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BACKGROUND The dysregulation of both myc gene expression and retinoid signaling pathways commonly occurs in small cell lung carcinoma (SCLC). Because preclinical data showed that all‐trans‐retinoic acid (RA) inhibited SCLC growth, altered myc expression, and blocked transition to a treatment‐resistant phenotype, a Phase II trial was designed to determine the effects of the combination of RA, cisplatin, and etoposide in patients with SCLC. METHODS Patients with untreated, extensive stage SCLC were treated with up to 8 cycles of cisplatin, 60 mg/m2, intravenously (i.v.) on Day 1 and etoposide, 120 mg/m2, i.v. on Days 1‐3 in addition to up to 1 year of oral RA, 150 mg/m2/day. RESULTS Of 22 assessable patients 1 had a complete response and 9 had a partial response, for an overall response rate of 45% (95% confidence interval, 24‐68%). The median survival was 10.9 months and the 1‐year survival was 41%. The median duration of chemotherapy was 6 cycles and the median duration of RA treatment was 2.8 months. Thirteen patients discontinued RA prematurely due to toxicity and only 4 responders were receiving RA at the time of recurrence. Toxicity‐limiting RA treatment mainly was comprised of mucocutaneous changes and headaches. CONCLUSIONS RA at a dose of 150 mg/m2/day was tolerated poorly in combination with cisplatin plus etoposide, leading to early discontinuation of RA in the majority of patients. The hematologic toxicity, response rate, and survival were similar to those associated with cisplatin and etoposide in prior trials. Further studies with more active and less toxic agents will be required to determine the role of retinoids in the treatment of SCLC. Cancer 1998;83:1102‐1108. © 1998 American Cancer Society.

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Horner's Syndrome (ptosis, anisocoria, and anhydrosis) developed in a 22-year-old woman. A mediastinal mass was noted on chest x-ray. Further evaluation led to a diagnosis of Hodgkin's disease, nodular sclerosis type. Horner's syndrome is an unusual initial manifestation of Hodgkin's disease, and, in this case, it was due to oculosympathetic damage from mediastinal compression. Because the potential for cure is high in Hodgkin's disease, this diagnosis should be considered in patients presenting with Horner's syndrome.