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"ABSTRAK Karsinoma ovarium adalah salah satu keganasan paling mematikan di bidang ginekologik. Penyebab keganasan belum diketahui pasti dan umumnya tidak memiliki gejala klinik yang jelas. Karsinoma ovarium tipe I khususnya karsinoma endometrioid dan karsinoma sel jernih diketahui dapat berasal dari endometriosis. Karsinoma yang berasal dari endometriosis dikenal sebagai endometriosis-associated ovarian carcinoma (EAOC). Pengembangan model hewan coba karsinoma ovarium yang berhubungan dengan endometriosis diperlukan untuk penelitian dasar dan uji klinik menggantikan jaringan manusia. Pada penelitian ini dikembangkan model hewan coba karsinoma ovarium dengan teknik autoimplantasi dan induksi DMBA. Penelitian ini mengunakan blok parafin dari tikus yang sebelumnya telah mendapatkan operasi plasebo (SHAM), autoimplantasi endometrium, kombinasi autoimplantasi endometrium dan induksi DMBA yang dikorbankan pada minggu ke-5,10, dan 20. Dilakukan penilaian histopatologik dan pulasan imunohistokimia ARID1A dengan penilaian persentase positivitas pada 200 sel. Penelitian ini menghasilkan lesi endometriosis atipik sebanyak 1 (20%) dan karsinoma sel jernih sebanyak 1 (20%) pada implantasi dan induksi DMBA 10 minggu dan karsinoma endometrioid sebanyak 100% pada kelompok induksi DMBA. Pulasan ARID1A tidak menunjukkan perbedaan bermakna (p=0,313) pada seluruh kelompok perlakuan.

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ABSTRACT Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause of malignancy is not known for sure and generally do not have clear clinical symptoms. Type I ovarian carcinoma especially endometrioid carcinoma and clear cell carcinoma is known to originate from endometriosis. Carcinoma originating from endometriosis is known as endometriosis-associated ovarian carcinoma (EAOC). The development of experimental animal models of ovarian carcinoma associated with endometriosis is needed for basic research and clinical trials replace human tissue. In this study an experimental model of ovarian carcinoma was developed with autoimplantation and DMBA induction techniques.This study used paraffin blocks from mice that had previously received placebo surgery (SHAM), endometrial autoimplantation, combination of endometrial autoimplantation and DMBA induction and were sacrificed at 5,10 and 20 weeks. Assessment of ARID1A expression by assessing the percentage of positivity in 200 cells.This study resulted in 1 (20%) atypical endometriosis lesions and 1 (20%) clear cell carcinoma in 10 weeks DMBA implantation and 100% endometrioid carcinoma in the DMBA induction group. ARID1A ekspression did not show a significant difference (p = 0.313) in all treatment groups.

 

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"Latar belakang: Karsinoma ovarium adalah salah satu keganasan paling mematikan di bidang ginekologik. Penyebab keganasan belum diketahui pasti dan umumnya tidak memiliki gejala klinik yang jelas. Karsinoma ovarium tipe I khususnya karsinoma endometrioid dan karsinoma sel jernih diketahui dapat berasal dari endometriosis. Karsinoma yang berasal dari endometriosis dikenal sebagai endometriosis-associated ovarian carcinoma (EAOC). Pengembangan model hewan coba karsinoma ovarium yang berhubungan dengan endometriosis diperlukan untuk penelitian dasar dan uji klinik menggantikan jaringan manusia. Pada penelitian ini dikembangkan model hewan coba karsinoma ovarium dengan teknik autoimplantasi dan induksi DMBA. Bahan dan cara kerja: Penelitian ini mengunakan blok parafin dari tikusyang sebelumnya telah mendapatkan operasiplasebo (SHAM), autoimplantasi endometrium, kombinasi autoimplantasi endometrium dan induksi DMBAyangdikorbankan pada minggu ke-5,10, dan 20. Dilakukan penilaian histopatologik dan pulasan imunohistokimia ARID1A dengan penilaian persentase positivitas pada 200 sel. Hasil: Penelitian ini menghasilkan lesi endometriosis atipik sebanyak 1 (20%) dan karsinoma sel jernih sebanyak 1 (20%)pada implantasi dan induksi DMBA 10 minggu dan karsinoma endometrioidsebanyak 100% pada kelompok induksi DMBA. Pulasan ARID1A tidak menunjukkan perbedaan bermakna (p=0,313) pada seluruh kelompok perlakuan.

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Background: Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause of malignancy is not known for sure and generally do not have clear clinical symptoms. Type I ovarian carcinoma especially endometrioid carcinoma and clear cell carcinoma is known to originate from endometriosis. Carcinoma originating from endometriosis is known as endometriosis-associated ovarian carcinoma (EAOC). The development of experimental animal models of ovarian carcinoma associated with endometriosis is needed for basic research and clinical trials replace human tissue. In this study an experimental model of ovarian carcinoma was developed with autoimplantation and DMBA induction techniques.

Materials and methods: This study used paraffin blocks from mice that had previously received placebo surgery (SHAM), endometrial autoimplantation, combination of endometrial autoimplantation and DMBA induction and were sacrificed at 5,10 and 20 weeks. Assessment of ARID1A expression by assessing the percentage of positivity in 200 cells.

Results: This study resulted in 1 (20%) atypical endometriosis lesions and 1 (20%) clear cell carcinoma in 10 weeks DMBA implantation and 100% endometrioid carcinoma in the DMBA induction group. ARID1A ekspression did not show a significant difference (p = 0.313) in all treatment groups."

"ABSTRAKLatar belakang: Endometriosis merupakan kelainan ginekologik yang paling sering ditemukan. Seperti halnya endometrium di uterus juga dapat terjadi berbagai perubahan pada epitel yang melapisi kista endometriosis di ovarium, antara lain metaplasia, hiperplasia, atipia bahkan perubahan ke arah keganasan. Saat ini banyak penelitian yang menghubungkan antara endometriosis dan kanker ovarium terutama jenis clear cell dan dikenal dengan istilah endometriosis-associated ovarian carcinoma (EAOC) dan dilaporkan adanya mutasi yang menginaktifkan gen supresor tumor (ARID1A), sehingga protein BAF250a tidak diekpresikan pada Clear cell carcinoma (CCC) ovarii.Bahan dan cara: Dilakukan pulasan imunohistokimia ARID1A pada sampel 20 kasus endometriosis non atipik, 20 kasus atipik dan 20 kasus CCC ovarii tahun 2012 hingga Maret 2015. Dari kelompok kasus CCC didapatkan 9 kasus EAOC. Selanjutnya dilihat adakah perbedaan persentase ekspresi ARID1A pada endometriosis non atipik, atipik, CCC ovarii serta endometriosis disertai CCC (EAOC).Hasil: Pada kelompok kasus endometriosis non atipik, atipik dan CCC ada perbedaan bermakna persentase ekspresi ARID1A (uji Kruskal-Wallis p=0,0035). Selanjutnya dilakukan analisis Post Hoc uji Mann-Whitney dan didapatkan perbedaan bermakna persentase ekspresi ARID1A antara endometriosis non atipik dan atipik dengan CCC ovarii (p=0,001 dan p=0,0015). Pada kelompok kasus endometriosis non atipik, atipik dan endometriosis pada EAOC, didapatkan ada perbedaan bermakna persentase ekspresi ARID1A (Uji Kruskal-Walis p=0,011). Selanjutnya dilakukan analisis Post Hoc uji Mann-Whitney dan ada perbedaan bermakna persentase ekspresi ARID1A antara endometriosis non atipik dan atipik dengan EAOC (p=0,005 dan p=0,008).Kesimpulan: Ekspresi ARID1A pada endometriosis non atipik dan atipik lebih tinggi bermakna dibanding CCC ovarii dan EAOC. Sehingga ekspresi ARID1A kemungkinan dapat digunakan sebagai petanda adanya transformasi ganas pada endometriosis.

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ABSTRACT

Background: Endometriosis is one of the most common gynecological abnormalities found. Endometriosis cyst in the ovary also exhibited changes in epithelial cyst just like endometrium in the uterus. Changes in the epithelial cells also include metaplasia, hyperplasia, atyphia even changes toward malignan characteristics. Nowadays, there are some research that linked endometriosis and clear cell ovarian cancer which is known with endometriosis-associated ovarian carcinoma (EAOC) it is reported that there?s a mutation that activated tumor suppressor gene (ARID1A), so protein BAF250a is not expressed in Clear Cell Carcinoma (CCC) in the ovarium.

Materials and Methods: Immunohistochemistry staining of ARID1A were done in 20 samples of non-atypical endometriosis, 20 samples of atypical endometriosis, 20 samples of CCC in the ovarium from the year 2012 until march 2015. From the group that experienced CCC we get 9 cases of EAOC. After that, we see if there?s any difference in the percentage of ARID1A expression in non-atypical endometrosis, atypical endometriosis, CCC in the ovarium and endometriosis with CCC( EAOC).

Results: In non-atypical endometriosis, atypical and CCC cases groups there are significant differences on the percentage of ARID1A expression (Kruskal-Walis test p=0,0035). Post Hoc analysis were done using Mann-Whitney test and there are significant differences on ARID1A expression between non-atypical and atypical endometriosis with CCC (p=0,001 and p=0,0015). In non-atypical endometriosis, atypical and EAOC groups there are significant differences on the percentage of ARID1A expression (Kruskal-Walis test p=0,011). Post Hoc analysis were done using Mann-Whitney test and there are significant differences on ARID1A expression between non-atypical and atypical endometriosis with EAOC (p=0,005 and p=0,008).

Conclusion: Expression of ARID1A in non atypical and atypical endometriosis are significantly higher compared to ovarian CCC and EAOC. So, we can say that ARID1A may be used as a marker for malignancy transformation in endometriosis."

"ABSTRAK Latar belakang: Endometriosis merupakan kelainan ginekologik yang palingsering ditemukan. Seperti halnya endometrium di uterus juga dapat terjadiberbagai perubahan pada epitel yang melapisi kista endometriosis di ovarium,antara lain metaplasia, hiperplasia, atipia bahkan perubahan ke arah keganasan.Saat ini banyak penelitian yang menghubungkan antara endometriosis dan kankerovarium terutama jenis clear cell dan dikenal dengan istilah endometriosisassociatedovarian carcinoma (EAOC) dan dilaporkan adanya mutasi yangmenginaktifkan gen supresor tumor (ARID1A), sehingga protein BAF250a tidakdiekpresikan pada Clear cell carcinoma (CCC) ovarii.Bahan dan cara: Dilakukan pulasan imunohistokimia ARID1A pada sampel 20kasus endometriosis non atipik, 20 kasus atipik dan 20 kasus CCC ovarii tahun2012 hingga Maret 2015. Dari kelompok kasus CCC didapatkan 9 kasus EAOC.Selanjutnya dilihat adakah perbedaan persentase ekspresi ARID1A padaendometriosis non atipik, atipik, CCC ovarii serta endometriosis disertai CCC(EAOC).Hasil: Pada kelompok kasus endometriosis non atipik, atipik dan CCC adaperbedaan bermakna persentase ekspresi ARID1A (uji Kruskal-Wallis p=0,0035).Selanjutnya dilakukan analisis Post Hoc uji Mann-Whitney dan didapatkanperbedaan bermakna persentase ekspresi ARID1A antara endometriosis non atipikdan atipik dengan CCC ovarii (p=0,001 dan p=0,0015). Pada kelompok kasusendometriosis non atipik, atipik dan endometriosis pada EAOC, didapatkan adaperbedaan bermakna persentase ekspresi ARID1A (Uji Kruskal-Walis p=0,011).Selanjutnya dilakukan analisis Post Hoc uji Mann-Whitney dan ada perbedaanbermakna persentase ekspresi ARID1A antara endometriosis non atipik dan atipikdengan EAOC (p=0,005 dan p=0,008). Kesimpulan: Ekspresi ARID1A pada endometriosis non atipik dan atipik lebihtinggi bermakna dibanding CCC ovarii dan EAOC. Sehingga ekspresi ARID1Akemungkinan dapat digunakan sebagai petanda adanya transformasi ganas padaendometriosis.ABSTRACT Background: Endometriosis is one of the most common gynecologicalabnormalities found. Endometriosis cyst in the ovary also exhibited changes inepithelial cyst just like endometrium in the uterus. Changes in the epithelial cellsalso include metaplasia, hyperplasia, atyphia even changes toward malignancharacteristics. Nowadays, there are some research that linked endometriosis andclear cell ovarian cancer which is known with endometriosis-associated ovariancarcinoma (EAOC) it is reported that there?s a mutation that activated tumorsuppressor gene (ARID1A), so protein BAF250a is not expressed in Clear CellCarcinoma (CCC) in the ovarium.Materials and Methods: Immunohistochemistry staining of ARID1A were donein 20 samples of non-atypical endometriosis, 20 samples of atypicalendometriosis, 20 samples of CCC in the ovarium from the year 2012 until march2015. From the group that experienced CCC we get 9 cases of EAOC. After that,we see if there?s any difference in the percentage of ARID1A expression in nonatypicalendometrosis, atypical endometriosis, CCC in the ovarium andendometriosis with CCC( EAOC).Results: In non-atypical endometriosis, atypical and CCC cases groups there aresignificant differences on the percentage of ARID1A expression (Kruskal-Walistest p=0,0035). Post Hoc analysis were done using Mann-Whitney test and thereare significant differences on ARID1A expression between non-atypical andatypical endometriosis with CCC (p=0,001 and p=0,0015). In non-atypicalendometriosis, atypical and EAOC groups there are significant differences on thepercentage of ARID1A expression (Kruskal-Walis test p=0,011). Post Hocanalysis were done using Mann-Whitney test and there are significant differenceson ARID1A expression between non-atypical and atypical endometriosis withEAOC (p=0,005 and p=0,008).Conclusion: Expression of ARID1A in non atypical and atypical endometriosisare significantly higher compared to ovarian CCC and EAOC. So, we can say thatARID1A may be used as a marker for malignancy transformation inendometriosis.;Background: Endometriosis is one of the most common gynecologicalabnormalities found. Endometriosis cyst in the ovary also exhibited changes inepithelial cyst just like endometrium in the uterus. Changes in the epithelial cellsalso include metaplasia, hyperplasia, atyphia even changes toward malignancharacteristics. Nowadays, there are some research that linked endometriosis andclear cell ovarian cancer which is known with endometriosis-associated ovariancarcinoma (EAOC) it is reported that there?s a mutation that activated tumorsuppressor gene (ARID1A), so protein BAF250a is not expressed in Clear CellCarcinoma (CCC) in the ovarium.Materials and Methods: Immunohistochemistry staining of ARID1A were donein 20 samples of non-atypical endometriosis, 20 samples of atypicalendometriosis, 20 samples of CCC in the ovarium from the year 2012 until march2015. From the group that experienced CCC we get 9 cases of EAOC. After that,we see if there?s any difference in the percentage of ARID1A expression in nonatypicalendometrosis, atypical endometriosis, CCC in the ovarium andendometriosis with CCC( EAOC).Results: In non-atypical endometriosis, atypical and CCC cases groups there aresignificant differences on the percentage of ARID1A expression (Kruskal-Walistest p=0,0035). Post Hoc analysis were done using Mann-Whitney test and thereare significant differences on ARID1A expression between non-atypical andatypical endometriosis with CCC (p=0,001 and p=0,0015). In non-atypicalendometriosis, atypical and EAOC groups there are significant differences on thepercentage of ARID1A expression (Kruskal-Walis test p=0,011). Post Hocanalysis were done using Mann-Whitney test and there are significant differenceson ARID1A expression between non-atypical and atypical endometriosis withEAOC (p=0,005 and p=0,008).Conclusion: Expression of ARID1A in non atypical and atypical endometriosisare significantly higher compared to ovarian CCC and EAOC. So, we can say thatARID1A may be used as a marker for malignancy transformation inendometriosis.;Background: Endometriosis is one of the most common gynecologicalabnormalities found. Endometriosis cyst in the ovary also exhibited changes inepithelial cyst just like endometrium in the uterus. Changes in the epithelial cellsalso include metaplasia, hyperplasia, atyphia even changes toward malignancharacteristics. Nowadays, there are some research that linked endometriosis andclear cell ovarian cancer which is known with endometriosis-associated ovariancarcinoma (EAOC) it is reported that there?s a mutation that activated tumorsuppressor gene (ARID1A), so protein BAF250a is not expressed in Clear CellCarcinoma (CCC) in the ovarium.Materials and Methods: Immunohistochemistry staining of ARID1A were donein 20 samples of non-atypical endometriosis, 20 samples of atypicalendometriosis, 20 samples of CCC in the ovarium from the year 2012 until march2015. From the group that experienced CCC we get 9 cases of EAOC. After that,we see if there?s any difference in the percentage of ARID1A expression in nonatypicalendometrosis, atypical endometriosis, CCC in the ovarium andendometriosis with CCC( EAOC).Results: In non-atypical endometriosis, atypical and CCC cases groups there aresignificant differences on the percentage of ARID1A expression (Kruskal-Walistest p=0,0035). Post Hoc analysis were done using Mann-Whitney test and thereare significant differences on ARID1A expression between non-atypical andatypical endometriosis with CCC (p=0,001 and p=0,0015). In non-atypicalendometriosis, atypical and EAOC groups there are significant differences on thepercentage of ARID1A expression (Kruskal-Walis test p=0,011). Post Hocanalysis were done using Mann-Whitney test and there are significant differenceson ARID1A expression between non-atypical and atypical endometriosis withEAOC (p=0,005 and p=0,008).Conclusion: Expression of ARID1A in non atypical and atypical endometriosisare significantly higher compared to ovarian CCC and EAOC. So, we can say thatARID1A may be used as a marker for malignancy transformation inendometriosis.;Background: Endometriosis is one of the most common gynecologicalabnormalities found. Endometriosis cyst in the ovary also exhibited changes inepithelial cyst just like endometrium in the uterus. Changes in the epithelial cellsalso include metaplasia, hyperplasia, atyphia even changes toward malignancharacteristics. Nowadays, there are some research that linked endometriosis andclear cell ovarian cancer which is known with endometriosis-associated ovariancarcinoma (EAOC) it is reported that there?s a mutation that activated tumorsuppressor gene (ARID1A), so protein BAF250a is not expressed in Clear CellCarcinoma (CCC) in the ovarium.Materials and Methods: Immunohistochemistry staining of ARID1A were donein 20 samples of non-atypical endometriosis, 20 samples of atypicalendometriosis, 20 samples of CCC in the ovarium from the year 2012 until march2015. From the group that experienced CCC we get 9 cases of EAOC. After that,we see if there?s any difference in the percentage of ARID1A expression in nonatypicalendometrosis, atypical endometriosis, CCC in the ovarium andendometriosis with CCC( EAOC).Results: In non-atypical endometriosis, atypical and CCC cases groups there aresignificant differences on the percentage of ARID1A expression (Kruskal-Walistest p=0,0035). Post Hoc analysis were done using Mann-Whitney test and thereare significant differences on ARID1A expression between non-atypical andatypical endometriosis with CCC (p=0,001 and p=0,0015). In non-atypicalendometriosis, atypical and EAOC groups there are significant differences on thepercentage of ARID1A expression (Kruskal-Walis test p=0,011). Post Hocanalysis were done using Mann-Whitney test and there are significant differenceson ARID1A expression between non-atypical and atypical endometriosis withEAOC (p=0,005 and p=0,008).Conclusion: Expression of ARID1A in non atypical and atypical endometriosisare significantly higher compared to ovarian CCC and EAOC. So, we can say thatARID1A may be used as a marker for malignancy transformation inendometriosis."