In the early 1900s, cervical cancer was . Doctors couldn’t see it early, couldn’t catch it early, and (too often) couldn’t do much about it once symptoms showed up.
Fast-forward to now, and we’re living in a different world. Today, cervical cancer is largely preventable, and in some countries, they are genuinely talking about elimination (as in: “we barely see this anymore”). That kind of public health success doesn’t happen because someone tweeted a good thread. It happens because of decades of patiently doing science, boring-but-brilliant logistics, and a few stubborn people who kept going when the room wasn’t clapping.
This story starts the way many great prevention stories do: with a microscope, some cells, and a researcher who notices something other people aren’t paying attention to. And, like many stories, it is not without its darker twists.
A Scientist’s Perseverance Against Doubt
Georgios (George) Papanicolaou was a Greek immigrant working in New York. In the 1910s and 1920s, . Then he tried the technique on humans (with his wife Mary as his first long-term volunteer), and over the years of careful observation, he realized something big: cancerous and precancerous cells looked different under the microscope—before a tumor was visible to the naked eye.
In 1928, he presented a paper on using vaginal smears to detect uterine/cervical cancer. And the response was… not exactly a standing ovation. The dominant mindset then was basically: Cells alone can’t tell you that story. Papanicolaou didn’t win the argument in one dramatic moment. He just kept collecting samples, refining his method, and building evidence—year after year after year.
That’s a theme in prevention: the breakthrough is rarely a fireworks show. It’s more like watching someone steadily stack bricks while everyone else is distracted by shiny objects.
An Unexpected Connection: HeLa Cells and Medical Progress
If you’ve ever heard of HeLa cells, you’ve heard a chapter of this story—even if it didn’t come labeled as “cervical cancer prevention.”
In 1951, Henrietta Lacks was diagnosed with cervical cancer in Baltimore, Maryland. Without her informed consent (a fact that matters, ethically and historically), cells from her tumor were taken and became the first human cells to grow robustly in a lab. Later, it was determined that her cells were infected with HPV-18, one of the more aggressive strains. .
HeLa cells that helped accelerate the polio vaccine era (including large-scale cell production for poliovirus work). And over the decades, her cells also contributed to virology, cancer biology, and (yes) the long arc of work that helped make HPV vaccines possible.
So if you ever want a reminder that science is a tangled web of human stories—some inspiring, some uncomfortable—HeLa is right there, quietly showing up in the background of modern medicine like the most underrecognized supporting actor of all time. Her story, like many others, deserves to be told in its entirety rather than just as a footnote.
Solving the Mystery: What Causes Cervical Cancer?
Even after Pap screening began saving lives, a central question lingered: why does cervical cancer happen in the first place?
For a while, herpes simplex virus type 2 (HSV-2) was a popular suspect. It’s sexually transmitted. It’s common. Some studies found it in cervical tissue. Case closed?
Not quite.
Harald zur Hausen, a German virologist, pushed a different hypothesis: . It took years of work, but the evidence piled up, including identifying HPV DNA in cervical tumors and isolating high-risk types like HPV 16 and 18, which are consistently associated with a large share of cervical cancers worldwide. That work earned zur Hausen the Nobel Prize in Physiology or Medicine for this discovery. It is interesting to note that when this relationship was first identified in the mid 1980s, Dr. zur Hausen and colleagues approached pharmaceutical companies to discuss the possibility of developing a vaccine, but . Nevertheless, the idea had been planted: an “aha!” moment that shifted cervical cancer from a disease we react to into a disease we can block at the source.
From Virus Discovery to Vaccine Development
Once HPV was identified as the necessary cause of most cervical cancers, prevention strategies basically got a turbo boost.
Here’s the key public-health magic trick: HPV infection is extremely common, but cancer is not. Most HPV infections clear on their own. The real danger is persistent infection with high-risk types—the slow burn that can lead to precancer and then cancer.
Enter vaccines.
HPV vaccines work extremely well at preventing infection from the HPV types they target—and the downstream precancers those infections can cause. The CDC notes that , and real-world U.S. data show large drops in vaccine-type HPV infections after vaccine introduction.
The public health analogy here is engineering and a smoke alarm. Fire-resistant materials keep the fire from starting in the first place. That’s the HPV vaccine. Screening (Pap/HPV testing) is the smoke alarm—catching trouble early. You want both.
Vaccine Safety and Common Concerns
Because HPV can be sexually transmitted, the vaccine has collected more social baggage than a perfectly normal medical product should ever have to carry. So let’s be blunt:
The HPV vaccine has been studied extensively and has a strong safety profile. The most common side effects are what you’d expect with lots of vaccines: sore arm, dizziness, headache, and nausea. And yes, fainting (syncope) happens sometimes in adolescents after shots (HPV vaccine included), which is why clinicians are encouraged to have people sit or lie down and to observe them for about 15 minutes afterward.
Two common “but what about…” concerns come up a lot:
- Infertility: The World Health Organization’s Global Advisory Committee on Vaccine Safety .
- “It’s too new” / “We don’t know long-term effects”: HPV vaccines have been in use for years (recommended in the U.S. since 2006), with ongoing safety monitoring and large-scale population data. That’s almost 20 years and millions of doses given to millions of people. It’s not new, and we do know the long-term effects.
If you want the shortest, least-dramatic takeaway: the HPV vaccine is like a seatbelt. It doesn’t guarantee that nothing bad ever happens, but it dramatically shifts the odds in your favor with a very low cost in risk and inconvenience.
The Two-Level Defense: Vaccination and Screening
Here’s the part that often confuses people: vaccination doesn’t replace screening. It reduces risk, but it doesn’t eliminate it—because no vaccine covers every cancer-causing HPV type, not everyone gets vaccinated before exposure, and because not every case of cervical cancer is caused by HPV.
:
- Routine vaccination at age 11–12 (can start at 9)
- Catch-up vaccination through age 26 if not adequately vaccinated
- Ages 27–45: vaccination may be considered via shared clinical decision-making (because benefit depends a lot on prior exposure)
On the screening side, guidelines evolve as tests improve. One very current example: the , explicitly including self-collection for HPV testing as an acceptable option (with clinician-collected cervical samples still preferred for primary HPV testing).
If you remember nothing else: the best screening test is the one you actually get.
Understanding Risk Factors Beyond HPV
HPV is the necessary ingredient in most cases—but it’s not the whole recipe. Other factors can increase the chance that an HPV infection persists and progresses.
:
- Smoking
- Immunosuppression (including HIV)
- Long-term oral contraceptive use (because you tend to use fewer condoms, if any)
- High parity / multiple full-term pregnancies
- Early age of sexual activity, including sexual abuse of any kind
- Certain co-infections and social determinants that affect access to screening and care
This is why a purely individual-level “just get screened” message isn’t enough. Risk is shaped by biology and systems: insurance coverage, clinic access, transportation, time off work, trust, and whether care is delivered in a culturally sensitive and trauma-informed way.
Prevention is infrastructure.
Early Detection Matters: Recognizing Symptoms
One of the cruel tricks of cervical cancer is that early stages often have no symptoms. That’s why screening matters: it catches precancerous changes and early cancer before anyone feels anything wrong.
Still, symptoms can appear—especially later—and they deserve attention. :
- Vaginal bleeding after sex or between periods
- An increase in menstrual bleeding patterns after the age of 40, or bleeding after menopause
- Unusual watery or bloody discharge (sometimes with a strong odor)
- Pelvic pain or pain during sex
Symptoms don’t automatically mean cancer, but they do mean “please don’t wait and see.”
Progress and Persistent Disparities
Cervical cancer mortality in the U.S. has dropped dramatically over time, largely because of screening and prevention. The the US death rate has dropped by more than half since the mid-1970s.
And yet—this is the part where public health gently clears its throat and points at the structural issues we keep trying to ignore—those benefits haven’t been evenly distributed.
The same ACS statistics highlight that death rates for Black women and Native American women are about 65% higher than for White women. And disparities are tied to later-stage diagnosis, differences in access to high-quality screening and follow-up, and inequities across the cancer care continuum.
If cervical cancer is preventable, then a big chunk of the remaining burden is, bluntly, preventable inequity.
The Global Picture
Globally, cervical cancer is still devastating, especially in places where screening and treatment aren’t widely available.
The that nearly 94% of cervical cancer deaths in 2022 occurred in low- and middle-income countries, where access to prevention services is often limited.
This is what “global health” looks like in practice: the tools exist, the biology is understood, and the outcomes still diverge because systems differ. It’s not a mystery. It’s a map of who gets access.
A Vision for Elimination
Here’s the hopeful ending, and it’s not a fairy tale one. It’s a targets-and-programs ending, the kind public health actually runs on.
WHO’s defines elimination as bringing incidence below 4 per 100,000 women, and it lays out the now-famous 90–70–90 targets:
- 90% of girls are fully vaccinated with the HPV vaccine by age 15
- 70% of women screened with a high-performance test by 35 and again by 45
- 90% of women with precancer are treated, and 90% of women with invasive cancer are managed.
In this plan, there is no mention of vaccination of men, but this is also an important component of preventing cancer for women when it comes to HPV transmission. This is because men can be infected with and transmit HPV. They are “vectors,” in a sense. of the throat, neck, penis, and rectum. This is why countries like Australia and others that are close to cervical cancer elimination have , much like the recommendations for vaccination of girls starting as early as age 9.
That’s the blueprint: prevent infections, find disease early, treat it effectively.
And here’s the quiet, practical punchline: this isn’t just a medical story. It’s a delivery story. Which means the heroes aren’t only scientists. They’re also the school nurses, clinic staff, vaccinators, lab professionals, data analysts, outreach workers, and policy folks who make sure the breakthrough doesn’t stay trapped in a journal article.
Even in the U.S., policy varies widely. For example, as of May 2025, Immunize.org lists only a small number of U.S. jurisdictions (including D.C., Hawaii, Rhode Island, and Virginia) .
So yes: we’ve gone from microscope slides to vaccine victory. But the “victory” part still depends on whether we actually build systems that get prevention to the people who need it on time, affordably, and without unnecessary obstacles.
Support Is Available
If you, or anyone you know, is affected by cervical cancer, there is support out there: