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Detection of latent tuberculosis infection in household contacts of drug-resistant tuberculosis patients using interferon-gamma release assay: a study at Universitas Indonesia Hospital Muhammad Faris Indratmo; Diah Handayani; Ardiana Kusumaningrum; Febriana Catur Iswanti; Mohamad Sadikin
Acta Biochimica Indonesiana Vol. 8 No. 2 (2025): Acta Biochimica Indonesiana
Publisher : Indonesian Society for Biochemistry and Molecular Biology

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32889/actabioina.214

Abstract

Background: Drug-resistant tuberculosis (DR-TB) poses significant public health challenges in Indonesia. Household contacts of DR-TB patients face elevated risk of Mycobacterium tuberculosis infection, which may remain latent and asymptomatic. Objective: This study aimed to assess the prevalence of latent tuberculosis infection (LTBI) among household contacts of DR-TB patients using interferon-gamma release assay (IGRA). Methods: This cross-sectional study was conducted at Universitas Indonesia Hospital from February to May 2023. Eighteen asymptomatic household contacts from six confirmed DR-TB index cases were enrolled. Participants underwent clinical evaluation, chest radiography, and LTBI screening using the QuantiFERON-TB Gold Plus (QFT-Plus) assay. Results: Among 18 participants (mean age 33.3 years; 55.6% female), 8 (44.4%) tested positive for LTBI, while 10 (55.6%) tested negative. The highest IGRA positivity rates were observed in adolescents aged 12–16 years (66.7%) and young adults aged 17–25 years (60.0%). All participants were clinically asymptomatic with normal chest radiographs. Conclusion: This study demonstrates substantial LTBI prevalence among household contacts of DR-TB patients. The findings underscore the importance of systematic contact tracing, IGRA-based screening, and timely tuberculosis preventive therapy to reduce disease transmission and progression in high-risk populations.
Temozolomide Resistance is Associated with Upregulated MICB mRNA Expression and Protein Secretion in Human Glioblastoma Cells Kevin Johanes Kawengian; Septelia Inawati Wanandi; Febriana Catur Iswanti; Remizar Alpaddli
The Indonesian Biomedical Journal Vol 18, No 3 (2026)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v18i3.4250

Abstract

BACKGROUND: Standard treatment for glioblastoma multiforme (GBM) chemotherapy with temozolomide (TMZ) is often limited by chemoresistance, which is correlated with cancer immune evasion caused by the dysregulation of natural killer group 2 member D ligands (NKG2DL). While suppression of NKG2DL facilitates cancer progression, how chemoresistance regulates NKG2DL expression remains unclear. This study was conducted to examine the association of TMZ resistance with the expression and secretion of the NKG2DL subtype, MHC class I chain-related protein B (MICB), in human GBM cells.METHODS: An experimental in vitro study was conducted using TMZ-sensitive (U87MG) and intrinsically TMZ-resistant (T98G) human GBM cell lines. MICB mRNA expression was analyzed via quantitative reverse transcription polymerase chain reaction (qRT-PCR). Surface protein expression and extracellular secretion of MICB were measured using flowcytometry and enzyme-linked immunosorbent assay (ELISA), respectively.RESULTS: Repeated TMZ exposure successfully induced resistance in U87MG-R (+TMZ) cells, yielding significantly higher cell viability (p<0.01) and slower proliferation rates compared to parental U87MG cells. Following 2-days TMZ treatment, both intrinsically resistant T98G and adaptively resistant U87MG-R (+TMZ) cells, demonstrated a significant increase in MICB mRNA levels (p<0.05 and p<0.0001, respectively) and extracellular secretion of soluble MICB protein (p<0.01 and p<0.01, respectively), compared to TMZ-sensitive counterparts. Conversely, MICB surface protein level after 2-days TMZ treatment was significantly reduced in both T98G (p<0.0001) and U87MG-R (+TMZ) (p<0.01) cells relative to the respective U87MG cells.CONCLUSION: GBM cell resistance to TMZ was associated with an upregulation of MICB mRNA transcription and extracellular protein secretion, and concurrently with a suppression of MICB expression on the cell surface. These conditions may lead to a cellular adaptive mechanism to develop resistance to TMZ and may represent a strategic route to evade native host immune. KEYWORDS: glioblastoma multiforme, temozolomide, cancer chemoresistance, MHC class I chain-related protein B (MICB), natural killer group 2D receptor (NKG2D)
Targeting tumor associated macrophages to alternate cancer stem cells and tumor microenvironment milieu Mahdaleny Mahdaleny; Septelia Inawati Wanandi; Noorwati Sutandyo; Febriana Catur Iswanti
Universa Medicina Vol. 45 No. 2 (2026)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2026.v45.310-321

Abstract

Macrophages in the tumor microenvironment are involved in promoting cancer growth and enabling it to evade therapies. By acting as something like a tumor's "underground," these cells dampen down the "calls for help" that chemotherapy or radiotherapy might otherwise trigger. They also appear to enable some cells in the cancers to reset themselves into cancer stem cells (CSCs), allowing them to divide and differentiate. Cancer stem cells are compelled to initiate tumors and maintain their growth. In part, the tumor-associated macrophages (TAMs) effect this by secreting cytokines with well-established roles in regulating stemness, as well as proteins that govern cell migration and are known to help keep CSCs in the niche where the tumor formed and maintain the tumor. Prognostic studies have found that TAMs are associated with worse patient outcomes. This article reviews the existing knowledge on TAMs in supporting the survival and maintenance of CSCs, increasing tumor resilience and resistance to therapy. We did a systematic review using the keywords CSC, TAM, tumor microenvironment (TME), and extracellular matrix remodeling from the following databases: ScienceDirect, PubMed, NCBI, Nature, Google Scholar, and Oxford Academic for articles published between 2010 to 2026. The underlying premise of the current investigation is that macrophages facilitate the maintenance of the "stemness" characteristics of CSCs. The TAM-CSC alliance must be interrupted to improve therapeutic outcomes and reduce tumor recurrence. Our review focuses on addressing the difficulties presented by CSCs and TME through advanced research techniques and specific combination treatments. This alternative method offers a less harsh and more effective therapy that will improve the patient’s outcomes by effectively eradicating tumor cells and modifying the tumor microenvironment to enhance the immune system's capability to combat the tumor.