ITGCN of the Testis Contralateral Testicular Biopsy and Bilateral Testicular Cancer

Michael E. Karellas, MDa, Ivan Damjanov, MD, PhDb, Jeffery M. Holzbeierlein, MDc*

aDepartment of Surgery, Division of Urology, Memorial Sloan Kettering Cancer Center, 353 E. 68th Street, New York, NY 10021, USA bDepartment of Pathology, University of Kansas School of Medicine, 2017 Wahl Hall West, Mailstop 3045, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA cDepartment of Urology, University of Kansas School of Medicine, 5017 Sudler Hall, Mailstop 3016, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA

Testicular cancer is the most common solid malignancy in the 20- to 34-year-old male age range. According to the most recent Surveillance Epidemiology and End Results (SEER) data, approximately 8000 men per year will be diagnosed with testicular cancer [1]. The mean age at diagnosis was 34 years of age, while the median age of death was 39.5 years old. The age-adjusted incidence of testicular cancer in the United States for the years from 1998 to 2002 was 5.3 per 100,000 men per year [1]. European data suggest the overall lifetime risk of developing testicular cancer is low at 0.5% to 1% [2]. The overwhelming majority (95%) of testicular tumors are of germ-cell origin (testicular germ-cell tumors [TGCTs]) and are divided into two main types: seminomas and nonse-minomas. Nonseminomas are further subdivided into five subtypes and usually consist of a mixture of these subtypes. Additionally, some tumors present as mixed lesions containing both seminoma-tous and nonseminomatous elements [3]. Despite the variety of TGCT types, it has been well established that almost all TGCTs develop from the precursor lesion of carcinoma in situ (CIS) (Fig. 1), otherwise known as intratubular germ-cell neopla-sia (ITGCN), or testicular intraepithelial neoplasia (TIN) [4]. In this review we will focus on the origins

* Corresponding author. E-mail address: [email protected] (J.M. Holzbeierlein).

of CIS and molecular genetics concerning expression and progression, as well as the current aspects of diagnosis and management of ITGCN, and bilateral TGCTs.

Skakkeb^k [5] was the first to describe the presence of a noninvasive precursor lesion that would progress to invasive TGCTs. He found atypical spermatogonia from testicular biopsies in two infertile patients who went on to develop testicular cancers. Over the past three decades since his early report, it is now well established that with the exception of pediatric testicular tumors (yolk sac, mature teratoma) as well as the rare finding of spermatocytic seminoma, almost all TGCTs arise from ITGCN [5]. The presence of ITGCN is present in the testis years before the ultimate tumor becomes clinically evident leading to speculation that early detection of TGCTs is possible with testicular biopsy and im-munohistological examination [6]. Multiple studies have shown the prevalence of ITGCN to be consistent with the lifetime risk of developing a TGCT [6,7].

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