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Testicular Germ Cell Tumours: a Review of Genetics, Morphology and Immunohistochemistry Pathology Section Review Article DOI: NJLM/2015/13783:2046 Testicular Germ Cell Tumours: A Review of Genetics, Morphology and Immunohistochemistry Pathology Section KANWARDEEP KAUR TIWANA, SARITA NIBHORIA, ASHISH YADAV, TANVI MONGA, AKANKSHA BAJAJ ABSTRACT cells from totipotent germ cell. The treatment modalities are Testicular Germ Cell Tumours (TGCTs) are rare tumours but different for TGCTs so pathologists must be very clear about the they are the most common solid malignancy in young males diagnosis, as the earlier correct diagnosis has high cure rate. and second leading cause of mortality. They exhibit biological This article reviews the genetics, histogenesis, morphological diversity making them interesting for academics. They are true details of TGCTs with stress on use of immunohistochemical experiments of nature making their genetics very interesting. stains to differentiate tumours and various dilemmas faced by They provide an apt model to study transformation of pluripotent the pathologist. Keywords: Genetics, Histogenesis, Testis INTRODUCTION a spatially and temporarily abnormal manner patterns of Testicular Germ Cell Tumours (TGCTs) are the most common differentiation that mimic stages normally undergone by solid malignancy in young men and second leading cause developing zygote. They provide us a model to study the of mortality [1,2]. However, they comprise only 2% of generation of a transformed pluripotent cell from totipotent human malignancies thus creating a lacunae in experience germ cell. Earlier it was thought that this pluripotentiality of pathologists, leading to various diagnostic challenges manifests as histological differentiation into germ cell like for the pathologists as their correct diagnosis has major undifferentiated (seminoma), primitive zygotic (epidermal therapeutic and prognostic implications. In this review we cyst), embryonal somatically differentiated (teratoma), extra highlight the recent insights on genetics, therapeutic role of embryonic differentiated (choriocarcinoma, yolk sac tumour). genetic mutations, pathogenesis and application of recent But according to Ulbright, histogenesis of teratomas is different immunohistochemical markers in the differential diagnosis of [5]. They are divided into two categories prepubertal and post TGCTs. pubertal. In former they arise directly from pluripotential germ cell. This is similar to ovarian teratomas. However, in the case Predisposing Factors of post pubertal teratomas they are derived from malignant TGCTs account for 95% of all testicular malignancies and germ cell (IGCNU) that gives rise to non teratomatous forms they show good therapeutic response if treated in early of germ cell tumours which in turn differentiates to form stages. They are broadly divided into two groups on the teratomatous elements. This theory is supported by genetic basis of their response to therapy as seminomas and analysis of teratomas and other TGCTs in post pubertal males Non-Seminomas (NSE), while the former is sensitive to [6]. Above model also explains one major issue i.e. association both radiation and chemotherapy while later responds to of pure teratomas in post pubertal males with IGCNU and chemotherapy only. Several risk factors have been identified metastases of non teratomatous types and uncommon which include cryptorchidism, spermatogenic and testicular occurrence of post pubertal testicular tumours without other dysgenesis, klienfelter`s syndrome, prior history of germ cell germ cell tumour type [Table/Fig-1]. tumour and family history [3]. Overall a 6-10 fold increased risk has been estimated for first degree male relative of Genetics patient [4]. Approximately 2% of TGCTs have another affected IGCNU is considered the precursor lesion for all adult TGCTs family member with rare families having three or more as explained by model of histogenesis. There are two models affected individuals [4]. Thus indicating a recessive mode of of origin of IGCNUs on the genetic basis. First model was inheritance. proposed by Skakkebaek et al., in which he described the role of kit receptor/SCF paracrine loop (skp Cullen f-box) Histogenesis & Genetics containing complex [7,8]. In this model they described that TGCTs are the true experiments of nature. They display foetal germ cells which escaped normal development into 30 National Journal of Laboratory Medicine. 2015 Jul, Vol 4(3): 30-35 www.njlm.jcdr.net Kanwardeep Kaur Tiwana et al., Testicular Germ Cell Tumours: A Review of Genetics, Morphology and Immunohistochemistry apoptosis. Zygotene –pachytene spermatocyte represent such stage in which recombination checkpoints appear [10]. This is temporally longest phase during spermatogenesis with cell machinery stopping still to permit recombinational events to complete. The aberrant chromatid exchange events during this stage may lead to increase 12p copy number and overexpression of cyclin D2. Such a cell may escape the recombination checkpoints leading to genetic instability and reinitiation of cell cycle. Sicinski et al., concluded that cyclin D2 plays an important oncogenic role in TGCTs [11]. The germ cells that enter the cell cycle after cyclin D2 activation downstream events such as loss of tumour suppressor [Table/Fig-1]: Flow chart depicting histogenesis of TGCTs (RB1, DCC, NME) gene bringing genomic instability leading to neoplastic progression. Further studies show role of spermatogonia, may undergo abnormal cell division mediated kit receptor and SCF. Kit receptor is expressed mainly by by kit/SCF paracrine loop leading to formation of ICGNU. This ICGNU and seminomas thus they are viewed in mitotically transformed germ cell been postulated to be susceptible to active transformed germ cells that have retained inhibitory subsequent invasive growth through the mediation of post mechanism [12]. On other hand NSEs (embryonal carcinoma, natal and prepubertal gonadotropin stimulation. This therapy teratomas) appear to down regulate kit and up regulate is supported by expression of same immunophenotype SCF, thus consistent with loss of germ cell phenotype and markers by gonocytes and IGCNU cells. acquisition of somatic fates [13]. Keywords: Genetics, Histogenesis, Testis Second model was proposed by Chaganti and Houldsworth Also due to deep understanding of genetics of TGCTs even which stresses on four genetic properties of TGCTs [3,9] i.e. cause of chemotherapy resistance has been identified i.e. 1) increased 12p copy number 2) expression of cyclin D2 in subset that harbours Tp53 gene mutation [14]. The reason for IGCNU 3) consistent near triploid-tetraploid chromosome this resistance is their inability to mount an apoptotic response numbers. 4) abundant expression of wild p53. They postulated after drug exposure because of an inactivity Tp53 gene that most likely target cell for transformation during germ cell mutation. Thus concluding that chemotherapy sensitive and development may be one with replicated chromosomes that resistance may be rooted in part in p53 dependent apoptotic express wild type p53, harbours DNA breaks and prone to pathway. Tumours IHC markers IGCNU Vs. Atypical germ cells OCT 3/4 NANOG PLAP D2-40 podoplanin SCF IGCNU Positive Positive Positive Positive Positive Atypical germ cells Negative Negative Negative Negative Negative Seminoma Vs. YCT OCT ¾ Cytokeratin AE1/AE3 AFP Glypican-3 Seminoma Positive Negative Negative Negative YCT Negative Positive Positive Positive Seminoma Vs. EC Podoplanin CD117 SOX117 Cytokeratin AE1/AE3 CD30 SOX2 Seminoma Diffusely positive Positive Positive Negative Negative Negative EC Negative Negative Negative Diffusely positive Positive Positive Spermatocytic Seminoma Vs. Classical Seminoma OCT 3/4 PLAP Spermatocytic seminoma Negative Negative Classical Seminoma Positive Positive Spermatocytic Seminoma Vs. EC CD30 Cytokeratin AE1/AE3 Spermatocytic Seminoma Negative Negative EC Positive Positive [Table/Fig-2]: IHC markers to differentiate various TGCTs National Journal of Laboratory Medicine. 2015 Jul, Vol 4(3): 30-35 31 Kanwardeep Kaur Tiwana et al., Testicular Germ Cell Tumours: A Review of Genetics, Morphology and Immunohistochemistry www.njlm.jcdr.net [Table/Fig-3]: Sections show classical seminoma exhibiting lobular arrangement with foci of dystrophic calcification (H&E X100) [Table/Fig-4]: Sections show high power view of classical seminoma showing clear cells with well-defined borders and large nuclei (H&E X450) [Table/Fig-5]: Sections show solid pattern in embryonal cell carcinoma (H&E X100). (Images from left to right) [Table/Fig-6]: Sections show Yolk Sac Tumour exhibiting Schiller Duval Bodies (H&E X100) [Table/Fig-7]: Sections show Epidermoid cyst (H&E X450) [Table/Fig-8]: Sections show immature teratoma exhibiting blastemal component (H&EX100) (Images from left to right) Histological Types of Testicular Germ Cell Tumours They may or may not be present in tubules with impaired (TGCTs) spermatogenesis which is in contrast with IGCNU which In TGCTs seminoma is most common followed by Mixed occurs in tubules lacking spermatogenesis. On IHC markers germ cell tumours. Embryonal carcinoma, teratomas and yolk OCT3/4, NANOG, placental alkaline phosphatase (PLAP), sac tumour as pure histological type are very low percentage podoplanin (D2-40) and Stem Cell Factor (SCF) are positive more frequently they are seen as component of mixed germ for IGCNU but doesn’t stain normal, hypertrophic or reactive cell tumours [Table/Fig-2]. spermatogonia. OCT3/4 (also known as POU5F1) is newly discovered nuclear transcription factor expressed
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