The Laws of Medicine by Siddhartha Mukherjee Read Free Book Online Page A

these could open new vistas for cancer treatment. If cancer cells were dependent on the mutant genes for their survival or growth—“addicted” to the mutations, as biologists liked to describe it—then targeting these addictions with specific molecules might force cancer cells to die. The battle-ax chemical poisons of cellular growth would become obsolete at last. The most spectacular example of one such drug, Gleevec, for a variant of leukemia, had galvanized the entire field. I still recall the first patient whom I treated with Gleevec, a fifty-six-year-old man whose bone marrow had been so eaten by leukemia that he had virtually no platelets left and would bleed profusely from every biopsy that we performed. A fellow had to meet Mr. K with a brick-size pack of sterile gauze pads in the exam room and press on his biopsy site for half an hour to prevent bleeding. About four weeks after he started treatment with Gleevec, it was my turn to perform his biopsy. I came prepared with the requisite armfuls of gauze, dreading the half-hour ordeal—except when I withdrew the needle, the wound stopped bleeding by itself. Through that nick of the skin, its edges furling with a normal-looking clot, I could see the birth of a revolution in cancer treatment.
    Around the first week of my fellowship, I learned that another such drug, a molecular cousin of Gleevec’s, was beingtested in our hospital for a different form of cancer. The drug had shown promising effects in animal models and in early human experiments—and an early trial was forging ahead with human patients.
    I had inherited a group of patients on the trial from a former fellow who had graduated from the program. Even a cursory examination of the trial patients on my roster indicated a spectacular response rate. One woman, with a massive tumor in her belly, found the masses melting away in a few weeks. Another patient had a dramatic reduction in pain from his metastasis. The other fellows, too, were witnessing similarly dramatic responses in their patients. We spoke reverentially about the drug, its striking response rate, and how it might change the landscape for the treatment of cancer.
    Yet six months later, the overall results of the study revealed a surprising disappointment. Far from the 70 or 80 percent response rates that we had been expecting from our data, the overall rate was an abysmal 15 percent. The mysterious discrepancy made no sense, but the reason behind it became evident over the next few weeks when we looked deeply at the data. The oncology fellowship runs for three years, and every graduating batch of fellows passes on some patients from his or her roster to the new batch and assigns the rest to the more experienced attending physicians in the hospital. Whether a patient gets passed on to a fellow or an attending doctor is a personal decision. The only injunction is that a patient who get reassigned to a new fellow must be a case of “educational value.”
    In fact, every patient moved to the new fellows was a drugresponder, while all patients shunted to the attending physicians were nonresponders. Concerned that the new fellows would be unable to handle the more complex medical needs of men and women with no drug response—patients with the most treatment-resistant, recalcitrant variants of the disease—the graduating fellows had moved all the nonresponding patients to more experienced attending physicians. The assignment had no premeditated bias, yet the simple desire to help patients had sharply distorted the experiment.
    ....

Every science suffers from human biases. Even as we train massive machines to collect, store, and manipulate data for us, humans are the final observers, interpreters, and arbiters of that data. In medicine, the biases are particularly acute for two reasons. The first is hope: we want our medicines to work. Hope is a beautiful thing in medicine—its most tender center—but it is