The aggressive cervical cancer tumor that murdered Henrietta Lacks, a 31-year-old African American woman, became a crucial instrument that helped the biomedical industry thrive in the twentieth century in an astonishing twist of fate.
Even as a cancer researcher who works with HeLa cells on a daily basis, I find it difficult to accept.
Lacks' cervical cancer cells, dubbed "HeLa" after her first and last names, are eternal, proliferating even when other cells would perish. This capacity to survive several generations of cells is what makes them so important to researchers working with human cells.
Why HeLa cells matter
Before HeLa cells, scientists needed a technique to grow and study human cells in the lab so that they could do experiments that would be difficult in a living person. When Lacks' cervical cancer cells were successfully cultured on a petri dish in 1951, scientists gained access to a new supply of low-cost, easy-to-use cells, allowing them to extend their research capabilities.
HeLa cells have been essential in many scientific breakthroughs and discoveries, from polio and COVID-19 vaccines to cancer research and genome sequencing.
Because these cells were extracted from Henrietta Lacks during a normal cervical cancer biopsy and subsequently provided to researchers without her knowledge, as was typical practice at the time, her tale is also an ongoing ethical issue.
The Lacks family has long sought legal redress against firms that they believe have gained unfairly from Henrietta's cells. Journalist Rebecca Skloot wrote a book in 2010 on how HeLa cells influenced science and the Lacks family.
But how did Lacks' cells become immortal?
Lacks had no idea that cells in her cervix were infected with the human papillomavirus, or HPV, a virus that causes one of the most prevalent sexually transmitted illnesses. Although there are more than 150 distinct varieties of HPV, only a limited number of them have been linked to cervical cancer. In fact, HPV is found in 99.7% of cervical malignancies.
Fortunately, most people who are infected with high-risk HPVs are able to get rid of the virus before it causes cancer. Vaccines against HPV can prevent over 90% of malignancies caused by the virus. However, 10% of women who have HPV infections on their cervix get cancer. Henrietta, unfortunately, was one of the unlucky ones.
Her suffering has aided in the understanding of how HPV operates. Many scientists, including myself, have been exploring how HPV causes cancer since the Nobel Prize-winning revelation of HPV's critical involvement in cervical cancer in 1976.
Two proteins
It turns out that the virus's capacity to cause cancer is tied to two proteins it creates. These viral proteins can attack and destroy two important cancer-fighting proteins in humans: p53 and retinoblastoma (Rb).
P53 and Rb serve as sentinels, ensuring that cells do not acquire detrimental genetic mutations and cease proliferating after a certain number of cycles. In numerous types of human cells, including HeLa, I've studied how HPV proteins interact with tumor-suppressing proteins.
Most cells divide between 40 and 60 times before becoming too old to function properly and dying spontaneously. Because HPV attacks the sentinels that hold uncontrolled division in check, cells can divide indefinitely.
Lacks' cervical cells lost the ability to make these sentinels when she was infected with HPV 18, the virus's second-most-common high-risk strain. Her cells were allowed to divide endlessly since there were no growth checks in place, and they became "immortal," surviving on to this day in test tubes and in the 70,000 research they enabled.
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