Radiotherapy after chemotherapy for metastatic seminoma--a diminishing role. MRC Testicular Tumour Working Party.

In a retrospective study, data from 302 patients with metastatic testicular seminoma treated with chemotherapy between 1978 and 1990 in 10 European centres were analysed to evaluate the role, if any, of postchemotherapy treatment with irradiation. The primary endpoint of this study was the progression-free survival rate after chemotherapy with or without additional radiotherapy. This was related to the type of primary chemotherapy, sites and sizes of pre- and postchemotherapy masses, the extent of surgical resection after chemotherapy and the use of radiotherapy. 174 patients had residual disease at the end of chemotherapy. The most important prognostic factors for progression were the presence of any visceral metastases or raised LDH prechemotherapy, and the presence of residual disease at visceral sites after chemotherapy. Approximately half the patients with residual masses underwent postchemotherapy radiotherapy, with selection based predominantly on institutional practice. In patients receiving platinum-based chemotherapy, no significant difference was detected in progression-free survival whether or not radiotherapy was employed. Patients receiving BEP (bleomycin, etoposide and cisplatin) had a progression-free survival rate of 88% (95% CI, 80-96%) uninfluenced by postchemotherapy radiotherapy. In patients with residual masses confined to the abdomen after platinum-based chemotherapy, the absolute benefit to radiotherapy was estimated to be 2.3%. The potential benefit of postchemotherapy radiotherapy is minimal, and so it is concluded that the use of adjuvant radiotherapy to residual masses after platinum-based chemotherapy for metastatic seminoma is unnecessary.

Triphasic locomotor response of a plant-parasitic nematode to avermectin: inhibition by the GABA antagonists bicuculline and picrotoxin.

The response of the plant parasitic nematode, Meloidogyne incognita (J2 stage) to avermectin B2a-23-one is triphasic, comprising an initial loss of locomotor activity where the juveniles remain sensitive to touch, a recovery phase and a final loss of activity where the juveniles are relatively insensitive to touch. In contrast, the acetylcholinesterase inhibitor, oxamyl, causes initial hyperactivity of juveniles followed by a progressive decline in movement. The addition of bicuculline and to a lesser extent picrotoxin, both antagonists of gamma-aminobutyric acid (GABA), blocks the action of avermectin on M. incognita.