CHAPTER FOUR

Abnormal Chromosomes and Abortions

Philadelphia, 1959

The practice of abortion in American hospitals is inequitable, inconsistent, and largely illegal. The basic reason for this is that this aspect of twentieth-century medicine is being governed by nineteenth-century laws.

—Robert E. Hall, an obstetrician and gynecologist at Columbia University in New York, 19671

ON AN EXCEPTIONALLY lovely weekend in April 1959, with the Wistar Institute’s impressive renovations recently completed, Koprowski threw his born-again institute a coming-out party. In typical Koprowski fashion, it was a big, bold, first-class affair, kicked off by a VIP dinner under the vaulted ceiling and among the hieroglyphic-inscribed pillars of the Egyptian Room of the university museum.

That weekend the institute’s new labs were formally opened, and five hundred biologists packed a two-day symposium entitled “The Structure of Science,” where they were treated to a star-studded list of speakers. These included dignitaries like the mayor of Philadelphia, the U.S. surgeon general, and the president of the National Academy of Sciences, as well as top scientists like Peter Medawar, the British transplantation expert who would win a Nobel Prize the following year—and whose younger partner, Rupert Billingham, Koprowski had already recruited to the Wistar as part of his A-team of scientists. But the most buzz may have been around the presence of Francis Crick, who, with James Watson, had described the structure of DNA only six years earlier. (Barbara Cohen, the young lab technician who was working for Koprowski at the time, asked to recall the event fifty-five years later, remembered only being dazzled by Crick’s presence.)

Hayflick also launched something new that April.2 He began pursuing a question that was swirling in the scientific air and that had begun to intrigue him too. Could viruses cause cancer in humans? The notion that viruses might be implicated in the dread disease was not a new one. As early as 1842, Domenico Rigoni-Stern, an observant surgeon in Padua, Italy, noted that nuns, shut away as they were from the world’s temptations, were afflicted with cervical cancer far more rarely than other women.3 There were no tools available to test the implication of his observation—that a sexually transmitted agent might cause the disease. The first hard evidence for a viral role in cancer didn’t come until 1908, when two scientists at the University of Copenhagen, Vilhelm Ellerman and Olaf Bang, showed that healthy chickens infected with fluid from chickens with leukemia—fluid filtered to remove cells and bacteria—contracted leukemia.4 Their finding might have garnered more notice if it had been more widely recognized at that time that leukemia was a cancer.

But three years later a young American pathologist named Peyton Rous, working at the Rockefeller Institute, showed that a virus caused chicken sarcoma—a malignant tumor of connective tissue. Rous had taken fluid from a sarcoma in one chicken, filtered it—again, the ultrafine filter caught bacteria but not viruses—and injected it into other chickens, which then grew the same cancer. The young scientist was greeted mostly with indifference to his discovery that cancer could be transmitted between the chickens “by an agent separable from the tumor cells.”5 It wasn’t thought that a finding about chicken cancer could be relevant to human beings. Rous’s “agent” would later be named Rous sarcoma virus and would play a huge role in the study of cancer causation.

Conventional wisdom among biologists in the first half of the twentieth century held that cancer was caused by environmental factors, like smoking or chimney soot or, according to others, by gene mutations. As late as the mid-1950s, the influential Australian biologist Frank Macfarlane Burnet, who in 1960 would win a Nobel Prize for his work in immunology, pointedly dismissed the notion that viruses could cause cancer.6 However, by 1959, when Hayflick tackled the question, many biologists were pushing back, even against the likes of Burnet. They had ammunition in the fact that, over the decades since Rous’s discovery, more than a dozen viruses had been discovered to cause either benign or malignant tumors in a variety of animals, including rats, mice, and cats—if not in humans. Then, in 1958, an Irish surgeon named Denis Burkitt threw a tantalizing new piece of information into the mix. He discovered an aggressive childhood lymphoma in sub-Saharan Africa. Its distribution, in malaria-ridden areas, suggested an infectious cause. The same year, the National Institutes of Health (NIH) launched a well-funded effort to track down human “cancer viruses.”

Koprowski began organizing, with other leading scientists including Rous, an American Cancer Society conference on the subject of viruses and cancer causation. In July 1959 Time magazine ran a cover story featuring two researchers from the NIH, Bernice Eddy and Sarah Stewart, who had discovered a mouse virus that caused tumors in hamsters, rabbits, and rats. “The hottest thing in cancer is research on viruses as possible causes,” John Heller, the chief of the NIH’s cancer institute told Time.7

Hayflick recognized that he had a skill set that equipped him well to tackle the topic: he knew a good deal about microbiology, and he knew more than most scientists about growing cells in the lab. He went at the question with the traits that defined his style: thoroughness, patience, determination, and an outsized tolerance for seemingly mundane, repetitive work. (Some former colleagues call his style unimaginative, dogged, and plodding.)

With the help of a surgeon named Robert Ravdin, across the street at the Hospital of the University of Pennsylvania, he got hold of 300 human tumor samples and coaxed 225 of them to grow in lab dishes bathed in nutritious medium.8

Hayflick’s next step was based on a reasoned assumption: if any of these tumors were caused by a virus, that virus was likely still lurking within them, replicating itself inside the cells and then bursting or budding out, flooding the surrounding fluid medium with millions of individual virus particles. Hayflick began collecting samples of that lab-dish fluid and freezing it.

When he was ready, his next step would be to thaw that fluid and pour it over noncancerous cells in culture. If cancer-causing viruses were in the fluid, then it stood to reason that they might infect some of the normal cells, causing them to become cancerous. But where to get certifiably noncancerous cells that could survive and multiply in the lab?

Fortunately for Hayflick, there was now a new benchmark for normalcy in cells. In a classic 1956 paper, “The Chromosome Number of Man,” Albert Levan and Joe Hin Tjio, two scientists working in Lund, Sweden, had used a new microscopic technique to pin down the normal number of human chromosomes.9 Biologists now knew beyond doubt that normal human cells had, residing in their nuclei, forty-six chromosomes: twenty-three inherited from each parent. A cell that carried this normal complement of chromosomes was called a “diploid” cell. (The only normal human cells that don’t carry forty-six chromosomes are sperm and eggs, which, because they carry half as many chromosomes, twenty-three, are called “haploid.”)

During the 1950s scientists had launched dozens of cell lines from apparently normal human tissue. But with time—sometimes with very little time—these cells began to behave strangely. They displayed bizarre, disorganized shapes and sizes and bloated nuclei. And they developed abnormal numbers of chromosomes. There were lab-grown knee-joint cells with 133 chromosomes, liver cells with anywhere between 65 and 90 chromosomes, and foreskin cells with 72 chromosomes—the last from a four-day-old baby.10 To Hayflick and his contemporaries, such changes signaled one thing: cancer.fn1

Abnormal chromosomes had first been associated with cancer seventy years earlier, in 1890, when a young German pathologist named David Paul von Hansemann first recognized chromosomes in abnormal configurations in dividing cancer cells.11 Von Hansemann, peering through a microscope, saw in cancer cells split, frayed, broken chromosomes and chromosomes that hadn’t doubled in number, as they normally should before cell division, but rather tripled or quadrupled. Not long after this, another German scientist, Theodor Boveri, after studying aberrantly fertilized sea urchin eggs, proposed that abnormal numbers of chromosomes resulted when the stringy DNA packages didn’t segregate themselves properly during cell division. The resulting cells, he suggested, might ultimately tilt into uncontrolled growth.12 But with the tools on hand at the time, he had no way of proving his hunch.

It would be 1960 before two researchers, working near Hayflick in Philadelphia, discovered the first link between a chromosomal aberration and a cancer. Peter Nowell, a tumor biologist at the University of Pennsylvania School of Medicine, and David Hungerford, a graduate student at the Fox Chase Cancer Center in Philadelphia, examined the bone marrow cells of adults with chronic myelogenous leukemia, a blood-cell cancer. In almost all of the patients, chromosome 22 was abnormally short. They christened this chromosome, with its lopped-off head, “the Philadelphia Chromosome.”13 Their discovery confirmed what many scientists had long suspected: cancer was, at least in part, a disorder of genes gone awry.

For Hayflick in 1959, even before the discovery of the Philadelphia Chromosome, the aberrant chromosome numbers in these dozens of lab-launched cell lines presented evidence enough that the cells were not normal and would not do for his experiment. Yet as he confronted a paucity of normal cells that had been launched in lab dishes, he did have some indication that the feat was not impossible. Tjio, the codiscoverer of the normal number of human chromosomes, had since moved from Sweden to the University of Colorado, to the lab of another leading scientist there named Theodore Puck. Together the pair had grown apparently normal cells from patients, or their leftover surgical tissues. They had created cell lines from the uterus, the testis, and the prepuce, a fold of skin surrounding the clitoris. They reported that the cells from each line still had forty-six chromosomes and that those chromosomes looked normal under the microscope, even after five months of vigorous dividing in lab dishes.14

Even so, Hayflick had reservations about using leftover surgical samples, or even skin samples from volunteers, to try to grow normal cells in lab bottles. As a microbiologist he was well aware that cells from any human being who has been on the planet for any length of time are potentially contaminated with disease-causing viruses. He had seen firsthand during his time in Galveston the adenoviruses that lurked in people’s tonsils and adenoids. Herpes simplex virus was known to lie latent in nerve cells. Hepatitis viruses were assumed to simmer quietly in livers, and scientists were discovering all manner of rhinoviruses—a major cause of the common cold—inhabiting human noses and throats. It would be pointless to expose cells obtained from adults to the fluid that had bathed his cancer cells in the lab. If the ostensibly normal cells became cancerous, he wouldn’t know if this was due to a virus from the fluid or to some hidden virus already residing in the cells. However, there was one obvious source of tissue that, while not absolutely guaranteed to be virus free, was far more likely to be clean.

A fetus is protected in the womb. Tucked away in its mother’s body, it isn’t exposed to the raft of illness-inducing microbes that babies and toddlers meet on diaper-changing tables, in preschool classrooms, and on kitchen floors. What’s more, when its pregnant mother is exposed to unwelcome bacteria and viruses, the fetus is protected from most of them by its mother’s germ-attacking antibodies and her invader-targeting immune cells. Those malevolent microbes that aren’t dispensed with in the mother’s throat, digestive tract, and blood can still be attacked in the fetus, because some maternal antibodies cross the placenta. There are exceptions: a handful of disease-causing viruses can escape immune defenses and infect the growing fetus. But compared with the viral exposures of adults, the odds of any one of these affecting a given fetus are remote. In particular, Hayflick in 1959 did not have to worry about one such virus that is notorious today: HIV. So as Hayflick cast about for the cleanest tissue he could find, he kept circling back to a conclusion that seemed inevitable: growing cells from aborted fetuses was his best bet for developing normal human cells.

As the work of Albert Sabin and John Enders and their colleagues in the 1930s and 1940s makes clear, Hayflick was not the first scientist to turn to aborted fetuses to probe a biological question. He himself, while working as a graduate student at the Wistar in the mid-1950s, had seen fetuses waiting to be taken to the incinerator in the Wistar courtyard after being dissected for experiments using cells from fetal pituitary glands. As he completed his graduate studies, scientists in Stockholm were using cells from aborted human fetuses in what became a failed effort to make the first human cell–based polio vaccine. And Levan and Tjio, also working in Sweden, had examined lung cells from four aborted fetuses to pin down the normal number of human chromosomes.

As he looked for a source of aborted fetuses, Hayflick was operating in one of two parallel universes that existed in the United States in 1959. According to the law, abortion was a criminal offense in every U.S. state. The 1939 statute that was on the books in Pennsylvania, unlike those in the other forty-nine states, didn’t even make an exception if the woman’s life would be endangered by carrying a pregnancy to term.15 It read:

Whoever, with intent to procure the miscarriage of any woman, unlawfully administers to her any poison, drug or substance, or unlawfully uses any instrument, or other means, with the like intent, is guilty of felony, and upon conviction thereof, shall be sentenced to pay a fine not exceeding three thousand dollars ($3,000), or undergo imprisonment by separate or solitary confinement at labor not exceeding five (5) years, or both.16

If the fetus died—in other words, if the abortion was successful—the penalty for the person who performed the abortion was doubled to $6,000 and ten years in solitary confinement at labor. The harsher penalty also applied if the mother died during the procedure.17

The law conspicuously failed to define an “unlawful” abortion; the very word suggested that if there were “unlawful” abortions there might also be “lawful” procedures. That ambiguity, however, did not stop Pennsylvania authorities from taking enforcement seriously. They prosecuted both unqualified, back-alley operators and physicians who operated as solo providers: people like Lamar T. Zimmerman in Montgomery County (which includes Philadelphia’s upscale northwestern suburbs), a physician who was convicted in 1967 of performing an illegal abortion; and Benjamin King, MD, of Allegheny County (which encompasses Pittsburgh), who was sentenced to two to five years in prison in 1968.18

At the same time in a different setting—the Hospital of the University of Pennsylvania and other major hospitals that comprised the other, parallel universe—legal authorities tolerated abortion. They were carrying on a tradition that had evolved over decades, beginning as early as 1867. Then, an Illinois law declared that abortion was criminal “unless done for bona fide medical or surgical purposes.” It didn’t define those purposes but left it to the medical profession to do so.19

The term “therapeutic abortion” came to be used to describe those abortions that were understood—at least by supportive physicians and legal authorities—not to be criminal. A therapeutic abortion was performed by a qualified doctor who judged it necessary, even if the reasons for that necessity floated in a legal gray zone that would not finally be dispelled until the 1973 Supreme Court decision in Roe v. Wade. In that landmark ruling, the high court struck down state criminal laws and said that, except to protect the mother’s health, states could not restrict abortions before fetuses became capable of meaningful life outside the womb.

In the early decades of the twentieth century, so-called therapeutic abortions were performed in doctors’ private offices and in homes. During the 1930s they migrated increasingly to clinics and hospitals, and their numbers grew as women responded to the crushing economics of the Depression.20 In Philadelphia, however, access was clearly limited: a survey presented to the Obstetrical Society of Philadelphia reported that 329 women died in the city from self-induced or nonphysician-induced abortions between 1931 and 1940, or about 10 women for every 1,000 babies born.21

The growing numbers of physician-assisted abortions led states to enact tighter abortion laws, like the 1939 statute in Pennsylvania.22 In turn, doctors and hospitals moved to try to protect themselves legally. In the 1940s and 1950s they set up what they called “therapeutic abortion committees” in hospitals. The committees were made up of small groups of doctors appointed to officially receive and evaluate abortion applications.

The Hospital of the University of Pennsylvania—HUP for short—was a huge, imposing institution whose sheer, ten-story brick facade towered over the south side of the Ivy League university’s campus in west Philadelphia and, at certain times of the day, literally cast its shadow on the Wistar Institute. The oldest university-owned teaching hospital in the country, HUP was established in 1874. By 1959 it had accrued all the power that came with being the most prestigious hospital in Philadelphia.

Like many major hospitals, HUP had put a therapeutic abortion committee in place by 1955, and possibly earlier.23 One doctor who performed abortions as an obstetrician/gynecologist at HUP in the late 1950s through 1962 recalled the committee as a casual group in a 2014 interview. “Frankly, if a patient wanted an elective abortion, you simply called a colleague or two and said, ‘Would you approve this?’ The committee never even really met…. If it ever came to a legal issue … we could say we talked on the phone” and approved it.24

But by 1963 that relaxed approach had changed, for reasons that aren’t clear. Written rules approved by the hospital’s medical board that year required that the committee receive written applications from physicians proposing to perform an abortion. Each of three anonymous obstetrician/gynecologists serving on the committee was required to issue a written opinion on each application. In cases where it was appropriate, a different kind of specialist, often a psychiatrist, could be enlisted to pass judgment on an application. If a member of the committee wished, he—and it was almost always a “he”—could interview and examine the patient.25

Women who saw private doctors—that is, women who were, in general, wealthier, whiter, and better connected—were far more likely to obtain abortions through the committee than so-called clinic patients—poorer, often black patients who were seen at the subsidized, hospital-based outpatient clinic that HUP operated. Still, by the late 1950s it was increasingly difficult for women of any color to get therapeutic abortions, whose numbers dwindled in the conservative climate of the 1950s.26 That did not change in the 1960s. One educated estimate published in 1967 put the ratio of illegal abortions to hospital abortions at one hundred to one.27

As Hayflick remembers it, he was able to begin obtaining fetuses in 1959 because of Hilary Koprowski’s connection to Isidor Schwaner Ravdin, HUP’s surgeon in chief and the vice president of medical affairs at the university.

If the Hospital of the University of Pennsylvania was the preeminent hospital in the city, I. S. Ravdin—“Rav,” as he was known to close colleagues—was the preeminent power in the hospital. He had been chair of HUP’s Department of Surgical Research since 1935—though he may have been prouder of his stint building and running a jungle hospital in Burma during World War II. A short, mustachioed man with dark, receding hair and preternatural energy—his secretary at the time, Betsy Meredith, remembers him as “like a pea on a hot griddle”—Ravdin terrified medical students and residents alike and was used to his orders being obeyed immediately, if not sooner.28 His influence extended well beyond HUP to the halls of power in Washington. In 1956 he was photographed on a podium at the Republican National Convention, triumphantly raising the hand of President Dwight D. Eisenhower.29 Two months earlier, Ravdin had been summoned to Washington to operate on Eisenhower, who had developed a life-threatening bowel obstruction. By 1959 Ravdin was busy hatching a grand, new 374-bed building extending HUP, named after himself.

Supplicants coming to see Ravdin would watch him pull out a Dictaphone and fire off a letter that would result in whatever string they wanted pulled in the vast machinery of the hospital getting pulled—or not. One of these requests, according to Hayflick, came from Koprowski, who asked for the ferrying of aborted fetuses to an obscure junior scientist at the Wistar Institute.

Ravdin was a consummate political player in matters of sexuality, contraception, and abortion. He had to be. In heavily Catholic Philadelphia the church was a hugely powerful presence, always hovering in the background of hospital and university politics. When the medical school set up a Division of Family Studies in 1952, the division’s affiliation with the liberal Marriage Council of Philadelphia caused the medical school dean to write to Ravdin, flagging concern “that this plan might be mis-interpreted by the Catholic Church as being concerned with birth control.”30

Still, by 1960 the church and society at large were confronting a wave of change. At HUP it appeared one morning in the form of bright orange flyers blanketing the hospital’s huge Gates Pavilion. THE ROMAN CATHOLIC CHURCH AND THE HOSPITAL OF THE UNIVERSITY OF PENNSYLVANIA, ran the title on the eight-by-eleven-inch sheets, which complained vociferously that even Jewish and Protestant patients seen by hospital doctors couldn’t get fitted for diaphragms owing to pressure from the church.31

The flyers provoked a flurry of letters between hospital higher-ups—not refuting their truth but trying to figure out who had used hospital paper and mimeograph machines to make them. (It appears that the culprits were never found out.) “It is, as you can see, an inflammatory statement and might very easily get the University into several embarrassing situations,” Ravdin wrote to Franklin Payne, the chairman of the Department of Obstetrics and Gynecology. “The paper which was used … has also been used in your Department, with a mimeograph machine similar to that which your Department has.”32

Privately Ravdin very likely agreed with the flyers. But his job was to protect his institution, and in the effort he steered a careful path between women’s-rights advocates on one side and, on the other, the church. He was photographed beaming at Pope Pius XII in Rome in 1958, in a moment that he recalled as a “wonderful occasion.”33 Still, when he was invited to a Planned Parenthood luncheon a few years later, he wrote to the organizers that he would be “very happy” to attend.34

Koprowski’s legendary charm had fallen flat with Ravdin, who in mid-1959 was rapidly coming to consider the ebullient Pole manipulative and untrustworthy; one year later Ravdin would lead the failed attempt by a faction of the Wistar Board of Managers to oust Koprowski.35 But Ravdin almost certainly agreed to Koprowski’s request that the hospital ferry fetuses to Hayflick for a simple reason: he believed in scientific progress and was not willing to let personal politics get in the way of it.

Ravdin had been helping Wistar scientists from his earliest days as surgeon in chief. “We can assist you in providing any amount of tumor tissue for your work. Just let me know what you want and when you want it,” he wrote to the elderly cancer scientist Margaret Lewis after she asked for samples from malignant tumors in 1947.36 A decade later William McLimans, a Wistar virologist, wrote to Ravdin that he had found interesting results in tissue that Ravdin had provided from the breast cancers of twelve HUP patients. He wondered if he could look at their medical records. “This letter will give you access to our Record Room in the Hospital,” Ravdin wrote back.37

Hayflick himself had likely already benefited from I. S. Ravdin’s support: when Hayflick needed tumor samples to begin his investigation of whether viruses might cause human cancers, it was I. S. Ravdin’s son, Robert Ravdin, then a young general surgeon at HUP with an office four doors down from his father’s, who provided them.38

In mid-1959 Hayflick began working with the first of a series of fetuses that would arrive, whole, in his lab after he received a phone call from HUP informing him that an abortion had been done and a fetus was available. The gynecological surgeons supplied fetuses from pregnancies of three to four months, so that their major organs were developed enough to be dissected and removed for Hayflick’s purposes.39

Hayflick’s receipt of the fetuses was not subject to paperwork or permissions beyond the go-ahead from I. S. Ravdin that had set the process in motion. The transfers were informal, as virtually all such arrangements were in those days. And while the physical movement of the fetuses was not hidden as one would hide an illicit transaction, it was not paraded openly either, legal realities and moral sensibilities being what they were.

At eighteen weeks of gestation—in medical parlance, this means eighteen weeks since the mother’s last menstrual period and therefore roughly sixteen weeks after sperm and egg meet at conception—a human fetus is roughly 5.5 inches long, from the top of its head to its rump. (Its legs are tucked up in the fetal position.) It has arms and legs, fully formed fingers and toes, a nose and mouth and lips and ears and fingernails. It can blink, grasp, sleep, move its mouth, and kick. Its skin is so new and translucent that the underlying vessels look like vivid red highways on a complicated road map. True, its eyes are still closed, and its head is huge compared with the rest of its body, giving it a slightly alien appearance. The nerve pathways in its brain that will lead to consciousness are just beginning to sprout.40 It cannot survive outside the womb. But there is no mistaking it for anything but an incipient human being.

“I remember receiving whole fetuses at three, four months’ gestation. A baby this big,” Hayflick said during a 2012 interview, holding his hands about six inches apart. “I remember distinctly not being disturbed by that—don’t ask me why—to dissect that. I can’t explain it. But my constitution was such that it didn’t affect me.

“It was definitely going to end up in an incinerator,” he added. “If it was used for research purposes, some good possibly could come out of it for people.”41

The first fetus that arrived in his lab was a male. After several hours’ work dissecting the lungs, breaking up the lung tissue with the enzyme trypsin, and spinning the resulting cells in a centrifuge, Hayflick planted the cells in four rectangular Pyrex flasks known as Blake bottles.42 He poured in nourishing medium, carefully plugged each glass bottle with an amber-colored silicone stopper, put the bottles on a tray, and walked them into the 36-degree heat behind the heavy door of the incubation room beside his lab. He placed the bottles on their flat sides on a wooden shelf. This allowed the maximum amount of “floor space” for the cells, which didn’t float in the fluid medium but sank to the bottom. They would multiply until they covered the floor in a single layer.

It was about three days later that Hayflick spotted signs of growth in the bottles of cells from that first fetus: a near-transparent haze on the bottom of the bottle where the cells, once attached to the glass floor of the bottle, had begun dividing.43 He poured off the growth medium in each bottle, replaced it with a fresh batch, closed the door, and waited. By ten days later the cells covered the bottom of each bottle in a single confluent layer. (Normal, noncancerous cells stop dividing at this point, rather than continuing to multiply and pile up on top of one another. This property is called “contact inhibition.”)

Now Hayflick delegated to his technician, Fred Jacks—a young military veteran who would eventually earn his MD and become the first African American resident at Abington Memorial, a suburban Philadelphia hospital—the tedious job of “splitting” the bottles so that the cells coating the bottom of one bottle were halved and half of them were placed in a new Blake bottle. This involved a long series of steps that required Jacks first to use trypsin, the “jackhammer” digestive enzyme, to loosen the cells from the side of the bottle, where they were firmly stuck. Later he would bathe the loosened cells in growth medium and redistribute half of them to a new bottle by sucking them up into and then shooting them out of a glass pipette. His mouth was protected only by a wad of cotton placed in the upper end of the pipette. Labs all over the country used this technique, occasionally leading to unsavory accidents. Today most pipettes are operated by thumb-controlled pistons, much like syringes.

Not long after the initial split, the lung cells seemed to kick into much higher gear, multiplying fast enough that Hayflick soon instituted a strict schedule of splitting the bottles every third or fourth day. (The frugal Hayflick would take the spent culture medium home in lab bottles and use it to fertilize his roses, daffodils, and tulips.)

As two bottles became four, and four became eight, and eight became sixteen, and sixteen became thirty-two, it became clear to Hayflick that the bottles would soon take over the communal incubation room next door to his lab. So he set Jacks to freezing the cells, transferring them first into tiny wine bottle–shaped glass ampules not quite two inches high, which he would seal by melting closed the neck of the ampule with a quick pass through a Bunsen burner. Each ampule contained a fraction of an ounce of growth medium. And floating in each were between three million and four million cells.44

Living human lung contains many types of cells, even just sixteen weeks after conception. In a fetus of this age, there are cubelike endothelial cells lining blood vessels; taller, columnlike epithelial cells lining the thousands of tiny airways called bronchioles; and underlying smooth-muscle cells giving them support, to name a few. But holding the lung together is connective tissue, and its components are made by fibroblasts: long, spindly cells with tapered ends, shaped something like a compass needle. Fibroblasts, it turned out, were the fittest when it came to survival in the lab. They were the only cells still living in Hayflick’s bottles after a few weeks of life in the lab.

In the summer of 1960 Hilary Koprowski published a sleek, eight-by-eleven-inch booklet that featured write-ups on the work of all the labs at his rejuvenated institute. The Wistar Institute’s biennial report for 1958 and 1959 featured just one photo on its cover. It showed Hayflick’s fibroblasts. Inside, a description of the photo read: “These cells are from a normal fetal human lung with a [normal] number of chromosomes.”45

Hayflick’s excitement comes through between the lines of his written report explaining the significance of the cover photo. It was possible, he wrote, to grow from human fetuses cells that had not—not yet, anyway—turned cancerous in lab bottles. The fetal cell line pictured on the cover had been growing in such bottles in his incubator for six continuous months. It was named WIHL, for “Wistar Institute Human Lung,” and while it had repeatedly outgrown its bottles, so that it had had to be halved and transferred to new bottles dozens of times, “it still retains the diploid number of chromosomes,” Hayflick wrote, referring to the normal number of human chromosomes: forty-six.46

What was more, he went on, these WIHL cells didn’t have any of the telltale microscopic hallmarks of cancer cells: disorganization, irregular sizes, and bloated nuclei. In fact, they looked no different under a microscope from how they had when freshly harvested from the fetus months earlier. They were classical fibroblasts: elongated cells with slightly thicker middles and tapered ends. The WIHL cell strain “is an extremely important tool in this investigation and has very important implications in other fields as well,” Hayflick reported. “It is, from all indications, a normal human cell.” That, he added, made it an ideal cell for use in his quest to discover cancer-causing viruses.

But Hayflick’s research into whether viruses caused cancer was about to get left behind, supplanted by a discovery that he didn’t anticipate and that would stand scientific wisdom on its head.