Medicine begins with storytelling. Patients tell stories to describe an illness; doctors tell stories to understand it. Science tells its own story to explain disease. (390)

Emperor of All Maladies is a book of many stories. Formally, it is a history of cancer, from its first recorded mention in 2500 B.C. among the hieroglyphic writings of the Egyptian doctor Imhotep, through twentieth-century research to present-day treatments. Mukherjee is a research physician, meaning he sees patients while engaging in cancer research, and he masterfully intersperses this history with stories of his patients as well as “stories” about genes and molecules that comprise our scientific understanding of cancer’s development.

The book’s subtitle is “A Biography of Cancer,” and Mukherjee treats his subject with the reverence due a career foe. Indeed, for reasons that will become clear, cancer holds a special place in the pantheon of disease. For one, it’s existed in humans as long as humans have existed. If it seems like a modern affliction that’s only because civilization has “unveiled” it (44). Cancer gains strength slowly, and throughout human history we tended to die from saber-toothed tigers, battle, or smallpox before cancer could get us. Ironically, as we cure other diseases and lengthen our lifespans, we give cancer unprecedented time to catch up.

What is Cancer?

The book reads at times like a detective story–with doctors and scientists chasing cancer through a winding and tragic history–and it sent a chill down my spine when we finally learn that the desperado is, in a single compelling word, us.

Cancer’s life is a recapitulation of the body’s life, its existence a pathological mirror of our own. Susan Sonntag warned against overburdening an illness with metaphor. But this is not a metaphor. Down to their innate molecular core, cancer cells are hyperactive, survival-endowed, scrappy, fecund, inventive copies of of ourselves. (388)

The most powerful medical realization in the book is that cancer cells do nothing that normal cells don’t–they just do it too much, too fast, and at the wrong time. When tumors send out blood vessels to feed their exponential growth, it’s the same process (angiogenesis) that normal organs engage. When cancer wickedly metastasizes throughout the body, it’s taking advantage of the same cellular mechanisms that allow our immune cells to travel within us to wherever they’re needed. This is why fighting cancer requires so much ingenuity: cancer cells are just broken normal cells–how do you kill one without hurting the other?

Cancer’s life

Every human cell is a machine of such staggering complexity that it’s a wonder we even exist at all. In order for human beings to grow and reproduce, our cells must do likewise, but it’s a tightly regulated process that depends on chemical signals (proteins) to tell cells when to start multiplying and when to stop (among thousands of other things). Our genes are the blueprints for these chemical signals, but when the DNA carrying our genes gets broken and the cell can’t fix it, the gene and thus the signal chemical it tells the cell to produce can become defective. If this defective gene, among roughly 26,000 others, is one of the hundred-or-so genes that regulate cell division, its broken signal may not be able to stop the cell from dividing. And since cells divide into exact copies of themselves, this one cell that can’t stop growing will turn into two cells that can’t stop growing, and then four, and eight, and on and on until it becomes a tumor.¹

The History of Cancer Treatment

2500 B.C.

Cancer’s first recorded appearance is in a parchment of the Egyptian physician Imhotep. He notes that “there is no treatment,” which at least makes him smarter than medieval European physicians three milennia later.

500 B.C.

The Persian queen Atossa has a tumor in her breast and orders a Greek slave to perform the first mastectomy. Miraculously, Atossa survives and rewards the slave with a Persian war against Greece so he can go home.

The Middle Ages

Medieval physicians think cancer is an excess of “black bile” (which doesn’t exist). They prescribe “frog’s blood…goat dung, holy water, crab paste” and some other useless crap.

1890s: The Surgical Age

William Halsted builds on the only thus-far viable method of removing cancer: the knife. He popularizes a method called radical surgery, from the Latin word radica, meaning root. He excises tumors plus as much around-the-tumor tissue as the patient can survive (and often sadly more), which tends to reduce rates of cancer recurrence. Scientists later learn that post-operative cancer recurrence has more to do with the stage of the cancer than with how much tissue you remove, meaning Halsted unnecessarily disfigured many women with early-stage breast cancer and performed hopeless surgery on many women with late-stage breast cancer.

Early 1900s: X-Rays

Scientists discover X-rays, which shatter DNA and prevent cells from dividing. For this reason, they’re tougher on rapidly-dividing cancer cells than they are on normal cells, but because they damage DNA they can also cause new cancer. Still, for small tumors that haven’t spread, X-rays prove an effective treatment.

The 1950s: Chemotherapy

A sea-change occurs with the emergence of chemotherapy. Scientists discover chemicals called antifolates that eat up folic acid, a vitamin essential to cellular reproduction. While antifolates damage all cells, Dr. Sidney Farber correctly reasons that they will especially damage rapidly-dividing cels like cancer (and hair follicles, hence the side-effect), making it an effective treatment. Cancer can grow resistant to such chemicals, however, leading doctors to try “cocktails” of several chemo drugs, bringing the body to the brink of death with hopes of it returning cancer-free.

The 1970s: Hormonal Therapy

Some prostate cancers depend on testosterone, and will shrink to nothingness when deprived of it by anti-testosterones. Likewise, some breast cancers depend on estrogen, and will shrink when given an anti-estrogen like Tamoxifen. While hormonal therapy is only effective against particular types of particular cancers, unlike chemo it has few side-effects.

The 1980s: Palliative Care

It was only in the 1980s that a movement emerged to treat the patient as well as the cancer. Called palliative care, this practice involves striving to reduce pain and suffering, both for those in treatment and with terminal cases, and looking to the psychological needs of patients.

The 1990s: Targeted Treatments

Only in the last 20 years have scientists gained an understanding of how cancer works at the molecular level. We’ve begun to identify the particular genes, proteins, and pathways that, when corrupted, can lead to cancer. And as a result, “targeted therapies” aim to attack specific molecules involved in cancer’s growth (as opposed to damaging all dividing cells like chemo does), resulting in more effective treatment with fewer to no side-effects. Targeted treatments are young, though: few are perfectly selective, and they haven’t yet been isolated for many types of cancer.

In the words of James Watson, Nobel laureate and co-discoverer of the structure of DNA:

Beating cancer now is a realistic ambition because, at long last, we largely know its true genetic and chemical characteristics. (393)

And indeed, looking back through the history of cancer treatment, it’s hard not to think we’re finally starting to figure cancer out. Targeted treatments hold great promise, even though they are now rather rare and unrefined. Yet it would seem that “beating cancer” means having effective treatments rather than eradicating it from our species, since life itself (i.e. normal cellular reproduction) is one of cancer’s causes. But even if we will always have to contend with cancer, there are still things it can teach us. In the words of the author, cancer cells are “more perfect versions of ourselves”: they thrive more easily, recover and adapt more quickly–and, on a final puzzling, perhaps thrilling note, cancer cells never die.

1. As with most biology, it’s of course more complicated than this. For one thing, we have two copies of every gene (one from mom and one from dad) and often both copies must get broken for the cell to truly become defective. And even then, it takes many broken signals for a cell to become cancerous. The odds are low, like rolling two million-sided dice, but we’re also constantly rolling these dice; genes get broken all the time by sunlight, chemicals in our environment, and even our cells making random copy-errors. ↩