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A History of HeLa Cells: How the Immortal Cells Advanced Biomedical Science

HeLa cells are the most famous human cells in science. Discover how cervical cancer, HPV proteins, and bioethics shaped one of medicine’s biggest breakthroughs.

Written byIvan Martinez, PhDBrought to you byThe Conversation
| 4 min read
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In an amazing twist of fate, the aggressive cervical cancer tumor that killed Henrietta Lacks, a 31-year old African American mother, became an essential tool that helped the biomedical field flourish in the 20th century. As a cancer researcher who uses HeLa cells in my everyday work, even I sometimes find it hard to believe.

In February 2026, over 70 years after doctors took Lacks’ cells without her consent or knowledge, her family reached a settlement with biotech company Novartis, which they’d sued in 2024 for making billions of dollars from her unethically harvested cells. Lacks’ descendants also filed lawsuits against several other biotech companies, including Thermo Fisher, which they reached a settlement with in August 2023. The family had not been previously compensated.

Lacks’ cervical cancer cells, called “HeLa” after the first two letters of her first and last name, are immortal, continuing to divide when most cells would die. This ability to survive through endless generations of cells is what makes them invaluable for scientists conducting experiments on human cells.

Why HeLa Cells Matter

Before HeLa cells, scientists wanted a way to grow and study human cells in the lab to conduct studies that are impossible to do in a living person. When Lacks’ cervical cancer cells were successfully grown in a petri dish in 1951, scientists now had a source of cost-effective and easy-to-use cells that expanded their ability to conduct research. From polio and COVID-19 vaccines to cancer research and sequencing the human genome, HeLa cells have played an enormous role in many scientific discoveries and advancements.1-4

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Henrietta Lacks’ story is also an ongoing bioethics case, because these cells were taken from her during a routine cervical cancer biopsy and were then given to researchers without her consent, as was common practice at the time.5 The Lacks family has long attempted legal action against companies they say have unfairly benefited from Henrietta’s cells. A 2010 book by journalist Rebecca Skloot details how HeLa cells affected both science and the Lacks family.

But how did Lacks’ cells become immortal?

Lacks didn’t know that cells in her cervix were infected with a virus that causes one of the most common sexually transmitted diseases: human papillomavirus, or HPV. There are more than 150 different types of HPVs, but only a small group are known to cause cervical cancer. In fact, 99.7 percent of cervical cancers are HPV positive.6

Fortunately, most people infected with high-risk HPVs are able to clear out the virus before it becomes cancerous. HPV vaccinations can prevent over 90 percent of HPV-related cancers. But 10 percent of people with HPV infections on their cervix develop cancer. Sadly, Henrietta Lacks was one of the unlucky ones.

Her misfortune has helped elucidate how HPV works. Since the Nobel Prize-winning 1976 discovery of HPV’s essential role in cervical cancer, many scientists, including me, have been investigating how HPV causes cancer.7,8

Two Proteins

It turns out that the virus’ cancer-causing ability is linked to two proteins it produces. These viral proteins can target and destroy two major human proteins that protect against cancer, p53 and retinoblastoma (Rb).9,10 P53 and Rb act as sentinels making sure cells don’t accumulate harmful genetic mutations and stop dividing after a set number of cycles. My research has focused on how HPV proteins interact with tumor-suppressing proteins in different types of human cells, including HeLa.11

Most cells divide around 40 to 60 times before they become too old to function properly and are naturally killed off.12 But HPV can allow cells to divide forever, because they attack the sentinels keeping uncontrolled division in check. After Lacks was infected with HPV 18, the second-most-common high-risk type of the virus, her cervical cells lost the ability to produce these sentinels.13 Without growth checks in place, her cells were able to divide indefinitely and became “immortal” – living on to this day both in test tubes and the well over 100,000 scientific publications they’ve made possible.

This article was updated to note the Lacks family’s settlement with Thermo Fisher in August 2023 and with Novartis in February 2026The Conversation

Ivan Martinez, Associate Professor of Microbiology, Immunology and Cell Biology, West Virginia University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

  1. Scherer WF, et al. Studies on the propagation in vitro of poliomyelitis viruses: IV. Viral multiplication in a stable strain of human malignant epithelial cells (strain HeLa) derived from an epidermoid carcinoma of the cervix. J Exp Med. 1953;97(5):695–710.
  2. Zhang NN, et al. A thermostable mRNA vaccine against COVID-19. Cell. 2020;182(5):1271-1283.e16.
  3. Bulzomi P, et al. The pro-apoptotic effect of quercetin in cancer cell lines requires ERβ-dependent signals. J. Cell. Physiol. 2012;227:1891-1898.
  4. Landry JJM, et al. The genomic and transcriptomic landscape of a HeLa cell line. G3 Genes|Genomes|Genetics. 2013;3(8):1213-1224.
  5. Beskow LM. Lessons from HeLa cells: The ethics and policy of biospecimens. Ann Rev Genomics Hum Genet. 2016;17:395-417.
  6. Walboomers JMM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J. Pathol. 1999;189:12-19.
  7. zur Hausen H. Condylomata acuminata and human genital cancer. Cancer Res. 1976;36(2 pt 2):794.
  8. Cooper GM. The cell: A molecular approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Tumor Viruses.
  9. Münger K, et al. Interactions of HPV E6 and E7 oncoproteins with tumour suppressor gene products. Cancer Surv. 1992;12:197-217.
  10. Barr JA, et al. Long non-coding RNA FAM83H-AS1 is regulated by human papillomavirus 16 E6 independently of p53 in cervical cancer cells. Sci Rep. 2019;9:3662.
  11. Martinez I, et al. miR-29 and miR-30 regulate B-Myb expression during cellular senescence. PNAS. 2011;108(2):522-7.
  12. Hayflick L. The limited in vitro lifetime of human diploid cell strains. Environmental Cell Research. 1965;37(3):614-636.
  13. Chen AA, et al. Human Papillomavirus 18 Genetic Variation and Cervical Cancer Risk Worldwide. J Virol 2015;89(20).
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Meet the Author

  • Ivan Martinez wears a grey vest over a white collared shirt with a blue tie in a research laboratory.

    Ivan Martinez, PhD, an Associate Professor of Microbiology, Immunology and Cell Biology at West Virginia University Cancer Institute, is investigating how RNA can influence lung cancer's response to radiation therapy.

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