ABSTRACT
Gastric cancer (GC) is one of the leading causes of cancer-related deaths globally. Gastritis caused by Helicobacter pylori (H. pylori) is a potent cause of gastrointestinal malignancies. The majority of all humans on the planet have H. pylori invasion in their stomachs, yet only a few diseased people develop GC. The human gastrointestinal system contains a broad population of microorganisms in addition to H. pylori. H. pylori heterogeneity has been studied because not all H. pylori diseases result in cancer. Individuals in the adult age group account for the bulk of gastric carcinoma cases. H. pylori has various strains, which is beneficial for its survival in host cell epithelium for a longer duration of time. Along with H. pylori, oral microbes have a major role in the pathogenicity of gastric carcinoma. The complex ecology of oral microbiota helps to defend against infections, preserve homeostasis, and regulate the immune system. In contrast, oral microbiota is involved in various mechanisms like anti-apoptotic activity, suppression of the immune system of the host, and initiation of chronic inflammation. These oral microbes are also responsible for the development of mutations. Interactions between the host immune system and bacteria promote the progression of cancer. For this review, various research articles were studied, and information was collected using databases like PubMed and Google Scholar. This review emphasizes on the role of H. pylori in gastric carcinoma, its pathogenesis, the role of various virulence factors and risk factors related to it, the role of oral microbiota in gastric carcinoma pathogenesis, diagnostic modalities, treatment options, and preventive measures for gastric carcinoma.
ABSTRACT
Glioblastoma multiforme (GBM) is a fourth-grade malignant glioma that continues to be the main contributor to primary malignant brain tumour-related death in humans. The most prevalent primary brain tumours are gliomas. The most dangerous of these neoplasms, GBM, has been shown to be one of the most lethal and refractory tumours. For those who have been diagnosed with GBM, the median time to progression, as determined by magnetic resonance imaging, is roughly six months, and the median survival is approximately one year. GBM is challenging to manage with old treatments like chemotherapy, tumour debulking, and radiation therapy. Treatment outcomes are poor, and due to this effect, the treatment is not up to the mark. GBM also shows diagnostic complexity due to limitations in the use of specific targeted therapies. The treatment protocol followed currently has an entire focus on safe resection and radiotherapy. Protein synthesis is not tightly regulated physiologically in malignant cells, which promotes unchecked growth and proliferation. An innovative, experimental technique for treating cancer uses polioviruses that have been genetically altered to target a fascinating aberration of translation regulation in cancer. This approach enables precise and effective cancer cell targeting based on the convergence of numerous variables. Oncolytic viruses have revolutionised cancer treatment. However, their effectiveness in glioblastoma remains restricted, necessitating more improvement. Oncolytic poliovirus has shown great potential in the treatment of GBM. Factors like the blood-brain barrier, immunosuppressive tumour microenvironment (TME), and tumour heterogeneity make treatment for malignant gliomas ineffective. In this review, we have focused on oncolytic viruses, specifically oncolytic poliovirus, and we explore malignant glioma treatments. We have also discussed currently available conventional treatment options for malignant glioma and other brain tumours.
