Background and Objectives. Cell lines serve as invaluable tools in studying lung cancer biology and developing new therapies to combat the disease. However, commercially available cell lines are typically of Caucasian origin and may be less representative of the local genetic background. To address this, our lab previously immortalized cells from pleural fluid of a Filipino non-small cell lung cancer (NSCLC) patient via CDK4 transduction. Copy number variations (CNVs) are a type of genetic variation which may affect physiology and disease by disrupting gene function or altering gene expression, and in cancer, these may be associated with patient outcomes. CNV profiling can be valuable for understanding the biology of our immortalized cells and identifying genes that could serve as potential targets for diagnostic, prognostic, and therapeutic interventions. This study aimed to characterize previously immortalized NSCLC-derived cells, GL01, in comparison with an established lung adenocarcinoma (LUAD) cell line, A549, through whole-genome microarray-based copy number profiling. Methods. DNA was extracted from GL01 and A549 cells using a commercially-available silica-based DNA extraction kit. DNA extracts were quantified and normalized for microarray analysis. Whole-genome copy number profiling was done using the OncoScan CNV Plus Assay following the manufacturer’s protocols, and data was analyzed using the Chromosome Analysis Suite software. Functional analysis of genes identified to be involved in copy number aberrations was done using the PANTHER Classification System. Results. Copy number aberrations span 1,592,737,105 bp in GL01 and 1,715,708,552 bp in A549, with a high degree of concordance between the two. Largescale and focal copy number aberrations previously identified to be recurrent in various LUAD cohorts were present in both GL01 and A549. Focal copy number aberrations associated with previously described lung cancer-related genes involve the PDE4D gene in GL01 and the SKIL and CDKN2A/CDKN2B genes in both GL01 and A549. PANTHER Pathway analysis of genes positively correlated with mRNA expression showed that the ubiquitin proteasome pathway was significantly overrepresented in both GL01 (FDR p = 0.000074) and A549 (FDR p = 0.000075), with 20 genes involved. Additionally, the KRAS:p.G12C/S:c.34G>T/A somatic mutation variant was detected in both GL01 and A549. Conclusion. This study provides a method for identifying potentially clinically-relevant genes associated with a sample’s copy number aberrations and the pathways they represent, providing personalized mechanistic, prognostic, and therapeutic insights into the cancer biology of our cells.

We sequenced and annotated the genome of Lactobacillus iners SPIN 2503V10-D, a human vaginal isolate previously sequenced as a reference genome for the Human Microbiome Project, to refine its existing genomic data.

Tuberculosis (TB) and human immunodeficiency virus (HIV) co-infection remains a major public health concern globally and in the Philippines. The country continues to face a high burden of TB, multidrug- and rifampicin-resistant TB (MDR/RR-TB), HIV, and HIV-associated TB. Since HIV increases the risk of TB and TB worsens HIV outcomes, co-infection hinders progress toward the End TB Strategy and the UNAIDS 95-95-95 targets. This review summarizes the current knowledge on the epidemiology, prevention, and treatment of TB–HIV co-infection with a focus on the Philippine setting. Key challenges include socioeconomic barriers to care and rising drug resistance. In addition, the lack of an integrated TB–HIV data system disrupts continuity of care and weakens surveillance. Closing these gaps requires a coordinated national response that integrates effective policy with active community engagement. Research-driven and locally adapted strategies will be essential to bring the Philippines closer to its elimination goals.