Hasil Pencarian  ::  Simpan CSV :: Kembali

"Kaitannya dengan ekspresi protein MLH1, MSH2, dan SMAD4, dan membandingkannya dengan pasien kanker kolorektal usia di atas 60 tahun.Metode: Data rekam medis pasien kanker kolorektal usia di bawah 40 tahun dan usia di atas 60 tahun , dikumpulkan dari 3 rumah sakit: Jakarta, Makasar, dan Bandung. Kelompok etnis dipilih dari suku bangsa Jawa, Makasar (Sulawesi Selatan, dan Minangkabau (Sumatera Barat) yang dikonfirmasi berdasarkan kuesioner. Pada spesimen tumor dilakukan pemeriksaan histopatologi, gradasi tumor, serta pemeriksaan imunohistokimia untuk penentuan ekspresi protein MLH1 dan MSH2 untuk menilai mutasi instabilitas mikrosatelit. Ekspresi protein SMAD4 diperiksa untuk memastikan bahwa jaringan tumor tidak berasal dari instabilitas mikrosatelit.Hasil: Telah dikumpulkan 121 penderita kanker kolorektal dari etnis Sunda, Jawa, Makasar, dan Minangkabau. Derajad keganasan antara pasien muda dan pasien tua berbeda secara bermakna (p = 0.001). Pewarnaan imunohistokimia untuk protein MSH2 dan MLH1 yang dilakukan pada masing-masing 92 dan 97 pasien, menunjukkan tidak terdapat perbedaan bermakna dalam hal ekspresi MLH1 dan MSH2 dan gradasi tumor, yang berarti tidak ada hubungan antara instabilitas mikrosatelit dan derajad tumor.Kesimpulan: Karakter kliniko patologi kanker kolorektal pada penduduk asli Indonesia, tidak berbeda antara pasien usia muda (< 40 tahun) dan pasien usia tua (>60 tahun) pada kelompok etnis yang sama. Juga tidak terdapat perbedaan dalam ekspresi protein MSH2 dan MLH1, yang merupakan indikator instabilitas mikrosatelit.

---

Aim: To obtain clinicopathological characteristics of colorectal cancer among young native Indonesians and to assess MLH1, MSH2, and SMAD4 protein expressions, comparing them with a matched population of colorectal cancer patients aged 60 years old and older.

Methods: Medical records of colorectal cancer patients aged 40 years or younger and 60 years or older from several hospitals in three Indonesian cities ? Jakarta, Makassar, and Bandung - were reviewed. The ?native? ethnic groups were selected from those originating from Java, Makassar (South Celebes), Miinangkabau (West Sumatra). Ethnicity of 121 colorectal carcinoma patients was confirmed by fulfilling requirements in a questionnaire. Tumor specimens of those patients underwent evaluation for histopathology, tumor grading as well as immunohistochemical analysis to assess MLH1, MSH2 protein expressions to detect microsatellite instability mutation pathway and SMAD4 protein expression to reconfirm that the specimens were not microsatellite instability origin.

Results: There were 121 colorectal carcinoma cases of Sundanese, Javanese, Macassarese and Minangkabau ethnic group. This study indicated that colorectal cancer has statistically different grade (p = 0.001) between the young and the older patients. Immunohistochemical staining for MSH2 protein and MLH1 were done for 92 and 97 specimens respectively. There was no significant difference between the expressions of MLH1 and MSH2 on tumor grading, indicated there was no correlation between microsatellite instability and tumor grading in this study.

Conclusion: Colorectal cancer in young native Indonesian patients (40 years old or less) was not different in clinicopathological characteristics compared to older patients (60 years old or more) in similar ethnic groups. There was also no difference in MSH2 and MLH1 protein expressions, important indicators of microsatellite instability."

"ABSTRAK Latar Belakang :Karsinoma kolorektal (KKR) merupakan penyebab kematian kedua di dunia dari seluruh jeniskanker. KKR dapat disebabkan oleh defek dari MMR DNA. Microsatellite instability (MSI)adalah penanda defek MMR DNA. KKR MSI-H memiliki gambaran karakteristik tertentu.Tumor-infiltrating-lymphocyte (TIL) merupakan faktor prognosis. Hilangnya ekspresi PMS2 danMSH6 dapat sebagai penanda MSI. Penelitian ini bertujuan untuk menilai terjadinya MSI padaKKR di sisi kiri dan sisi kanan kolon melalui Hilangnya ekspresi PMS2 dan MSH6, sertamengetahui hubungan antara TIL dengan MSI-H.Bahan dan Metode :Dilakukan pulasan IHK PMS2 dan MSH6, serta penghitungan TIL. Penilaian dilakukan denganmenghitung hilangnya ekspresi PMS2 dan MSH6 pada inti sel dan dikelompokkan ke dalamkelompok mutasi dan tidak mutasi .Penghitungan TIL juga dikelompokkan ke dalam TIL tinggidan rendah, berdasarkan nilai titik potong Hasil : Didapatkan 27,8% kasus menunjukkan hilangnya ekspresi PMS2 dan MSH6 dengan 14,4%kasus di distal kolon. TIL terbanyak di distal kolon 30% kasus. Tidak terdapat perbedaanbermakna antara mutasi PMS2 dan MSH6 dengan lokasi (p=0,829) dan TIL (p=0,187). Terdapatperbedaan bermakna antara usia dan lokasi (p=0,020) serta peningkatan ekspresi PMS2 denganMSH6 (p=0,06).Kesimpulan :MSI-H ditemukan pada 27,8% kasus. Penggunaan PMS2 dan MSH6 pada penelitian ini belumdapat menggantikan 4 panel IHK. Terdapat kecenderungan dimana adenokarsinoma NOSmemiliki frekuensi mutasi lebih tinggi dari adenokarsinoma musinosum.ABSTRACT Background : Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. ;Background :Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. ;Background :Colorectal carcinoma (CRC) is the world second leading cause of death from all types of cancer.CRC can be caused by a defect of MMR DNA. Microsatellite instability (MSI) is a marker ofDNA MMR defect. CRC MSI-H has a certain characteristic figures. Tumor-infiltratinglymphocytes (TIL) isone of prognostic factor. Loss expression of the PMS2 and MSH6 can beuse as a marker of MSI. This study aims to assess the occurrence of MSI in CRC on the left sideand the right side of the colon through the loss of expression of PMS2 and MSH6, anddetermine the relationship between TIL with MSI-H. Materials and Methods :Immunohistochemical staining using two marker, there is PMS2 and MSH6. We also countingthe number of TIL. Assessment by calculating the loss expression of PMS2 and MSH6 in the cellnuclei and divided into two groups, the mutations and non mutations . TIL result also groupedinto high and low, based on the cutoff point. Result :There are 27.8% of cases showed loss of expression of PMS 2 and MSH6 with 14.4% of cases inthe distal colon. About 30% TIL cases located in distal colon. There were no significantdifferences between PMS2 and MSH6 mutation with the location (p = 0.829) and TIL (p =0.187). There are significant differences between age and location (p = 0.020) and increasedexpression of PMS2 with MSH6 (p = 0.06). \ Conclusion :MSI-H was found in 27.8% of cases. The use of PMS2 and MSH6 in this study have not beenable to replace 4 panels of IHC. There is a tendency where the adenocarcinoma NOS have ahigher mutation frequency than mucinous adenocarcinoma. "

"Latar belakang: Pada kanker nasofaring, tingginya angka kegagalan metastasis jauh paska terapi masih menimbulkan masalah. Sehingga, penelitian mengenai penggunaan terapi sistemik novel pada kanker nasofaring seperti imunoterapi perlu dilakukan. Terdapat beberapa biomarker yang dapat diperiksa untuk dapat memprediksi respon dari pemberian imunoterapi, salah satunya adalah microsatellite instability (MSI). Mikrosatelit merupakan area pada DNA yang memiliki banyak pengulangan kodon, sehingga rentan terjadi gangguan coding dan mengakibatkan akumulasi mutasi. Pada keadaan normal, kerusakan ini akan diperbaiki dengan sistem mismatch repair. Namun, jika terdapat gangguan atau mutasi terkait sistem ini, atau yang disebut dengan deficient mismatch repair (dMMR), akan menghasilkan fenotipe MSI. Pada kanker kolorektal dan endometrium. Namun sampai saat ini, hanya terdapat 3 penelitian yang melakukan pemeriksaan status MSI pada kanker nasofaring. Penelitian ini bertujuan untuk melihat gambara status MSI pada pasien kanker nasofaring pada pasien di RSCM, Indonesia.Metode: Penelitian ini merupakan penelitian eksploratif dengan 36 subjek penelitian. Dilakukan pemeriksaan status instabilitas mikrosatelit menggunakan pemeriksaan berbasis polymerase chain reaction (PCR) Idylla MSI. Dilakukan pula pemeriksaan MMR menggunakan pemeriksaan berbasis imunohistokimia (IHK) menggunakan 4 antibodi untuk mendapatkan keselerasan antara pemeriksaan MSI dan MMR pada pasien kanker nasofaring di RSCM.Hasil : Menggunakan pemeriksaan Idylla MSI, ditemukan MSI pada 2 dari 36 pasien (5,6%) dan dMMR menggunakan pemeriksaan IHK pada 3 dari 36 pasien (8,34%). Hasil yang konsisten ditemukan pada 2 metode pemeriksaan sebesar 96,97%.Kesimpulan: Pada kanker nasofaring ditemukan frekuensi MSI yang rendah baik menggunakan pemeriksaan IHK dan Idylla MSI. Ditemukan keselerasan yang tinggi antara pemeriksaan berbasis IHK dan pemeriksaan berbasis PCR Idylla MSI.

---

Background: Despite high probability of local control after treatment, high rate of distant metastases-failure still pose as problem in the management of locally advanced nasopharyngeal carcinoma. Thus, research for novel systemic therapies for nasopharyngeal cancer, such as immunotherapy, needs to be done. There are several biomarkers that may predict the response to immunotherapy, one of which is microsatellite instability (MSI) phenotype. Microsatellites defined by areas in DNA that are prone to mutations due to repetition of 1-3 nitrogen base. However, under normal circumstances, there are repair systems that can identify and correctly repairs DNA mutations in microsatellite area, a system called mismatch repair (MMR) system. Microsatellite instability is a condition of accumulating mutations in microsatellite area due to defect in MMR system. In colorectal and endometrial cancer, MSI are known as one of prognostic and predictive markers, especially with the usage of immunotherapy immune checkpoint blockade PD-1/PD-L1. To this date, only 3 studies are available in exploring the role of MSI in nasopharyngeal cancer, and no study was done in Indonesia. We conduct this study to assess the MSI status of Indonesia's nasopharyngeal cancer patients in Ciptomangunkusumo Hospital.

Methods: This is the first explorative study in exploring the role of MSI in Indonesia's nasopharyngeal cancer patients. A total of 36 subjects were recruited, and both MSI assessment using immunohistochemistry (IHC) and polymerase chain reaction (PCR) Idylla MSI was done on all study subjects.

Results: MSI was found in 2 patients (5,6%) using PCR based Idylla MSI, and dMMR was found in 3 patients (8,34%). Consistent results between IHC and PCR based MSI assessment was found in 32 patients (96,97%).

Conclusion: MSI was a rare event in Indonesia's nasopharyngeal cancer patients. High concordance was found between IHC and PCR MSI assessment in nasopharyngeal cancer."

"Latar belakang: Penderita kanker ovarium umumnya datang berobat pada stadium lanjut, sehingga kekambuhan pasca pembedahan dan pemberian kemoterapi mencapai 70-80%. EGFR mengaktifkan jalur sinyal yang menginduksi onkogenesis dan proliferasi sel. Tujuan penelitian ini adalah untuk menganalisis peran EGFR dalam patogenesis tumor serosum ovarium dan peluangnya untuk digunakan sebagai penanda keganasan.Metode: Penelitian ini menggunakan metode potong lintang. Sampel terdiri atas 15 kasus tumor jinak, 15 kasus borderline dan 15 kasus adenokarsinoma di Departemen Patologi Anatomik FKUI/RSCM tahun 2008-2012. Dilakukan pulasan imunohistokimia EGFR dan penilaian dengan H score.Hasil: Terdapat perbedaan ekspresi EGFR yang bermakna antara kelompok tumor serosum jinak (H score = 15), borderline (H score = 60) dan adenokarsinoma (H score = 120), dengan p=0,000.Kesimpulan. Ekspresi EGFR pada tumor serosum ovarium meningkat seiring peningkatan derajat keganasan.

---

Background: Most of ovarian cancer patients are diagnosed in already advanced stage, therefore 70-80% of cases having recurrence after surgical staging and chemotherapy. EGFR activates signaling pathways which induce oncogenesis and cell proliferation. The aim of this study is to analyze the role of EGFR in the pathogenesis of serous ovarian tumors and its possibility to be used as a malignant marker.Methods: This was a cross-sectional study on each 15 cases of benign, borderline and malignant serous ovarian tumors from Anatomical Pathology Department FMUI/CMH in 2008-2012. EGFR status was assessed by immunohistochemistry technique and the expression was evaluated using H score.Results: There was significant difference between EGFR expression in benign (H score = 15), borderline (H score = 60) and malignant serous ovarian tumors (H score = 120), p=0,000.Conclusion: The EGFR immunoexpression was increased along with the higher degree of serous ovarian tumor malignancy."

"Tujuan: Mengetahui pengaruh mutasi patogenik BRCA1/2 tumor terhadap kesintasan pasien advanced stage-high grade serous epithelial ovarian cancer di RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, dan RS MRCCC Siloam Jakarta.Metode: Sejumlah 68 sampel dari 144 pasien diagnosis high-grade serous epithelial ovarian cancer (HGSOC) stadium FIGO IIB-IV, periode 1 Januari 2015 sampai 31 Maret 2021, di RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, dan RS MRCCC Siloam Jakarta, menjalani pemeriksaan NGS mutasi patogenik BRCA1/2 tumor, dilibatkan dalam penelitian kohort historikal ini. Kami membandingkan karakteristik klinikopatologis pasien, dan hasil luaran kesintasan, setelah pasien menjalani tatalaksana primer, berdasarkan status mutasi patogenik BRCA1/2 tumor. Faktor terkait tatalaksana, yang diperkirakan berpengaruh terhadap hasil luaran kesintasan pasien, juga turut dianalisis dalam penelitian ini.Hasil: Angka kejadian mutasi patogenik BRCA1/2 tumor diketahui sebesar 27,94% (19/68). Antara kelompok mutasi patogenik BRCA1/2 tumor, dengan kelompok tanpa mutasi patogenik, tidak terdapat perbedaan statistik signifikan berdasarkan usia, paritas, indeks massa tubuh (kg/m2), riwayat kanker payudara, stadium FIGO 2014, kadar CA125 serum pre operatif (U/mL), volume cairan ascites intra operatif (mL), lesi residual pasca laparotomi debulking, pemberian neoadjuvant chemotherapy (NACT), pemberian kemoterapi adjuvant. Riwayat kanker keluarga terkait HBOC, merupakan variabel paling berpengaruh terhadap mutasi patogenik BRCA1/2 tumor. Kelompok dengan riwayat kanker keluarga terkait HBOC, berisiko 5,212 kali lebih besar mengalami mutasi patogenik BRCA1/2 tumor, dibandingkan dengan kelompok tanpa riwayat kanker tersebut (RR adjusted 5,212; 95%CI 1,495-18,167; nilai p=0,010).Pada kelompok mutasi patogenik BRCA1/2 tumor, kemungkinan meninggal 86% lebih rendah (RR adjusted 0,149; 95%CI 0,046-0,475; nilai p=0,001), dan median survival yang lebih baik (median 46 bulan; 95%CI 34,009-57,991; nilai p=0,001), apabila dibandingkan dengan kelompok tanpa mutasi patogenik (median 23 bulan; 95%CI 15,657-30,343; nilai p=0,001). Analisis multivariat menunjukkan mutasi patogenik BRCA1/2 tumor merupakan faktor prognostik independen yang baik terhadap hasil luaran kesintasan (RR adjusted 0,149; 95%CI 0,046-0,475; nilai p=0,001).Kesimpulan: Pasien advanced stage-high grade serous epithelial ovarian cancer, dengan mutasi patogenik BRCA1/2 tumor, memiliki kesintasan lebih baik, dibandingkan pasien tanpa mutasi patogenik BRCA1/2 tumor.

---

Objective: To evaluate the impact of pathogenic BRCA1/2 tumor mutational status on advanced stage- high grade serous epithelial ovarian cancer survival outcome at RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, and RS MRCCC Siloam Jakarta.

Methods: A total 68 of 144 patients diagnosed with FIGO 2014 stage IIB-IV high grade serous epithelial ovarian cancer (HGSOC) between January 1st, 2015 until March 31st, 2021, at RSUPN Dr. Cipto Mangunkusumo, RSUP Persahabatan, and RS MRCCC Siloam Jakarta, underwent NGS tumor BRCA1/2 gene testing, and were included in this cohort hystorical study. We compared patients clinicopathological characteristics, and survival outcomes after primary treatment, according to pathogenic BRCA1/2 tumor mutational status. Treatment-related factors that might affect patients’ survival outcome were also investigated.

Results: The BRCA1/2 pathogenic tumor mutations prevalence was observed in this study 27.94% (19/68). There were no significant statistical differences in age, parity, body mass index (kg/m2), previous breast cancer history, FIGO 2014 staging, pre-operative serum CA 125 level (U/mL), intra operative ascites volume (mL), post cytoreductive surgery residual lesion, neoadjuvant chemotherapy (NACT), and adjuvant chemotherapy administration, between the pathogenic tumor BRCA1/2 mutation, and no pathogenic tumor BRCA1/2 mutation groups. The hereditary breast ovarian cancer family history (HBOC) variable has the strongest correlation with pathogenic tumor BRCA1/2 mutation. The group with a family history of HBOC-related cancer had a 5.212 times greater risk of developing pathogenic BRCA1/2 tumor mutations, compared with the group without a history of those cancer (RR adjusted 5.212; 95%CI 1.495-18.167; p value=0.010).

The pathogenic BRCA1/2 tumor mutation group displayed better survival outcome. In the pathogenic BRCA1/2 tumor mutation group, the likelihood of dying was 86% lower (RR adjusted 0.149; 95%CI 0.046-0.475; p-value=0.001), and the median survival was better (median 46 months; 95%CI 34.009- 57.991; p value=0.001), than without pathogenic BRCA1/2 tumor mutations group (median 23 months; 95%CI 15.657-30.343; p value=0.001). The multivariate analyses identified pathogenic BRCA1/2 tumor mutation as an independent favorable prognostic factor for survival outcome (RR adjusted 0.149; 95%CI 0.046-0.475; p-value=0.001).

Conclusions: In advanced stage-HGSOC, patients with pathogenic BRCA1/2 tumor mutations have a better prognosis with longer survival outcome than those without pathogenic BRCA1/2 tumor mutations."

"Latar belakang Sisplatin merupakan pengobatan utama untuk karsinoma nasofaring KNF , tetapi berpotensi menimbulkan nefrotoksisitas. Selain kadar BUN dan kreatinin serum, KIM-1 dan NGAL diduga cukup sensitif untuk mendeteksi nefrotoksisitas. Penelitian ini bertujuan untuk mengevaluasi kadar KIM-1 dan NGAL dalam urin untuk mendeteksi gangguan fungsi ginjal pada pasien KNF stadium lanjut yang mendapatkan kemoterapi berbasis sisplatin.Metode: Penelitian ini merupakan penelitian kohort prospektif. Subyek penelitian dibagi dalam 3 kelompok: pasien yang belum pernah terpapar dan yang sudah pernah mendapatkan kemoterapi berbasis sisplatin 75-100 mg/m serta pasien yang belum pernah mendapatkan kemoterapi sisplatin dan kemudian diberi sisplatin 40 mg/m 2 . Kadar KIM-1, NGAL dalam urin serta kadar BUN dan kreatinin dalam serum diukur pada saat sebelum dan sesudah mendapatkan sisplatin pada ketiga kelompok. Analisis statistik yang digunakan adalah uji ANOVA, uji Pearson, Spearman, Kolmogorov-Smirnov dan SPSS versi 22,0.Hasil: Terdapat perbedaan selisih kadar BUN yang bermakna antara sebelum dan sesudah diterapi pada ketiga kelompok p=0.0001 . Perbedaan selisih kadar NGAL dalam urin pada penelitian ini juga berbeda bermakna antara sebelum dan sesudah diterapi terhadap ketiga kelompok p=0,025 , tetapi ada perbedaan rerata pada sepasang kelompok yang bermakna hanya didapatkan pada kelompok yang belum pernah dikemoterapi 40 mg/m 2 dan kelompok yang sudah pernah diberi kemoterapi 75-100 mg/m 2 p=0,02. Perbedaan selisih kadar KIM-1 tidak bermakna pada ketiga kelompok p=0,275.Kesimpulan: Sisplatin menunjukkan akumulasi nefrotoksisitas yang tergantung pada dosis dose-dependent manner . Pengukuran kadar NGAL dalam urin dapat mendeteksi nefrotoksisitas tahap dini, tetapi belum bisa menggantikan peran BUN. Pengukuran kadar KIM-1 dalam urin tidak dapat mendeteksi gangguan fungsi ginjal.

---

Background: Cisplatin is the main treatment for nasopharyngeal carcinoma NPC with a potency of causing nephrotoxicity. In addition to serum BUN and creatinine levels, KIM 1 and NGAL levels is assumed to be quite sensitive in detecting nephrotoxicity. The study was aimed to evaluate urinary KIM 1 and NGAL level to detect kidney dysfunction in patients with advanced stage NPC who received cisplatin based chemotherapy.

Method: The study was a cohort prospective study. Subjects were categorized into 3 groups, i.e. patients who had never received and who had received 75 100 mg m2 cisplatin based chemotherapy as well as those who had never received any cisplatin based chemotherapy and were subsequently received 40 mg m cisplatin. The levels of urinary KIM 1, NGAL and serum level of BUN and creatinine were measured before and after receiving cisplatin in the three groups. Statistical analysis used in our study were ANOVA, Pearson, Spearman, KolmogorovSmirnov test and SPSS version 22.0.

Results: There was a significant difference of delta BUN level before and after treatment in all three groups p 0.0001 . Delta urinary NGAL level was also significantly different between before and after treatment in all groups p 0.025 however, a significant mean difference of a pair group was only found between those who never had 40 mg m 2 chemotherapy and those who had received 75 100 mg m 2 chemotherapy p 0.02 while delta KIM 1 level showed no significant difference in all three groups p 0.275.

Conclusion: Cisplatin may cause accumulated nephrotoxicity, which has dosedependent manner. Measuring urinary NGAL level can detect an early stage of kidney dysfunction however, it still cannot replace the role of BUN. Measurement of urinary KIM 1 level cannot detect kidney dysfunction."

"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.

---

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."