<![CDATA[ABSTRAK Latar belakang Adenokarsinoma serosum ovarium tipe II (high grade) lebih sering ditemukan dibandingkan tipe I (low grade). Tumor tipe II bersifat agresif, namun lebih sensitif kemoterapi. Hal sebaliknya terjadi pada tumor tipe I. Mutasi p53 berperan dalam patogenesis berbagai jenis keganasan, termasuk organ genitalia wanita. Ki67 terlibat dalam semua fase aktif pada siklus sel (G1, S, G2 dan mitosis). EGFR mengaktifkan jalur sinyal yang menginduksi onkogenesis dan proliferasi sel. Tujuan penelitian ini untuk mengetahui peran p53, Ki67 dan EGFR dalam patogenesis adenokarsinoma serosum ovarium dan peluang penggunaannya sebagai alat bantu diagnostik untuk membedakan tumor tipe I dan tipe II. Metode Penelitian observasional analitik potong lintang, pada 25 kasus adenokarsinoma serosum ovarium dari arsip Departemen Patologi Anatomik FKUI/RSCM 2011-2013, dengan bahan blok parafin. Dilakukan pulasan imunohistokimia p53, Ki67 dan EGFR dengan metode indirect. Pada kedua kelompok dihitung dan dibandingkan persentase positivitas pulasan inti p53 dan Ki-67, serta H score ekspresi EGFR. Hasil Median ekspresi p53, Ki67 dan H score EGFR pada kelompok tipe I adalah 15 (4-50), 15 (5-30), dan 46,5 (30-180); sedangkan pada tipe II adalah 80 (0-90), 20 (10-60), dan 40 (0-160). Perbandingan ekspresi p53, Ki67 dan H score EGFR pada kedua kelompok tumor: p=0,03, 0,37 dan 0,05. Kesimpulan Protein p53 berperan penting dalam patogenesis adenokarsinoma serosum ovarium tipe II (high grade). Ekspresi p53 dapat digunakan untuk membedakan adenokarsinoma serosum tipe II dari tipe I, sedangkan ekspresi Ki67 maupun EGFR tidak. Kata kunci: adenokarsinoma serosum, EGFR, Ki-67, ovarium, p53. ABSTRACK Background Serosum ovarian adenocarcinoma tipe II (high grade) is more common than type I (low grade). Type II tumors are aggressive, but more sensitive to chemotherapy. The opposite occurs in tumor type I. p53 mutation plays a role in the pathogenesis of a variety of malignancies, including female genital organs. Ki67 actively involved in all phases of the cell cycle (G1, S, G2 and mitosis). EGFR activate signaling pathways that induce oncogenesis and cells proliferation. The aim of this study are to determine the role of p53, Ki67 and EGFR in the pathogenesis of serosum ovarian adenocarcinoma and to determine the possibilities to use them as diagnostic tool to differentiate tumor type I and type II. Methods A consecutive cross-sectional observational study, in 25 cases of serosum ovarian adenocarcinoma from archives in Department of Anatomical Pathology Faculty of Medicine University of Indonesia/RSCM 2011-2013, with material paraffin blocks. Indirect immunohistochemical staining of p53, Ki67 and EGFR were performed. Results in both groups were calculated and compared the percentage of core outward positivity p53 and Ki-67, and H scores EGFR expression. Results Median expression of p53 , Ki67 and EGFR score in group H type I was 15 (4-50), 15 (5-30), and 46.5 (30-180); where as in type II was 80 (0-90), 20 (10-60), and 40 (0-160). Comparison of expression of p53, Ki67 and H score of EGFR in both tumor groups: p=0.03, 0.37 and 0.05 . Conclusions P53 protein plays an important role in the pathogenesis of type II serosum ovarian adenocarcinoma (high grade). P53 expression can be used to distinguish the type II adenocarcinoma serosum of type I, neither the EGFR nor Ki-67 expressions can be used. Key words : EGFR, Ki67, ovarian, p53, serosum adenocarcinoma.]]>
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