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"Latar Belakang: Survivin merupakan inhibitor protein apoptosis yang diekspresikan sangat tinggi pada kanker payudara dan berkaitan dengan agresivitas kanker yang ditandai oleh progresi cepat dan prognosis buruk. Peran utama survivin adalah untuk mengatur pembelahan sel dan mencegah apoptosis. Namun, mekanisme survivin lainnya sangat kompleks dan belum sepenuhnya dipahami. Tujuan dari penelitian ini adalah untuk mengevaluasi efek knockout survivin terhadap agresivitas kanker yang berkaitan dengan mekanisme proliferasi, apoptosis, stemness, respons stres seluler, dan metastasis, serta volume nodul tumor payudara.Metode: Sistem CRISPR/Cas9 digunakan untuk knockout survivin pada studi in vitro dan in vivo. Pada studi in vitro, sel knockout dan wild–type digunakan untuk menganalisis efek hilangnya survivin dalam berbagai mekanisme biologis. Protein yang berkaitan dengan apoptosis, pluripotensi, dan stres seluler diperiksa menggunakan proteomik array. Siklus sel, apoptosis, dan ekspresi penanda sel punca kanker payudara dianalisis menggunakan flowcytometry. Penanda yang berkaitan dengan metastasis dievaluasi melalui qRT‒PCR. Pada studi in vivo, plasmid CRISPR/Cas9 diberikan melalui injeksi intratumor sebanyak tiga kali dengan rentang tiga hari antar injeksi. Tikus dikorbankan 14 hari setelah injeksi terakhir, kemudian nodul diukur dan diisolasi untuk validasi tingkat DNA dan protein.Hasil: Sel knockout survivin menunjukkan laju proliferasi yang lebih lambat dan persentase apoptosis yang lebih tinggi dibandingkan dengan sel wild–type. Sel knockout survivin juga menunjukkan persentase penanda sel punca kanker payudara yang lebih kecil, mendorong perubahan aktivasi respons terhadap stres seluler, seperti stres genotoksik, hipoksik, dan oksidatif, serta penurunan ekspresi protein dan mRNA yang berkaitan dengan metastasis. Selain itu, knockout survivin menunjukkan penghambatan pertumbuhan tumor mencapai 50%.Kesimpulan: Ketidakhadiran survivin menyebabkan penurunan agresivitas kanker payudara dengan menghambat proliferasi, menginduksi apoptosis, menekan stemness, mengubah berbagai respons stres seluler, dan menurunkan protein yang berkaitan dengan metastasis. Selain itu, ketidakhadiran survivin juga menyebabkan penurunan volume tumor nodul payudara.

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Introduction: Survivin, an inhibitor of apoptosis proteins, is highly expressed in breast cancer and closely associated with its aggressiveness, characterized by its rapid progression and poor prognosis. The main role of survivin is to regulate cell division and prevent apoptosis. However, other survivin mechanisms are complex and not fully understood. The aim of this study was to evaluate the effects of knocking out survivin on cancer aggressiveness relating to mechanisms of proliferation, apoptosis, stemness, cellular stress response, and metastasis, as well as volume of nodule breast tumor.

Method: The CRISPR/Cas9 system was utilized to establish knockout survivin both in the in vitro and in vivo study. In in vitro study, knockout and wild–type cells were used to analyse the loss of survivin in various biological mechanisms. Apoptosis–, pluripotency–, and cellular stress–related proteins were examined using proteomic arrays. Cell cycle, apoptosis, and expression of breast cancer stem cell markers were analyzed via flow cytometry. Metastasis–related markers were evaluated via qRT‒PCR. In in vivo study, CRISPR/Cas9 plasmid was given as intratumor injection three times with an interval of three days between injections. The rat was sacrificed 14 days after the last injection, then the nodule was measured and isolated for validation in DNA and protein levels.

Results: Knockout survivin cells exhibited slower proliferation rate and higher percentage of apoptosis. Knockout survivin cells also showed smaller percentage of breast cancer stem cells markers, promoted a shift toward activation response to cellular stress, such as genotoxic, hypoxic, and oxidative stress, as well as decreased of protein and mRNA expression–related metastasis. Additionally, survivin knockout demonstrated around 50% of the tumor growth inhibition.

Conclusion: The absence of survivin leads to attenuation of breast cancer aggressiveness by inhibiting proliferation, inducing apoptosis, suppressing stemness, altering various cellular stress response, and reducing protein related to metastasis. Moreover, the absence of survivin also leads to a reduced volume of nodule breast tumor."

"Insidensi kanker payudara terus meningkat secara global setiap tahun. Di negara berpendapatan menengah ke bawah, meningkatnya insidensi ini diikuti dengan meningkatnya angka kematian akibat kanker payudara yang disebabkan oleh keterlambatan diagnosis yang sering terjadi, sehingga pengobatan dan perawatan kanker payudara tidak lagi efektif dilakukan. Pada penelitian ini dilakukan analisis metode peningkatan deteksi dini terencana kanker payudara yang telah dilakukan di beberapa negara berpendapatan menengah ke bawah dengan menggunakan systematic review. Systematic review dilakukan dengan melakukan identifikasi literatur dari Google scholar, ProQuest, ScienceDirect, Scopus, dan Pubmed dengan menggunakan kata kunci improve, early detection, screening, breast cancer, low middle-income countries, dan LMIC, lalu dilakukan pencarian lanjutan dengan teknik snowball dari literatur yang sudah didapatkan. Kriteria inklusi pada pencarian literatur adalah artikel full text berbahasa Inggris yang diterbitkan pada tahun 2010 – Juni tahun 2020 dan memiliki lokasi studi di negara berpendapatan menengah ke bawah. Sebelas artikel didapatkan dari pencarian dan proses seleksi menggunakan diagram alir PRISMA. Ditemukan 5 jenis program dalam upaya peningkatan deteksi dini kanker payudara di negara berpendapatan menengah ke bawah, yaitu program skrining berbasis populasi, program skrining oportunistik, program peningkatan pengetahuan dan kesadaran, program pengalihan tugas, dan pelaksanaan program nasional deteksi dini kanker payudara. Program-program tersebut diketahui berhasil meningkatkan deteksi dini kanker payudara pada latar negara berpendapatan menengah ke bawah. Program peningkatan pengetahuan dan kesadaran, dan program pengalihan tugas dinilai sebagai program yang paling sesuai untuk dilaksanakan di negara berpendapatan menengah ke bawah. Meski begitu, perlu dilakukan pilot studi dan evaluasi biaya untuk melihat keefektifan program deteksi dini ini.

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Incidence of breast cancer keeps increasing globally every year, and in low-and middle-income countries it followed by increased mortality rate. This phenomenon could be associated with late-stage diagnosis that made treatments no longer effective. This study aimed to analyse methods to increase early detection for breast cancer that has been done in several low-and middle-income countries by using systematic review. Systematic review was carried out by identifying literatures from online databases such as Google scholar, ProQuest, ScienceDirect, Scopus, and Pubmed using “improve”, “early detection”, “screening”, “breast cancer”, “low middle-income countries", and “LMIC” as keywords, and followed by manually searching literatures using snowball technique from the literatures that had been identified earlier. Inclusion criterias in this study were English full text that were published between 2010 – June 2020 with low-and middle-income countries setting. Eleven articles were obtained using PRISMA flow diagram and 5 types of programs were found to increase early detection for breast cancer in low-and middle-income countries; population-based screening program, oportunistic screening program, program to improve knowledge and awareness about breast cancer and early detection, task shifting program, and implementation of national breast cancer early detection program. These programs were known to be able to improve early detection in their respective study location. Improving knowledge and awareness, and task shifting program were the most suitable program to be executed in low-and middle-income countries setting. These countries shall do some pilot studies and cost evaluation to identify and analyse the effectivity of these programs before implementing it widely."

"Latar Belakang: Kanker payudara merupakan jenis kanker invasif yang paling banyak menyerang wanita. Kejadian dan kematian akibat kanker ini tinggi, baik secara global maupun di Indonesia. Subtipe molekuler kanker payudara, terutama kanker payudara triple-negative (TNBC), berperan penting dalam menentukan pilihan pengobatan. Namun, TNBC belum memiliki terapi target khusus dan berpotensi resisten terhadap pengobatan standar. Senyawa alami semakin banyak diteliti sebagai alternatif pengobatan kanker. Asam galat (GA), menunjukkan potensi sebagai antikanker, terutama untuk kanker payudara. Daun Mangifera foetida kaya akan GA dan berpotensi menjadi sumber pengobatan. Metode: Penelitian in-vitro ini menggunakan sel TNBC MDA-MB-231 yang diberi GA murni dan ekstrak daun M. foetida. Setelah nilai IC50 didapatkan, sekuensing RNA dilakukan untuk analisis bioinformatika. Hasil: DEG signifikan setelah pemberian kedua jenis perlakuan. Gen yang mengalami peningkatan ekspresi pada kedua perlakuan sebagian besar terkait dengan respons terhadap stres sel. Gen-gen yang ekspresinya meningkat meliputi MRI1, AKR1B15, NQO1, GSTA3, SRXN1, sedangkan gen-gen yang ekspresinya menurun meliputi ISG15 dan SERPINE1. Analisis jalur menunjukkan adanya pengayaan pada jalur yang berkaitan dengan daur ulang metionin, biosintesis estrogen, respons imun, stres oksidatif, dan kematian sel. Kesimpulan: Baik GA maupun ekstrak M. foetida memengaruhi ekspresi gen pada sel TNBC. Ekstrak M. foetida menunjukkan pengaruh yang lebih besar terhadap beberapa gen yang berkaitan dengan respons stres oksidatif seluler, kemungkinan karena adanya interaksi sinergis dengan metabolit lain dalam ekstrak tersebut

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Introduction: Breast cancer is the most prevalent invasive cancer in women, with high incidence and mortality rates globally and in Indonesia. Molecular subtyping, particularly triple-negative breast cancer (TNBC), guides treatment, but TNBC lacks targeted therapies. Chemotherapy with agents like anthracyclines is standard, but with severe side effects and potential resistance. Natural compounds are increasingly explored as alternative anticancer agents. Gallic acid (GA), a phenolic compound, shows promising anticancer activity, especially against breast cancer. Mangifera foetida leaves are a rich source of GA, potentially offering a cost-effective treatment option. Method: This in-vitro study used TNBC MDA-MB-231 cells treated with pure GA and M. foetida leaf extract. IC50 values were determined, and cells were treated at these concentrations. RNA sequencing was performed, followed by bioinformatic analysis of differentially expressed genes (DEGs) and pathway enrichment analysis. Results: Significant DEGs were identified after both treatments. Upregulated genes in both treatments were mainly related to stress response. Upregulated DEGs included MRI1, AKR1B15, NQO1, GSTA3, SRXN1, while downregulated genes included ISG15 and SERPINE1. Pathway analysis revealed enrichment in pathways related to methionine salvage, estrogen biosynthesis, immune response, oxidative stress, and cell death. Conclusion: Both GA and M. foetida extract affected gene expression in TNBC cells, with the extract showing greater effects on several genes linked to stress response, potentially indicating synergistic interactions with other metabolites"

"In recent years, cancer stem cells have been recognized as important component in carcinogenesis and they seem to form the basis of many (if not all) tumor types. Cancer stem cells or "cancer cell like stem cells" have been isolated from various cancers of different origin (blood, breast, brain, skin, head and neck, thyroid, cervix, lung, retina, colon, pancreas and so on). Cancer stem cells - rare cells with indefinite proliferative potential that drive the formation and growth of tumours- seem to show intriguing relationships with physiological stem cells. Specifically, these cancer cells show significant similarities in the mechanisms that regulate self-renewal of normal stem cells. Moreover, tumour cells might directly arise from normal stem cells. Further, the cellular biology of cancer stem cells show a lot of similarities with normal stem cells."

"Latar Belakang: Prognosis pasien kanker payudara Triple Negative (TNBC) lebih buruk dibandingkan dengan kanker payudara tipe lain. Hal ini seringkali dikaitkan dengan terjadinya peningkatan ekspresi PD-L1 pada pasien TNBC. Hubungan PD-L1 dengan kesintasan pada kanker payudara triple negative masih belum sepenuhnya dipahami dan beberapa penelitian menyatakan hasil yang masih berbeda-beda. Penelitian ini dilakukan untuk mengetahui pola ekspresi PD-L1 dihubungkan dengan kesintasan pasien TNBC.Metode : Penelitian ini merupakan penelitian kohort retrospektif. Subjek penelitian adalah pasien TNBC yang berobat di RSUPN Dr. Cipto Mangunkusumo Jakarta, dilakukan pemeriksaan ekspresi PD-L1 dari jaringan kanker payudara dengan menggunakan pewarnaan PD-L1, ditentukan follow-up selama tiga tahun. Kemudian dilanjutkan analisa survival untuk mendapat data prognosis PD-L1 dan dinilai juga faktor klinikopatologi yang berpengaruh terhadap ekspresi PD-L1. Analisis statistik dilakukan menggunakan software SPSS 20.Hasil : Dari 40 sampel yang diteliti, sebagian besar sampel memiliki ekspresi PD-L1 positif (67,5%). Sebanyak 14 subjek (51,9%) dengan PD-L1 positif dan 5 subjek (38,5%) dengan PD-L1 negatif meninggal pada pengamatan selama 36 bulan. Subjek yang meninggal memiliki rata-rata waktu survival sebesar 19 bulan dengan waktu terpendek 3 bulan dan paling lama 35 bulan serta paling sering muncul adalah 11 bulan. Rata-rata durasi overall survival didapatkan sebesar 27,78 ± 1,69 bulan. Sementara itu, pada kelompok PD-L1 positif rata-rata durasi survival sebesar 26,56 ± 2,15 bulan dan pada kelompok PD-L1 negatif rata-rata durasi survival sebesar 30,31 ± 2,57 bulan.Kesimpulan : Durasi rata-rata survival pasien TNBC dengan ekspresi PD-L1 positif lebih rendah dibandingkan ekspresi PD-L1 negatif. Akan tetapi ekspresi PD-L1 secara statistik tidak berhubungan signifikan dengan survival pasien TNBC selama tiga tahun massa follow up.

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Background: Triple Negative Breast Cancer (TNBC) prognosis is the worst compared to other types of breast cancer. This is often associated with an increase PD-L1 expression in TNBC patients. The PD-L1 relationship with survival in the negative triple breast cancer is still not fully understood and some studies declare the results that are still different. This research was conducted to determine the pattern of PD-L1 expression associated with the survival of TNBC patients.

Methods: This research was a retrospective cohort study. The subjects were TNBC patients who were treated at Dr. Cipto Mangunkusumo Jakarta, examined the expression of PD-L1 from breast cancer tissue using PD-L1 staining, was determined by three years follow-up. Then proceed with survival analysis to obtain prognostic data for PD-L1 and also clinicopathological factors that affect PD-L1 expression. Statistical analysis was performed using SPSS 20 software.

Results: Of the 40 samples studied, most of the samples had positive PD-L1 expressions (67.5%). A total of 14 subjects (51.9%) with PD-L1 positive and 5 subjects (38.5%) with PD-L1 negative died on observation for 36 months. The subjects that did not survive had an average of 19 months of survival time with the shortest time of 3 months and a maximum of 35 months and most often appears is 11 months. The average duration of overall survival was 27.78 ± 1.69 months. In the PD-L1 positive group, mean overall survival was 26.56 ± 2.15 months and in the PD-L1 negative group, mean overall survival was 30.31 ± 2.57 months.

Conclusion: The average duration of survival of TNBC patients with positive PD-L1 expression was lower than that of negative PD-L1 expression. However, PD-L1 expression was not significantly associated with the survival of TNBC patients during the three-year follow-up period."

"Latar Belakang: Kanker payudara triple negatif dikenal sebagai jenis kanker yang memiliki prognosis yang lebih buruk daripada jenis kanker payudara lainnya karena kurangnya terapi target dan tingkat kekambuhan dini dan metastasis yang lebih tinggi. Manganese superoxide dismutase (MnSOD), pertahanan utama melawan superoksida, telah ditemukan untuk memiliki peran ganda dalam kanker. Meskipun MnSOD mungkin memiliki peran penekan tumor pada tahap awal tumorigenesis, MnSOD akan kemudian mempunyai peran penting untuk kelangsungan hidup sel kanker saat tumor berkembang. Sel punca kanker, ditemukan dalam tingkat yang tinggi dalam kanker payudara triple negatif, adalah subpopulasi sel tumor yang memiliki kapasitas tumorigenisitas dan stress oksidatif yang tinggi. Sel punca kanker mengekspresikan faktor transkripsi seperti Oct4 dan Sox2 yang mengatur gen yang diperlukan untuk pembaruan diri dan pluripotensi sel punca kanker ini. Penelitian ini bertujuan untuk mengetahui pengaruh penekanan ekspresi MnSOD melalui gen knockout terhadap pluripotensi sel punca kanker payudara triple negatif dengan mengukur ekspresi protein Oct4 dan Sox2. Metode: Penelitian ini menggunakan satu kelompok kontrol BT-549 sel punca kanker payudara triple negatif dan dua kelompok BT549 sel punca kanker payudara triple negatif yang telah diberi perlakuan knockout gen MnSOD. Untuk setiap kelompok sampel, tiga pasase digunakan (P2, P3, P4). Protein Oct4 dan Sox2 yang diekspresikan oleh setiap pasase dari setiap kelompok dideteksi menggunakan Western blot dan area pita masing-masing protein kemudian dianalisis menggunakan program ImageJ.Hasil: Ditemukan adanya tren penurunan ekspresi protein Oct4 dan tren peningkatan ekspresi protein Sox2. Kesimpulan: Penekanan ekspresi MnSOD mungkin bisa menjadi target untuk mengubah tingkat pluripotensi sel punca kanker payudara triple negatif melalui interaksi tidak langsung dengan Oct4 dan Sox2.

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Introduction: Triple negative breast cancer is considered to have a poorer prognosis than other subtypes of breast cancer due to the lack of targeted therapies and its higher rate of early recurrence and distant metastasis. Manganese superoxide dismutase (MnSOD), the primary defense against superoxides, have been found to have a dual role in cancer. Although MnSOD may have a tumor-suppressing role in the early stages of tumorigenesis, it later becomes essential for the survival of the cancer cells as the tumor progresses. Cancer stem cells (CSCs), enriched in triple negative breast cancer, are a population of tumor cells that possess high capacity of tumorigenicity and oxidative stress. They express transcription factors such as Oct4 and Sox2 which regulate genes necessary for the self-renewal and pluripotency of these CSCs. This study aims to determine the impact of suppressing MnSOD expression through gene knockout on the pluripotency of triple negative breast cancer stem cells by measuring Oct4 and Sox2 protein expression.

Methods: A control group of wild type BT-549 BCSCs and two groups of treated BT549 BCSCs were used in this study, with the treated groups having their MnSOD gene knocked out. For each group of samples, three passages were used (P2, P3, P4). The Oct4 and Sox2 proteins expressed by each passage number from each group were detected using Western blot and their respective area densities were then analyzed using the ImageJ program.

Results: There was a decreasing trend in Oct4 protein expression and an increasing trend in Sox2 protein expression.

Conclusion: Suppression of MnSOD expression may be a target to alter the pluripotency of triple negative BCSCs through its indirect interaction with Oct4 and Sox2. "

"Latar belakang: Terapi farmakologi kanker payudara triple negative (KPTN)terbatas pada obat sitostatika seperti doksorubisin. Namun, resistensi doksorubisinsulit dihindari. Salah satu jalur pensinyalan yang penting pada resistensiKPTN terhadap doksorubisn adalah TGF-β. TMEPAI (transmembran prostatandrogen-induced protein), regulator negatif sekaligus gen target pada jalur TGF-β diduga merupakan salah satu kunci dalam resistensi KPTN terhadapdoksorubisin.Metode: Teknik CRISPR-Cas9 digunakan untuk menghilangkan TMEPAI padagalur sel KPTN, BT549. Sel diberi perlakuan TGF-β 2 ng / mL dan doksorubisinselama 24 jam. Pengukuran konsentrasi sitotoksik doksorubisin pada 50%populasi sel (CC50) dilakukan terhadap sel KPTN wildtype (WT) dan knock out(KO). Setelah itu, sel dipanen dan dihitung. Rantai Polimerase Waktu NyataReaction (RT-PCR) dan western blot (WB) digunakan untuk mengukur tingkatekspresi penande proliferasi, apoptosis, EMT, dan transporter. Selain itu, SMADyang terfosforilasi dan aktivitas PI3K / Akt juga belajar.Hasil: Galur sel yang tidak memiliki TMEPAI (KO) berhasil diperoleh dari selKPTN, BT549. Sel WT terbukti lebih resistan terhadap doksorubisindibandingkan sel KO yang ditunjukkan dengan peningkatan CC50 dan Ki-67.TMEPAI menurunkan efek apoptosis doksorubisin dengan memodulasi ekspresibcl-2 dan kaspase-3, namun tidak kaspase-9 dan bax. Efek TMEPAI mengurangidoksorubisin dengan menekan fosforilasi SMAD. Namun TMEPAI meningkatkanpenghambatan PI3K / Akt oleh doksorubisin. TMEPAI juga meningkatkan EMTdan transporter efluks yang diinduksi oleh doksorubisin.Kesimpulan: TMEPAI terhadap pertarungan dalam resistensi sel KPTNdoksorubisin melalui aktivasi jalur sinyal TGF-β non-canonical beserta proteindan gen targetnya.Background: Triple negative breast cancer (KPTN) pharmacological therapylimited to cytostatic drugs such as doxorubicin. However, doxorubicin resistancehard to avoid. One of the important signaling pathways of resistanceKPTN against doxorubisn is TGF-β. TMEPAI (transmembrane prostateandrogen-induced protein), a negative regulator as well as a target gene in the TGF-β is thought to be one of the keys in the resistance of KPTN todoxorubicin.Method: The CRISPR-Cas9 technique was used to remove TMEPAI onKPTN cell lines, BT549. Cells were treated with TGF-β 2 ng / mL and doxorubicinfor 24 hours. Measurement of the cytotoxic concentration of doxorubicin at 50%cell population (CC50) was carried out against wildtype KPTN (WT) cells and knockout(KO). After that, cells are harvested and counted. Real Time Polymerase ChainReaction (RT-PCR) and western blot (WB) were used to measure levelsexpression markers of proliferation, apoptosis, EMT, and transporters. Apart from that, SMADthe phosphorylated and PI3K / Akt activities also learn.Results: Cell lines that did not have TMEPAI (KO) were obtained from the cellsKPTN, BT549. WT cells have been shown to be more resistant to doxorubicincompared to cell knockout shown with increased CC50 and Ki-67.TMEPAI decreases the apoptotic effect of doxorubicin by modulating expressionbcl-2 and caspase-3, but not caspase-9 and bax. TMEPAI reducing effectsdoxorubicin by suppressing SMAD phosphorylation. However TMEPAI is improvingPI3K / Akt inhibition by doxorubicin. TMEPAI also increases EMTand doxorubicin-induced efflux transporters.Conclusion: TMEPAI against the fight against KPTN cell resistancedoxorubicin via activation of the non-canonical TGF-β signaling pathway along with proteinsand its target genes."

"Latar Belakang: Potensi lunasin dari ekstrak kedelai telah banyak diketahui memberikan manfaat dalam terapi kanker melalui efek antipoliferatifnya. Bcl-2 merupakan protein antiapoptosis yang ekspresinya meningkat pada kanker payudara dan dapat mencegah kejadian apoptosis dari sel kanker. Tujuan dari penelitian ini adalah untuk mengetahui pengaruh pemberian ekstrak kedelai kaya lunasin terhadap ekspresi protein Bcl-2 sel kanker payudara tikus yang diinduksi DMBA. Metode: Penelitian menggunakan bahan biologi tersimpan dari jaringan kanker payudara tikus jenis Sprague-Dawley (SD) yang telah diberi perlakuan dalam 5 kelompok percobaan dan dipulas dengan pewarnaan imunohistokimia. Identifikasi ekspresi Bcl-2 dilakukan dengan aplikasi ImageJ dan dikuantifikasi menggunakan metode H-score untuk dianalisis secara statistik. Hasil: Hasil H-score setiap kelompok secara berurutan dari tertinggi adalah kontrol negatif (171,61%), lunasin kuratif (156,28%), kontrol positif (147,92%), adjuvan (142,12%), dan kelompok normal (127,22%). Terdapat perbedaan bermakna pada uji perbandingan tiap dua kelompok kecuali pada kelompok normal-adjuvan, kontrol positif-adjuvan, kontrol positif-kuratif, serta adjuvan-kuratif. Kesimpulan: Pemberian ekstrak kedelai kaya lunasin mampu menunrunkan ekspresi protein Bcl-2 sel kanker payudara payudara tikus yang diinduksi DMBA. Tidak terdapat perbedaan yang signifikan secara statistik antara kelompok lunasin dengan tamoksifen. Kelompok adjuvan lebih efektif dalam menurunkan ekspresi Bcl-2 dengan hasil yang tidak berbeda secara statistik dengan kelompok normal.

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Background: The potential of lunasin from soybean extract has been widely known to provide benefits in cancer therapy through its antiproliferative effect. Bcl-2 is an antiapoptotic protein whose expression increases in breast cancer and can prevent apoptosis in cancer cells. The purpose of this study was to determine the effect of administration of lunasin-rich soybean extract on the expression of Bcl-2 protein in DMBA-induced rat breast cancer cells. 

Methods: The study used stored biological material from breast cancer tissue of Sprague-Dawley (SD) rats that had been treated in 5 experimental groups and stained immunohistochemically. Identification of Bcl-2 expression was carried out using ImageJ application and quantified using the H-score method for statistical analysis. 

Results: The results of the H-scores of each group sequentially from the highest were negative control (171.61%), curative lunasin (156.28%), positive control (147.92%), adjuvant (142.12%), and group normal (127.22%). There were significant differences in the comparison test of each of the two groups except for the normaladjuvant, positive-adjuvant control, positive-curative control, and adjuvant-curative group. 

Conclusion: The administration of lunasin-rich soybean extract was able to reduce the expression of Bcl-2 protein in DMBA-induced rat breast cancer cells. There was no statistically significant difference between the lunasin and tamoxifen groups. The adjuvant group was more effective in reducing Bcl-2 expression with results that were not statistically different from the normal group."

"Kanker payudara menjadi penyebab kematian utama akibat kanker pada wanita. Metastasis dan kekambuhan menjadi faktor penyebab utama kematian akibat kanker. Metastasis menyebabkan sel tumor menginvasi dan menyebar melalui pembuluh darah menuju organ tubuh lain dan resistensi disebabkan karena sel punca yang memiliki kemampuan untuk self-renewal. Gen EpCAM dan CD44 dilaporkan memiliki kaitan dengan kepuncaan sel kanker. Sampai saat ini, pengembangan pengobatan kanker payudara masih terus dilakukan. Penggunaan kultur primer dalam studi in vitro terus dikembangkan karena hasil kultur primer homogen dengan lingkungan kanker primer. Optimasi kultur primer masih perlu dikembangkan. Selain itu, untuk melihat kepuncaan sel kanker diperlukan studi ekspresi gen terkait sel punca, yaitu EpCAM dan CD44. Penelitian ini bertujuan untuk mengoptimasi kultur primer kanker payudara dan mendeteksi sel punca menggunakan gen EpCAM dan CD44. Sampel kanker payudara didapatkan dari 10 pasien RS Cipto Mangunkusumo. Sampel yang digunakan adalah sampel high proliferative dan low proliferative. Metode kultur primer yang digunakan adalah metode enzimatis dan eksplan. Pengamatan kultur sel dilakukan selama 30 hari. Pada pengamatan molekuler, jaringan asal kanker dan sel hasil kultur primer digunakan untuk melihat ekspresi gen menggunakan metode qPCR. Hasil yang diperoleh menunjukkan bahwa metode yang berhasil untuk menumbuhkan sel kanker payudara adalah metode eksplan dan karakteristik sampel high proliferative. Sel sferoid (3D) didapatkan pada kultur kanker payudara. Hasil ekspresi gen menunjukkan ekspresi EpCAM dan CD44 tidak berbeda nyata (P>0,05) antara hasil kultur dan jaringan asal. Ekspresi gen yang tinggi diketahui berkorelasi dengan kehadiran sel punca

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Breast cancer is the leading cause of death from cancer in women. Metastases and relapses are the main contributing factors to death from cancer. Metastases cause tumor cells to invade and spread through blood vessels to other organs of the body and resistance is caused due to stem cells having the ability to self-renew. The EpCAM and CD44 genes are reported to be associated with cancer cell stemness. To date, the development of breast cancer treatment is still being developed. The use of primary culture in in vitro studies continues to be developed because the results of the primary culture are homogeneous with the primary cancer environment. However, optimization of primary culture is still required to be developed. In addition, to see the cancer stemness, studies of stem cell-related gene expression are needed, namely EpCAM and CD44. This study aims to optimize the primary culture of breast cancer and detect stem cells using the EpCAM and CD44 genes. Breast cancer samples were obtained from 10 patients at Cipto Mangunkusumo Hospital. The samples used were high proliferative and low proliferative samples. The primary culture methods used were enzymatic and explanatory methods. Observation of cell cultures was carried out for 30 days. In molecular observations, cancer origin tissue and primary cultured cells were used to see gene expression using the qPCR method. The results obtained showed that the successful method for growing breast cancer cells is the explant method. Spheroid (3D) cells were obtained in breast cancer cultures. Gene expression results showed that EpCAM and CD44 expression did not differ significantly (P>0.05) between culture results and tissue origin. High gene expression is known to correlate with the presence of stem cells."

"Latar belakang: Kanker payudara (KP) termasuk penyebab umum kematian pada wanita di dunia. Salah satu tumor marker yang digunakan sebagai penanda proliferasi sel kanker payudara yakni Ki-67. Ki-67 merupakan protein yang mudah diekspresikan di inti sel selama siklus sel, ekspresi Ki-67 yang tinggi menandakan semakin banyak sel yang berproliferasi. Terapi KP yang dijalani sekarang masih banyak ditemukan efek samping sehingga dibutukan terapi adjuvant dalam pengobatan KP yakni kedelai, kedelai dipilih karena murah, mudah dijangkau serta diyakini mampu menurunkan angka kejadian KP. Riset ini dilakukan untuk mengetahui efek lunasin dalam menurunkan ekspresi Ki-67 pada kelenjar payudara tikus. Metode: : Tikus jenis Sprague dewlay (SD) berjumlah 25 ekor dibagi secara acak ke dalam 5 kelompok yakni kelompok normal, kelompok kontrol negatif atau hanya dinduksi DMBA saja, kelompok tamoksifen, kelompok lunasin + tamoksifen dan kelompok lunasin kuratif. Setiap sedian jaringan kanker payudara diberi pewarnaan immunohistokimia terhadap Ki-67 kemudian akan dilihat dibawah mikroskop cahaya dengan pembesaran 400x,perhitungan jumlah sel dilakukan pada 5 lapang pandang untuk menilai ekspresi Ki-67.Perhitungan jumlah sel dengan menggunakan aplikasi Image J dan IHC profiler Hasil: Lunasin mampu menurunkan ekspresi Ki-67. Terdapat perbedaan bermakna pada setiap kelompok uji jika dibandingkan dengan kontrol negatif (p=0,000). Akan tetapi tidak terdapat perbedaan bermakna antara kelompok tamoksifen dengan kelompok terapi lunasin+ tamoksifen (p=0,961). Kesimpulan: Pemberian lunasin, tamoksifen dan lunasin+tamoksifen mampu menurunkan ekspresi Ki-67 pada sel kanker payudara tikus SD yang diinduksi DMBA. Kata kunci: DMBA, kanker payudara, lunasin, kedelai, protein Ki-67, tamoksifen.

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Introduction: Background: Breast cancer (KP) is a common cause of death in women around the world. One of the tumor markers used as a marker for breast cancer cell proliferation is Ki-67. Ki-67 is a protein that is easily expressed in the cell nucleus during the cell cycle, high Ki-67 expression indicates more cells are proliferating. There are still many side effects of KP therapy currently being carried out, so adjuvant therapy is needed in the treatment of KP, namely soybeans, soybeans were chosen because they are cheap, easy to reach, and are believed to be able to reduce the incidence of KP. This research was conducted to determine the effect of lunasin in reducing the expression of Ki-67 in the breast glands of rats. Method: 25 Sprague dewlay (SD) rats were randomly divided into 5 groups namely the normal group, negative control group or DMBA-induced only, tamoxifen group, lunasin + tamoxifen group and curative lunasin group. Each breast cancer tissue preparation was given immunohistochemical staining of Ki-67 and then viewed under a light microscope with 400x magnification, cell counts were performed in 5 fields of view to assess Ki-67 expression. Cell counts were performed using Image J and IHC profiler applications. Result: Lunasin was able to reduce the expression of Ki-67. There was a significant difference in each test group when compared to the negative control (p=0.000). However, there was no significant difference between the tamoxifen group and the lunasin + tamoxifen therapy group (p=0.961). Conclusion: Administration of lunasin, tamoxifen and lunasin+tamoxifen was able to reduce Ki-67 expression in DMBA-induced SD rat breast cancer cells. Keywords: DMBA, breast cancer, lunasin, soybean, Ki-67 protein, tamoxifen"