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Differences of Bone Marrow Features and BCR-ABL Variants in Chronic Granulocytic Leukemia Post Tyrosine Kinase Inhibitor Therapy Wivina Riza Devi; M Darwin Prenggono; Purwanto AP; Imam B
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 26, No 2 (2020)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v26i2.1457

Abstract

Chronic Granulocytic Leukemia (CGL) occurs due to chromosomal translocation (9;22) known as Philadelphiachromosome. p210 BCR-ABL1 oncogenes are classified into b2a2 and b3a2 transcripts which possibly lead to differentclinical manifestations and response to therapy. This study was aimed to prove that there is a difference in bone marrowfeatures and BCR-ABL between remissive and resistant CGL after Tyrosine Kinase Inhibitor (TKI) therapy. This research wasan observational study with a cross-sectional design carried out at Ulin Hospital Banjarmasin on 32 subjects. BCR ABL wasdetected by using PCR and bone marrow features were assessed by using bone marrow aspiration technique. The differencebetween bone marrow features and BCR-ABL variants was analyzed by using the T-test (p < 0.005) and Chi-Square(p < 0.005), respectively. There was a difference of BCR-ABL variants with p=0.091 and characterized by M:E ratio (p=0.124),myeloblast count (p=0.063), and eosinophil count (p=0.055). Also, there was a difference of bone marrow cellularity(p=0.000) and basophil count (p=0.016) between remissive CGL and resistant CGL patients. There was no difference in BCRABL variants, myeloblast count and eosinophil count between remissive CGL and resistant CGL patients. However, there wasdifferent of bone marrow cellularity and basophil count between remissive CGL and resistant CGL patients.
Eritropoetin dan Penggunaan Eritropoetin pada Pasien Kanker dengan Anemia Muhammad Darwin Prenggono
Cermin Dunia Kedokteran Vol 42, No 1 (2015): Neurologi
Publisher : PT. Kalbe Farma Tbk.

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.55175/cdk.v42i1.1049

Abstract

Eritropoetin (Epo) adalah hormon glikoprotein 30,4 kDa yang merupakan regulator utama produksi eritrosit sebagai respons terhadap penurunan oksigenasi jaringan. Produksi Epo terutama terjadi di ginjal dan sebagian kecil di hati, juga oleh sel-sel jaringan dan tumor. Efek Epo pada sel diperantarai oleh reseptor eritropoetin (EpoR). Aktivasi EpoR dimulai saat Epo berikatan dengan EpoR dan membentuk dimerisasi EpoR yang kemudian mengaktivasi jalur pensinyalan JAK2. Aktivasi JAK2 menyebabkan aktivasi jalur-jalur pensinyalan intraseluler, seperti STAT, Ras/MAPK, dan PI3-K. Pada sel-sel kanker, aktivasi jalur-jalur pensinyalan tersebut diduga mengakibatkan peningkatan proliferasi sel dan penurunan apoptosis. Ekspresi EpoR pada sel-sel kanker masih merupakan kontroversi. Penelitian dengan Epo-binding assay tidak dapat mengkonfirmasi keberadaan EpoR di membran sel kanker dan aktivasinya. Hubungan antara ekspresi EpoR dan progresivitas kanker diduga terjadi melalui efek parakrin ke sel-sel lain dalam lingkungan mikrotumor, seperti endotel dan trombosit. Efek Epo pada EpoR di sel-sel endotel dan trombosit tersebut dapat memicu angiogenesis dan mikrometastasis, sehingga menyebabkan perburukan kanker. Peran Epo dan EpoR pada progresivitas sel-sel kanker masih kontroversial dan memerlukan pembuktian lebih lanjut. Sejauh ini pedoman penatalaksanaan anemia terkait kanker yang dikeluarkan oleh NCCN dan ASCO tetap merekomendasikan penggunaan eritropoetin untuk pasien kanker dengan pembatasan-pembatasan tertentu.Erythropoetin (Epo) is a glycoprotein hormone of 30.4 kDa, is the main regulator of erythrocyte production in response to decreased tissue oxygenation. Epo production occurs mainly in the kidney and to a much lesser degree in the liver, it is also produced by other tissues and tumor cells. Activation of EpoR starts when Epo binds to EpoR resulting dimerization which then activates the JAK-2 signaling pathway. JAK2 activation triggers the activation of other intracellular signaling pathways, such as STAT, Ras/MAPK, and PI3-K. In cancer cells, activation of those signaling pathways could lead to increased cell proliferation and reduced cell apoptosis. The expression of EpoR on cancer cells is still an open debate. Studies using Epo-binding assay could not confirm the existence of EpoR on the cell membrane nor its activation. The association between EpoR expression and cancer progression is thought to occur through the paracrine effect on other cells within the tumor microenvironment, such as endothelial cells and platelets. The effect of Epo on the EpoR in endothelial cells and platelets could induce angiogenesis and micrometastasis, which then could lead to cancer progression. Role of Epo and EpoR in cancer progression has been controversial and further research is needed. Cancer-related anemia guidelines from NCCN and ASCO still recommend the use of Epo in cancer patients with certain restrictions.
Perbedaan Kadar Kreatinin Sebelum dan Sesudah Kemoterapi Berbasis Platinum Rusyda Taqiya Rahmi; Sasongko Hadi Priyono; Azma Rosida; M. Darwin Prenggono; FX Hendriyono
Homeostasis Vol 3, No 3 (2020)
Publisher : Homeostasis

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (260.52 KB)

Abstract

Abstract: Platinum analog has a potential cytostatic effect and causing nephrotoxicity or a decrease in kidney function. This study used creatinine level to assess kidney function that are carried out routinely before the patient starts the chemotherapy cycle. This study aimed to determine the differences in creatinine levels before and after platinum-based chemotherapy. This an analytical study used retrospective cohort design with a total sample of 70 people according to inclusion criteria. The result showed a median creatinine level of breast cancer patients before and after platinum-based chemotherapy is 0,63 mg/dL and 0,75 mg/dL. Wilcoxon test results obtained”p=0,000 (p <0.05), considered as a significant difference between creatinine level  before and after platinum-based chemotherapy in breast cancer patients period January 2018-June 2019 in Ulin Hospital Banjarmasin, but the change of creatinine levels remain in the normal range. Keywords: platinum, based” chemotherapy, creatinine” levels, breast cancer” Abstrak: Analog platinum memiliki efek sitostatika poten dan efek samping nefrotoksisitas atau penurunan fungsi ginjal. Penilaian fungsi ginjal menggunakan parameter kadar kreatinin yang dilakukan secara rutin sebelum pasien memulai siklus kemoterapi. Penelitian bertujuan untuk mengetahui perbedaan kadar kreatinin sebelum dan sesudah kemoterapi berbasis platinum. Ini adalah penelitian observasional analitik dengan pendekatan Kohort Retrospektif dengan subjek penelitian 70 orang sesuai kriteria inklusi. Didapatkan median kadar kreatinin sebelum dan sesudah kemoterapi berbasis platinum sebesar 0,63 mg/dL dan 0,75 mg/dL. Uji Wilcoxon menunjukkan nilai p=0,000 (p<0,05), disimpulkan terdapat perbedaan bermakna kadar kreatinin sebelum dan sesudah kemoterapi berbasis platinumpada pasien kanker payudara periode Januari 2018-Juni 2019 di RSUD Ulin Banjarmasin meskipun perubahan kadar kreatinin masih dalam rentang normal. Kata-kata kunci: kemoterapi berbasis platinum, kadar kreatinin, kanker payudara
Enhancing the Anticancer Activity of Squamocin for Breast Cancer Treatment Using Nanodiamond Nanoparticles: An In Vivo Study Firli Rahmah Primula Dewi; Sri Puji Astuti Wahyuningsih; Rasyidah Fauzia Ahmar; Na'ilah Insani Alifiyah; Vuanghao Lim; Muhammad Darwin Prenggono
HAYATI Journal of Biosciences Vol. 30 No. 1 (2023): January 2023
Publisher : Bogor Agricultural University, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.4308/hjb.30.1.131-139

Abstract

Squamocin is one of the annonaceous acetogenins produced by the Annonaceae family and displays potent anti-cancer activity against cancer cell lines. This study aimed to investigate the growth inhibition activity of squamocin coupled with nanodiamond on rats (Rattus norvegicus)-induced breast cancer. Twenty-five female R. norvegicus were divided into five groups (n = 5), including normal control (without any treatment), negative control, group treated with nanodiamond only (ND), group treated with squamocin only (SQ), and the group treated with squamocin coupled with nanodiamond (NDSQ). All of the animal models were induced for breast cancer, except for the normal control group. Breast cancer induction was performed using two doses of N-nitroso-N-methylurea (NMU) injection (50 and 30 mg/kg body weight) intraperitoneally and waited for 22 weeks until the tumor was detected to formed. Nanodiamond coupled with squamocin were administered by intraperitoneal injection (1.5 mg/kg body weight) for 5 weeks, one injection per 3 days. This study showed that the treatment with squamocin coupled with nanodiamond (NDSQ) significantly reduced the proliferation (Ki-67) and induced apoptosis (Caspase-3) of breast cancer cells, corresponding to the reduction of the thickness of the mammary ductal epithelium (p<0.001) and the lower level of CA-153 in serum. In addition, the treatment significantly reduced the malondioldehyde (MDA) and PI3KCA and increased the p53 level significantly. Altogether, in this study, we are the first to report the anti-cancer activity of squamocin in rat-induced breast cancer and the potency of nanodiamond as a carrier of squamocin to increase its anti-cancer activity.
Differences of Bone Marrow Features and BCR-ABL Variants in Chronic Granulocytic Leukemia Post Tyrosine Kinase Inhibitor Therapy Wivina Riza Devi; M Darwin Prenggono; Purwanto AP; Imam B
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol. 26 No. 2 (2020)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v26i2.1457

Abstract

Chronic Granulocytic Leukemia (CGL) occurs due to chromosomal translocation (9;22) known as Philadelphia chromosome. p210 BCR-ABL1 oncogenes are classified into b2a2 and b3a2 transcripts which possibly lead to different clinical manifestations and response to therapy. This study was aimed to prove that there is a difference in bone marrow features and BCR-ABL between remissive and resistant CGL after Tyrosine Kinase Inhibitor (TKI) therapy. This research was an observational study with a cross-sectional design carried out at Ulin Hospital Banjarmasin on 32 subjects. BCR ABL was detected by using PCR and bone marrow features were assessed by using bone marrow aspiration technique. The difference between bone marrow features and BCR-ABL variants was analyzed by using the T-test (p < 0.005) and Chi-Square (p < 0.005), respectively. There was a difference of BCR-ABL variants with p=0.091 and characterized by M:E ratio (p=0.124), myeloblast count (p=0.063), and eosinophil count (p=0.055). Also, there was a difference of bone marrow cellularity (p=0.000) and basophil count (p=0.016) between remissive CGL and resistant CGL patients. There was no difference in BCR ABL variants, myeloblast count and eosinophil count between remissive CGL and resistant CGL patients. However, there was different of bone marrow cellularity and basophil count between remissive CGL and resistant CGL patients.
Effect of Mercury Administration as an Oxidative Stress Trigger in Hepato-Renal Injuries Yuliana, Ida; Triawanti; Prenggono, Muhammad Darwin; Oktaviyanti, Ika Kustiyah; Irfan Maulana; Fahrina Ulfah
JURNAL KESEHATAN LINGKUNGAN Vol. 17 No. 2 (2025): JURNAL KESEHATAN LINGKUNGAN
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jkl.v17i2.2025.159-167

Abstract

Introduction: Mercury as the source of free radicals can trigger the activation of oxidative stress pathways. With its high toxicity, it can cause hepato-renal injuries. There have been many studies on mercury toxicity in various organs, but there are still few scientific studies that examine the hepato-renal injuries caused by mercury through the oxidative stress pathway. This study was conducted to investigate the triggering of the oxidative stress pathway due to mercury exposure in hepato-renal injuries. Methods: Research using randomized true laboratory experiment method with post-test control group design. The number of samples used was 28 Wistar rats. The research group consisted of 2 groups, control group was given aquadest ad libitum, and intervention group was given water contaminated with mercury per oral once a day (15 kg/WB). The treatment period was 14 consecutive days and on the 15th day, blood samples were taken. Oxidative stress marker was assessed by examining MDA and GPx levels and hepato-renal injuries were assessed by examining liver function (ALT and AST) and kidney function (ureum and creatinine). The collected data were analyzed by independent t-test with 95% confidence level; significant if p>0.05. Results and Discussion: The study found that mercury can trigger the activation of oxidative stress pathways and have an impact on hepato-renal function. Conclusion: Research still needs to be continued to prove that impaired hepato-renal injuries also occur at the cellular histomorphologic and discover other biomolecular mechanisms such as activation of inflammatory pathways that can also cause organ damage.
The Effects of Heavy Metal Contamination on Liver Function in a Rat Model Yuliana, Ida; Triawanti, Triawanti; Prenggono, Muhammad Darwin; Oktaviyanti, Ika Kustiyah; Asnawati, Asnawati; Ulfah, Fahrina; Maulana, Irfan
MAGNA MEDIKA Berkala Ilmiah Kedokteran dan Kesehatan Vol 11, No 2 (2024): August
Publisher : Universitas Muhammadiyah Semarang

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.26714/magnamed.11.2.2024.145-153

Abstract

Background:  Mining activities in South Kalimantan have been widely associated with the emergence of various health issues through heavy metal contamination in the water. Previous studies have demonstrated that the presence of heavy metals has an impact on physiological alterations inside many organs, notably the liver.Objective: The study aimed to determined the impact of liver damaged from heavy metal of lead (Pb), cadmium (Cd), and mercury (Hg), and the combination of the three in rat model.Methods: Our research used the true experiment laboratory method with a post-test group design. Male white rats (Rattus norvegicus), aged 2–6 months and weighing 250–300 grams, were assigned to the control group and the treatment group. Treatment groups were administered orally with water contaminated with heavy metals of Pb, Cd, and Hg orally for 28 days. The serum markers of liver damaged were then measured.Results: The levels of transaminase enzymes (AST and ALT) in the heavy metal-exposed group were increased compared to the control group. However, the increase was not statistically significant (p = 0.247; p = 0.349, respectively). The group exposed to Hg exhibited the highest levels of AST and ALT in comparison to the other groups.Conclusion: Heavy metal exposure tend to raise transaminase enzyme levels, indicating liver damage. Hg exhibited the greatest transaminase value increase of all heavy metals, indicating its highest potential for liver toxicity.