What is cancer?

Cancer is a group of diseases characterized by the uncontrolled growth and spread of abnormal cells in the body. These abnormal cells, called cancer cells, can invade and destroy surrounding tissues and organs, leading to serious health problems. Cancer can occur in almost any part of the body and can arise from various types of cells.


The development of cancer typically involves multiple stages, including initiation, promotion, and progression. During initiation, genetic mutations or alterations occur within normal cells, leading to their transformation into cancer cells. These mutations may be caused by factors such as exposure to carcinogens (e.g., tobacco smoke, ultraviolet radiation), genetic predisposition, or other environmental factors.


Following initiation, cancer cells undergo uncontrolled growth and proliferation, a process known as promotion. This stage may be influenced by factors such as hormones, chronic inflammation, or immune system dysfunction. As the cancer cells continue to proliferate, they may acquire additional genetic changes that enable them to invade nearby tissues and spread to distant sites in the body, a process known as metastasis.


What is the relationship between cancer and oxidative stress?

Oxidative stress plays a significant role in the development, progression, and treatment response of cancer. Here’s how oxidative stress is related to cancer:


  • DNA Damage: Oxidative stress can lead to the generation of reactive oxygen species (ROS) within cells. ROS are highly reactive molecules that can damage cellular components, including DNA. DNA damage caused by oxidative stress can lead to mutations and genetic alterations that contribute to the initiation and progression of cancer. These mutations may affect genes involved in cell growth regulation, DNA repair, and cell death pathways, leading to uncontrolled cell proliferation and tumor formation.


  • Tumor Growth and Metastasis: Oxidative stress can promote tumor growth and metastasis through various mechanisms. ROS can activate signaling pathways involved in cell proliferation, survival, and angiogenesis (formation of new blood vessels). Additionally, oxidative stress can induce epithelial-mesenchymal transition (EMT), a process that enables cancer cells to acquire invasive and metastatic properties. By promoting tumor growth and metastasis, oxidative stress contributes to the spread of cancer to distant organs and tissues, leading to advanced disease and poorer outcomes.


  • Resistance to Therapy: Oxidative stress can contribute to resistance to cancer therapy, including chemotherapy, radiation therapy, and targeted therapies. Cancer cells exposed to oxidative stress may activate survival pathways and develop mechanisms to evade the cytotoxic effects of therapy. For example, ROS can activate cell survival pathways such as nuclear factor kappa B (NF-κB) and PI3K/Akt, which promote cell survival and resistance to apoptosis (programmed cell death). By enhancing cancer cell survival and resistance to therapy, oxidative stress can limit the effectiveness of cancer treatment and contribute to treatment failure.


  • Inflammation and Immune Response: Oxidative stress is closely linked to inflammation, which plays a critical role in cancer development and progression. Chronic inflammation can generate ROS and reactive nitrogen species (RNS), leading to oxidative stress and DNA damage within cells. Additionally, oxidative stress can modulate the immune response, impairing the function of immune cells such as T cells, natural killer (NK) cells, and dendritic cells. By promoting inflammation and immune suppression, oxidative stress can create a tumor-promoting microenvironment that supports cancer growth and progression.


Overall, oxidative stress is intimately involved in the pathogenesis of cancer and influences various aspects of tumor biology, including DNA damage, tumor growth, metastasis, therapy resistance, inflammation, and immune response.