Malaria elimination remains a global public health priority, particularly in low- and middle-income countries. India has set a target of eliminating malaria by 2030, making it essential to understand gaps in healthcare access, utilization, and preventive practices in endemic areas to guide focused interventions to achieve national and global malaria elimination targets. A subnational, cross-sectional study surveying 37,849 households in ten malaria-endemic states in India, which covered 177,644 individuals, was carried out to estimate the health service and long-lasting insecticidal net (LLIN) utilization for febrile illness and malaria. The study found that the accessibility of a government healthcare facility was within 2.5 km (interquartile range [IQR] 1–5 km), with 57.4
Cancer cell characteristics are determined by gene expression, influenced by genomic, epigenetic, and transcriptional modifications. Genomic rearrangements and transcriptional splicing can result in the formation of fusion genes. BCR-ABL1 is an established fusion gene employed as a biomarker in leukemia. A single gene can amalgamate with several other genes and may impact cellular fate. Ethnicity-specific variants of fusion genes have been identified, such as the TMPRSS2-ERG variation observed in prostate malignancies among African-American, Caucasian, and Japanese populations in research studies. Next-generation sequencing has provided a new method for predicting genomic and transcriptomic changes. We aim to identify fusion genes in the Indian population using cancer samples to enhance diagnostic outcomes. This study performed a meta-analysis of tumor-specific RNA sequencing data for liver, tongue, and ovarian cancers, which are available online. It identified known fusion genes, including TRO-MAGED2, KRT14-S100A9, RNASE10-CD38, ACTN4-ACTN1, RGPD1-RANBP2, CTSC-RAB38, C15orf57-CBX3, AMBRA1-CKAP5, ATP2B3-ATP2B4, CNKSR3-IPCEF1, E2F4-RPL14, and MZT2A-MZT2B, along with 101 novel fusion genes. Novel fusion genes GABRP_SCGB3A2 and WWOX_FUT1 were identified in all three tumor tissues. GABRP acts as a tumor inducer, whereas SCGB3A2 functions as a tumor suppressor. WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.
Malaria, a persistent global health challenge, claimed 610,000 (estimated) lives in 2024, predominantly in sub-Saharan Africa. Effective control hinges on accessible data for prevention, surveillance, diagnosis, and treatment, yet critical intervention data remain restricted, hindering research and equitable outcomes. We advocate for a global policy mandating open access to malaria intervention data (e.g., number of rapid diagnostics used, antimalarial drugs used, distribution of insecticide-treated nets, and other vector control tools), arguing that it is a public health good essential to innovation, transparency, and resource allocation. Using India as a case study, we highlight gaps in data availability at district levels and propose actionable strategies, including standardized data platforms. This policy shift can accelerate malaria elimination, ensuring that data drive health equity worldwide.
Oral cancer, a major form of head and neck cancer (HNC), remains clinically challenging due to its aggressiveness, and therapeutic resistance. Tumor microenvironment (TME) is one of the key factors of cancer progression which strongly influences how cancer cells survive, spread, and respond to treatment. However, the molecular factors underlying its dysregulation are not fully understood. Recent data suggest that oncogenic forms of p53, particularly the mutant R273H and its amyloidogenic conformer, display gain-of-functon(GOF) phenotype. In this study, we investigated how oncogenic p53 remodel the secretome to affect the extracellular matrix (ECM) organization. Proteomic analysis of conditioned media from AW13516 (tongue carcinoma) cells show distinct ECM-related secreted proteins. Among the differentially enriched proteins, Inter-Alpha-Trypsin Inhibitor Heavy Chain H2 (ITIH2) and Clusterin (CLU) were secreted in amyloid p53 and mutant p53 expressing cells. Super-resolution microscopy revealed spatial co-localization of both ITIH2 and CLU with intracellular mutant p53 aggregates. Further, exosome isolation and analysis confirmed that both proteins are actively packaged and released through exosomes. Functional studies showed that ITIH2 silencing induced apoptosis through inhibition of the AKT/NF-κB pathway. Similarly, the CLU silencing reduced Vimentin and mTOR levels, while increasing BAX and E-cadherin levels, indicating loss of stemness, induction of apoptosis and partial restoration of epithelial features. To identify potential therapeutic vulnerabilities, molecular docking analysis revealed that methotrexate (MTX) binds strongly and specifically to both ITIH2 and CLU. Consistent with these predictions, MTX treatment combined with ITIH2 or CLU silencing produced a synergistic effect on the suppression of proliferation and migration. Overall, our findings identify ITIH2 and CLU as exosome-associated downstream effectors of oncogenic p53 that contribute to tumor microenvironment dysregulation. Thus, targeting this secretome axis, particularly, in combination with MTX may offer a promising strategy to limit oral cancer progression.
Cancer is the greatest cause of mortality, and tobacco smoking has been identified as the most significant risk factor for developing oral cancer. Nicotine is a primary addictive constituent of tobacco, and it is responsible for the development of cigarette addiction by stimulating the nicotinic receptor, which promotes the release of neurotransmitters in the brain, giving the smoker a pleasurable experience. A preponderance of evidence supports that tobacco smoking is the most important leading cause of cancer which is preventable. Tobacco cessation is a key component of a comprehensive approach to prevent and reduce tobacco use and save people from cancer. However, cessation programs are not found that efficient.
