Honnavara N. Ananthaswamy

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The ultraviolet (UV) radiation present in sunlight is immune-suppressive. Recently we showed that solar-simulated UV radiation (UVA + UVB; 295-400 nm), applied after immunization, suppressed immunological memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in(More)
DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed "cellular proofreading." Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found(More)
The ultraviolet radiation present in sunlight is the primary cause of nonmelanoma skin cancer and has been implicated in the development of cutaneous malignant melanoma. In addition, ultraviolet is immune suppressive and the suppression induced by ultraviolet radiation has been identified as a risk factor for skin cancer induction. Ultraviolet also(More)
The ultraviolet radiation present in sunlight is immune suppressive. Recently we showed that solar-simulated ultraviolet radiation (ultraviolet A + B; 295-400 nm), applied after immunization, suppressed immunologic memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that(More)
One of the major targets for breast cancer therapy is the epidermal growth factor receptor (EGFR) and related receptors, which signal via different signal transduction pathways including the mitogen-activated protein kinase (MAPK) pathway. This study determined whether there is a correlation between EGFR/HER2 status and MAPK (ERK1/2) phosphorylation in(More)
The cellular and molecular events that contribute to the development of UV-induced skin cancer is a complex process involving at least two distinct pathways that interact or converge to cause skin cancer (Figure 1). One pathway involves the action of UV on target cells (keratinocytes) for neoplastic transformation, and the other involves the effects of UV(More)
UV radiation is a potent DNA-damaging agent and a known inducer of skin cancer in experimental animals. To elucidate the role of oncogenes in UV carcinogenesis, we analyzed UV-induced murine skin tumors for mutations in codon 12, 13, or 61 of Ha-ras, Ki-ras, and N-ras oncogenes by amplification of genomic tumor DNAs by the polymerase chain reaction followed(More)
Basal cell nevus syndrome (BCNS) is an autosomal dominant genetic disorder in which the afflicted individuals are extremely susceptible to sunlight-induced skin cancers, particularly basal cell carcinomas. How ever, the cellular and molecular basis for BCNS is unknown. To ascertain whether there is any relationship between genetic predisposition to skin(More)
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