Merkel Cell Carcinoma in Patients withLong-Term Ingestion of Arsenic: Sheng-Yow HO, et al. Departments of Radiation Oncology, Sin-Lau Christian Hospital, Taiwan-Merkel cell carcinoma (MCC) is a rare primary neuroendocrine carcinoma of the skin, mostly occurring late in life on sun-exposed body parts. Little is known about the specific etiological factors in the pathogenesis of MCC. A previous report indicated that arsenic exposure might cause MCC, which might be another specific type of skin cancer associated with arsenic exposure. On the southwest coast of Taiwan, high arsenic levels in artesian well water have been documented, and various diseases associated with arsenic exposure have been found to be prevalent in this area. We report two pathologically confirmed cases of MCC in patients who had histories of long-term ingestion of arsenic from drinking water. The tumors were on the anterior chest wall, an area less exposed to the sun, in both cases. The literature on the dose-response relationship between arsenic exposure and MCC is limited. We estimated that the total arsenic ingested by these two cases was around 14.7 and 2.6 gm, respectively. We also tried to assess the cancer risk on the basis of the estimated doses of arsenic exposure and the cancer risk model developed by the U.S. Environmental Protection Agency (EPA). The estimated lifetime target cancer risk was 1.3 × 10 -2 in Case 1 and 2.3 × 10 -3 in Case 2. Both are much higher than the 10 -6 upper limit on lifetime cancer risk put forth by the U.S. EPA health protection standard. We believe that arsenic intoxication played an important role in the carcinogenic process of MCC in our cases. (J Occup Health 2005; 47: 188-192) Field Study
The mouse skin carcinogenesis model provides a conceptual framework to study the carcinogenesis process. It has been used extensively to assess whether a chemical or physical agent carries a carcinogenic hazard to humans and to define the mechanism involved with the carcinogenic effects. We conducted a study to evaluate whether the tumor-promoting activity of pentachlorophenol (PCP) is mainly from its major metabolite tetrachlorohydroquinone (TCHQ). We applied the mouse skin model to CD-1 mice and the results showed that PCP and TCHQ are much weaker promoters than 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin during a 25-wk experiment. Both PCP and TCHQ could induce mice skin epidermal hyperplasia and proliferating cell nuclear antigen (PCNA) labeling index in the epidermis. However, TCHQ caused a more significant induction of epidermal hyperplasia and PCNA positive cells than PCP. Topical application of PCP, but not TCHQ, induced significant organ enlargement and lymphoma in mice, whereas short-term treatment of TCHQ increased tumor necrosis factor-alpha (TNF-alpha) gene expression in mouse skin. We did not observe a significant association between the carcinogenic process and serum TNF-alpha or interleukin-1 beta (IL-1 beta) levels in mice.
The detection of monoclonal expansions of the immunoglobulin heavy chain (IgH) or the T-cell receptor-gamma (TCRgamma) chain genes is an important supplement for the diagnosis of the non-Hodgkin's lymphomas (NHLs). Detection of monoclonality by polymerase chain reaction (PCR) method has offered an efficient approach for rapid diagnosis and monitoring of the therapeutic effects. Here we conducted a retrospective PCR clonality study on 49 cases of NHLs including 23 B-cell lymphomas (BCLs), 20 peripheral T-cell lymphomas (PTCLs), 6 natural killer (NK)/T-cell lymphomas and 3 reactive lymphoid tissues from southern Taiwan. Genomic DNAs from paraffin sections were extracted and analyzed by the IgH- and TCR-specific PCR reactions. The results showed that 20 of 23 (87.5%) BCLs exhibited IgH gene rearrangements and were all germline for TCRgamma. 15 of 20 (75.0%) PTCLs exhibited TCRgamma gene rearrangements while 1 case (5%) was positive for IgH gene rearrangement. The 6 NK/T-cell lymphomas and 3 reactive lymphoid tissues were all germline for either IgH or TCRgamma genes. Our results were similar to other Western reports in terms of sensitivity and cell-lineage specificity. This is the first large series of PCR clonality study of IgH and TCRgamma gene rearrangements on NHLs from Taiwan. We have confirmed that this rapid method is a sensitive diagnostic tool for NHLs.
This study illustrates a paradigm using molecular genetic approach in identifying chromosome 14q32 that may harbor a tumor suppressor gene involved in the pathogenesis of a subset of gastrointestinal and ampullary malignancies.
The intratumoral blood flow by transvaginal color Doppler ultrasound correlated with a reduced tumor size and tumor volume, but did not correlate with cell proliferation or angiogenesis.
Secondhand smoke (SHS) is an important health issue worldwide. Inhaling SHS during pregnancy could cause abnormalities in the internal tissues of newborns, which may then impair fetal development and even cause severe intrauterine damage and perinatal death. However, the understanding of cytopathic mechanisms of SHS by maternal passive smoking on fetus liver during pregnancy is still limited. This study analyzed the effects of high-dose SHS (SHSH) on fetus liver using a maternal passive smoking animal model. Experiments showed that hepatic matrix metalloproteinase-9 activity and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling-positive cells were significantly increased in livers from fetuses of hamsters treated with SHSH. Similarly, expressions of both extrinsic and intrinsic apoptotic molecules were significantly higher in livers from fetuses of hamsters exposed to SHSH. Additionally, significantly increased inflammatory proteins, including transforming growth factor β, inducible nitric oxide synthase, and interleukin 1β, and fibrotic signaling molecules, including phosphorylated Smad2/3, SP1, and α-smooth muscle actin, were observed in the fetus livers from hamsters treated with SHSH. This study revealed that SHSH not only increased apoptosis through intrinsic and extrinsic pathways in the livers of fetuses from hamsters exposed to SHSH but also augmented hepatic fibrosis via Smad2/3 signaling.
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