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Curr Opin Oncol. 1999 May;11(3):236-41.

Germ cell cancer.

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St. Bartholomew's Hospital and The Royal London School of Medicine, Queen Mary and Westfield College, West Smithfield, UK.


The publication of the proceedings of Fourth Workshop on Carcinoma in situ was an impressive leap in our understanding of the interaction between prenatal and postpubertal factors in the development of germ cell cancer as well as increased insight into the molecular events that are involved in the development of these tumors. From this work, physicians are increasingly accepting that estrogen-mediated prenatal priming of germ cells generates a predisposition to postpubertal cyclin D2-driven initiation of full mitotic cell cycle replication of a tetraploid p53-expressing meiotically arrested pachytene spermatocyte that is under increased gonadotrophin drive because of testicular atrophy inducing events. From this new knowledge, new markers, eg, FGF4, CD30, and OCT-4, of embryonal carcinoma cells are identifying alternative ways of identifying poor risk tumors and leading to renewed interest in study of histopathology of these tumors. With greater attention to late events and increasing confirmation that chemotherapy is better than radiation even in seminoma and that seminoma is more chemosensitive than nonseminoma, a renewed clinical need exists for improved pathologic definition to reduce unnecessary usage of chemotherapy and maximize its benefits. With the failure of vinblastine, ifosfamide, and cisplatin to show any benefit over BEP (bleomycin, etoposide, and cisplatin) in the Southwest Oncology Group trial, re-examination of approaches to treatment of poor risk disease is emphasized as the priority for future trials.

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