisms analysed, an insertional variant in p53 (P53PIN3) and two polymorphisms in the 3'-end and exon 7 of CYP1A1 showed significant association with enhanced endometrial cancer risk.
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PMID:Susceptibility to endometrial cancer: influence of allelism at p53, glutathione S-transferase (GSTM1 and GSTT1) and cytochrome P-450 (CYP1A1) loci. 915 64

Apoptosis is a process of single-cell deletion requiring active participation of the cell in its own demise. First described in 1972, it is now known to play a major role in embryogenesis, tissue homeostasis and neoplasia. Apoptosis can be initiated when DNA damage occurs causing the cell to pause in its reproductive cycle. If the DNA damage is beyond repair, the cell proceeds to apoptotic cell death. When the genetic mechanism(s) involved in the pathway of apoptosis is altered, the cell does not die. Further mutations occur by proliferation and such multiple mutational events can lead to a malignant phenotype and cancer growth. The tumour suppressor gene p53 causes a DNA-damaged cell to rest and attempt repair. If damage is irreparable, p53 levels will continue to increase, initiating apoptosis. Mutation of p53, found in approximately 50% of cancers, can stop the apoptotic process. Increased bcl-2 expression, an apoptosis inhibitor, also plays a role in cellular transformation and cancer growth. Its altered expression occurs in the presence of oncogene expression. This paper reviews the role of apoptosis in malignant transformation, cancer growth, and response to therapy for gynaecological cancers. For cervical cancer and its precursors, data on apoptotic index, bcl-2 and Bax expression are presented and discussed in relationship to human papillomavirus expression. In ovarian epithelial malignancies, the role that apoptosis plays in chemotherapeutic responses is reviewed. The data for endometrial cancer are currently limited to apoptotic index.
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PMID:The role of apoptosis in gynaecological malignancies. 918 26

bcl-2 protein is expressed in normal endometrium and seems to be under hormonal control. Its role in endometrial carcinoma (EC) is largely unknown. EC can serve as a good model to investigate the role of bcl-2 in hormone-dependent neoplasia, because EC shows a spectrum of hormonally induced changes in which bcl-2 might have a potential role. p53, a tumor suppressor gene, is the most commonly mutated gene in human cancer and is a frequent abnormality in advanced EC. There is interaction between p53 and bcl-2 proteins in the regulation of physiological programmed cell death and in malignant processes. In this study, we performed immunohistochemical investigations of the expression of bcl-2 and p53 in 57 ECs, along with estrogen and progesterone receptors (ERs, PRs), to correlate the expression patterns of bcl-2 and p53 in different grades of EC with relation to clinicopathologic parameters. The average age of the patients was 61 years. Among 57 ECs, there were 13 noninvasive ECs and 44 ECs with various depths of invasion. p53 was positive in 21 of 57 cases, and bcl-2 was positive in 42 of 57. ER and PR were positive in 24 of 57 cases; PR and ER alone were positive in 15 and 2 cases, respectively. bcl-2 expression is present in ECs, and its expression is related to grade and stage. bcl-2 expression is strongly associated with PR, whereas p53 is associated with higher grade and is inversely related to PR positivity.
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PMID:bcl-2 and p53 in endometrial adenocarcinoma. 923 85

Expression of the HER-2/neu proto-oncogene product was looked for immunohistochemically in 222 endometrial carcinomas in a retrospective follow-up study. The intensity of protein expression was correlated with patient survival. Median follow-up time was 4.8 years. In 109 (49%) of 222 endometrial carcinomas there was aberrant expression of HER-2/neu. HER-2/neu-expression did not correlate with p53-expression and proliferation rate, as determined immunohistochemically by the monoclonal antibody Ki-S1. In univariate statistical analysis aberrant HER-2/neu expression was not predictive of adjusted survival (p = 0.18) and of disease-free survival (p = 0.42). In multivariate analysis HER-2/neu-expression was not found to be an independent prognosticator (p = 0.099) as compared to FIGO-stage (p = 0.0001), histologic grade (p = 0.00099) and proliferation rate (p = 0.0013). Therefore immunohistochemically detected expression of HER-2/neu seems not to be a clinical prognosticator in endometrial cancer.
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PMID:Immunohistochemically detected HER-2/neu-expression and prognosis in endometrial carcinoma. 927 38

We studied 54 patients diagnosed with endometrial cancer between 1981 and 1994 following a diagnosis of breast cancer. We used a case-case analysis, comparing tumors with and without overexpression of the p53 gene product to evaluate the association of putative p53 mutations with tamoxifen use and other risk factors for endometrial cancer. Twenty-four % of the tumors showed strong positive staining for the p53 gene product. Tumors in a more advanced stage (stage 2, 3, or 4, compared to stage 1) were more likely to overexpress p53 [odds ratio (OR) = 4.2; 95% confidence interval (CI), 1.1-16.2], as were tumors with serous or clear cell, compared to endometrioid, histology (OR = 5.8; 95% CI, 1.3-26.5). There was a small association between p53 overexpression and treatment with tamoxifen for breast cancer (OR = 2.6; 95% CI, 0.69-9.8). There was a strong relationship between overexpression of p53 and having a first-degree relative with breast cancer (OR = 12.3; 95% CI, 2.6-57.4) and between overexpression of p53 and having an additional cancer, i.e., at sites other than breast or endometrium (OR = 7.9; 95% CI, 1.6-40.1). In this group of women, genetic predisposition to cancer, as reflected in family history of breast cancer and personal history of an additional primary cancer, was strongly associated with overexpression of p53 in endometrial tumors. The results suggest that use of tamoxifen may be associated with an increase in tumors that overexpress p53, although the results could be due to chance.
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PMID:A case-case analysis of factors related to overexpression of p53 in endometrial cancer following breast cancer. 933 64

During the past decades, the expansion of molecular biology has had a pivotal role in understanding the basis of cancer development and progression. In addition, real advances have been made in the application of DNA recombinant technology to cancer therapy and patient management. In gynecologic oncologic fields, there are also many investigations to explore the basic pathogenesis of gynecologic cancer, such as cervical cancer, ovarian cancer, and endometrial cancer. It is now known that specific types of human papilloma virus (HPV) are the principal etiologic agents for both cervical cancer and its precursors. However, the various kinds of alterations in oncogenes and tumor suppressor genes may play additional roles in carcinogenesis of cervical cancer. Although ovarian carcinoma is the most frequent cause of death from gynecologic malignancies, the histogenesis and biological characteristics of these tumors are not well understood. During the last several years, many key observations have been made concerning the genetic alterations associated with ovarian cancer. Recent researches including some dominant oncogenes and tumor suppressor gene mutations common to these malignancies are providing bases to elucidate the mechanisms underlying this cancer. The most important basis of endometrial cancer is that K-ras and p53 mutations are also frequently observed.
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PMID:Molecular genetics of gynecologic cancer. 936 94

Each year, about 25,000 new cases of ovarian cancer are diagnosed in the US. Because ovarian cancer has few symptoms in its early stages and there is no effective screening test, most patients have widespread metastases at diagnosis. Epidemiologic studies have demonstrated that OC use can protect against ovarian cancer for at least 15 years after pill use is discontinued. The most likely mechanism of this protective effect is inhibition of ovulation. A strong association between total number of lifetime ovulations and mutation of the p53 gene in ovarian cancers has been reported. Use of the pill for 5 years decreases the risk of ovarian cancer by 40% but decreases lifetime ovulations by only about 15%, suggesting that factors other than prevention of proliferation-associated mutations contribute to the protective effect of ovulation inhibition. The pill also decreases the incidence of endometrial cancer by about 50%. At present, OCs represent the best option for US women from both the contraceptive and cancer prevention perspectives.
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PMID:Oral contraceptive pills. Prevention of ovarian cancer and other benefits. 939 51

The predictive value of p53 and K-ras-2 mutational genotyping in determining tumor aggressiveness and survival in patients with endometrial carcinoma (EC) was retrospectively evaluated using a molecular genotyping approach on fixative treated tissue specimens. Two groups of patients with EC were selected based upon length of survival. Group A consisted of 14 patients that died within 3 years of initial diagnosis and treatment (mean survival of 1.1 years). Group B consisted of 18 patients that survived beyond 3 years (mean survival of 4.7 years). Clinicopathologic features including clinical stage, histologic type, and combined nuclear and architectural grade of each tumor were statistically analyzed with respect to oncogene/tumor suppressor gene alterations. The majority of carcinomas in group A were serous (57%), stage III or IV (93%), and high combined grade (93%). Group B consisted mostly of endometrioid (89%) and low-grade carcinomas (83%); 56.1% were stage III or IV. K-ras-2 point alterations were found in 2 (14%) and 4 (22%) patients from group A and B respectively; the spectrum of K-ras-2 genotypes was similar in both groups. p53 gene mutations were identified in 9 (64%) and 1 (6%) patient from group A and B respectively. p53 staining in group A tended to be of strong intensity and diffuse distribution, being associated with the presence of point mutations, mainly in exon 8. Only a single group B tumor exhibited point mutational change. The presence of p53 mutations strongly correlated with short survival (p <0.05) but the finding of K-ras-2 alterations did not. p53 genotyping has potential prognostic value in EC and can be used along with histopathologic type and histologic grade to identify subsets of more aggressive tumors and to guide the treatment.
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PMID:Prognostic value of p53 and K-ras-2 topographic genotyping in endometrial carcinoma: a clinicopathologic and molecular comparison. 942 Oct 75

Expression of the tumor suppressor gene product p53 and the cyclin-dependent kinase inhibitor p21, which is transcriptionally activated by p53, was investigated and compared with patient survival in a retrospective longitudinal study of 202 cases of endometrial carcinoma. The median duration of follow-up was 4.3 years. P53 was observed immunohistochemically in 63 (31%) of the tumors and was found by univariate analysis to be related to reduced adjusted survival (p = 0.00028) and disease-free survival (p = 0.04). However, p53 expression was not found by multivariate analysis to be an independent prognostic factor when compared with FIGO stage, histologic grade, and proliferative activity, as determined by immunoreactivity for topoisomerase IIalpha with the antibody Ki-S1. Overexpression of p53 was related to histologic grade (p < 0.00001), proliferative activity (p = 0.0071), and inversely to progesterone receptor content (p = 0.042). Immunohistochemical identification of p21 was investigated in 95 cases and found to be positive in 19 (39%) of 49 tumors with p53 overexpression and in 13 (28%) of 46 tumors without p53 overexpression (p = 0.28). Expression of p21 is therefore not related to p53 expression, nor was it found to be related to proliferative activity. Strong expression of p21 was observed in tumors negative for progesterone receptors (p = 0.0028). P53 in endometrial carcinoma is not associated with induction of the cell cycle inhibitor p21, but is associated with an enhanced proliferative activity. The findings of multivariate analysis suggest that the prognostic significance of p53 is related mainly to cell proliferation.
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PMID:p53 protein in endometrial cancer is related to proliferative activity and prognosis but not to expression of p21 protein. 942 Oct 76


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