Stepwise abnormality of sex steroid hormone receptors, tumor suppressor gene products (p53 and Rb), and cyclin E in uterine endometrioid carcinoma

Li, Shuanfang; Shiozawa, Tanri; Nakayama, Kohzo; Nikaido, Toshio; Fujii, Shingo

doi:10.1002/(sici)1097-0142(19960115)77:2<321::aid-cncr15>3.0.co;2-3

Cited by 66 publications

(5 citation statements)

References 34 publications

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“…The present study also demonstrates that there are no apparent differences in p53 gene in UL. A similar observation was reported in another sex steroid-dependent tumor, uterine endometrioid carcinoma, in which there were no changes in p53 level between endometrioid carcinoma and the adjacent tissue (Li et al, 1996). Ours and other some studies have confirmed that there has been no significant association between p53 loss and UL.…”

Section: Discussionsupporting

confidence: 90%

Chromosome Imbalances and Alterations in the p53 Gene in Uterine Myomas from the Same Family Members: Familial Leiomyomatosis in Turkey

Hakverdı

Demırhan²,

Tunç³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Uterine leiomyomas (UL) are extremely common neoplasms in women of reproductive age, and are associated with a variety of characteristic choromosomal aberrations (CAs). The p53 gene has been reported to play a crucial role in suppressing the growth of a variety of cancer cells. Therefore, the present study investigated the effects of CAs and the p53 gene on ULs. We performed cytogenetic analysis by G-banding in 10 cases undergoing myomectomy or hysterectomy. Fluorescence in situ hybridization (FISH) with a p53 gene probe was also used on interphase nuclei to screen for deletions. In patients, CAs were found in 23.4% of 500 cells analysed, significantly more frequent than in the control group (p<0.001). In the patients, 76% of the abnormalities were structural aberrations (deletions, translocations and breaks), and only 24% were numerical. Deletions were the most common structural aberration observed in CAs. Among these CAs, specific changes in five loci 1q11, 1q42, 2p23, 5q31 and Xp22 have been found in our patients and these changes were not reported previously in UL. The chromosome breaks were more frequent in cases, from high to low,

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Section: Discussionsupporting

confidence: 90%

Chromosome Imbalances and Alterations in the p53 Gene in Uterine Myomas from the Same Family Members: Familial Leiomyomatosis in Turkey

Hakverdı

Demırhan²,

Tunç³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…4) Thus, overexpression of cyclin E/CDK2 is theoretically oncogenic. In our study, only a limited number of cyclin E-positive cells was observed in the normal squamous epithelia, whereas considerable numbers of cells in severe epithelial dysplasia and SCCs overexpressed cyclin E. While overexpression of cyclin E has also been noticed in breast, 39) endometrial, 40) uterine, 22) and lung 20,41) cancers, the role of this protein is not clear.…”

Section: Discussioncontrasting

confidence: 71%

Overexpression of CDK2 Is a Prognostic Indicator of Oral Cancer Progression

Mihara

Shintani

Nakahara

et al. 2001

Japanese Journal of Cancer Research

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Cyclins and cyclin-dependent kinases (CDKs) play key roles in cell cycle regulation, a process of which dysregulation can lead to uncontrolled cell growth and hence to cancer. We have already reported the alteration of CDK4 and cyclin D1 expression in oral cancer. In this study, we examined by immunohistochemistry the expression of CDK2, and cyclins A and E in 20 normal oral mucosa, 42 dysplastic epithelia, and 103 oral squamous cell carcinomas (SCCs). The expressions of CDK2, and cyclins A and E were not detected in the normal epithelium and significantly altered from epithelial dysplasia to SCC. While there were no significant correlations between the expression of cyclins A, E and the patients' survival, CDK2 expression was significantly correlated with lymph node involvement (P = = = =0.025), tumor differentiation (P = = = =0.032), mode of tumor invasion (P = = = =0.017), and shorter survival period (P = = = =0.0173). These results suggest that the elevated expression of CDK2 is a critical factor in oral cancer progression and can be used as a negative predictive marker of the patients' prognosis. Key words: CDK2 -Cyclin A -Cyclin E -Oral cancer -PrognosisCell proliferation is ultimately dependent on cell cycle control, and the decision to continue to proliferate is made mainly during G1 phase as a result of the activities of G1 cyclins and cyclin-dependent kinases (CDKs) complexes.1-8) Among those kinases that regulate G1 progression, CDK4 and CDK6 are activated by association with cyclin D in the mid G1.9, 10) CDK2 is activated by binding to cyclin E, and its activity is essential for transition through the restriction point in the late G1. 7,8,11,12) Subsequently, cyclin A is expressed and is thought to be required, in association with CDK2, for progression through the S phase.13) Amplification and/or overexpression of cyclin E has been reported in colorectal, breast, lung, ovarian and uterus carcinomas.14-22) Overexpression of cyclin A has been reported in lung 20) and uterus carcinomas. 22) In the head and neck, amplification of cyclin D in oral squamous cell carcinoma (SCC) has recently been reported. 23,24) There are few reports on CDK2, and cyclins A and E in oral SCC, and the molecular events that underlie the histological progression are not well understood. In this study, we focused our attention on the G1/S and S to G2 transitions in the cell cycle and examined by immunohistochemistry the expression of CDK2, as well as its regulatory partners, cyclins A and E, in oral premalignant lesions and cancers. We also performed western blot analysis in matched sets of tumors and normal tissues. Furthermore, we analyzed the relationship between the expressions of CDK2 and cyclins A and E, and the clinicopathological parameters and patients' survival outcome. MATERIALS AND METHODSPatients Tissue samples of 20 normal oral mucosa specimens, 42 epithelial dysplasia specimens, and 103 oral SCC patients were investigated. The patients underwent surgery at the Department of Oral and Maxillofacial Surgery II, Okay...

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“…Cyclin E immunostaining is a feature of most endometrial carcinomas (90). As has been demonstrated in breast cancers, an inverse correlation between positive estrogen receptor status and cyclin E immunostaining appears to exist in endometrial carcinomas, but not in adjacent normal or hyperplastic epithelium from the same patients (91). Although cyclin E is not restricted to neoplastic endometrial disorders, since increased levels of cyclin E are noted during the normal proliferative phase (92), there does appear to be an accumulation of this protein from normal through simple and complex hyperplasia to malignancy (91,93).…”

Section: Genito-urinary Tract Cancersmentioning

confidence: 72%

“…Although cyclin E is not restricted to neoplastic endometrial disorders, since increased levels of cyclin E are noted during the normal proliferative phase (92), there does appear to be an accumulation of this protein from normal through simple and complex hyperplasia to malignancy (91,93). Although correlations with serous type, grade, and stage have been suggested (91,93), the prognostic implications of cyclin E need to be studied in greater detail (90).…”

Section: Genito-urinary Tract Cancersmentioning

confidence: 99%

Cyclin E in human cancers

1999

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Regulators of the cell cycle such as cyclin E play an important part in neoplasia. The cyclin E protein forms a partnership with a specific protein kinase. This complex phosphorylates key substrates to initiate DNA synthesis. Cyclin-dependent kinase inhibitors (CKIs) are able to suppress the activity of cyclin E. Various substances (including proteins produced by oncogenic viruses) affect cyclin E directly or indirectly through an interaction with CKIs. These interactions are important in elucidating the mechanisms of neoplasia. They may also provide prognostic information in a wide range of common cancers. Cyclin E may even be a target for treatment of cancers in the future.

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Stepwise abnormality of sex steroid hormone receptors, tumor suppressor gene products (p53 and Rb), and cyclin E in uterine endometrioid carcinoma

Abstract: In the development of endometrial carcinoma, stepwise abnormalities of sex steroid receptors, tumor suppressor gene products, and cyclins apparently exist, and may correlate with the progression of the malignant process.

Cited by 66 publications

References 34 publications

Chromosome Imbalances and Alterations in the p53 Gene in Uterine Myomas from the Same Family Members: Familial Leiomyomatosis in Turkey

Chromosome Imbalances and Alterations in the p53 Gene in Uterine Myomas from the Same Family Members: Familial Leiomyomatosis in Turkey

Overexpression of CDK2 Is a Prognostic Indicator of Oral Cancer Progression

Cyclin E in human cancers

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