Henrietta Lacks’s Cancer Cells


eLa is an “immortal” cancer cell line used extensively in research. It is named after Henrietta Lacks, a 31-year-old African American and mother of five


children who died of cervical cancer in 1951. Harvested at Johns Hopkins, the cell line is widely available, and the University never sold it, but has offered it freely to cancer researchers around the world. The cells are noted for active growth associated with the enzyme telomerase during cell division. Telomeres stop the ends of chromosomes from fraying or sticking during cell


division, like the plastic tip (aglet) at the end of shoelaces. The cell’s DNA repair system includes a single strand overlap that “looks like”damaged DNA. It makes sure that DNA is copied accurately, and telomerase helps reverse the loss of DNA from each round of replication. Longer telomeres are associated with anti-aging and are encouraged by healthy


lifestyles, including intermittent fasting, and dietary intake of legumes, nuts, seaweed, omega-3 fatty acids, vitamin D, fruit, dairy, and coffee. On the other hand, alcohol, red and processed meat may shorten them. A longitudinal 10-year follow-up study of 1,014 elderly patients, looked at telomere lengths and physical activity, and found higher leisure time physical activity in women, but not men, was associated with more rapid telomere attrition (Jantunen et al., 2020). The discovery of telomerase led to awarding the 2009 Nobel Prize in


Physiology/Medicine to three scientists, Elizabeth Blackburn, Carol Greider, and Jack Szostalc. Telomerase is widely expressed in 85% of human cancers, which are immortal


because the telomere mechanism is damaged. Human cells are not, and are subject to apoptosis (self-programmed death). Too much telomerase increases the number of cancer cells, and too little also increases cancer by depleting healthy regenerative potential, and shortening of telomeres. It is a fine balance. Want to learn more? Check out The Immortal Life ofHenrietta Lacks by Rebecca Skloot; 2010, Crown Publ.


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