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Oncogenesis and Metastasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Other examples of precursors include:Penile intraepithelial neoplasia (PeIN) in penile cancer.Atypical small acinar proliferation (ASAP) and high-grade prostatic intraepithelial neoplasia (HGPIN) in prostate cancer.Germ cell neoplasia in situ (GCNIS) in testicular cancer.
Testicular cancer
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
The aetiology of testicular cancer is unknown, but almost all cases of testicular cancer display amplification of the short arm of chromosome 12 (3). This suggests that genes in this region are important in the development of GCT. GCTs are thought to be derived from cells in the germ cell lineage that are blocked in maturation. In adults, GCTs are thought to be initiated during fetal development and involve changes to the primordial germ cells. All GCT progress through a non-invasive lesion called germ cell neoplasia in situ (GCNIS). GCNIS was formerly named carcinoma in situ (CIS) or testicular intraepithelial neoplasia (TIN) (8).
Testicular Cancer
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Nkwam Nkwam, Chitranjan J. Shukla, David A. Manson-Bahr, Taimur T. Shah, Farooq Khan
Regarding germ cell neoplasia in situ (GCNIS), which of the following is TRUE?Overall incidence in the contralateral testis is approximately 10%.Incidence of a contralateral metachronous tumour is approximately 10%.Biopsy of the contralateral testis is mandatory in most cases.Chemotherapy is more effective than radiotherapy in its treatment.Five-year risk of developing testicular cancer is 90% with a normal contralateral testis.
A stroll through the present and future of testicular germ cell tumour biomarkers
Published in Expert Review of Molecular Diagnostics, 2023
Nuno Tiago Tavares, Rui Henrique, Aditya Bagrodia, Carmen Jerónimo, João Lobo
In 2005, Oosterhuis and Looijenga proposed a broad classification of GCTs by considering a developmental model of the disease and the cell and categorizing these tumors according to cell of origin, developmental potential, and epigenomic background [3]. In this classification, seven types of GCTs are proposed, from type 0 to type VI GCTs. Testicular germ cell tumors (TGCTs) may include types I-III tumors, but the vast majority fit into the type II category, which will be the focus of this review. More recently, the World Health Organization (WHO) Classification divided TGCTs into those derived from precursor lesion germ cell neoplasia in situ (GCNIS), corresponding to postpubertal-type (type II) tumors, and those unrelated to GCNIS, including both prepubertal-type tumors (type I) and spermatocytic tumors (type III) [4]. GCNIS-derived TGCTs show malignant behavior and are divided into two major subtypes, with clinical implications: the seminomas (SE) and the non-seminomatous tumors (NST) [4,5]. While SEs represent a more homogeneous group, with overall better prognosis, NSTs are truly heterogeneous, mostly assuming the form of mixed tumors (rather than pure forms), composed by one or more GCT histological components: embryonal carcinoma (EC), an undifferentiated component approximating pluripotent embryonic stem cells (ESC), yolk sac tumor (YST) and choriocarcinoma (CHC), composed by extra-embryonic elements, and teratoma (TE), made up by differentiated somatic tissues (Figure 1) [5,6].
18-Year-old patient with Klinefelter syndrome (47, XXY) and complete androgen insensitivity syndrome (CAIS) – case report
Published in Gynecological Endocrinology, 2021
Karolina Skalska, Maciej Ziółkowski, Adrian Skoczylas, Marta Teleon, Monika Grymowicz, Agnieszka Pollak, Roman Smolarczyk, Rafał Płoski, Błażej Męczekalski
Since there is no causal treatment [5], the most important management in patients with CAIS is bilateral gonadectomy due to a greater risk of germ cell tumors (GCT) associated with the presence of the Y chromosome. Such tumors include gonadomas, seminomas, teratomas, yolk sac tumors, choriocarcinomas, and embryonal carcinoma from stem cells. The precancerous conditions that precede these tumors are termed benign germ cell neoplasia in situ (GCNIS). In this patient, however, neither germ cell tumors nor GCNIS were found. Although, in the case of complete androgen insensitivity syndrome, the risk of neoplasm is much lower than in the partial form, it is not insignificant [5]. An additional factor related to the higher risk of other neoplasms in this patient is the coexistence of Klinefelter syndrome, as the peripheral conversion of the excessive androgens to estrogens is primarily favorable for breast cancer [17]. Thus, the removal of the gonads is an additional protective factor.
Molecular characteristics of testicular germ cell tumors: pathogenesis and mechanisms of therapy resistance
Published in Expert Review of Anticancer Therapy, 2020
Khaleel I. Al-Obaidy, Michal Chovanec, Liang Cheng
Pluripotency is defined as the ability of stem cells to differentiate into various tissue types. It is a characteristic feature of GCNIS, seminoma and embryonal carcinoma to a variable extent. Only embryonic stem cells (ESCs) are known to have pluripotency-specific genes. Like ESCs, embryonal carcinoma is also found to have overexpression level of these genes [16]. Pluripotency is related directly to the gain of 12p where some of the crucial genes are located [1,2]. Increased NANOG levels due to 12p gain may be enough to up-regulate the remaining pluripotency regulators, OCT3/4 and SOX2, breaking the balance between pluripotency and malignancy. The shift in the NANOG: OCT3/4 ratio is believed to influence the progression of GCNIS into an invasive tumor. On the other hand, GCNIS and seminoma have similar genetic expression profiles to embryonal carcinoma, but they lack the expression of SOX-2. SOX17 is located at the short arm of chromosome 8 (8p23) and is often overexpressed in these tumors where it cooperates with OCT3/4 in place of SOX2 (Figure 2).