Journal of Clinical Oncology, Vol 19, Issue 6
(March), 2001: 1610-1618
© 2001 American Society for Clinical Oncology
Lung Cancer After Hodgkin’s Disease: A Nested Case-Control Study of the Relation to Treatment
By A. J. Swerdlow,
M. J. Schoemaker,
R. Allerton,
A. Horwich,
J. A. Barber,
D. Cunningham,
T. A. Lister,
A. Z.S. Rohatiner,
G. Vaughan Hudson,
M. V. Williams,
D. C. Linch
From the Section of Epidemiology, Academic Unit of Radiotherapy and Oncology, and Lymphoma Unit, Institute of Cancer Research, Royal Marsden Hospital, and Royal Marsden National Health Service Trust, Sutton, Surrey; Radiotherapy and Oncology Department, Deanesly Centre, New Cross Hospital, Wolverhampton; Department of Medical Statistics and Evaluation, Imperial College School of Medicine; Imperial Cancer Research Fund Medical Oncology Unit, St Bartholomew’s Hospital; British National Lymphoma Investigation, University College Hospital, London; and Oncology Centre, Addenbrooke’s National Health Service Trust, Cambridge, United Kingdom.
Address reprint requests to A.J. Swerdlow, DM, Institute of Cancer Research, Section of Epidemiology, D Block, Cotswold Rd, Sutton, Surrey SM2 5NG, United Kingdom.
PURPOSE: To investigate the causes of the raised risk of lung cancer in patients who have had Hodgkin’s disease, and in particular the relationship to treatment.
PATIENTS AND METHODS: A nested case-control study was conducted within a cohort of 5,519 patients with Hodgkin’s disease treated in Britain during 1963 through 1993. For 88 cases of lung cancer and 176 matched control subjects, information on treatment and other risk factors was extracted from hospital case-notes, and odds ratios for lung cancer in relation to these factors were calculated.
RESULTS: Risk of lung cancer was borderline significantly greater in patients treated with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) chemotherapy than those who did not receive this treatment (relative risk [RR] = 1.66; 95% confidence interval [CI], 0.99 to 2.82), and increased with number of cycles of MOPP (P = .07). Exclusion of lung cancers for which histologic confirmation was not available strengthened these associations (RR = 2.41; 95% CI, 1.33 to 4.51; P = .004 for any MOPP and P = .007 for trend with number of cycles of MOPP). Risks were not raised, however, after chlorambucil, vinblastine, procarbazine, and prednisone treatment. There was evidence that the raised risk of lung cancer occurring in relation to radiotherapy was restricted to histologies other than adenocarcinoma.
CONCLUSION: The results suggest that MOPP chemotherapy may lead to elevated risk of lung cancer, at least in certain subgroups of patients. The role of chemotherapy in the etiology of lung cancer after Hodgkin’s disease deserves further investigation.
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