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Scientific research underscores the critical role of inflammation in tumor development, with chronic inflammation from persistent infection sites serving as a key contributor to carcinogenesis. Inflammatory cells drive the tumor microenvironment, promoting neoplastic growth through cell proliferation, survival, and migration. This persistent state leads to DNA damage, free radical formation, and growth factor secretion, significantly elevating the risk of developing neoplasms. Thus, this chapter delves into the intricate relationship between inflammation and genetic mutations, highlighting the role of inflammatory cells in promoting reactive oxygen species production and cell growth. Tumors are portrayed as unhealed wounds, emphasizing the connection between inflammation and cancer development. Anti-inflammatory agents, particularly NSAIDs like aspirin, show promise in cancer treatment. NSAIDs exhibit efficacy in reducing colorectal cancer incidence and mortality, offering a diversified approach by limiting cell migration, enhancing chemotherapy sensitivity, and reducing primary and secondary tumor incidence. Integration of anti-inflammatory agents with traditional treatments presents a potential paradigm shift in cancer management. Further exploration of the inflammation-cancer relationship includes a focus on key inflammatory mediators and targets for inflammation reduction. Thus, this chapter also discusses recent developments in anti-inflammatory agents and cancer treatment, pointing toward future research directions. Cancer’s multifaceted nature involves inflammation in promoting tumor growth and metastasis, with the tumor microenvironment playing a crucial role. Triggers for inflammation, such as hypoxia, cell death, and genetic/epigenetic factors, are investigated. Understanding the molecular and cellular mechanisms governing inflammation’s role in tumor initiation, metastasis, and therapy resistance is vital. As immune-targeted cancer therapies gain prominence, examining immune and inflammatory pathways in therapy resistance becomes crucial. Therefore, the chapter concludes by emphasizing the need to unravel inflammation’s dual role in immunity and cancer, guiding efforts to overcome resistance to modern cancer treatments.

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Targeting Inflammatory Proteins for Inhibition of Cell Proliferation in Tumor Microenvironment

  • 章节

  • 发表日期：

    2024年

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  • Ankita Khataniar,
  • Sanchaita Rajkhowa,
  • Aparoop Das,
  • Magdi E. A. Zaki

摘要

Scientific research underscores the critical role of inflammation in tumor development, with chronic inflammation from persistent infection sites serving as a key contributor to carcinogenesis. Inflammatory cells drive the tumor microenvironment, promoting neoplastic growth through cell proliferation, survival, and migration. This persistent state leads to DNA damage, free radical formation, and growth factor secretion, significantly elevating the risk of developing neoplasms. Thus, this chapter delves into the intricate relationship between inflammation and genetic mutations, highlighting the role of inflammatory cells in promoting reactive oxygen species production and cell growth. Tumors are portrayed as unhealed wounds, emphasizing the connection between inflammation and cancer development. Anti-inflammatory agents, particularly NSAIDs like aspirin, show promise in cancer treatment. NSAIDs exhibit efficacy in reducing colorectal cancer incidence and mortality, offering a diversified approach by limiting cell migration, enhancing chemotherapy sensitivity, and reducing primary and secondary tumor incidence. Integration of anti-inflammatory agents with traditional treatments presents a potential paradigm shift in cancer management. Further exploration of the inflammation-cancer relationship includes a focus on key inflammatory mediators and targets for inflammation reduction. Thus, this chapter also discusses recent developments in anti-inflammatory agents and cancer treatment, pointing toward future research directions. Cancer’s multifaceted nature involves inflammation in promoting tumor growth and metastasis, with the tumor microenvironment playing a crucial role. Triggers for inflammation, such as hypoxia, cell death, and genetic/epigenetic factors, are investigated. Understanding the molecular and cellular mechanisms governing inflammation’s role in tumor initiation, metastasis, and therapy resistance is vital. As immune-targeted cancer therapies gain prominence, examining immune and inflammatory pathways in therapy resistance becomes crucial. Therefore, the chapter concludes by emphasizing the need to unravel inflammation’s dual role in immunity and cancer, guiding efforts to overcome resistance to modern cancer treatments.