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www.thelancet.com/oncology Vol 14 September 2013 e395

Righting a long-standing wrong for Henrietta LacksIn 1951, Henrietta Lacks attended Baltimore’s Johns Hopkins Hospital (MD, USA) for radiotherapy. While she was under anaesthetic, the surgeon cut a sample from the tumour that was to kill her that same year. He was not required to obtain prior permission, and did not do so.

The resultant cell line, HeLa, remains in existence today; a continually regenerating collection of cells that, massed together, would weigh in excess of 50 million tonnes. HeLa has contributed to tens of thousands of scientifi c papers, amounting to some 1300 Gb of data, and played a crucial role in the development of all kinds of research.

On Aug 7, 2013, the US National Institutes of Health (NIH) announced that the contribution of Henrietta Lacks and her family to medical science would be formally recognised. The decision was prompted by the publication earlier

this year of the genetic sequence of the HeLa genome. “It quickly became apparent that the publicly posted HeLa genome data and what it might reveal about Ms Lacks’ disease risks could have implications for her descendents”, commented NIH director Francis Collins. Representatives from the NIH held a series of meetings with the Lacks family to fi nally defi ne how their genetic information should be used.

They opted for a closed access database. Scientists wishing to obtain the data will have to apply to the NIH (declaring any commercial interests and agreeing not to contact the family). Those who use HeLa data will also be required to acknowledge the Lacks family in the publication. The new rules are only enforceable for NIH-funded researchers but the NIH hope that other scientists will abide by them.

“It is a historic moment”, said Rebecca Skloot, author of the best-selling 2010

book that brought Henrietta’s case to prominence. She notes that the Lacks family have endured some appalling treatment. “Scientists tracked down Henrietta’s children in the 1970s and published research on them without their consent, and in the 1980s they had their medical records published”, she told The Lancet Oncology.

Whether the decision has wider relevance is moot. “The Henrietta Lacks case is unique because members of the Lacks family are now well known public fi gures”, explains Amy McGuire (Baylor College of Medicine, Houston, TX, USA). “When sequence data are publicly released, it creates privacy risks”, she added. “Risks to individuals are typically addressed through informed consent requirements, but current policy does not adequately address risks to family members.”

Talha Khan Burki

A new biomarker for graft-versus-host diseaseScientists in the USA have identifi ed a plasma biomarker that can predict the response to therapy for acute graft-versus-host disease (GVHD) after allogeneic haemopoietic stem-cell transplantation.

Suppression of tumorigenicity 2 (ST2) is a member of the interleu-kin 1 receptor family. The researchers measured its concentration in 381 patients at the beginning of their treatment for GVHD, and in 673 patients during the fi rst month after transplantation. They noted that patients with high levels of ST2 at therapy initiation were 2·3 times (95% CI 1·5–3·6) more likely to have treatment-resistant GVHD than those with low levels of ST2, and were 3·7 times (2·3–5·9) more likely to die within 6 months of commencement of therapy.

Levels of ST2 proved a more accurate predictor of mortality than

did disease grading. Patients with low levels of ST2 had substantially lower mortality than did individuals with high levels of the protein, irrespective of GVHD grade (11% vs 31% for grades 1–2, and 14% vs 67% for grades 3–4). Furthermore, whereas clinical signs of GVHD typically appear about 1 month after transplantation, raised levels of ST2 after 14 days are associated with increased risk. “Clinical signs are less important than the biomarker”, explains lead investigator Sophie Paczesny (Indiana University Melvin and Bren Simon Cancer Center and Wells Center for Pediatric Research, Indianapolis, IN, USA). “It means that we can diagnose GVHD before the clinical signs, and we can begin pre-emptive treatment.”

Alois Gratwohl, former head of Basel University Hospital’s Stem Cell Trans-plantation Team (Basel, Switzerland), off ers cautionary words. “From a basic

science perspective, it is a fascinating piece of work, but this is just the latest in a series of markers that are predictive of outcome.” He notes that, from a clinical perspective, knowing whether or not a patient will respond to therapy for GVHD is of limited use, in view of the scarcity of treatment options aside from glucocorticoids. He believes that understanding why some patients develop GVHD is more important than identifi cation of biomarkers.

Paczesny points out that establish-ment of the mechanism by which ST2 is implicated in GVHD might have implications for future treatment regimens. But she concedes that this will be a sizeable undertaking. “ST2 is involved in a lot of immune responses”, she said. Meanwhile, the ST2 fi ndings need to be validated in a large-scale prospective trial.

Talha Khan Burki

Published OnlineAugust 15, 2013 http://dx.doi.org/10.1016/S1470-2045(13)70393-0

Published OnlineAugust 15, 2013 http://dx.doi.org/10.1016/S1470-2045(13)70394-2

For the study see N Engl J Med 2013; 369: 529–39

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