How to kill a cancer cell
An oncologist today can choose from least 100 different cancer drugs, all of them aimed at killing dangerous cells or halting their growth without lethal harm to the patients. Most current drugs aren't that selective, but they exploit a weakness of cancer cells — they're more vulnerable than normal ones to damage because their self-repair mechanisms aren't as effective.
Cancer drugs attack malignant cells in a number of ways. Among them:
- Blocking metabolic reactions on which the cell's life depends.
- Damaging the DNA in the cell, causing it to self-destruct by apoptosis (natural cell death).
- Shutting down the cell's ability to divide. Some compounds disrupt chemical reactions needed for DNA to copy itself, while others break the DNA strands. Still others, like taxanes (Taxol® and related drugs) and vincristine, "freeze" the miniature tubes forming the cell's framework so they can't disassemble themselves for cell division.
- Turning off overactive cell growth signals caused by genetic mutations. Among these "targeted" drugs are Gleevec®, Erbitux™, Herceptin®, and Rituxan®. Because they selectively pinpoint cancer cells (normal cells lack the growth-gene mutations), they have fewer toxic side effects than most conventional agents.
- Prodding the body's immune system to recognize and attack cancer cells. Experimental cancer vaccines are made with bits of the patient's own tumor, combined with compounds that trigger a strong immune response.
- Antiangiogenesis — slowing or halting a tumor's growth by disrupting the network of blood vessels that feeds it (see related story). Antiangiogenic drugs include Avastin™, the first of its kind approved for commercial sale.
Despite this array of clever drug strategies, researchers are constantly hunting for new and better ones. Time will tell whether therapies based on the findings of Stanley Korsmeyer, MD,'s lab at Dana-Farber will add a new dimension to the fight against cancer, the nation's leading killer.
