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Background. The purpose of this study was to evaluate the utility of positron emission tomography‐ (PET) 2‐[18F]‐fluoro‐2‐deoxy‐D‐glucose (FDG) imaging in extra‐cranial head and neck cancers. Methods. Sixty patients with biopsy‐proven cancers were studied using PET‐FDG. Thirty‐four patients were studied before therapy (staging), of which 15 patients received primary radiotherapy and serial PET‐FDG imaging (monitoring). Seven patients with advanced disease had laser excision (monitoring), and 19 patients were evaluated for recurrent disease (recurrence). Results. Four patients had unknown primary lesions. PET‐FDG imaging located the primary tumor in two of four patients, and magnetic resonance imaging (MRI) in none of four. In the remaining patients (staging), PET‐FDG imaging detected the primary tumor in 29 of 30 patients, and MRI in 23 of 30. In the staging group, PET‐FDG imaging identified the presence or absence of lymph node involvement in 32 of 34 patients, and MRI in 31 of 34. PET‐FDG imaging was helpful in evaluating tumor response to radiation therapy or laser excision. Ten patients evaluated for recurrent disease had biopsy‐confirmed recurrences, and 7 had no recurrence. PET‐FDG imaging results were positive for primary tumor recurrence in 9 of 10 patients, and MRI results were positive in 6 of 10. MRI results were negative for lymph node disease in one of these patients with recurrent primary tumor where PET‐FDG imaging and biopsy demonstrated nodal involvement. PET‐FDG results were negative for recurrent disease in seven of seven patients, and MRI results were negative for recurrent disease in in four of seven. Conclusion. In this series, the authors found that PET‐FDG is a useful diagnostic modality for evaluating the patient with an unknown primary, monitoring response to therapy, and in detecting recurrent tumors. Cancer 1994; 73:3047–58.

Background. Radiation recall refers to a tissue reaction produced by a chemotherapeutic agent in a previously irradiated field that would not occur in a nonirradiated field. A number of agents have been reported to cause radiation recall. Recently, there have been case reports of recall dermatitis from paclitaxel treatment. Methods. A patient with metastatic lung cancer received palliative radiation to her mediastinum and ribs. Because of disease progression, she subsequently received paclitaxel. Results. After paclitaxel administration, the patient became acutely dyspneic. A subsequent chest X‐ray revealed a parenchymal opacity in a region that corresponded with the patient's radiation portal. She also developed a severe skin reaction in the previously treated electron field. Conclusions. This is one of few reported cases of recall dermatitis from paclitaxel and is also suggestive of recall pneumonitis, a phenomenon previously unreported to the authors' knowledge. Given paclitaxel's ability to function as a radiosensitizer, this response is not unexpected. As the frequency of paclitaxel administration increases, its potential as a radiation sensitizer and radiation recall should be considered. Cancer 1995;76: 1069–72.

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Dedifferentiation of human thyroid tumors is frequently found in humans. The effect of retinoids (13 cis-RA) was studied on the proliferation and differentiation of a human follicular cell line in vitro (UCLA R0 82 W-1). A significant and dose-dependent reduction (P less than 0.001) in cell number and [3H] thymidine uptake was found in cells exposed to 13 cis-RA up to 10 microM. Higher concentrations of 13 cis-RA, however, led to a dose-dependent restoration of cell proliferation. Various parameters of differentiation increased under the influence of 13 cis-RA (10 microM) over nonexposed cells. The 125I uptake increased 4-fold over that in control nonexposed cells (P less than 0.05). [125I] Epidermal growth factor binding increased 5-fold, and [125I] human TSH binding increased significantly after exposure to 13 cis-RA (P less than 0.02). Deiodinase activity, however, was significantly lower in 13 cis-RA exposed cells than in control cells. The present study shows that 13 cis-RA (10 microM) drives the tumor cells toward a more normal state of proliferation and differentiation.