Co-expression of p53 by epithelial and stromal elements in carcinosarcoma of the female genital tract: an immunohistochemical study of 19 cases

Szukala,; Маркс,; Burchette,; Elbendary,; Krigman,

doi:10.1046/j.1525-1438.1999.09905.x

Cited by 42 publications

(30 citation statements)

References 25 publications

(41 reference statements)

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“…19,20 p53 overexpression has been associated with biological aggressiveness in endometrioid adenocarcinomas as well as in papillary serous carcinomas of the endometrium. 21,22 As uterine carcinosarcomas are clinically aggressive malignancies and approximately 54% of the patients in our cohort had metastatic disease at presentation, it was not surprising to find a high rate of p53 overexpression in these tumors.…”

Section: Discussionmentioning

confidence: 99%

DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

et al. 2006

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Growing molecular evidence shows that uterine carcinosarcomas are clonal tumors. The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defective DNA mismatch repair in the histiogenesis of uterine carcinosarcomas remains controversial. We studied the pattern and frequency of defective DNA mismatch repair and TP53 alterations in the epithelial and mesenchymal components of 28 uterine carcinosarcomas. We found evidence of defective DNA mismatch repair in six cases (21%) with a concordance rate of 83% for carcinoma-sarcoma pairs (j ¼ 0.887, Po0.001). Lack of immunostaining for the MLH1 protein was demonstrated in both components in two of these tumors. TP53 defects were evaluated by 17p deletion analysis and p53 immunostaining. Nineteen carcinoma (68%) and 18 sarcoma (64%) components had evidence of either TP53 allelic loss or p53 overexpression. These defects proved clonal in 76% of cases (j ¼ 0.602, P ¼ 0.003). Our results indicate that defective DNA mismatch repair and TP53 defects are common early events in carcinosarcoma tumorigenesis. The high rate of concordance for these molecular defects between the carcinoma and sarcoma components adds to existing molecular evidence that carcinosarcomas are clonal malignancies. Keywords: carcinosarcoma; malignant mixed mü llerian tumor; microsatellite instability; DNA mismatch repair; TP53; clonality Carcinosarcomas of the uterus account for 1-2% of all malignancies of the uterine corpus. The pathologic hallmark of these tumors is the presence of malignant epithelial and mesenchymal components. These mixed malignancies can affect any of the mü llerian derivatives of the female reproductive tract. Despite their relatively low incidence, these aggressive tumors represent a significant clinical problem. 1The overall survival at 5 years for all patients with cancer of the uterine corpus is 84% and only 31% for patients with a uterine carcinosarcoma. 2,3 There is clinical and molecular evidence suggesting that uterine carcinosarcomas are clonal malignancies. [4][5][6][7][8][9][10]

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Section: Discussionmentioning

confidence: 99%

DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

et al. 2006

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“…Immunohistochemical studies demonstrate that both the sarcomatous and carcinomatous components in CS coexpress cytokeratins and vimentin [31,32,33,34,35,36]. Additionally, both the carcinomatous and sarcomatous components in CS stain for p53 [37, 38]. These observations support a common origin for the epithelial and mesenchymal components because, if these were true collision tumors, such concordance in all cases would be extremely unlikely.…”

Section: Discussionmentioning

confidence: 99%

Prognoses and Prognostic Factors of Carcinosarcoma, Endometrial Stromal Sarcoma and Uterine Leiomyosarcoma: A Comparison with Uterine Endometrial Adenocarcinoma

et al. 2006

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Aims: The aims of this study were to evaluate the factors affecting prognosis in patients with uterine sarcomas and to demonstrate that carcinosarcoma bears a similarity to high-grade endometrial carcinoma in terms of its prognosis and clinicopathological parameters. Methods: In June 2004, 17 Japanese institutions received questionnaires regarding uterine sarcomas. Study patients had uterine sarcomas initially treated at each institution between January 1990 and May 2004. Survival analyses and comparisons were performed by univariate methods. Patient data of 921 cases of endometrial adenocarcinoma were also analyzed and compared to the data with the uterine sarcomas. Results: One hundred twenty-one patients with uterine sarcomas were identified who met study eligibility criteria. In uterine sarcomas, carcinosarcoma had a worse prognosis than other sarcomas, but the difference was not significant (p = 0.302). In carcinosarcoma, significant differences were observed with age (p = 0.0388), stage (p < 0.01) and surgical procedure (with or without pelvic lymphadenectomy, p = 0.0316). In carcinosarcoma and G3 adenocarcinoma, no significant difference was identified with regard to overall survival in univariate (p = 0.191) and multivariate (p = 0.168) analyses. Conclusion: Our results demonstrate that the clinical behavior of carcinosarcoma strongly resembles that of G3 endometrial adenocarcinoma, setting it apart from other ‘pure’ uterine sarcomas.

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“…Moreover, p53 expression was similar in primary uterine tumors and paired metastatic lesions [49]. Altogether, most studies published worldwide report a p53 pattern concordance between the epithelial and mesenchymal CS components, with both components being either positive or negative [49,51,84,85,86,87,88,89,90,91,92,93,94,95] (fig. 2).…”

Section: P53 Alterations/expression In Uterine Cssmentioning

confidence: 99%

Role of p53 Pathway Alterations in Uterine Carcinosarcomas (Malignant Mixed Müllerian Tumors)

et al. 2014

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Carcinosarcomas (CSs; malignant mixed Müllerian tumors) of the uterus are highly malignant neoplasms characterized by an unfavorable outcome. They represent less than 5% of all uterine malignancies, and the median patient survival rate is only 21 months. p53 pathway alterations have been studied in CSs originating from the uterus, supporting the monoclonal nature of most but not all of these neoplasms. This paper gives an overview of the current knowledge of p53 pathway distortions in patients with uterine CSs. The survival of patients with uterine CSs in relation to p53 pathway alterations is also briefly summarized.

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Co-expression of p53 by epithelial and stromal elements in carcinosarcoma of the female genital tract: an immunohistochemical study of 19 cases

Cited by 42 publications

References 25 publications

DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

Prognoses and Prognostic Factors of Carcinosarcoma, Endometrial Stromal Sarcoma and Uterine Leiomyosarcoma: A Comparison with Uterine Endometrial Adenocarcinoma

Role of p53 Pathway Alterations in Uterine Carcinosarcomas (Malignant Mixed Müllerian Tumors)

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