Cell proliferation and nasal carcinogenesis.

Abstract

The nasal passages of rodents provide valuable opportunities for research on relationships between cell proliferation and cancer. The nose, which has multiple functions, possesses a diverse range of tissue types, each with its own morphologic, physiologic, and metabolic characteristics and site-specific cell turnover rates. Moreover, for inhaled materials deposited in the nose, complex regional uptake or deposition patterns can result in site-specific responses, including cancer. Presented here are important criteria necessary for undertaking cell proliferation studies in the nasal passages. The current literature concerning nasal toxicity and the toxicant-induced proliferative response are also reviewed. Rodent nasal epithelium provides a fruitful area for research on the role of cell proliferation in carcinogenesis.

Cell Proliferation and Chemical Carcinogenesis: summary and future directions

“…3). Data from the new mechanisms-based bioassay reported at this meeting (5) replicates the initial bioassay, but has an additional important exposure group of 10 ppm. This provides new information on the concentration response for tumor induction and clearly demonstrates that the nonlinear response is a straight line from 6 to 15 ppm.…”

“…The exact temporal association between increased cell proliferation and the induction of neoplasia is unknown at this time. It is clear from the data presented at this meeting on formaldehyde that a minimum of 3 months of sustained cell proliferation is needed to sharply increase the slope for nasal cancer incidence (5). Likewise, it took 12 months for the nongenotoxic agent ethyl acrylate to induce forestomach tumors in rats (8).…”

Transitional carcinoma with extensive invasion of the bony orbit in a dog

“…Occupational exposure in the lumber industry, nickel refineries, boot and shoe making, urban pollution as well as the textile industry, increases cell proliferation and have, therefore, been suggested as additional causative factors for malignant transformation. In several studies a substantial number of patients were addicted to alcohol and smoking (Monticello et al, 1993;Calderón-Garcidienas et al, 1999;Dubey et al, 1999;Choong and Vokes, 2008). It is known that the metabolism of xenobiotics into reactive intermediate molecules may play a role in neoplastic transformation (Caswell and Williams, 2007).…”

Absence of Morphologic Correlation between Chemical Toxicity and Chemical Carcinogenesis

“…Similarly, in the other example, relating to nasal cancer, Monticello et al (77) stress "that cell proliferation in response to cell death is not the sole determinant in nasal carcinogenesis, since other inhaled irritant gases, such as dimethylamine, induce severe nasal cytotoxicity, inflammation, and squamous metaplasia, yet do not induce nasal tumors following chronic exposure. Additional work is needed to delineate the correlation between nasal toxic responses, epithelia proliferation, and the carcinogenic process.…”