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)

Histopathologic changes ranging from simple cystic hyperplasia to carcinoma in situ may be observed in adenomyotic foci in patients with endometrial carcinoma. These changes can be an area of concern and physicians should be aware of their clinicopathologic significance. We studied a total of 94 patients, including endometrial carcinoma with (28 patients) and without adenomyosis (56 patients), and control group of adenomyosis cases (10 patients) without endometrial carcinoma. The histopathological changes in adenomyosis in patients with endometrial carcinoma varied from endometrial glands resembling the basal endometrium (13 of 28) through simple hyperplasia (8 of 28) to complex atypical hyperplasia, resembling carcinoma in situ (7 of 28). Formalinfixed paraffin-embedded tissues from 55 patients (45 endometrial carcinomas and 10 control adenomyosis) were stained with monoclonal antibodies against P53. P53 positivity was not detected in adenomyosis cases without endometrial carcinoma but was present in 7 of the endometrial carcinoma-related cases. P53 positivity was found in 14 of 45 endometrial carcinomas studied. In all of the adenomyosis-positive cases, the endometrium was also positive. In conclusion, adenomyosis with a range of hyperplastic to atypical changes is not uncommon in adenocarcinoma patients. Our findings regarding P53 positivity in adenomyosis are consistent with the hypothesis that hyperplastic and atypical changes in adenomyosis might be due to a carcinogenic field effect in the vicinity of endometrial carcinoma rather than by direct invasion.
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PMID:P53 expression in adenomyosis in endometrial carcinoma patients. 875 56

The role of p53 and bcl-2 apoptosis related proteins in the pathogenesis of endometrial cancer remains unclear. We immunohistochemically examined 133 surgically removed tumour specimens from patients with stage I endometrial cancer for p53 oncoprotein nuclear expression and bcl-2 cytoplasmic reactivity. 114/133 (86%) cases were of the endometrioid histological sub-type. A cut-off point of 10% of cells with strong reactivity was used for positivity. Positive p53 expression was observed in 12/133 (9%) and positive bcl-2 in 40/133 (30%) cases. p53 expression was not related to bcl-2 expression. No association of p53 and bcl-2 with depth of myometrial invasion, vascular invasion or histological grade was observed. However, continuous variable analysis revealed a trend of low grade cases to have a higher percentage of bcl-2 positive cells (16.3 + 27% vs. 7.8 + 16%; p = 0.09, unpaired two tailed t-test). Interestingly, a statistically significant association of p53 positivity with age was also observed (p = 0.03). A strong association of high grade with depth of myometrial invasion (p = 0.006) and vascular invasion (p = 0.0001) was also noticed. In addition, the presence of adenomyosis was also associated with low grade (p = 0.01) and absence of vascular invasion (p = 0.02). We conclude that although loss of bcl-2 protein expression and p53 mutant protein nuclear accumulation are early events in the endometrial cancer progression, histological grade and vascular invasion remain the most important factors defining local invasive behaviour of endometrial cancer.
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PMID:Bcl-2 and p53 expression in stage I endometrial carcinoma. 985 78

A case of endometrioid adenocarcinoma arising from adenomyosis is reported. The patient was a 53-year-old woman who complained of vulvar itching. Smear cytology of the endometrium revealed adenocarcinoma. Magnetic resonance imaging of the pelvis revealed a lesion with a slightly high intensity in the uterine fundus on a T2-weighted image. Semiradical total hysterectomy and bilateral adnexectomy were performed, followed by chemotherapy. Histologically, the lesion in the uterine fundus was composed mostly of adenocarcinoma with stromal invasion. There were many adenomyotic foci in and around the carcinoma, including some showing transition to adenocarcinoma. There was no malignant finding in the normally situated endometrium. The carcinoma invaded in the myometrium, involving the uterine serosa, but no dissemination to the peritoneal cavity was found. The carcinoma was, therefore, considered to be endometrioid adenocarcinoma arising from adenomyosis. Immunohistochemistry showed expression of p53 oncoprotein and Ki-67 antigen in the carcinoma cells. The value of immunohistochemistry in predicting prognosis is discussed.
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PMID:Endometrioid adenocarcinoma arising from adenomyosis: report and immunohistochemical analysis of an unusual case. 1135 Jun 16

Adenocarcinomas arising from adenomyosis uteri are rare. This study reports four such cases and characterizes them clinically and microscopically. In all four patients, the endometrial cytology was negative, and MR imaging and ultrasound sonography did not detect the tumors preoperatively. The histological subtypes of the four tumors were endometrioid (one grade 1, one grade 3), serous, and clear cell. In three cases, the adenocarcinomas were present exclusively in the myometrium, and a transition between the carcinomas and the adenomyotic glands was observed in all cases. The eutopic endometrium was normal except in one case in which there was a small focus of invasive carcinoma. In two of four cases, pelvic or paraaortic lymph node metastases were present. In the carcinomas, ER immunoreactivity was not found in any tumor and PR positivity was found in only one tumor. In contrast, p53 immunopositivity was found in three of four carcinomas. Adenocarcinomas arising from adenomyosis are difficult to diagnose preoperatively, and their aggressive behavior in some cases seems to be related to the histological subtype.
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PMID:Adenocarcinomas arising from uterine adenomyosis: a report of four cases. 1206 69

This study presents a case of endometrial clear cell adenocarcinoma complicated by complex atypical glandular hyperplasia surrounded by adenomyosis in the uterine myometrium. The former was immuno-negative for estrogen receptor (ER) and positive for p53, whereas both of the latter were immuno-positive for ER and negative for p53. Therefore, there were two kinds of neoplasia arising from different origins in the uterine corpus.
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PMID:Two kinds of endometrial neoplasia arising from different origins in the uterine corpus: comparison of p53 expression and sex steroid receptor status. 1220 33

Our objective was to investigate the presence of focal p53 expression in relation to proliferation rates in adenomyotic lesions during the menstrual cycle and in women on oral contraception. Fifty-nine perimenopausal patients with menorrhagia and adenomyosis were submitted to endometrial resection. The procedure was carried out during menstruation (n = 14), during the proliferative phase (n = 15), during the luteal phase (n = 20) or following the use of oral contraceptives (n = 10). The number of Ki-67-positive cells was low during menstruation, during the luteal phase and following the use of progestins. In the proliferative phase, on the other hand, there was a significant increase in the percentage of Ki-67-positive cells. Focal p53 expression was detected mainly during the proliferative phase of the menstrual cycle when proliferation rates were high. PTEN expression was detected in all cases irrespective of the phase of the menstrual cycle or use of oral contraception. We conclude that proliferation rates in adenomyotic lesions undergo marked cyclic variations and this affects the percentage of cases showing focal p53 expression in the glandular epithelium.
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PMID:Proliferation kinetics in adenomyosis during the menstrual cycle and during oral contraceptive use. 1519 2

We report a case of a clear cell adenocarcinoma arising from a giant cystic adenomyosis, with immunohistochemical analysis of p53 and laminin-5 gamma2 chain overexpression. Microscopically, not only clear cell adenocarcinoma showing myometrial invasion but also single-layered clear cell adenocarcinoma cells lining the cyst wall were observed. Transition from these single-layered tumor cells to papillary proliferative lesions of various degrees was recognized. Moreover, these tumor cells were continuous with minimal atypical cells. Although the tumor cells within the uterus showed a low positive cell ratio for p53, the metastatic foci showed a remarkable p53 overexpression. Laminin-5 gamma2 chain expression was low in papillary proliferation and high in myometrial invasion and metastatic foci. The single-layered tumor cells showing non-invasive proliferation also contained laminin-5 gamma2 chain-positive cells. When non-invasive tumor cells were considered to be at an early stage in tumor progression, some tumor cells had already acquired an invasive feature. p53 overexpression was not related to expression of the laminin-5 gamma2 chain.
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PMID:Clear cell adenocarcinoma arising from a giant cystic adenomyosis: a case report with immunohistochemical analysis of laminin-5 gamma2 chain and p53 overexpression. 1846 37

Serous endometrial intraepithelial carcinoma (serous EIC) arising in adenomyosis is rare. It may be underrecognized because of its deceiving morphology when embedded in the foci of adenomyosis. Although there is no connection to peritoneal cavity, some cases may be associated with extrauterine disease. It is currently unknown what the etiology for such a disease is. More studies are in need to elucidate the pathogenesis of such a grave malady. We report a series of 5 cases of serous EIC, which may arise in adenomyosis. The 5 cases are in 5 different patients or whom on histopathological examination of their hysterectomy specimens, the finding of adenomyosis involved with serous intraepithelial neoplasia was identified. The finding of interest was the presence of multifoci of adenomyosis; some of those foci were involved in serous EIC. In addition to EIC, lesions of endometrial glandular dysplasia were present in the foci of adenomyosis. To rule out the possibility of endometrial serous carcinoma (ESC) invading into the areas of the adenomyosis, all of the 5 uteri were extensively examined. Among the 5 uteri, the eutopic endometirum showed 1 invasive ESC, 2 serous EIC, and 2 benign resting endometrium without any cancer or precancerous lesions. In 1 uterus with ESC, we did not see any direct spatial connection between the invasive component of ESC and the areas of EIC in the foci of adenomyosis. In 2 uteri with serous EIC within the endometrial cavity, there was a distance of at least 0.5 cm between the lesions within the endometrial cavity and the serous EIC in adenomyosis. The remaining 2 uteri showed no evidence of endometrial malignancy in the endometrial cavity, whereas serous EIC was present only in areas of adenomyosis. Clinicopathologic data including characterized immunohistochemical stainings and p53 gene sequence analysis are presented and clinical significance is discussed.
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PMID:Serous endometrial intraepithelial carcinoma arising in adenomyosis: a report of 5 cases. 2146 26

The aim of this review article was to evaluate the relationship and the possible etiological mechanisms between endometriosis, leiomyoma (LM) and adenomyosis and gynecological cancers, such as ovarian and endometrial cancer and leiomyosarcoma (LMS). MEDLINE was searched for all articles written in the English literature from July 1966 to May 2013. Reports were collected systematically and all the references were also reviewed. Malignant transformation of gynecologic benign diseases such as endometriosis, adenomyosis and LM to ovarian and endometrial cancer remains unclear. Hormonal factors, inflammation, familial predisposition, genetic alterations, growth factors, diet, altered immune system, environmental factors and oxidative stress may be causative factors in carcinogenesis. Early menarche, low parity, late menopause and infertility have also been implicated in the pathogenesis of these cancers. Ovarian cancers and endometriosis have been shown to have common genetic alterations such as loss of heterozygosity (LOH), PTEN, p53, ARID1A mutations. MicroRNAs have also been implicated in malignant transformation. Inflammation releases proinflammatory cytokines, and activates tumor associated macrophages (TAMS) and nuclear factor kappa b (NF-KB) signaling pathways that promote genetic mutations and carcinogenesis. MED12 mutations in LM and smooth muscle tumors of undetermined malignant potential (STUMP) may contribute to malignant transformation to LMS. A hyperestrogenic state may be shared in common with pathogenesis of adenomyosis, LM and endometrial cancer. However, the effect of these benign gynecologic diseases on endometrial cancer should be studied in detail. This review study indicates that endometriosis, LM, adenomyosis may be associated with increased risk of gynecological cancers such as endometrial and ovarian cancers. The patients who have these gynecological benign diseases should be counseled about the future risks of developing cancer. Further studies are needed to investigate the relationship between STUMPs, LMS and LM and characteristics and outcome endometrial carcinoma in adenomyotic patients.
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PMID:Endometriosis, leiomyoma and adenomyosis: the risk of gynecologic malignancy. 2428 48

Papillary proliferations of the endometrium, without atypia have been uncommonly documented, including on cytology specimens. Herein, we present an uncommon case of a 55-year-old obese lady, on antihypertensive medications, who presented with history of irregular perimenopausal bleeding. A year ago, she was diagnosed with simple cystic hyperplasia on dilation and curettage specimen. Presently, she underwent endometrial aspiration. Cytology smears were prepared from the collected tissue specimen that was further submitted for histopathological analysis. Although the smears were initially diagnosed as negative for malignancy, the tissue sections were reported as a uterine papillary serous carcinoma (UPSC). Review of the smears revealed prominent overlapping clusters and papillary arrangements of relatively banal endometrial cells exhibiting focal metaplasia. Histopathology sections confirmed diagnosis of complex papillary hyperplasia (CPH). Immunohistochemical (IHC) stains reinforced this impression with diffuse estrogen receptor positivity, low Ki-67/MIB1, and lack of diffuse p53 immunostaining. Subsequent hysterectomy, at the time of intraoperative consultation showed a small residual focus of CPH, restricted to endometrium with intramural leiomyomas and adenomyosis. This case is presented to highlight the fact that despite lack of significant atypia, cytological features like overlapping, clustering, and papillary formations are indicators of papillary lesions of the endometrium, including CPH, especially in postmenopausal women. On histopathology, in spite of conspicuous papillary formations, lack of significant nuclear pleomorphism, and tumor invasion are helpful features in avoiding an overdiagnosis of UPSC in such cases. IHC stains are supportive. Correct identification has significant therapeutic implications.
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PMID:Complex papillary hyperplasia of the endometrium: an uncommon case report with cytopathological features and diagnostic implications. 2482 43


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