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"This book in order to stimulate the discussion of how the knowledge gained in the emerging field of oxidative stress in cancer biology can be utilized to more effectively design interventions to enhance therapeutic responses while causing fewer treatment limiting complications. The chapters contained in this volume provide highly informative emerging perspectives on how that selective enhancement of oxidative stress in cancerous tissues can be used as a target for enhancing therapeutic outcomes as well as how selective inhibition of oxidative stress could spare normal tissue damage and inhibit carcinogenesis. "

"ABSTRAKLatar Belakang: Keberadaan sel punca kanker payudara diduga berkontribusi dalam timbulnya resistensi terapi. Beberapa mekanisme yang mempengaruhi respons terapi pada kanker yaitu aktifnya jalur sinyal embrionik, hambatan apoptosis dan tingginya perbaikan DNA serta adaptasi sel punca kanker terhadap hipoksia dan stres oksidatif.Tujuan: Menganalisis profil ekspresi gen kepuncaan pada kanker payudara setelah terapi neoajuvan hormonal dan kemoterapi dilihat hubungannya dengan jalur apoptosis p53, jalur stres oksidatif NFkB dan penanda hipoksia HIF- serta respons terapi.Metode: Penelitian ini menggunakan sampel jaringan kanker payudara stadium IIIB dan IV sebelum terapi neoajuvan 46 sampel pre dan setelah terapi neoajuvan 46 sampel post . Total RNA diekstraksi kemudian dilakukan pengukuran ekspresi dengan menggunakan teknik Next Generation Sequencing Truseq targeted RNA expression Illumina dengan menggunakan panel sel punca, p53 dan NFkB. Selain itu juga ekspresi HIF-1 dan HIF-2 diukur dengan menggunakan qRT-PCR.Hasil: Setelah terapi neoajuvan, profil ekspresi gen kanker payudara yang memiliki respons molekuler yang baik pada jalur kepuncaan adalah CCNE1, CDC42, CTNNB1, HDAC2, PSEN1, PSENEN, pada jalur apoptosis adalah BIRC5, CASP8, CASP9, CDK1 dan PCNA, pada jalur stres oksidatif adalah SOD2, STAT1 dan TBK1, serta pada jalur hipoksia yaitu HIF-1 dan HIF-2 . Profil ekspresi gen dengan respons molekuler yang buruk pada jalur kepuncaan adalah ALDH1A1, ALDH2, CCND2, CXCL12, FZD7, IGF1, sedangkan pada jalur apoptosis adalah ATM dan BID. Respons histopatologis Miller Payne berkorelasi positif bermakna dengan ekspresi gen jalur apoptosis dengan respons molekuler yang baik BIRC5, CASP8, CDK1 , namun berkorelasi negatif bermakna dengan ekspresi gen ALDH1A1. Survival pasien kanker payudara berkorelasi negatif bermakna dengan ekspresi ALDH1A1 dan SOD2.Kesimpulan: Ekspresi gen ALDH1A1 dan SOD2 merupakan faktor penting untuk prediksi prognosis terapi neoajuvan sistemik pada pasien kanker payudara stadium lanjut.

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ABSTRACTIntroduction: The presence of breast cancer stem cells is considered to contribute to therapeutic resistance. There are some mechanisms affected therapy response in the cancer, such as active embryonic signaling pathways, inhibition of apoptosis and high DNA repair, adaptation to hypoxia and oxidative stress.Aim: to analyse the stemness gene expression profile in breast cancer after neoadjuvant chemotherapy and hormonal therapy correlated with apoptotic p53 , oxidative stress NFkB and hypoxia HIF- signaling pathways and also therapeutic responses.Methods: This study used breast tissue samples IIIB and IV before neoadjuvant therapy 46 pre samples and after neoadjuvant therapy 46 post samples . Total RNA was measured the expression profile using Next Generation Sequencing Truseq targeted RNA expression Illumina with stem cell, p53 and NFkB panels. In addition, HIF-1 and HIF-2 expression were measured using qRT-PCR. Results: After neoadjuvant therapy, the expression profiles of breast cancer genes that have good molecular responses in stem cells pathway are CCNE1, CDC42, CTNNB1, HDAC2, PSEN1, PSENEN, in apoptotic pathway are BIRC5, CASP8, CASP9, CDK1 and PCNA, in oxidative stress pathway are SOD2, STAT1 and TBK1, as well as in the hypoxic pathway HIF-1 and HIF-2 . Expression profiles with poor molecular responses in stem cells pathway are ALDH1A1, ALDH2, CCND2, CXCL12, FZD7, IGF1, while in apoptotic pathway are ATM and BID. Histopathologic response Miller Payne was significantly positively correlated with apoptotic pathway gene expression with good molecular response BIRC5, CASP8, CDK1 , but negatively significant correlated with ALDH1A1 gene expression. Survival of breast cancer patients significantly negatively correlated with ALDH1A1 and SOD2 expression. Conclusion: ALDH1A1 and SOD2 gene expression is an important factor for predicting the prognosis of systemic neoajuvan therapy in patients with advanced breast cancer."

"Latar Belakang: Pada ODHA didapatkan peningkatan inflamasi dan stres oksidatif. Puasa Ramadan dapat memperbaiki inflamasi dan stres oksidatif, namun penelitian pada ODHA yang mendapat antiretroviral belum pernah dilakukan. Tujuan: Mengetahui pengaruh puasa Ramadan terhadap high sensitivity Creactive protein (hs-CRP) dan status antioksidan total (SAT) pada ODHA yang mengonsumsi antiretroviral. Metode: Penelitian ini merupakan penelitian prospektif pada 29 orang ODHA dengan ARV yang berpuasa dan 29 yang tidak berpuasa. Kriteria inklusi yaitu pria, 20-40 tahun, mendapat ARV lini 1 minimal 6 bulan, serta tidak dalam fase inisiasi pengobatan untuk infeksi oportunistik. Pasien yang mendapat steroid atau imunosupresan lain atau pasien dengan adherens minum ARV kurang dari 95% dieksklusi. Pemeriksaan kadar hs-CRP dan SAT dilakukan sebelum dan saat puasa Ramadan (setelah 14 hari puasa). Hasil: Karakteristik baseline usia, hitung CD4, HIV-RNA, kombinasi ARV, status hepatitis B dan C, serta kadar hs-CRP tidak berbeda antara kelompok berpuasa dengan kontrol. Setelah dua minggu, terdapat penurunan signifikan hs-CRP pada kelompok yang berpuasa dibandingkan kontrol (p=0,004). Median perubahan hs-CRP pada kelompok puasa adalah -0,41 (IQR -1; 0,1) mg/L, sedangkan pada kelompok kontrol adalah 0,2 (IQR -0,3; 1,5) mg/L. Konsumsi polyunsaturated fatty acid, berat badan, jumlah rokok, dan jumlah jam tidur per hari menurun selama puasa Ramadan (berturut-turut p=0,029; p<0,001; p<0,001; dan p<0,001). Tidak ditemukan perbedaan bermakna perubahan SAT antara kelompok yang berpuasa dengan kontrol (p=0,405). Median perubahan SAT pada kelompok puasa adalah 0,05 (IQR -0,03; 0,12) mmol/L, sedangkan pada kelompok kontrol adalah 0,04 (IQR -0,13; 0,36) mmol/L. Simpulan: Puasa Ramadan menurunkan kadar hs-CRP pada ODHA yang mengosumsi antiretroviral. Puasa Ramadan belum meningkatkan kadar SAT pada ODHA yang mengonsumsi antiretroviral.

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Background: Inflamation and oxidative stress were increased among HIV patients. Studies had showed Ramadan fasting could improve inflammation and oxidative stress, but not one of them had been conducted in HIV patients receiving antiretroviral therapy.

Aim: to know the effect of Ramadan fasting on hs-CRP level and total antioxidant status among HIV patients on highly active antiretroviral therapy.

Methods: A prospective cohort study comparing 29 HIV-infected patients on stable ART doing Ramadan fasting versus 29 non-fasting patients. Inclusion criteria were male, 20-40 years old, receiving first line ART for at least six months, and not on initial phase of opportunistic infection?s treatment. Patients who consumed steroid or other immunosuppressant or patients with poor ART adherence were excluded. Level of hs-CRP was obtained before and during Ramadan after at least 14 days fasting.

Results: Baseline age, CD4 cell count, HIV-RNA, ART combination, hepatitis B and hepatitis C status, and hs-CRP level were similar for both fasting and control groups. After 2 weeks, a significant hs-CRP decrease was found in fasting group compared to non-fasting one (p=0.004). Median difference of hs-CRP in fasting group was -0.41 (IQR -1 and 0.1) mg/L, while in control group the median difference was 0.2 (IQR -0.3 and 1.5) mg/L. Polyunsaturated fatty acid consumption, body weight, amount of cigarette smoking, and total sleep hours per day were decreased significantly during Ramadan fasting (p=0.029; p<0.001, p<0.001, p<0.001 respectively). There was no statistically significant changes in total antioxidant status between the two groups (p=0.405). Median total antioxidant status changes in fasting group was 0.05 (IQR -0.03;0.12) mmol/L. Median total antioxidant status changes in control group was 0.04 (IQR -0.13; 0.36) mmol/L.

Conclusion: Ramadan fasting decreased hs-CRP level among HIV patients on antiretroviral therapy. Ramadan fasting had not increased total antioxidant status among HIV patients on antiretroviral therapy."

"Pendahuluan: Endometriosis merupakan suatu kelainan jinak ginekologi yang dapat mengalami transformasi menjadi kanker. Stres oksidatif diduga berperan dalam perkembangan penyakit endometriosis. Gen supresor tumor ARID1A banyak ditemukan termutasi dan inaktif pada kanker ovarium yang berhubungan dengan endometriosis. Tujuan penelitian adalah untuk menganalisis peran stres oksidatif terhadap ekspresi gen supresor tumor ARID1A dalam transformasi endometriosis menjadi ganas. Metoda: Penelitian dimulai dengan 10 sampel jaringan kanker ovarium, 10 sampel endometriosis dan3 jaringan endometrium eutopik sebagai kontrol yang diisolasi mRNA dan proteinnya. Analisis ekspresi gen ARID1A pada tingkat mRNA dilakukan dengan pemeriksaan RT-qPCR dan pada tingkat protein dengan ELISA. Pada sel endometriosis dan kanker ovarium dilakukan analisis stres oksidatif dengan pemeriksaan aktivitas antioksidan MnSOD dan pemeriksaan kadar MDA sebagai salah bukti kerusakan salah satu komponen sel. Setelah itu dilakukan uji eksperimental pada kultur sel endometriosis dan endometrium eutopik sebagai kontrol. Kedua sel kultur diinduksi dengan H2O2 konsentrasi 0 nM, 100 nM, dan 1000 nM. Analisis dilakukan terhadap ketahanan hidup sel, kadar ROS dan ekspresi gen ARID1A pada tingkat mRNA dan protein. Hasil: Efek induksi H2O2 dalam menekan ekspresi gen ARID1A sel endometriosis dan sel endometrium eutopik pada tingkat mRNA dan protein, bermakna, meskipun pada kanker ovarium tidak bermakna pada penelitian ini. Kesimpulan: Stres oksidatif berperan dalam menekan ekspresi gen supresor tumor ARID1A ditingkat mRNA dan protein pada endometriosis.

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Introduction: Endometriosis as a gynecologic benign lesion, can transform itself into cancer. Oxidative stress is considered as an important factor in endometriosis development. Studies found that ARID1A as tumor suppressor gene, was frequently mutated and inactivated in endometriosis associated ovarian cancer. The aim of the study is to analyze the role of oxidative stress on ARID1A expresion in endometriosis malignant transformation.

Methods: This study started with ten samples of ovarian cancer, ten samples of endometriosis, and 3 samples of eutopic endometrioid tissues as control. They were analyzed for the expression of ARID1A by RT-qPCR and ELISA, then analyzed for the activity of MnSOD as antioxidant enzyme and level of malondialdehyde as one of the oxidative stress damage effect evidence on cell's components. The second part of the study was experimental study on cultured eutopic endometrial and endometriosis cells. They were induced by H2O2 of 0, 100, and 1000 nM concentration. Analysis of the expression of ARID1A by RTqPCR and ELISA, and the DCFH-DA for the level of Reactive oxygen species were done.

Result: The impact of the H2O2 induction in repressing ARID1A gene expression on the endometriosis as well on the eutopic endometrium cells are significant, but not on the ovarian cancer in this study.

Conclusion: Oxidative stress has a role in repressing the expression of ARID1A gene at the mRNA and protein levels on the endometriosis."

"Mortalin biology : life, stress and death” is a remarkable compilation of the research outcomes on the stress protein mortalin, a member of heat shock 70 family of proteins. The book is unique as it describes mortalin playing essential role in life, stress response and death either from cancer, when it becomes hyperactive or from neuro-degeneration, when it becomes hypoactive. The book provides up-to-date knowledge on mortalin with respect to its discovery, structure, evolutionary conservation, function and signal transduction in different organisms in a simple, but most comprehensive way, that besides offering an enjoyable and in-depth reading, prompts the reader to ask further questions to explore this protein with new ideas, approaches and experiments. Twenty-one chapters by the world leaders on the specific areas of mortalin research throw light on its multi-functionality, potentials for biotechnology, diagnostics and therapeutic values. Avenues of mortalin biology, yet unexplored, hold immense promises for future, and reading this volume provides an easy, enthusiastic and energetic head-on start."

"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."