What are HeLa cells?  Cancer biologist explains the 'You can't die' controversy

What are HeLa cells? Cancer biologist explains the ‘You can’t die’ controversy

In a stunning 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 field of biomedicine flourish in the 20th century.

As a cancer researcher who uses HeLa cells in my daily work, I sometimes find this hard to believe.

Cervical cancer cells that lack precancerous cells called “HeLa” after the first letters of their first and last name, are immortal, and continue dividing when most cells die. This ability to survive through endless generations of cells is what makes them invaluable to scientists experimenting with human cells.

Why are HeLa cells important

Before HeLa cells, scientists wanted a way to grow and study human cells in the lab for studies that would be impossible to perform on a living person. When Lax cervical cancer cells were successfully grown in a Petri dish in 1951, scientists now had a source of cost-effective, easy-to-use cells that expanded their ability to conduct research.

From polio and COVID-19 vaccines to cancer research and human genome sequencing, HeLa cells have played a huge role in many scientific discoveries and developments.

Henrietta Lacks’ story is also an ongoing bioethical issue, because these cells were taken from her during a routine cervical biopsy that were then given to researchers without her consent, as was common practice at the time.

The Lacks family has long tried to take legal action against companies they say have unfairly profited from Henrietta’s cells. A 2010 book by journalist Rebecca Sklott details how HeLa cells have affected science and the Lacks family.

But how did Lax cells become immortal?

Little did she know that the cells of 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 HPV, but only a small group are known to cause cervical cancer. In fact, 99.7% of cervical cancers are HPV-positive.

Fortunately, most people with high-risk HPV are able to clear the virus before it becomes cancerous. HPV vaccines can prevent more than 90 percent of HPV-related cancers. But 10 percent of people with HPV infection in the cervix develop cancer. Unfortunately, Henrietta was one of the unlucky ones.

Her misfortune helped explain how HPV works. Since the 1976 Nobel Prize-winning discovery of the essential role of HPV in cervical cancer, many scientists, including myself, have investigated how HPV causes cancer.

Two types of proteins

The virus’s ability to cause cancer has been shown to be linked to two proteins it produces. These viral proteins can target and destroy two key human proteins that protect against cancer, p53 and retinoblastoma (Rb).

P53 and Rb act as guards to ensure that cells do not accumulate harmful genetic mutations and stop dividing after a specified number of cycles. My research has focused on how HPV proteins interact with tumor suppressor proteins in different types of human cells, including HeLa.

Most cells divide about 40 to 60 times before they are too old to function properly and are killed naturally. But HPV can allow cells to divide forever, as it attacks the sentinels while keeping uncontrolled division in check.

After Laks was infected with HPV-18, the second most common and high-risk virus, her cervical cells lost the ability to produce these guards. Without growth assays, her cells were able to divide indefinitely and became “immortal” — surviving to this day in both test tubes and the 70,000 studies that made them possible.

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

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

2022-06-02 01:55:52

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