Shui-Sang Hsue

Sialolipoma of the Floor of the Mouth: A Case Report

Intra‐oral lipoma is a well‐known entity, but lipomatous tumors including salivary gland tissue containing clustered or peripherally located ducts and acinar cells are uncommon. They are a newly recognized entity of salivary gland lipoma, designated sialolipoma. We describe a case of sialolipoma arising in the floor of the mouth presenting with apparently normal salivary gland tissue, as demonstrated by both histologic and immunohistochemical findings, in a 67‐year‐old female. Complete surgical removal of the tumor with preservation of the sublingual gland was implemented after a careful examination confirming that the lesion did not originate from the sublingual gland.

Increased expression of inducible nitric oxide synthase for human buccal squamous-cell carcinomas: Immunohistochemical, reverse transcription-polymerase chain reaction (RT-PCR) and in situ RT-PCR studies

The inducible nitric oxide synthase (iNOS) is involved primarily in inflammatory and carcinogenesis processes. An enhanced expression of iNOS at the protein level has been reported previously for human oral squamous cell carcinoma; however, the expression of iNOS at the mRNA level has not yet been demonstrated. Furthermore, no studies have addressed whether iNOS expression at mRNA level correlates with cervical lymph node metastasis.

p73 expression for human buccal epithelial dysplasia and squamous cell carcinoma: Does it correlate with nodal status of carcinoma and is there a relationship with malignant change of epithelial dysplasia?

TP73, a p53 homologue gene, shares similar structural sequences with p53. The aim of this study was to investigate the p73 expression for human buccal epithelial dysplasia (ED) and squamous cell carcinoma (SCC).

The mRNA expression of placental glutathione S-transferase isoenzyme in hamster buccal-pouch carcinomas using reverse transcription-polymerase chain reaction

Placental glutathione S-transferase (GST-P) may facilitate cell proliferation and inhibit apoptosis, hence allowing for the expansion of a population of initiated tumor cells. The enhanced expression of GST-P at the protein level has been reported previously in chemically induced oral carcinomas in hamster buccal-pouch mucosa but the expression of GST-P at the mRNA level has not yet been demonstrated. The purpose of the present study was to assess the GST-P mRNA expression in 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal-pouch carcinomas using a reverse transcription-polymerase chain reaction (RT-PCR). Thirty-five outbred, young (6 weeks old), male, Syrian golden hamsters (Mesocricatus auratus) were randomly divided into one experimental group (15 animals), and two control groups (10 animals each). Bilateral pouches of a group of 15 animals of the experimental group were painted with a 0.5% DMBA solution three times a week for 12 weeks while each animal of one of the control groups was similarly treated with mineral oil. Another control group of 10 animals was untreated throughout the experiment. Areas of dysplasia and squamous-cell carcinomas with a 100% tumor incidence developed in all of the DMBA-treated buccal pouches. The mineral oil-treated and untreated pouches revealed no obvious changes. Placental glutathione S-transferase mRNA was demonstrated to be present amongst all the 12-week DMBA-treated hamster buccal-pouch mucosa animals, but not for the untreated animals or the animals for which the buccal pouch was treated with mineral oil. Multiple potential regulatory pathways including gene amplification, enhanced mRNA stability, chromosomal translocation/gene rearrangement, and hypomethylation of the promoter region can contribute to the overexpression of GST-P mRNA in DMBA-induced hamster buccal-pouch carcinomas. Further study is necessary to completely understand which candidate mechanism(s) will contribute principally to the increased GST-P mRNA expression in oral experimental carcinogenesis.

Immunohistochemical demonstration of p73 protein in the early stages of DMBA-induced squamous-cell carcinogenesis in hamster buccal pouch

The identification of a new protein, p73, with structural and functional similarities to p53 protein suggests that a family of p53-like proteins is likely to exist. This study investigated the status of p73 protein in the early stages of 7,12-dimethyl benz[a]anthracene (DMBA)-induced carcinogenesis. Outbred young (6-week-old) male Syrian golden hamsters (Mesocricatus auratus; 40 animals) were randomly divided into four equal groups: a 3-week DMBA-treated experimental group, a 6-week DMBA-treated experimental group, a mineral oil-treated control group, and a non-treated control group. Following this, a total of 80 specimens of pouch mucosa were obtained from the 40 animals in the four groups. Positive nuclear staining for p73 protein was randomly distributed throughout the whole epithelial layer of the DMBA-treated specimens and was absent in controls. Positive p73 staining was observed in 8 of the 20 (40%) 3-week, and 14 of the 20 (70%) 6-week DMBA-treated specimens. None of the 3-week DMBA-treated specimens revealed more than 25% p73-positive keratinocytes, but, in 12 (60%) of the 6-week-treated specimens, more than 25% of the keratinocytes examined were p73-positive. This suggests that the longer the DMBA painting period, the higher the proportion of p73-stained pouch keratinocytes. Furthermore, a p73-dependent mechanism may be associated with the early stages of oral carcinogenesis. Such a mechanism could be very important to an understanding of the participation of p73 in the development of oral squamous-cell carcinomas.

Expression of inhibitors of apoptosis family protein in 7,12‐dimethylbenz[a]anthracene‐induced hamster buccal‐pouch squamous‐cell carcinogenesis is associated with mutant p53 accumulation and epigenetic changes

Fifty outbred Syrian golden hamsters were equally divided into three experimental groups and two control groups. The pouches of the experimental groups were painted bilaterally with a 0.5% 7,12‐dimethylbenz[a]anthracene (DMBA) solution thrice a week for 3, 7 and 14 weeks. One of the control groups was applied with mineral oil while another control group remained untreated throughout the experiment. Neither survivin nor cIAP2 could be detected in any of the control tissues, whereas survivin and cIAP2 were found to be significantly increased in 3‐, 7‐ and 14‐week DMBA‐treated pouches compared with the control pouches. Expression of XIAP, cIAP1 and NAIP were noted for both the control and 3‐, 7‐ and 14‐week DMBA‐treated pouches, but levels were found to be significantly elevated in the experimental groups compared with the control pouches. p53 was not detected in any control tissues, but was significantly increased in 3‐, 7‐ and 14‐week DMBA‐treated pouches. Direct sequencing revealed a point mutation (C→G) of p53 for pouch tissues treated with DMBA for 3 and 7 weeks, and there was a wide variation in the p53 sequence of the 14‐week DMBA‐treated pouch tissues, as compared with the control tissues. The control tissues had a survivin‐ and cIAP2‐methylated allele, whereas the DMBA‐treated tissues showed no evidence of survivin‐ and cIAP2‐methylation. Neither the control nor DMBA‐treated pouches showed evidence of XIAP‐, cIAP1‐ or NAIP‐methylation. Our results suggest that the expression of inhibitors of apoptosis family in DMBA‐induced hamster buccal‐pouch squamous‐cell carcinogenesis may be modulated by both genetic (mutant p53) and epigenetic mechanisms.