Anticancer drugs are pharmaceutical agents developed to eliminate or slow the growth of malignant cells. These treatments focus on the unique characteristic of cancer cells: rapid and uncontrolled proliferation, which distinguishes them from most healthy tissues. Historically, treatment involved generalized agents toxic to any rapidly dividing cell. Modern oncology now uses increasingly precise methods, shifting from broad cellular destruction toward specific molecular and immunological manipulation, resulting in greater efficacy and reduced harm.
Traditional Chemotherapy
Traditional chemotherapy operates on the principle of cytotoxicity, targeting rapidly dividing cells. Malignant cells divide faster than most normal cells, making them disproportionately vulnerable. This approach targets the cellular machinery responsible for replication and division, not the cell’s molecular identity.
One common mechanism involves interfering with the cell’s genetic material. Alkylating agents create cross-links or breaks in the DNA strands, preventing accurate replication. Antimetabolites mimic the natural building blocks of DNA and RNA, halting synthesis when incorporated into the genetic material.
Another class of drugs disrupts mitosis, the final stage of cell division. Anti-microtubule agents interfere with the formation of the mitotic spindle, a structure necessary for separating chromosomes. By damaging DNA or blocking cell division, these drugs initiate programmed cell death (apoptosis) in cancer cells. This non-specificity means healthy, quickly dividing cells are also affected, leading to systemic side effects.
Targeted Therapies
Targeted therapies represent a shift toward precision medicine by acting on specific molecular features that drive cancer growth. These drugs inhibit proteins, enzymes, or pathways that are overactive or mutated in cancer cells. The goal is to block the specific signaling mechanisms that allow the tumor to thrive, rather than broadly killing dividing cells.
One major type involves small molecule inhibitors, which are compounds small enough to enter the cell and block specific enzymes, such as tyrosine kinases. These enzymes function as switches in signaling cascades that instruct a cell to grow and divide; blocking them halts proliferation. Another form uses monoclonal antibodies, which attach to receptors on the cancer cell surface or to growth factors in the surrounding environment.
These antibodies can block growth factor receptors (e.g., HER2 or EGFR), preventing the cell from receiving growth signals. Targeted agents can also inhibit angiogenesis, the process by which tumors generate new blood vessels for nutrients and oxygen. Blocking factors like Vascular Endothelial Growth Factor (VEGF) starves the tumor. Due to their specificity, these therapies require biomarker testing to identify unique genetic mutations or protein overexpression before treatment begins.
Immunotherapies
Immunotherapies utilize the patient’s own immune system to recognize and eliminate malignant cells, representing a fundamentally different strategy. Instead of directly attacking the tumor, these drugs enhance the host’s immune cells to fight cancer. Immunotherapy works by disabling the sophisticated mechanisms cancer cells use to evade immune detection.
A prominent class is immune checkpoint inhibitors, which block molecules on immune cells or cancer cells that act as “brakes” on the immune response. For example, a T-cell has a checkpoint protein (PD-1) that can be activated by the cancer cell’s ligand (PD-L1), effectively deactivating the T-cell. Checkpoint inhibitors disrupt this binding, releasing the brake and allowing T-cells to become active and target the tumor.
Another specialized form is Chimeric Antigen Receptor (CAR) T-cell therapy. This involves extracting a patient’s T-cells, genetically modifying them in a laboratory to express a synthetic receptor (the CAR), and then reinfusing them. The CAR receptor is designed to lock onto a protein on the cancer cell surface, turning the engineered T-cells into targeted fighters. This leverages the immune system’s memory and specificity to create a sustained anti-cancer response.
Administration Methods and Common Side Effects
Administration Methods
Anticancer drugs are administered through several routes depending on the drug, cancer type, and patient health. The most common method is intravenous (IV) infusion, delivered directly into a vein. This systemic delivery ensures the medication is quickly distributed throughout the bloodstream to reach cancer cells.
Many newer targeted therapies and some chemotherapy agents are formulated as oral medications, which patients can take at home. Less common methods include subcutaneous injection or local administration, such as intrathecal injection into the fluid surrounding the spinal cord to treat CNS cancers. The choice of administration method balances efficacy, patient convenience, and safety.
Common Side Effects
The side effects experienced vary significantly based on the drug’s mechanism of action.
Chemotherapy Side Effects
Because traditional chemotherapy targets all rapidly dividing cells, common adverse effects stem from damage to healthy tissues. This damage often leads to:
- A drop in blood cell counts due to bone marrow damage, increasing the risk of infection.
- Nausea, vomiting, and inflammation of the mouth (mucositis) due to digestive tract lining damage.
- Hair loss due to damage to hair follicles.
Targeted Therapy Side Effects
Targeted therapies cause fewer generalized effects due to their precision, but they can still lead to issues such as skin rash, diarrhea, or liver enzyme abnormalities depending on the specific molecular pathway inhibited.
Immunotherapy Side Effects
Immunotherapies introduce a unique set of side effects by activating the immune system, sometimes excessively. This can lead to immune-related adverse events, characterized by inflammation in various organs, such as the lungs, colon, or endocrine glands. General symptoms like fatigue or fever may also occur.