CONNECTION BETWEEN CANCER AND INFLAMMATION: COMPREHENSIVE REVIEW
Authors: Baidya M , DE S AND SHIL P

ABSTRACT
Inflammation is often associated with the development and progression of cancer. The cells responsible for cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance; therefore, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammations can result in immune suppression, thereby providing a preferred background for tumor development. The current review provides a link between inflammation and cancer development. Inflammation that promotes cancers is one of the hallmarks of cancer. Research has demonstrated that inflammation, both acute and chronic, has a significant impact on the development of cancer. Advances in the study of inflammation have demonstrated a link between inflammatory processes and tumor growth, neoplastic transformation, and the productionof metastases and recurrences. Furthermore, the invasive procedures for tumors (biopsy and surgery) impact the residual tumor cells by promoting their migration, proliferation, and survival. In this review, we concentrate on the state of our understanding on inflammation and how inflammatory processes may induce cancer. Keywords: Inflammation, cancer, cell signalling, immunotherapy’s, cyclooxygenase-2
Publication date: 01/07/2025
    https://ijbpas.com/pdf/2025/July/MS_IJBPAS_2025_9185.pdf
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https://doi.org/10.31032/IJBPAS/2025/14.7.9185