Dan-Ning Hu

Population-based incidence of conjunctival melanoma in various races and ethnic groups and comparison with other melanomas.

PURPOSEnTo investigate racial and ethnic differences in the incidence of conjunctival melanoma in a large population-based study.nnnDESIGNnObservational cross-sectional study.nnnMETHODSnUsing data from 1992 through 2003 provided by the National Cancer Institutes Surveillance, Epidemiology, and End Results (SEER) program, we calculated age-adjusted incidence rates of conjunctival melanoma in various racial and ethnic groups (Black, American Indian, Asian and Pacific Islander, Hispanic, and non-Hispanic White). In addition, we calculated the standard incidence ratios (risk ratios) and 95% confidence intervals to describe the differences within these racial and ethnic groups.nnnRESULTSnFrom 1992 through 2003, there were a total of 168 conjunctival melanomas diagnosed in 13 SEER registries with known racial and ethnic groups. The annual age-adjusted incidence rates (per million population) of conjunctival melanoma was 0.18 (Blacks), 0.17 (American Indians), 0.15 (Asians), 0.33 (Hispanics), and 0.49 (non-Hispanic Whites). The difference in the incidence of conjunctival melanoma between Whites and Blacks or Asians was statistically significant, but was not significant between Blacks and Asians.nnnCONCLUSIONSnThe overall White-to-Black incidence ratio in conjunctival melanoma was 2.6:1, which is much less than that of uveal melanoma (18:1) and cutaneous melanoma (13:1 to 26:1), but is similar to that of mucosal melanoma (2.2:1 to 2.3:1). The cause and significance of this difference of racial and ethnic incidence in various melanomas are discussed.

Effect of TGF-β and cAMP-elevating Agents on the Growth of Human Scleral Fibroblasts In Vitro

Previous reports regarding the effects of transforming growth factor (TGF-β) on the growth of fibroblasts have been very conflicting. The present studies indicate that the confusion may be caused by performing studies at different cell densities. At a low cell density (similar to the in vivo situation), TGF-β inhibits the growth of cultured human scleral fibroblasts. Some neurotransmitters or hormones known to influence the development of myopia work through cAMP system. The effect of cAMP on the growth of scierai fibroblasts is not clear. We found that cAMP-elevating agents inhibit the growth of fibroblasts in vitro.

Role of Uveal Melanocytes in the Development of Myopia

Reduction of nitric oxide (NO) may inhibit the development of experimental myopia. Uveal melanocytes reduced the amount of exogenous NO in culture medium provided by a NO donor (S-nitroso-N-acetylpenicillamine, SNAP). Uveal melanocytes have the receptors of various neurotransmitters, melatonin, basic fibroblast growth factor (bFGF) and transforming growth factor-s (TGF-s) and can respond to most of these factors, all of which are known to play a role in the development of myopia. These factors may bind to and modulate the functions of uveal melanocytes and thus influence the development of myopia.

Hepatocyte Growth Factor Protection of Retinal Pigment Epithelial Cells

Hepatocyte growth factor (HGF) is a pleiotropic growth factor that is mainly expressed in mesenchymal cells. MET (mesenchymal–epithelial transition factor) is a membrane receptor that binds HGF. The receptors for HGF (MET) are primarily found in epithelial cells and several stromal cells. Activation of MET by HGF promotes migration, mitosis, and survival of various cells. HGF protects various cells from oxidative stress-induced apoptosis mainly via the phosphorylation of phosphoinositide 3-kinase/Akt pathway. HGF also plays a role in embryogenesis, tissue repair, and angiogenesis. HGF levels in the ocular fluids are elevated in various ocular diseases related to cell proliferation and angiogenesis. HGF protects retinal pigment epithelial (RPE) cells from hydrogen peroxide-induced apoptosis by inhibition of the mitochondrial apoptotic pathway. In ceramide- and glutathione depletion-induced apoptosis of RPE cells, studies have also demonstrated that HGF can protect RPE cells in these oxidative stress models. These studies suggest that HGF is a natural protective factor for RPE cells and plays an autocrine role protecting RPE cells against oxidative stress.