In 1989, we reported the immunologic identification of a prognostic molecule in the tumor cells of breast cancer patients with a poor prognosis for recurrence and death due to their disease (1). This prognostic factor was statistically independent ofimportant clinical parameters including tumor size, lymph node involvement, and assessment of estrogen and progesterone receptors; subsequent studies also showed it to be independent of other prognostic molecules including c-erb-B2 and cathepsin D (2). Tumors marked by this prognostic molecule were nearly 4 times more likely to recur and metastasize than tumors not so marked, representing a prognostic power as strong as the presence of cancer in the axillary lymph nodes ofpatients with T1 or T2 primaries (1-3).We

Tumors express peptide antigens capable of being recognized by tumor-specific cytotoxic T lymphocytes (CTL)

pp32 is a nuclear protein found highly expressed in normal tissues in those cells capable of self-renewal and in neoplastic cells. We report the cloning of cDNAs encoding human and murine pp32. The clones encode a 28.6-kDa protein; approximately two-thirds of the N-terminal predicts an amphipathic a helix containing two possible nuclear localization signals and a potential leucine zipper motif. The C-terminal third is exceptionally acidic, comprised of approximately 70% aspartic and glutamic acid residues; the predicted pl of human pp32 is 3.81. Human and murine pp32 cDNAs are 88% identical; the predicted proteins are 89% identical and 95% similar. Although the structure of pp32 is suggestive of a transcription factor, pp32 did not significantly modulate transcription of a reporter construct when fused to the Gal4 DNA-binding domain. In contrast, in cotransfection experiments, pp32 inhibited the ability of a broad assortment of oncogene pairs to transform rat embryo fibroblasts, including ras + myc, ras + jun, ras + Ela, ras + mutant p53, and E6 + E7. In related experiments, pp32 inhibited the ability of Rat la-myc cells to grow in soft agar, whereas it failed to affect ras-induced focus formation in NIH3T3 cells. These results suggest that pp32 may play a key role in self-renewing cell populations where it may act in the nucleus to limit their sensitivity to transformation.