To test the involvement of the telomeres in the senescent phenotype, we used telomerase-immortalized human foreskin fibroblasts (hTERT-BJ1). We exposed hTERT-BJ1 and parental BJ cells to either UVB or H2O2 subcytotoxic stress(es). Both cell lines developed biomarkers of replicative senescence: loss of replicative potential, increase in senescence-associated β-galactosidase activity, typical senescence-like morphology, overexpression of p21WAF-1 and p16INK-4a, and decreased level of the hyperphosphorylated form of pRb. Telomere shortening was slightly higher under stress for both BJ and hTERT-BJ1 but still much lower than that reported for other cell lines. We conclude that pathways alternative to telomere shortening must cause the appearance of the senescence phenotype. © 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.