Differential expression of P16 and P21 in benign and malignant uterine smooth muscle tumors

Ünver, Nurcan; Açıkalın, Mustafa Fuat; Öner, Ülkü; Çiftçi, Evrim; Özalp, Sinan; Çolak, Ertuğrul

doi:10.1007/s00404-010-1690-z

Cited by 34 publications

(24 citation statements)

References 24 publications

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“…Significance was also observed in the expression of p16 among LMS, AUSMT, and leiomyomas (LM) [12] . Thus, the combination of p16 and p53 IHC profiles could represent a useful tool to identify high-risk AUSMT which may potentially recur as LMS [13][14][15][16] . Notably, missense mutations in the TP53 gene represent more than 75% of all p53 mutations in solid tumors.…”

Section: Introductionmentioning

confidence: 99%

Atypical Uterine Smooth Muscle Tumors: A Retrospective Evaluation of Clinical and Pathologic Features

et al. 2017

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Background: Clinical characteristics combined with new biomarkers help discriminate between atypical uterine smooth muscle tumors (AUSMT) and leiomyosarcomas (LMS). Patients and Methods: We retrospectively collected a series of leiomyomas (LM), AUSMT, and LMS. Estrogen receptors (ER), progesterone receptors (PR), p16, Ki-67, and p53 expression were assessed by immunohistochemistry. For AUSMT patients, immunohistochemistry evaluations were performed at the time of diagnosis and at recurrences. Results: A total of 27 cases of AUSMT, 22 LM, and 31 LMS were identified. The expression of ER and PR decreased from LM to LMS (ER+: LM 95.5%, AUSMT 88.9%, LMS 41.9%, p < 0.001; PR+: LM 100%, AUSMT 88.9%, LMS 38.2%, p = 0.002). By contrast, p16 and p53 expression increased (p16+: LM 4.5%, AUSMT 40.7%, LMS 45.2%, p = 0.004; p53: LM 9.1%, AUSMT 33.3%, LMS 58.1%, p = 0.001). At a median follow-up of 33.47 months, 40.7% of patients with AUSMT experienced recurrent disease, 6 patients relapsed as AUSMT and 5 as LMS. In univariate analysis was observed that ER status (p = 0.027) and p53 expression (p = 0.015) predicted risk of relapse. Conclusions: Treatment of AUSMT should be centralized in dedicated centers. International collaborations are needed to optimize research strategy, which may lead to the identification of new useful biomarkers and to improvement in the clinical management of this rare disease.

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Section: Introductionmentioning

confidence: 99%

Atypical Uterine Smooth Muscle Tumors: A Retrospective Evaluation of Clinical and Pathologic Features

et al. 2017

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“…Several studies have reported that p16 is overexpressed in LMS; therefore, p16 may be useful for distinguishing between benign and malignant USMTs (3,6,7,22). Chen and Yang (7) compared among LMS, STUMP, and other LMs and reported that a strong/moderate-to-significant staining pattern was observed in all LMS and STUMP cases that were positive for p16, whereas weak focal staining was observed in some UL and CL cases.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic and Prognostic Significance of p16, p53, and bcl-2 Expressions and Ki-67 Proliferation Index in Benign and Malignant Uterine Smooth Muscle Tumors

Akkalp¹,

Tetikkurt²,

Koy³

et al. 2017

Erciyes Med J

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Objective: This study aimed to evaluate diagnostic parameters such as mitotic count and tumor size in; leiomyosarcomas (LMSs) and benign uterine smooth muscle tumors (USMTs) and to define the diagnostic value and prognostic significance of the Ki-67 proliferation index and p16, p53, and bcl-2 expressions by immunohistochemical (IHC) methods. Materials and Methods:In total, 44 cases diagnosed as LMS, atypical leiomyoma, or cellular leiomyoma at our pathology department from January 2010 to December 2015 were included. IHC staining was performed for bcl-2, p16, p53, and Ki-67 using standard techniques.Results: Tumor size and mitotic index were significant prognostic factors (p=0.008 and p=0.001, respectively). The rate of diffuse p16 expression was significantly higher in the LMS group than in the other LM group (p=0.001). A Ki-67 positivity rate of >10% (increased proliferation) was statistically significantly higher in the LMS group than in the benign USMT group (p=0.0001). No statistically significant difference was found between the LMS and benign USMT groups with respect to bcl-2 expression (p=0.892). Mitotic count and high Ki-67 expression (>%10) were statistically high in cases with relapse/ metastasis (+) (p=0.0001 and p=0.0002, respectively). Conclusion:In addition to histopathological findings (tumor size and mean mitotic count), diffuse p16 expression and p53 overexpression can be used to distinguish between benign and malignant USMTs. A high mitotic index [≥10/10 (high-power field)] and high Ki-67 expression (>10%) can serve as useful indicators for diagnosing LMS, distinguishing benign tumors, and predicting an aggressive clinical course.

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“…Significantly downregulated were alcohol dehydrogenase 1A polypeptide, alcohol dehydrogenase 1B polypeptide, insulinlike growth factor 1, c-Jun, c-Fos, and TU3A. Further, p16 and p21 genes [47] were differentially expressed in benign and malignant tumors. There was no difference in p16 and p21 expressions between leiomyomas, atypical leiomyomas, and STUMPs.…”

Section: Mesenchymal Tumorsmentioning

confidence: 94%

Malignant tumors of the uterine corpus: molecular background of their origin

et al. 2015

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Tumors of the uterine corpus can be divided into two main groups: endometrial tumors and mesenchymal tumors. The former ones are common gynecological diseases, whereas malignant mesenchymal tumors, which behave in a much more aggressive way, are quite rare with a poorer prognosis. The most common type of endometrial tumors is endometrioid adenocarcinomas, and in case of mesenchymal tumors, these are carcinosarcomas, or leiomyosarcomas, if only clear types of tumors are taken into account. The objective of this article is to review molecular-genetic abnormalities associated with tumorigenesis of both types of tumors, with focus on the most aggressive forms. This view includes a different expression pattern of genes, usually aberrant in cases of uterine cancer that can arise due to epigenetic modifications, mostly hypermethylation of promoters or microRNA (miRNA)'s interference with concrete genes. Furthermore, clinical predispositions of tumorigenesis, involving hormonal factors, age, and ethnicity, are also mentioned.

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Differential expression of P16 and P21 in benign and malignant uterine smooth muscle tumors

Abstract: Our findings suggested that p16 and p21 may be of value as an adjunct to conventional morphologic criteria in the assessment of problematic uterine smooth muscle tumors.

Cited by 34 publications

References 24 publications

Atypical Uterine Smooth Muscle Tumors: A Retrospective Evaluation of Clinical and Pathologic Features

Atypical Uterine Smooth Muscle Tumors: A Retrospective Evaluation of Clinical and Pathologic Features

Diagnostic and Prognostic Significance of p16, p53, and bcl-2 Expressions and Ki-67 Proliferation Index in Benign and Malignant Uterine Smooth Muscle Tumors

Malignant tumors of the uterine corpus: molecular background of their origin

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