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Journal of Clinical Oncology, Vol 25, No 28 (October 1), 2007: pp. 4494-4496 © 2007 American Society of Clinical Oncology. DOI: 10.1200/JCO.2007.12.7530
Enlarging Residual Mass After Treatment of a Nonseminomatous Germ Cell Tumor: Growing Teratoma Syndrome or Cancer Recurrence?Nuclear Medicine Department, and Bioticla Unit, GRECAN, François Baclesse Comprehensive Cancer Center and Caen University, Caen, France
Pathology Department, University Hospital, Caen, France
Medical Oncology Department, François Baclesse Comprehensive Cancer Center, Caen, France An 18-year-old patient underwent orchidectomy followed by three cycles of chemotherapy (bleomycin plus cisplatin and etoposide) for a stage IIIA mixed nonseminomatous germ cell tumor (NSGCT) containing teratocarcinoma and choriocarcinoma. At the time of initial staging, retroperitoneal and inframediastinal nodal involvement was observed on computed tomography (CT) data. Figure 1A shows the pretherapeutic mediastinal lesion (open arrow, maximum diameter: 15 mm), close to the esophagus (dotted arrow) and the azygos vein (closed arrow). Serum tumor markers were normalized after the first cycle of chemotherapy. Restaging after completion of chemotherapy revealed retroperitoneal (maximum diameter 47 mm, data not shown) and inframediastinal residual masses (Fig 1B, maximum diameter 16 mm). Retroperitoneal lymph node dissection was performed and pathology revealed mature teratoma and necrosis, without viable tumor. Four months later, an enlargement of the residual inframediastinal lesion was observed on a CT scan (maximum diameter: 34 mm; Fig 1C). No increase in tumor marker blood level was observed. The patient was therefore referred for an [18F]-fluorodeoxyglucose (FDG) positron emission tomography examination which revealed no abnormal foci in the area of the developing mass. Figure 2 displays the maximum intensity (A) projection view and a (B) transverse slice at the level of the mediastinal lesion. False negative result was unlikely, the lesion measuring more than 1 cm, and no hyperglycemia having being observed before FDG injection. Moreover, review of CT scans revealed cystic and low densities on post-treatment scans, in contrast with pretherapeutic CT scan revealing tissular densities. Such CT patterns have been shown to be associated with mature teratoma.1,2 Given the negative tumor marker and the imaging features, growing teratoma syndrome3 was hypothesized, and surgery was planned for 10 weeks later after multidisciplinary consensus. Pathological examination of the resected lesion confirmed the diagnosis of mature teratoma (Fig 3). The tumor contained several cysts lined by glandular epithelium of enteric or respiratory type. The stromal tissues consisted of hypocellular fibrous tissue with few smooth muscle fibers (Fig 3A). Immunohistochemistry showed a weak and focal stain for MIB 1 (Fig 3B).
Whereas residual masses of seminomatous germ cell tumors (SGCT) may contain either necrosis or viable tumor,4 those observed in NSGCT may also contain mature teratoma in up to 30% of cases. This latter histological component may enlarge during2 or after3 the course of chemotherapy (growing teratoma syndrome), thus mimicking treatment failure or relapse. Growing mature teratoma is unresponsive to chemotherapy and requires surgical excision to avoid complications such as compression of adjacent structures or malignant transformation, surgery in this situation being, however, less urgent than in the case of suspected relapse.5 FDG positron emission tomography is not capable of differentiating necrosis from mature teratoma,4,6 but can accurately detect viable tumor in both SGCT7 and NSGCT8 residual masses. This case highlights the fact that the negativity of FDG imaging, considered concurrently with negative tumor marker and specific CT scan features, may help to suspect a growing teratoma syndrome and to adapt treatment planning in case of enlarging NSGCT residual mass. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest.
REFERENCES
1. Husband JE, Hawkes DJ, Peckham MJ: CT estimations of mean attenuation values and volume in testicular tumors: A comparison with surgical and histologic findings. Radiology 144:553-558, 1982 2. Panicek DM, Toner GC, Heelan RT, et al: Nonseminomatous germ cell tumors: Enlarging masses despite chemotherapy. Radiology 175:499-502, 1990 3. Lorigan JG, Eftekhari F, David CL, et al: The growing teratoma syndrome: An unusual manifestation of treated, nonseminomatous germ cell tumors of the testis. Am J Roentgenol 151:325-329, 1988[Abstract] 4. De Santis M, Pont J: The role of positron emission tomography in germ cell cancer. World J Urol 22:41-46, 2004[CrossRef][Medline] 5. Schmoll HJ, Souchon R, Krege S, et al: European consensus on diagnosis and treatment of germ cell cancer: A report of the European Germ Cell Cancer Consensus Group (EGCCCG). Ann Oncol 15:1377-1399, 2004 6. Hain SF, Maisey MN: Positron emission tomography for urological tumours. BJU Int 92:159-164, 2003[CrossRef][Medline] 7. De Santis M, Becherer A, Bokemeyer C, et al: 2-18fluoro-deoxy-D-glucose positron emission tomography is a reliable predictor for viable tumor in postchemotherapy seminoma: An update of the prospective multicentric SEMPET trial. J Clin Oncol 22:1034-1039, 2004 8. Hain SF, O'Doherty MJ, Timothy AR, et al: Fluorodeoxyglucose positron emission tomography in the evaluation of germ cell tumours at relapse. Br J Cancer 83:863-869, 2000[CrossRef][Medline]
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Copyright © 2007 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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