PubMed · 14113760
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R B MULVEY. 1964. PERIPHERAL BONE METASTASES.. https://pubmed.ncbi.nlm.nih.gov/14113760/
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We describe a case of osteoid osteoma in the tibia of a 3-year-old patient who presented with a clinical and radiographic picture that suggested an exostosis. The formation of osteoid osteoma with a radiographic picture similar to that of osteophytes or exostosis has been previously documented only rarely. The authors hypothesize that the exostosis-like formation observed was actually the calcification of soft tissues that formed after the intense periosteal inflammatory reaction caused by the osteoid osteoma. As a result of its peculiar clinical and radiographic presentation, diagnosis of this lesion was delayed. Being located close to the medial growth plate of the tibia, it caused lengthening of the limb with a pronounced valgus deviation of the knee. An excisional biopsy provided histological evidence, clinical resolution and immediate pain relief, but incomplete resolution of the valgus deformity of the knee.
BACKGROUND: Prostate cancer (PC) has a propensity to metastasize to the skeleton, inducing an osteoblastic response in the host. Recent epidemiological studies have suggested that circulating IGF-I may be important for both the pathogenesis and dissemination of PC. We have postulated that tumor secreted IGF-I in conjunction with endogenous IGF-I contributes to the osteoblastic phenotype characteristic of metastatic PC. METHODS: To test this thesis we studied the established LNCaP PC progression model consisting of three genetically related human PC cell lines. RESULTS: Using RIA, we found serum-free conditioned media (CM) of LNCaP and C4-2 had no measurable IGF-I, whereas IGF-I was easily detected in CM from C4-2B cells at 24 hr (i.e., 1.8 +/- 0.53 ng/mg cell protein). Real-time PCR of IGF-I mRNA showed that C4-2B expressed 100-fold more IGF-I mRNA than LNCaP cells. In addition, C4-2B expression of IGF-I mRNA was substantially increased in the presence of exogenous IGF-I to nearly twofold. While IGFBP-3 and IGFBP-1 were not detectable in the CM of any PC line, all cells secreted IGFBP-2. C4-2B cells produced 40% more IGFBP-2 than LNCaP or C4-2 cells (C4-2B at 167 +/- 43 ng/mg cell protein). RANKL, a product of bone stromal cells, was also differentially expressed: LNCaP had threefold higher RANKL mRNA compared to C4-2 and C4-2B and at least equivalent protein expression. CONCLUSIONS: Our results suggest that PC cells that have metastasized to bone have an upregulated IGF-I regulatory system. This suggests an activated IGF-I axis contributes to the host-PC interaction in promoting osteoblastic metastases.
Tubulin, the subunit protein of microtubules, has generally been thought to be exclusively a cytoplasmic protein in higher eukaryotes. We have previously shown that cultured rat kidney mesangial cells contain the betaII isotype of tubulin in their nuclei in the form of an alphabetaII dimer [Walss et al., 1999: Cell Motil. Cytoskeleton 42:274-284, 1999]. More recently, we examined a variety of cancerous and non-cancerous cell lines and found betaII in the nuclei of all of the former and only a few of the latter (Walss-Bass et al., 2002: Cell Tissue Res. 308:215-223]. In order to determine if betaII-tubulin occurs in the nuclei of actual cancers as well as in cancer cell lines, we used the immunoperoxidase method to look for nuclear betaII in a variety of tumors excised from 201 patients. We found that 75% of these tumors contain betaII in their nuclei. Distribution of nuclear betaII was highly dependent on the type of cancer, with 100% of the colon and prostate cancers, but only 19% of the skin tumors, having nuclear betaII. Nuclear betaII was particularly marked in tumors of epithelial origin, of which 83% showed nuclear betaII, in contrast to 54% in tumors of non-epithelial origin. In many cases, betaII staining occurred very strongly in the nuclei and not in the cytoplasm; in other cases, betaII was present in both. In many cases, particularly metastases, otherwise normal cells adjacent to the tumor also showed nuclear betaII, suggesting that cancer cells may influence nearby cells to synthesize betaII and localize it to their nuclei. Our results have implications for the diagnosis, biology, and chemotherapy of cancer.