cover
Contact Name
Bayu Brahma
Contact Email
journal.cancer@gmail.com
Phone
+628176389956
Journal Mail Official
admin@indonesianjournalofcancer.or.id
Editorial Address
National Cancer Center - Dharmais Cancer Hospital Research and Development Building, 3rd-floor Jl. Letjen S. Parman Kav. 84-86, Slipi West Jakarta
Location
Kota adm. jakarta barat,
Dki jakarta
INDONESIA
Indonesian Journal of Cancer
ISSN : 19783744     EISSN : 23556811     DOI : https://www.doi.org/ 10.33371
Core Subject : Health, Science,
Indonesian Journal of Cancer is a peer-reviewed and open-access journal. This journal is published quarterly (in March, June, September, and December) by Dharmais Cancer Hospital - National Cancer Center. Submissions are reviewed under a broad scope of topics relevant to experimental and clinical cancer research. Articles are original research that needs to be disseminated and written in English. All submitted manuscripts will go through the double-blind peer review and editorial review before being granted acceptance for publication. The journal publishes original research articles, case reports, and review articles under the following categories: cancer management, cancer prevention, cancer etiology, epidemiology, molecular oncology, cancer diagnosis and therapy, tumor pathology, surgical oncology, medical oncology, radiation oncology, interventional radiology, as well as early detection.
Arjuna Subject : Kedokteran - Onkologi
Articles 4 Documents
Search results for , issue "Vol 4, No 3 (2010): Jul - Sep 2010" : 4 Documents clear
Total Kolektomi pada Adenomatous Poliposis Kolon Ganas DUKUT RESPATI KASTOMO
Indonesian Journal of Cancer Vol 4, No 3 (2010): Jul - Sep 2010
Publisher : National Cancer Center - Dharmais Cancer Hospital

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v4i3.109

Abstract

Polyp hyperplasia is a neoplastic lession, abnormal gen hidding beyond the cell and developed to be malignant. Most of lession founded in rectum and sigmoid, and almost multiple, the smaller size 2 mm, appearance like a normal mucous colour and a little pale. Proportion in male and female is 13 : 1, most often in boy under 10 year-old (about four year-old), in adult around 18 year-old. Endoscopicaly incidens non adenomatous 15% - 86% under five mm in size, but 97% is adenoma if the size more than one cm. Familial Adenomatous Polyposis (FAP) 100% is became a malignancy.
Ekspresi Protein Gen p53 yang Bermutasi pada Jaringan Sediaan Blok Parafin Kanker Paru Karsinoma Bukan Sel Kecil ARIF R HANAFI; ELISNA SYAHRUDDIN; AHMAD HUDOYO
Indonesian Journal of Cancer Vol 4, No 3 (2010): Jul - Sep 2010
Publisher : National Cancer Center - Dharmais Cancer Hospital

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v4i3.101

Abstract

The tumor supressor gen p53 mutation encodes a protein that inhibits programmed cell death (apoptosis). The protein is expressed in basal cells in normal human epithelium, but no data are available on the frequency or clinical importance of its expression in carcinoma. We studied p53 mutation protein expression in post surgery tissues of patients with non-small cell lung carcinoma (NSCLC) and evaluated the correlation between protein expressions with prognosis of diseases. We have performed a retrospective study using 43 parafin block samples of NSCLC patients who were underwent surgery in Persahabatan Hospital during 1997 to 2008. The p53 mutation protein expression were analyzed by immunohystochemical method using a monoclonal antibody specific for p53 mutation protein. The possibility that p53 mutation expression correlated with survival was investigated with the log-rank test Kaplan Meier. Patients characteristic we found male 25/43 (58.1%) female 18/43 (41.9%) with mean age 56.19 + 8.3 y.o and mostly age 40 to 60 y.o 33/43 (76.7%). Number of smoker patiens were 31/43 (72.1%). We also detected p53 mutation protein in 16/43 (37,2%) in NSCLC tissues. Regarding histopatology types were 9/18 (50%) in squamous-cell carcinomas and 7/25 (28%) in adenocarcinomas. The corellation between positive p53 mutation protein expressions with pathological staging was significant p 0,004, according to T status T1-T2 62,5% and T3-T4 23,8% have had positive p53 mutation protein. Favorable prognostic significance of p53 mutation in patients with NSCLC stage I II, patients in the positive p53 mutataion survived longer than those in negative with respective median survival durations 28 and 18 months p 0,019. Adenocarcinomas type with p53 mutation have had median survival 11 months compared with squamose cell carcinomas 14 months.
Cancer Stem Cell: Target Baru Obat Antikanker DANNY HALIM; TONO DJUWANTONO; TRI HANGGONO AHMAD
Indonesian Journal of Cancer Vol 4, No 3 (2010): Jul - Sep 2010
Publisher : National Cancer Center - Dharmais Cancer Hospital

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v4i3.108

Abstract

Relaps, resistance and metastasis has become prominent problems that oncologists and cancer patients have to dealt with. Various studies have been done previously concluded that there are a subpopulation of cancer cells, identified as cancer stem cell, most likely to be the cause of relaps, resistance and metastasis of cancer. Cancer stem cell is a subpopulation of cancer cells that possess tumorigenicity, hence it can initiate the growth of tumor. Cancer stem cell has been suspected to be originated from normal stem cells reside in mature tissues, or from progenitor cells that gone through some series of alterations on its characteristics, including mutagenic and non-mutagenic changes. As seen in normal stem cells, cancer stem cell is also oftenly found in its inactive state. Therefore, cancer stem cell is not affected when it treated with many chemotherapeutic agents that are targeting cancer cells that proliferate extensively. Eventually, this event leads to the incidence of cancer relaps on cancer patients who already had series of cancer therapy. Based on this knowledge, it can be concluded that the only absolute way to overcome the incidence of metastasis, resistance and relaps on cancer patients, is to targeting cancer stem cell. Therefore, optimization on protocols of cancer stem cell identification and isolation strived continously. Some molecular markers that are oftenly used as a standard on cancer stem cell isolation are CD34, CD44 and CD133. In line with that, isolation methods that are based on sphere formation and the absorption of coloring dye could also be done to obtain cancer stem cell population. This review article would like to explain the nature of cancer stem cell existence, the pathology underlies its formation, characteristics and identification techniques that are commonly used, and challenges that have to be faced by scientists and physicians in order to optimize the application of cancer stem cell theory for the progress of science and patients sake.
Analisis Hambatan Siklus Sel Kanker Lidah Manusia SP-C1 yang Diinduksi oleh Biskoklaurin Alkaloid Cepharantine Menggunakan flow cytometry SUPRIATNO -
Indonesian Journal of Cancer Vol 4, No 3 (2010): Jul - Sep 2010
Publisher : National Cancer Center - Dharmais Cancer Hospital

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33371/ijoc.v4i3.103

Abstract

Flow cytometry has been widely used for detecting of apoptosis and cell cycle arrest on several human cancer cells. Supris clone-1 (SP-C1) cell is an oral tongue squamous cell carcinoma cell line which has rapidly growth, highly migration-invasion and metastatic to regional and distant lymph nodes. The aim of the study was to analyze the cell cycle arrest of SP-C1 inducted by cepharantine (CE) using flow cytometry. Treatment of SP-C1 cells with CE concentration 0, 5, 10 and 20 g/ml was carried out for 72 hours. The examination of cell cycle arrest of SP-C1 by flow cytometry revealed that CE with concentration 10 and 20 g/ml was significantly arrested of SP-C1 cell cycle in G1-S phase. Moreover, apoptosis was detected in G0 phase on the cells treated by CE 20 g/ml. These results concluded that CE had a potency to increase apoptosis with suppressing SP-C1 cell cycle phases.

Page 1 of 1 | Total Record : 4


Filter by Year

2010 2010


Filter By Issues
All Issue Vol 19, No 4 (2025): December Vol 19, No 3 (2025): September Vol 19, No 2 (2025): June Vol 19, No 1 (2025): March Vol 18, No 4 (2024): December Vol 18, No 3 (2024): September Vol 18, No 2 (2024): June Vol 18, No 1 (2024): March Vol 17, No 4 (2023): December Vol 17, No 3 (2023): September Vol 17, No 2 (2023): June Vol 17, No 1 (2023): March Vol 16, No 4 (2022): December Vol 16, No 3 (2022): September Vol 16, No 2 (2022): June Vol 16, No 1 (2022): March Vol 15, No 4 (2021): December Vol 15, No 3 (2021): September Vol 15, No 2 (2021): June Vol 15, No 1 (2021): March Vol 14, No 4 (2020): December Vol 14, No 3 (2020): September Vol 14, No 2 (2020): June Vol 14, No 1 (2020): March Vol 13, No 4 (2019): December Vol 13, No 3 (2019): September Vol 13, No 2 (2019): June Vol 13, No 1 (2019): March Vol 12, No 4 (2018): October-December Vol 12, No 3 (2018): July-September Vol 12, No 2 (2018): April-June Vol 12, No 1 (2018): Jan - Mar Vol 11, No 4 (2017): October- December 2017 Vol 11, No 3 (2017): July - September 2017 Vol 11, No 2 (2017): April - June Vol 11, No 1 (2017): Jan-Mar Vol 10, No 4 (2016): October - December 2016 Vol 10, No 3 (2016): July - September 2016 Vol 10, No 2 (2016): April - June 2016 Vol 10, No 1 (2016): Jan - Mar 2016 Vol 9, No 4 (2015): Okt - Des 2015 Vol 9, No 3 (2015): Jul - Sept 2015 Vol 9, No 2 (2015): April-Juni 2015 Vol 9, No 1 (2015): Jan - Mar 2015 Vol 8, No 4 (2014): Oct - Dec 2014 Vol 8, No 3 (2014): Jul - Sep 2014 Vol 8, No 2 (2014): April-Juni 2014 Vol 8, No 1 (2014): Jan - Mar 2014 Vol 7, No 4 (2013): Oct - Dec 2013 Vol 7, No 3 (2013): Jul - Sep 2013 Vol 7, No 2 (2013): Apr - Jun 2013 Vol 7, No 1 (2013): Jan - Mar 2013 Vol 6, No 4 (2012): Oct - Dec 2012 Vol 6, No 3 (2012): Jul - Sep 2012 Vol 6, No 2 (2012): Apr - Jun 2012 Vol 6, No 1 (2012): Jan - Mar 2012 Vol 5, No 4 (2011): Oct - Dec 2011 Vol 5, No 3 (2011): Jul - Sep 2011 Vol 5, No 2 (2011): Apr - Jun 2011 Vol 5, No 1 (2011): Jan - Mar 2011 Vol 4, No 4 (2010): Oct - Dec 2010 Vol 4, No 3 (2010): Jul - Sep 2010 Vol 4, No 2 (2010): Apr - Jun 2010 Vol 4, No 1 (2010): Jan - Mar 2010 Vol 3, No 4 (2009): Oct - Dec 2009 Vol 3, No 3 (2009): Jul - Sep 2009 Vol 3, No 2 (2009): Apr - Jun 2009 Vol 3, No 1 (2009): Jan - Mar 2009 Vol 2, No 4 (2008): Oct - Dec 2008 Vol 2, No 3 (2008): Jul - Sep 2008 Vol 2, No 2 (2008): Apr - Jun 2008 Vol 2, No 1 (2008): Jan - Mar 2008 Vol 1, No 4 (2007): Oct - Dec 2007 Vol 1, No 3 (2007): Jul - Sep 2007 Vol 1, No 2 (2007): Apr - Jun 2007 Vol 1, No 1 (2007): Jan - Mar 2007 More Issue