BACKGROUNDHuman papillomavirus (HPV)-mediated oropharyngeal squamous cell carcinoma is a subset of head and neck cancer with a unique mechanism of carcinogenesis. Local disease is treated ...definitively with a multimodal approach. Navigating recurrences can be challenging, as they are sometimes indiscernible from de novo primary malignancies. Identification of dynamic biomarkers that are specific to HPV-mediated disease may assist in disease monitoring. We present a 78-year-old man who developed a squamous cell carcinoma in the lung 7 years after completing definitive chemoradiation for his p16+ head and neck squamous cell carcinoma. METHODSA novel assay for plasma circulating tumor HPV DNA was employed and provided a tool for longitudinal disease monitoring during therapy. CONCLUSIONWe bring attention to a novel assay and highlight its potential for use in the treatment paradigm of HPV-mediated oropharyngeal carcinoma.
BACKGROUND: Exposure to environmental tobacco smoke (ETS) is considered to be a major lung cancer risk factor for never smokers. We investigated the hypothesis that never-smoking women who are ...exposed to ETS and develop lung cancer are a genetically susceptible population. METHODS: Archival tumor tissues were analyzed from 106 never-smoking women enrolled in a case-control study of ETS (and other personal and environmental factors) and lung cancer risk. We analyzed germline polymorphisms in genes that have been associated with cancer susceptibility and whose products activate (cytochrome P450 1A1 CYP1A1) and detoxify (glutathione S-transferases M1 GSTM1 and T1 GSTT1) chemical carcinogens found in tobacco smoke. RESULTS: When compared with never smokers who had no ETS exposure and developed lung cancer (n = 55), never smokers with exposure to ETS who developed lung cancer (n = 51) were more likely to be deficient in GSTM1 activity (i.e., were GSTM1 null) because of a genetic polymorphism in the GSTM1 gene (odds ratio = 2.6; 95% confidence interval = 1.1-6.1). A statistically significant rising trend in risk occurred with increasing ETS exposure (two-sided P = .02), reaching a more than sixfold excess risk in those exposed to 55 pack-years of ETS (ETS pack-year = ETS produced by an active smoker, within a confined space such as a room, who smokes one pack of cigarettes a day for a year). No evidence was found of associations between GSTT1 deficiency or the CYP1A1 valine variant and lung cancer risk due to ETS exposure. CONCLUSIONS: A common genetic polymorphism divides the population of never smokers into two groups of approximately equal size, one (homozygous carriers of the GSTM1 null allele) that has a statistically significant greater risk of lung cancer from ETS than the other (heterozygous or homozygous carriers of the wild-type GSTM1 allele).
Lung cancer is the leading cause of cancer death in the world; over 1.2 million new cases and 1.1 million worldwide deaths were predicted for 2004.1 These statistics are astounding given the rarity ...of lung cancer during the first half of the 20th century, when lung cancer had a lower incidence than liver, prostate, colon, stomach, uterine, breast, and even ovarian cancer. Only a sound understanding of the complex epidemiologic, etiologic, and clinicopathologic aspects of lung carcinoma will enable clinical and scientific progress against this deadly disease regardless of technological advances. Recent modifications in the World Health Organization (WHO) classification of non-small-cell lung cancer (NSCLC) reflect our greater understanding of lung cancer pathology. This chapter provides the necessary information for sound pathologic diagnoses by reviewing general aspects of lung carcinoma as well as the clinicopathologic features of the most common types of NSCLC, namely squamous cell carcinoma (SCC), adenocarcinoma, large cell carcinoma (LCC), and their variants.
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