Testicular cancer.
Despite the overall cure rate now in excess of 90%, innovation in management of germ cell tumors continues. The report that 80% of patients with extragonadal germ cell tumors have either carcinoma in situ or atrophic tubules as evidence of tumor rejection emphasizes the need to investigate the testis in patients with undiagnosed primary cancer because even today treatment delay is worsening prognosis. The evidence that testicular atrophy is a precursor of malignancy may explain why testis cancer has increased while normal sperm count has fallen over the past 50 years and why there is an association between exposure during service in Vietnam to agents that damage spermatogenesis and development of testis cancer. The improved prognostication from analysis of large databases and salvage with high-dose chemotherapy and bone marrow rescue are giving confidence to explore new innovations, eg, carboplatin instead of cisplatin. In addition, as the database on patients with stage I disease on surveillance enlarges, so does interest in adjuvant chemotherapy, encouraging the search for better markers to predict poor response. Linkage between overproduction of the tumor marker lactate dehydrogenase-1 and the increased copy number of the isochrome 12p in the tumor may be of use in this respect. Reports that germ cell tumor patients exposed to etoposide, eg, leukemic, lung, and ovarian cancer patients, can develop an acute myeloid leukemia with a marker on chromosome 11 are tempering enthusiasm for its use in adjuvant therapy. However, the observation that radiotherapy or chemotherapy may reduce second testis tumor incidence more effectively than surgery does encourages more detailed exploration of the results of adjuvant treatment.