Abstract

Yolk sac tumour of testis configures as a germ cell neoplasm comprised of cellular articulations or structures simulating embryonic or foetal yolk sac, allantois and extra-embryonal mesenchyme. Testicular yolk sac tumour is pre-eminently comprised of prepubertal subtype which is non-concordant to germ cell neoplasia in situ, emerges as a ‘pure’ neoplasm and demonstrates multiple gains within chromosome 1q, 20q or 22 and losses within chromosomes 1p, 4 or 6q. Postpubertal subtype is concurrent to germ cell neoplasia in situ (GCNIS), preponderantly configures as a component of ‘mixed tumour’ and occurs due to testicular dysgenesis syndrome, subfertility or as single nucleotide polymorphism (SNP) variants within KITLG, SPRY4 or DMRT1 genes and expounds gain of isochromosome 12p. Upon microscopy, neoplasm may configure distinctive configurations as microcystic or reticular pattern, macrocystic pattern, myxomatous pattern, sarcomatoid or spindle shaped cellular pattern, solid pattern, glandular or alveolar pattern, endodermal sinus or perivascular pattern, hepatoid pattern, papillary pattern, parietal pattern or poly-vesicular vitelline pattern. Yolk sac tumour appears immune reactive to alpha fetoprotein (AFP), glypican 3, SALL4, pancytokeratin, villin or CK7. Neoplastic cells appear immune non-reactive to OCT3/4, CD30, CD117, placental alkaline phosphatase (PLAP), podoplanin (D2-40), inhibin, GATA3 or p63. Testicular yolk sac tumour requires segregation from neoplasms as teratoma, seminoma, embryonal carcinoma, rete testis with hyaline globules and microcystic leydig cell tumour. Tumefaction preponderantly depicts elevated levels of serum alpha fetoprotein (AFP). Testicular yolk sac tumour may be optimally subjected to surgical manoeuvers as orchiectomy.

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