Testicular cancer

The human genome project has revolutionized technology for the study of DNA. Several of this yearʼs papers have applied these techniques to the study of testicular cancer, especially the use of double-fluorescence in situ hybridization to identify the germ cell tumor marker isochrome 12p in tissue sections, and loss-of-heterozygosity studies to demonstrate a candidate suppressor gene on the long arm of the same chromosome that may be a ligand for the c-kit protooncogene. The report of a solitary case of a patient with a tumor (in a solitary testis) who was treated by partial orchiectomy and then fathered two children emphasizes the need for more information on fertility of patients with carcinoma in situ before the highly effective low-dose radiation to the testis can be accepted. The confirmation of the occurrence of acute myeloid leukemia as a late effect of etoposide and stomach cancer as a late effect of radiotherapy for stage I seminoma has drawn attention to the need to reduce treatment in good-risk patients. Results of trials substituting cisplatin with carboplatin and a trial eliminating bleomycin are particularly disappointing, and the 10% lower cures with the experimental regimen in these studies is an object lesson of the risks involved in such studies. Two other issues that continue to be debated include the increasing recognition of the value of lactate dehydrogenase-1 for identifying poor-risk patients, and the benefits of referral to a unit specializing in testicular cancer. There is an increasing trend to use high-dose chemotherapy for previously untreated patients who have poor risk factors.