Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium

Yvette P. Geels, Louis J M Van Der Putten, Angela A G Van Tilborg, Irene Lurkin, Ellen C. Zwarthoff, Johanna M A Pijnenborg, Saskia H. Van Den Berg-Van Erp, Marc P L M Snijders, Johan Bulten, Daniel W Visscher, Sean Christopher Dowdy, Leon F A G Massuger

Research output: Contribution to journalArticle

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Abstract

Objective. Endometrial carcinomas are divided into type I endometrioid endometrial carcinomas (EECs), thought to arise fromhyperplastic endometrium, and type II nonendometrioid endometrial carcinomas, thought to arise fromatrophic endometrium. However, a minority (20%) of EECs have atrophic background endometrium, which was shown to be a marker of a worse prognosis. This study compares the immunohistochemical and genetic profiles of this possible third type to that of the known two types. Methods. 43 patients with grade 1 EEC and hyperplastic background endometrium (type I), 43 patients with grade 1 EEC and atrophic background endometrium (type III) and 21 patients with serous carcinoma (type II) were included (n = 107). Tissue microarrays of tumor samples were immunohistochemically stained for PTEN, L1CAM, ER, PR, p53, MLH1, PMS2, β-catenin, E-cadherin and MIB1. The BRAF, KRAS, and PIK3CA genes were analyzed for mutations. Results. A significantly higher expression of ER and PR, and a lower expression of L1CAM, p53 and MLH1 were found in type I and III compared to type II carcinomas. Expression of E-cadherinwas significantly reduced in type III compared to type I carcinomas. Mutation analysis showed significantly less mutations of KRAS in type III compared to type I and II carcinomas (p < 0.01). Conclusion. There appear to be slight immunohistochemical and genetic differences between EECs with hyperplastic and atrophic background endometrium. Carcinogenesis of EEC in atrophic endometrium seems to be characterized by loss of E-cadherin and a lack of KRAS mutations. As expected, endometrioid and serous carcinomas were immunohistochemically different.

Original languageEnglish (US)
Pages (from-to)245-251
Number of pages7
JournalGynecologic Oncology
Volume137
Issue number2
DOIs
StatePublished - 2015

Fingerprint

Endometrioid Carcinoma
Endometrial Neoplasms
Endometrium
Neural Cell Adhesion Molecule L1
Carcinoma
Mutation
Cadherins
Catenins
Carcinogenesis

Keywords

  • Background endometrium
  • Endometrial carcinoma
  • Endometrioid
  • Genetical
  • Immunohistochemistry

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Oncology

Cite this

Geels, Y. P., Van Der Putten, L. J. M., Van Tilborg, A. A. G., Lurkin, I., Zwarthoff, E. C., Pijnenborg, J. M. A., ... Massuger, L. F. A. G. (2015). Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium. Gynecologic Oncology, 137(2), 245-251. https://doi.org/10.1016/j.ygyno.2015.03.007

Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium. / Geels, Yvette P.; Van Der Putten, Louis J M; Van Tilborg, Angela A G; Lurkin, Irene; Zwarthoff, Ellen C.; Pijnenborg, Johanna M A; Van Den Berg-Van Erp, Saskia H.; Snijders, Marc P L M; Bulten, Johan; Visscher, Daniel W; Dowdy, Sean Christopher; Massuger, Leon F A G.

In: Gynecologic Oncology, Vol. 137, No. 2, 2015, p. 245-251.

Research output: Contribution to journalArticle

Geels, YP, Van Der Putten, LJM, Van Tilborg, AAG, Lurkin, I, Zwarthoff, EC, Pijnenborg, JMA, Van Den Berg-Van Erp, SH, Snijders, MPLM, Bulten, J, Visscher, DW, Dowdy, SC & Massuger, LFAG 2015, 'Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium', Gynecologic Oncology, vol. 137, no. 2, pp. 245-251. https://doi.org/10.1016/j.ygyno.2015.03.007
Geels YP, Van Der Putten LJM, Van Tilborg AAG, Lurkin I, Zwarthoff EC, Pijnenborg JMA et al. Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium. Gynecologic Oncology. 2015;137(2):245-251. https://doi.org/10.1016/j.ygyno.2015.03.007
Geels, Yvette P. ; Van Der Putten, Louis J M ; Van Tilborg, Angela A G ; Lurkin, Irene ; Zwarthoff, Ellen C. ; Pijnenborg, Johanna M A ; Van Den Berg-Van Erp, Saskia H. ; Snijders, Marc P L M ; Bulten, Johan ; Visscher, Daniel W ; Dowdy, Sean Christopher ; Massuger, Leon F A G. / Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium. In: Gynecologic Oncology. 2015 ; Vol. 137, No. 2. pp. 245-251.
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abstract = "Objective. Endometrial carcinomas are divided into type I endometrioid endometrial carcinomas (EECs), thought to arise fromhyperplastic endometrium, and type II nonendometrioid endometrial carcinomas, thought to arise fromatrophic endometrium. However, a minority (20{\%}) of EECs have atrophic background endometrium, which was shown to be a marker of a worse prognosis. This study compares the immunohistochemical and genetic profiles of this possible third type to that of the known two types. Methods. 43 patients with grade 1 EEC and hyperplastic background endometrium (type I), 43 patients with grade 1 EEC and atrophic background endometrium (type III) and 21 patients with serous carcinoma (type II) were included (n = 107). Tissue microarrays of tumor samples were immunohistochemically stained for PTEN, L1CAM, ER, PR, p53, MLH1, PMS2, β-catenin, E-cadherin and MIB1. The BRAF, KRAS, and PIK3CA genes were analyzed for mutations. Results. A significantly higher expression of ER and PR, and a lower expression of L1CAM, p53 and MLH1 were found in type I and III compared to type II carcinomas. Expression of E-cadherinwas significantly reduced in type III compared to type I carcinomas. Mutation analysis showed significantly less mutations of KRAS in type III compared to type I and II carcinomas (p < 0.01). Conclusion. There appear to be slight immunohistochemical and genetic differences between EECs with hyperplastic and atrophic background endometrium. Carcinogenesis of EEC in atrophic endometrium seems to be characterized by loss of E-cadherin and a lack of KRAS mutations. As expected, endometrioid and serous carcinomas were immunohistochemically different.",
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T1 - Immunohistochemical and genetic profiles of endometrioid endometrial carcinoma arising from atrophic endometrium

AU - Geels, Yvette P.

AU - Van Der Putten, Louis J M

AU - Van Tilborg, Angela A G

AU - Lurkin, Irene

AU - Zwarthoff, Ellen C.

AU - Pijnenborg, Johanna M A

AU - Van Den Berg-Van Erp, Saskia H.

AU - Snijders, Marc P L M

AU - Bulten, Johan

AU - Visscher, Daniel W

AU - Dowdy, Sean Christopher

AU - Massuger, Leon F A G

PY - 2015

Y1 - 2015

N2 - Objective. Endometrial carcinomas are divided into type I endometrioid endometrial carcinomas (EECs), thought to arise fromhyperplastic endometrium, and type II nonendometrioid endometrial carcinomas, thought to arise fromatrophic endometrium. However, a minority (20%) of EECs have atrophic background endometrium, which was shown to be a marker of a worse prognosis. This study compares the immunohistochemical and genetic profiles of this possible third type to that of the known two types. Methods. 43 patients with grade 1 EEC and hyperplastic background endometrium (type I), 43 patients with grade 1 EEC and atrophic background endometrium (type III) and 21 patients with serous carcinoma (type II) were included (n = 107). Tissue microarrays of tumor samples were immunohistochemically stained for PTEN, L1CAM, ER, PR, p53, MLH1, PMS2, β-catenin, E-cadherin and MIB1. The BRAF, KRAS, and PIK3CA genes were analyzed for mutations. Results. A significantly higher expression of ER and PR, and a lower expression of L1CAM, p53 and MLH1 were found in type I and III compared to type II carcinomas. Expression of E-cadherinwas significantly reduced in type III compared to type I carcinomas. Mutation analysis showed significantly less mutations of KRAS in type III compared to type I and II carcinomas (p < 0.01). Conclusion. There appear to be slight immunohistochemical and genetic differences between EECs with hyperplastic and atrophic background endometrium. Carcinogenesis of EEC in atrophic endometrium seems to be characterized by loss of E-cadherin and a lack of KRAS mutations. As expected, endometrioid and serous carcinomas were immunohistochemically different.

AB - Objective. Endometrial carcinomas are divided into type I endometrioid endometrial carcinomas (EECs), thought to arise fromhyperplastic endometrium, and type II nonendometrioid endometrial carcinomas, thought to arise fromatrophic endometrium. However, a minority (20%) of EECs have atrophic background endometrium, which was shown to be a marker of a worse prognosis. This study compares the immunohistochemical and genetic profiles of this possible third type to that of the known two types. Methods. 43 patients with grade 1 EEC and hyperplastic background endometrium (type I), 43 patients with grade 1 EEC and atrophic background endometrium (type III) and 21 patients with serous carcinoma (type II) were included (n = 107). Tissue microarrays of tumor samples were immunohistochemically stained for PTEN, L1CAM, ER, PR, p53, MLH1, PMS2, β-catenin, E-cadherin and MIB1. The BRAF, KRAS, and PIK3CA genes were analyzed for mutations. Results. A significantly higher expression of ER and PR, and a lower expression of L1CAM, p53 and MLH1 were found in type I and III compared to type II carcinomas. Expression of E-cadherinwas significantly reduced in type III compared to type I carcinomas. Mutation analysis showed significantly less mutations of KRAS in type III compared to type I and II carcinomas (p < 0.01). Conclusion. There appear to be slight immunohistochemical and genetic differences between EECs with hyperplastic and atrophic background endometrium. Carcinogenesis of EEC in atrophic endometrium seems to be characterized by loss of E-cadherin and a lack of KRAS mutations. As expected, endometrioid and serous carcinomas were immunohistochemically different.

KW - Background endometrium

KW - Endometrial carcinoma

KW - Endometrioid

KW - Genetical

KW - Immunohistochemistry

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