Krebs

Cancer results from mutations in genes that regulate cell division. When genes encoding positive regulators are mutated, they become oncogenes producing over-active proteins. Conversely, mutations in tumor suppressor genes disable negative regulation, allowing unchecked proliferation. These genetic changes disrupt the normal balance that keeps cells dividing only when appropriate.

p53 is a multifunctional tumor suppressor protein essential for cell cycle control and apoptosis. Up to 50% of human tumors have mutations in the gene coding for p53. When mutated, this negative regulator loses function, allowing cells to divide unchecked and preventing damaged cells from undergoing programmed death, accelerating cancer progression.

A benign tumor is a mass of cells that remains localized and does not invade nearby tissues. Once a tumor begins invading surrounding tissues, it becomes malignant. Malignant tumors are dangerous because they can spread to other body parts through metastasis, which accounts for nearly 90% of cancer-related deaths.

As tumors grow, cells require more oxygen and nutrients. Through a process called angiogenesis, cancer cells produce growth factors that promote new blood vessel formation within the tumor. This increased blood supply enables continued tumor growth and provides a pathway for cancer cells to enter circulation and spread to distant sites.

Cancer is not one disease but many distinct diseases. Each patient has specific gene mutations, and every tumor contains different mutated cells. As tumors grow, new random mutations accumulate, making cells increasingly varied. Two patients with identical initial mutations develop tumors that respond differently to the same treatment, requiring personalized therapeutic approaches.

Some viruses cause cancer by inserting their own oncogene copies into healthy cells. For example, the viral version of the SRC enzyme lacks the regulatory domain present in the human version. Without this regulatory control, the viral protein triggers uncontrolled cell division in host cells, transforming them into cancer cells.

Chemotherapy targets cell division processes by using cytotoxic drugs—chemicals toxic to cells—that slow proliferation or kill fast-growing cells throughout the body. Different drug combinations are used depending on cancer type and stage. This approach exploits the characteristic feature shared by all cancers: abnormal cell proliferation.