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All Journal Medical Journal of Indonesia Damianus Journal of Medicine Indonesian Journal of Cancer The New Ropanasuri Journal of Surgery Generics: Journal of Research in Pharmacy

Rianto Setiabudy

Department of Pharmacology, Faculty of Medicine, Universitas Indonesia, Jakarta

Author-ID : 376426

Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology Public Health

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Evaluation of Kidney Injury Molecule-1 (KIM-1) and Neutrophil Gelatinase-Associated Lipocalin (NGAL) Urinary Levels for Detecting Kidney Dysfunction in Patients With Nasopharyngeal Cancer Treated With Cisplatin-Based Treatment Rejeki, Marliana Sri; Arozal, Wawaimuli; Setiabudy, Rianto; Atmakusuma, Djumhana
Indonesian Journal of Cancer Vol 12, No 2 (2018): April-June
Publisher : National Cancer Center - Dharmais Cancer Hospital

Background: Cisplatin has a potency of causing nephrotoxicity. Serum BUN and creatinine levels have been well-known for detecting kidney dysfunction; while KIM-1 and NGAL urine levels are relatively new measurements. 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.Methods: The study was a cohort-prospective study with 3 subject 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 40 mg/m2 cisplatin-based chemotherapy. The levels of urinary KIM-1, NGAL and serum level of BUN and creatinine were measured before and after receiving cisplatin. Statistical analyses were ANOVA, Pearson, Spearman, Kolmogorov-Smirnov test and SPSS version 22.0.Result: There was a significant difference of delta BUN level (p=0.0001) and delta urinary NGAL level (p = 0.025) before and after treatment in all three groups; while delta KIM-1 level showed no significant difference in all three groups (p=0.275). Cisplatin may cause accumulated nephrotoxicity, which has dose-dependent manner.Conclusion: 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.

Steroid response as prognostic factor and its correlation with molecular assessment of childhood acute lymphoblastic leukemia Andriastuti, Murti; Gatot, Djajadiman; Wirawan, Riadi; Setiabudy, Rianto; Mansyur, Muchtaruddin; Ugrasena, I Dewa G.
Medical Journal of Indonesia Vol 24, No 4 (2015): December
Publisher : Faculty of Medicine Universitas Indonesia

Background: Survival rate of children with acute lymphoblastic leukemia (ALL) in Indonesia remains low. Risk stratification accuracy is important to improve survival. In developed countries, risk stratification is determined based on gene fusion that is known related to steroid resistency. Steroid response at day-8 correlates with prognosis. The assessment can be applied in centers that cannot perform molecular assessment. This study aims to evaluate whether steroid response correlated to molecular assessment. Methods: A cross-sectional study was performed at Child Health Department, Cipto Mangunkusumo Hospital (January 2013-March 2014), a total of 73 patients were enrolled. Steroid was given for 7 days. Peripheral blast count at day 8 was evaluated, good response if blast count <1000 /µL and poor if ≥1000 /µL. Fusion gene detection was also performed. The data was analysed using Statistical Package for Social Sciences (SPSS) version 20.0.Results: Fusion gene was detected in 45 patients. In 1–10 years age group, 26/32 (81%) subjects had good response, while 75% in <1 year age group and 7/9 (78%) in ≥10 years age group had poor response. 5/7 (71%) subjetcs had leukocyte count >100,000 /µL and 7/8 (88%) with T-cell showed poor response. Age, leukocyte count, and T-cell were statistically correlated with steroid response (p<0.05). E2A-PBX1 fusion gene was the most common 19/45 (42%), followed by TEL-AML1 17/45 (38%), BCR-ABL 5/45 (17%), and MLL-AF4 1/45 (3%). Four of five subjects (80%) with BCR-ABL and one subject with MLL-AF4 had poor steroid response. On the other hand, 12/19 (63%) with E2A-PBX1 and 13/17 (77%) with TEL-AML1 had good response. There was no correlation between steroid response and molecular assessment.Conclusion: Steroid response correlates with age, leukocyte count, and T-cell but not with molecular assessment.

Knock-out transmembrane prostate androgen-induced protein gene suppressed triple-negative breast cancer cell proliferation Wardhani, Bantari W.K.; Puteri, Meidi U.; Watanabe, Yukihide; Louisa, Melva; Setiabudy, Rianto; Kato, Mitsuyasu
Medical Journal of Indonesia Vol 26, No 3 (2017): September
Publisher : Faculty of Medicine Universitas Indonesia

Background: Triple negative breast cancer (TNBC) tends to grow more rapidly and has poorer prognosis compared to others. High expression of transmembrane prostate androgen-induced protein (TMEPAI) correlates with poor prognosis in TNBC patients. However, the mechanistic role of TMEPAI in tumorigenic remains unknown. This study aimed to knock-out TMEPAI in TNBC cell line to determine its function further in cells proliferation.Methods: CRISPR-Cas9 has been used previously to knock-out TMEPAI in Hs857T TNBC cell line. Hs587T TNBC parental cell line (wild-type/WT) and TMEPAI knock out Hs 586T cell lines were cultured in Dulbecco’s modified eagle medium (DMEM) supplemented with 10% fetal bovine serum, 1% penicillin-streptomycin and amphotericin B. Both cell lines were seeded in 24-well plates and counted every two days, then proliferation rates were plotted. Afterwards, total RNA were isolated from the cells and Ki-67, and TGF-β mRNA expression levels as proliferation markers were determined.Results: Cell proliferation rates as displayed in growth curve plots showed that WT-TMEPAI cell line grew more rapidly than KO-TMEPAI. In accordance, mRNA expression levels of Ki-67 and TGF-β were significantly decreased KO-TMEPAI as compare to TMEPAI-WT.Conclusion: Knock-out of TMEPAI attenuates cell proliferation in TNBC.

TMEPAI genome editing in triple negative breast cancer cells Wardhani, Bantari W.K.; Puteri, Meidi U.; Watanabe, Yukihide; Louisa, Melva; Setiabudy, Rianto; Kato, Mitsuyasu
Medical Journal of Indonesia Vol 26, No 1 (2017): March
Publisher : Faculty of Medicine Universitas Indonesia

Background: Clustered regularly interspaced short palindromic repeats/CRISPR-associated 9 (CRISPR/Cas9) is a powerful genome editing technique. It consists of RNA-guided DNA endonuclease Cas9 and single guide RNA (gRNA). By combining their expressions, high efficiency cleavage of the target gene can be achieved, leading to the formation of DNA double-strand break (DSB) at the genomic locus of interest which will be repaired via NHEJ (non-homologous end joining) or HDR (homology-directed repair) and mediate DNA alteration. We aimed to apply the CRISPR/Cas9 technique to knock-out the transmembrane prostate androgen-induced protein (TMEPAI) gene in the triple negative breast cancer cell line.Methods: Designed gRNA which targets the TMEPAI gene was synthesized, annealed, and cloned into gRNA expression vector. It was co-transfected into the TNBC cell line using polyethylenimine (PEI) together with Cas9-GFP and puromycin resistant gene vector. At 24-hours post-transfection, cells were selected by puromycin for 3 days before they were cloned. Selected knock-out clones were subsequently checked on their protein levels by western blotting.Results: CRISPR/Cas9, a genome engineering technique successfully knocked-out TMEPAI in the Hs578T TNBC cell line. Sequencing shows a frameshift mutation in TMEPAI. Western blot shows the absence of TMEPAI band on Hs578T KO cells.Conclusion: TMEPAI gene was deleted in the TNBC cell line using the genomic editing technique CRISPR/Cas9. The deletion was confirmed by genome and protein analysis.

The Role of Melatonin in Improving Hypoxia in Malignant Tumor: A Mini-Review Kartini, Diani; Taher, Akmal; Panigoro, Sonar S.; Setiabudy, Rianto; Jusman, Sri W; Haryana, Sofia M; Abdullah, Murdani; Rustamadji, Primariadewi
The New Ropanasuri Journal of Surgery
Publisher : UI Scholars Hub

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KADAR 2,3-DINOR-6-KETO-PROSTAGLANDIN-F1 DALAM URIN WANITA PASCAMENOPAUSE ALAMI DAN PRAMENOPAUSE YANG MINUM ASPIRIN 100 MG Arieselia, Zita; Setiawati, Arini; Setiabudy, Rianto; Baziad, Ali
Bahasa Indonesia Vol 10 No 2 (2011): Damianus Journal of Medicine
Publisher : Atma Jaya Catholic University of Indonesia

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Background: The prevalence of cardiovascular diseases in women increases sharply after menopause. In postmenopausal women, thromboxane production increases while prostacyclin production decreases. Low dose aspirin (75- 150 mg) has long been known as an antiplatelet aggregator. Aspirin reduces the production of both thromboxane (potent thrombocyte aggregator and vasoconstrictor) and prostacyclin (anti thrombocyte aggregator and potent vasodilator).Methods: The present study was an open-label clinical trial with 2 parallel groups. One group consisted of 15 premenopausal women (age > 40 years) while the other group 15 postmenopausal women (for 3 - 5 years). Twenty-four hours urine was collected from each subject before and after aspirin 100 mg daily for 7 days. The concentration of prostacyclin was measured as its metabolite (2,3-dinor-6-keto-prostaglandin-F1) in urine using EIA (Enzyme Immunoassay). Thromboxane as its urinary metabolites (11-dehidrotromboksan-B2) was also measured in these same urine samples in the previous study.Results: Previous study showed that aspirin significantly reduced thromboxane in both groups, with significantly larger percentage reduction in postmenopausal women compared to premenopausal women. Results of the present study showed that aspirin reduced prostacyclin significantly in both premenopausal women (mean difference = 78.44 ng/g creatinine; p = 0.001) and postmenopausal women (mean difference = 35.71 ng/g creatinine; p <0.001), but the percentage reduction between the groups was not significantly different (46,26% vs. 40,94%; p = 0,574). The decrease in thromboxane and prostacyclin should be compared (as the decrease in the ratio of 11-dehidrotromboksan-B2 / 2,3-dinor-6-keto-prostaglandin-F1) to assess aspirin efficacy as an antithrombotic. Calculation of the ratio of 11-dehidro-tromboksanB2 / 2,3-dinor-6-keto-prostaglandin-F1 before aspirin consumption was much higher in postmenopausal women compared to that in premenopausal women (4.09 vs. 1.13; p = 0.001). The decrease in 11-dehidro-tromboksan-B2 / 2,3- dinor-6-keto-prostaglandin-F1? ratio by aspirin was found much larger in postmenopausal women compared to that in premenopausal women (1.91 vs.0.17; p = 0.022).Conclusions: It was concluded that aspirin reduced prostacyclin significantly in each group with nonsignificant percentage reduction between groups, but reduced the 11-dehidro-tromboksan-B2/2,3-dinor-6-keto-prostaglandin-F1? ratio much larger in post-menopausal women compared to that in premenopausal women.

Implikasi Klinis Variasi Jumlah Copy Gen CYP2D6 Gayatri, Anggi; Ascobat, Purwantyastuti; Setiabudy, Rianto
Generics: Journal of Research in Pharmacy Vol 3, No 2 (2023): Generics: Journal of Research in Pharmacy, Volume 3, Edisi 2, 2023
Publisher : Faculty of Medicine, Diponegoro University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14710/genres.v3i2.19085

Enzim CYP2D6 adalah salah satu varian sitokrom P450 (CYP450) yang berperan dalam metabolisme obat di hati. Isoform ini berperan dalam memetabolisme 25% obat yang saat ini beredar di pasaran. Aktivitas CYP450 dapat dipengaruhi oleh berbagai faktor seperti usia, jenis kelamin, fungsi organ pemetabolisme, jenis dan derajat penyakit, serta variasi genetik. Salah satu faktor penentu aktivitas CYP2D6 adalah sifat gene CYP2D6 yang sangat polimorfik. Faktor penentu polimorfisme gen CYP2D6 adalah mutasi pada nukleotida tunggal (single nucleotide polymorphisms (SNPs)) dan variasi jumlah copy (copy number variation (CNV)) gen CYP2D6. Kejadian mutasi gen dan variasi jumlah copy gen CYP2D6 dapat meningkatkan atau menurunkan aktivitas enzim CYP2D6 yang selanjutnya dapat menurunkan atau meningkatkan efikasi obat yang merupakan substrat CYP2D6 ataupun dapat menimbulkan toksisitas obat. Berbagai penelitian telah dilakukan untuk mengevaluasi hubungan mutase SNPs gen CYP2D6 dengan efek obat. Dalam tinjauan kali ini akan dibahas mengenai pengaruh variasi jumlah copy (copy number variation) gen CYP2D6 terhadap efek terapi ataupun efek samping obat.

Co-Authors Adi K Aman, Adi K Ahmad Sulaeman Akmal Taher Ali Baziad Ali Sulaiman Alida Harahap Arini Setiawati Aru W Sudoyo Ascobat, Purwantyastuti Bernardus Philippi Beti E. E Dewi, Beti E. E Cosphiadi Irawan Daldiyono H Dalima A.W. Astrawinata Dewi Muliaty Diani Kartini Djajadiman Gatot Djumhana Atmakusuma, Djumhana Frans D. Suyatna Gayatri, Anggi Harry Isbagyo, Harry Haryana, Sofia M Hidayati, Anggi Puspa Nur Husniah Th-Akib I Dewa Gede Ugrasena Imam Effendi Indra Kusuma INDRAYANI, LENNY Inge A. Kristanti Instiaty, Instiaty Irawan Yusuf Iwan Darmansjah Jason Sriwijaya Johannes Hudiono Jusman, Sri W Kato, Mitsuyasu Laurentius A. Lesmana Lina Lasminingrum Madoka Takeuchi Marulam M. Panggabean Masahiro Takeuchi Melva Louisa Muchtaruddin Mansyur Murdani Abdullah Murti Andriastuti, Murti Nafrialdi Nafrialdi Nurul Akbar Nuzirwan Acang Primariadewi Rustamadji Priyono, Harim Puteri, Meidi U. Putri, Pingkan Permata Rahajuningsih Dharma Rejeki, Marliana Sri Restuti, Ratna Dwi Riadi Wirawan Rikarni Rikarni Robby Zulkarnain Saukani Gumay Septelia I. Wanandi Sjaifoellah Noer Soehartati Gondowiardjo Sonar S. Panigoro Suyanto Sidik Tambunan L Tambunan, Tambunan L Toar J.M. Lalisang Unggul Budihusodo Vera Yuwono Vivian Soetikno Wardhani, Bantari W.K. Watanabe, Yukihide Wawaimuli Arozal Yefta Moenadjat Zita Arieselia

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