Ureteral obstruction in a patient with Burkitt's lymphoma and AIDS.

Burkitt's lymphoma presenting as an intrinsic ureteral mass is rare. We report on an immunocompromised patient with hydronephrosis secondary to direct involvement of the ureter by this non-Hodgkin's lymphoma. This case illustrates one of the manifestations of AIDS and the treatment of this manifestation. The relationship of AIDS and its sequela to the genitourinary system is discussed.

Clinical follow-up in 24 nonfamilial renal tumors cytogenetically characterized in tissue culture.

OBJECTIVE: This study investigates the relationship between clonal chromosomal abnormalities detected in nonfamilial renal cell carcinoma and the clinical outcome, specifically, whether or not patients whose tumors had karyotypic changes have a different prognosis than those whose tumors did not. METHOD: Fresh tumor tissue obtained from 32 cases was grown in tissue culture. Twenty four grew successfully and were harvested and multiple cells of each karyotyped. Clinical follow-up was obtained for at least five years or until the time of death. RESULTS: Fourteen of 24 cases demonstrated karyotypic abnormalities including loss of Y chromosome (64%), trisomy 7 (50%), trisomy 12 (14%), trisomy 9, 10, 14, 15, 16, and 17, monosomy 9 and 20, and long-arm deletion of chromosome 16 (1 case each). Tumors were well-differentiated in 16 cases, moderately differentiated in 5 cases, and poorly differentiated in 1 case; 13 cases were pathologic Stage I, 5 Stage II, and 6 Stage III. Thirty-three percent of the patients demonstrated clinical progression. CONCLUSIONS: No significant difference in prognosis could be found between patients with and without karyotypic abnormalities. The only clinical or pathologic difference which could be established was sex distribution. Significantly greater numbers of males had karyotypic abnormalities than females, but this could be explained by the high number of Y chromosome deletions that were detected. The lack of correlation between karyotypic abnormalities and clinical outcome may reflect a confounding factor in genetic evolution such that clinically determining chromosomal changes present early in a tumor's growth in vivo may no longer be present when the tumor is diagnosed, treated, or after it is grown in culture. This may make demonstration of such clinically significant chromosomal changes very difficult.