MITOGEN-INDUCED LYMPHOPROLIFERATIVE RESPONSE AND PHAGOCYTIC-ACTIVITY OF MONOCYTES IN RENAL-CELL CARCINOMA PATIENTS TREATED BY INTERFERON A ALONE OR IN COMBINATION WITH VINBLASTINE
N. Stanojevicbakic et al., MITOGEN-INDUCED LYMPHOPROLIFERATIVE RESPONSE AND PHAGOCYTIC-ACTIVITY OF MONOCYTES IN RENAL-CELL CARCINOMA PATIENTS TREATED BY INTERFERON A ALONE OR IN COMBINATION WITH VINBLASTINE, Oncology Reports, 2(5), 1995, pp. 891-895
The functions of T cells and monocytes were studied in relation to the
clinical stage and clinical course of renal cell carcinoma (RCC) pati
ents, treated by interferon alpha (LFN-alpha). Lymphoproliferative res
ponse (LPR) to phytohemagglutinin and phagocytic activity of periphera
l blood monocytes were estimated before, immediately after, and six mo
nths after completion of therapy with IFN-alpha alone (applied in stag
e II RCC) or in combination with vinblastine (in stages III and IV). T
he number of total T cells and their mitogen-induced proliferative res
ponse were diminished in all patient groups before therapy, the decrea
se of LPR being more pronounced in advanced (III and IV) stages of the
disease. The pretreatment number of monocytes and their phagocytic ac
tivity were increased in RCC patients regardless of clinical stage. Th
e initial level of the lymphocyte and monocyte functions did not corre
late with the clinical course of the disease. The pretreatment levels
of LPR and phagocytic activity were not changed immediately after IFN
treatment, irrespective of the clinical response to therapy. Similar r
esults were obtained six months after therapy; the only exception was
the increased LPR in stage III patients, which was unrelated to clinic
al response to the therapy, since it was seen in patients with progres
sion of the disease. These findings suggest that the pretreatment leve
l of LPR and monocyte phagocytic activity in RCC patients in different
clinical stages of RCC were not predictive of the clinical response t
o IFN therapy. IFN-alpha, as used in this study, had no major influenc
e on LPR and phagocytic activity of monocytes irrespective of the clin
ical stage or clinical course of the disease.