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  1. Kathiresan N, Selvaraj C, Pandian S, Subbaraj GK, Alothaim AS, Safi SZ, et al.
    Adv Protein Chem Struct Biol, 2024;138:275-300.
    PMID: 38220428 DOI: 10.1016/bs.apcsb.2023.06.001
    Osteosarcoma is a malignant osseous neoplasm. Osteosarcoma is a primary bone malignancy capable of producing osteoid tissue or immature bones. A subsequent malignant degeneration of the primary bone pathology occurs less frequently in adults. The over-expression of several proteins, including Heat shock proteins, Cofilin, Annexins, Insulin-like growth factor, transforming growth factor-β, Receptor tyrosine kinase, Ezrin, Runx2, SATB2, ATF4, Annexins, cofilin, EGFR, VEGF, retinoblastoma 1 (Rb1) and secreted protein, has been associated to the development and progression of osteosarcoma. These proteins are involved in cell adhesion, migration, invasion, and the control of cell cycle and apoptosis. In genomic studies, osteosarcoma has been associated with several genetic abnormalities, including chromosomal rearrangements, gene mutations, and gene amplifications. These differentially expressed proteins could be used as early identification biomarkers or treatment targets. Proteomics and genomics play significant parts in enhancing our molecular understanding of osteosarcoma, and their integration provides essential insights into this aggressive bone cancer. This review will discuss the tumour biology that has assisted in helping us better understand the causes of osteosarcoma and how they could potentially be used to find new treatment targets and enhance the survival rate for osteosarcoma patients.
  2. B S, Thanigai Arasu A, Ravichandar S, Ganapathy P, Rajagopal RE, Murali U, et al.
    Ophthalmic Genet, 2026 Oct 30.
    PMID: 42960599 DOI: 10.1080/13816810.2026.2749870
    BACKGROUND: Age-related macular degeneration (AMD) is a progressive retinal disorder and a major cause of irreversible blindness in the elderly, with complement pathway dysfunction playing a key role in its pathogenesis.

    METHODS: The present aims to examine the impact of CFH rs1061170 (Y402H), C2 rs9332739 (E318D), and C3 rs2230199 (R102G) gene polymorphisms and AMD risk, in addition, Deleterious missense SNPs in CFH, C2, and C3 were analyzed for stability, conservation, and structural impact using multiple computational approaches. Relevant studies were searched in PubMed, Web of Science, and Google Scholar databases between the years Jan 2020 and 30 April 2026 and covered a total of nine case-control articles.

    RESULTS: Meta-analysis demonstrated significant associations of CFH rs1061170 and C3 rs2230199 polymorphisms with AMD susceptibility under specific genetic models (p 

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