The never-ending story of HeLa
Re: "HeLa Herself"
HeLa was not originally grown as a monolayer but as an explant, and not in a "nutrient solution of chicken plasma" but in a clot formed from chicken plasma and chicken embryo extract. The latter supplied the main source of nutrients. This technique had been used since the nineteen twenties by Alexis Carrel.
HeLa may have been sent to researchers "studying the effects of zero gravity in space,"...
Terry Sharrer replies: I thank the correspondents for their helpful remarks. Hayflick is quite right about the first "immortal" cells being Earle's mouse line, and he raises another interesting point about the WI-38 human embryo cell line used for vaccine production. Enders, Weller, and Robbins also used human fetal tissue to first grow poliovirus (as Weller's notebook reads for March 30, 1948: "Tissue consisted of the arm and scapula of a 4-month of [sic, old] fetus obtained at therapeutic abortion because of rubella at three months' gestation.").
George Gey, who developed the roller tube method Enders and others used to grow virus in tissue cultures, showed (with William Scherer and Jerome Syverton) that poliovirus could infect HeLa cells,
Consent to culture HeLa cells was neither asked nor given while Mrs. Lacks was alive nor later from her family. Despite the Nurenberg Code (1947) which established voluntary consent as "absolutely essential" for medical experiments, Gey and colleagues did not consider biopsy material as experimental. Readers will have to decide for themselves whether Johns Hopkins School of Medicine kept Henrietta Lacks' identity secret for decades because of proper concern for patient confidentially or for not wanting to expose itself under an issue where the norms changed. The Lacks family wonders about this, too.
References1. T. Sharrer, "HeLa Herself," The Scientist, 20(7):22, July 2006. 2. T. Sharrer, "The First Immortal Cell Line," The Scientist, 20(7):88, July 2006. 3. W.R. Earle, "Production of malignancy in vitro: IV. The mouse fibroblast cultures and changes seen in the living cells" J Natl Cancer Inst, 4:165, 1943. 4. P. Montgomery et al., "The response of single human cells to zero gravity," In Vitro, 14:165-73,1978. 5. M.A. Fletcher et al., "Human diploid cell strains (HDCS) viral vaccines," Dev Biol Stand, 93:97-107, 1998. 6. L. Hayflick, "The illusion of cell immortality," Brit J Cancer, 83:841-6, 2000. 7. Notebook page reproduced in: T.H. Weller, Growing Pathogens in Tissue Cultures, Boston: Boston Medical Library, 2004, p. 247. 8. W.F. Scherer et al., "Studies on the propagation in vitro of poliomyelitis viruses," J Exp Med, 97:695-715, 1953. 9. R.W. Brown, J.H. Henderson, "The mass production and distribution of HeLa cells at the Tuskegee Institute, 1953-55," J Hist Med Allied Sci, 38:415-31, 1983.
The inequality of science
While there are inequalities in the plains states with regard to funding from the NIH, you paint too bleak a picture in your August feature, "The Inequality of Science."1 I have been on the faculty of the Department of Pharmacology, Physiology, and Therapeutics at the University of North Dakota since August of 2000. My own laboratory has been quite successful over the past six years, but it hasn't been easy. I use my own success to attract quality postdoctoral fellows, flying them to Grand Forks for an interview, providing relocation money, cosigning car loans, helping them establish credit, getting them inexpensive university housing, but most important, providing them with quality projects and the tools to complete these projects.
These three outstanding postdoctoral fellows have published 16 papers in the past two and a half years and have six to eight manuscripts in the review process. My laboratory has exceptionally good equipment. But the key to success is that we have worked hard to provide the evidence that we can indeed compete. In the world of lipids, my laboratory has continued to gain recognition on the national and world stage.
Eric J. Murphy
University of North Dakota
Setting the record straight on antibiotic resistance
Re: "Chromosome copies confer resistance."1 Contrary to your story, we first reported aneuploidy of a specific chromosome conferring resistance to fluconazole in the human opportunistic pathogen Candida albicans.2 In this paper, we established for the first time that either diminution of chromosome 4 or a combination of chromosome 4 diminution and chromosome 3 duplication conveys the resistance. This control represented a novel mechanism, which did not involve either the gene ERG11, a target of fluconazole, or the genes for cellular pumps that reside on chromosome 5.
Our publication was part of a more general effort being used to demonstrate that C. albicans uses changes in copy number of specific chromosomes to survive in specific adverse environments. Our results on C. albicans survival on a toxic sugar L-sorbose, nonutilized sugar D-arabinose, as well as toxic 5-fluoro-orotic acid and fluconazole, were presented in numerous experimental and review papers. In fact, Berman cited the paper in a 2002 review,3 but failed to acknowledge it in her most recent paper.4
University of Rochester, New York