Malignant melanoma is a highly malignant tumor derived from melanocyte. Malignant melanoma of the oral cavity occurs mainly in the palatine mucosa and the maxillary gingiva in men in their 50s. Malignant melanoma can be divided into pigmented and non-pigmented(amelanotic). Among them, non-pigmented malignant melanoma accounts for 2-8% of all malignant melanomas. Pigmented malignant melanoma is detected through changes in pigmentation, whereas non-pigmented malignant melanoma is characterized by no pattern of color change. In this study, at the initial visit, a malignant lesion was suspected and a biopsy was performed. According to the biopsy results, it was diagnosed as polymorphic sarcoma, but the histological examination performed during the operation revealed that it was amelanotic melanoma. As such, the differential diagnosis is important because there is no clinical change in non-pigmented malignant melanoma. Diseases to be differentially diagnosed when non-pigmented malignant melanoma occurs in the oral cavity include squamous cell carcinoma, lymphoma, sarcoma, inflammation, and osteomyelitis. In this study, we report a case that showed the histopathological characteristics of malignant melanoma without superficial pigmentation.

Oral lichen planus (OLP) is a chronic inflammatory disease observed in approximately 0.5–2.2% of the population, and it is recognized as a premalignant lesion that can progress into oral squamous cell carcinoma (OSCC). The rate of malignant transformation is approximately 1.09–2.3%, and the risk factors for malignant transformation are age, female, erosive type, and tongue site location. Malignant transformation of OLP is likely related to the low frequency of apoptotic phenomena. Therefore, apoptosis-related genetic factors, like p53, BCL-2, and BAX are reviewed. Increased p53 expression and altered expression of BCL-2 and BAX were observed in OLP patients, and the malignant transformation rate in these patients was relatively higher. The involvement of microRNA (miRNA) in the malignant transformation of OLP is also reviewed. Because autophagy is involved in cell survival and death through the regulation of various cellular processes, autophagy-related genetic factors may function as factors for malignant transformation. In OLP, decreased levels of ATG9B mRNA and a higher expression of IGF1 were observed, suggesting a reduction in cell death and autophagic response. Activated IGF1-PI3K/AKT/mTor cascade may play an important role in a signaling pathway related to the malignant transformation of OLP to OSCC. Recent research has shown that miRNAs, such as miR-199 and miR-122, activate the cascade, increasing the prosurvival and proproliferative signals.

Differential diagnosis of the malignant lesion and the benign lesion is critically important for the precise treatment. A clinician should diagnose in a comprehensive manner considering clinical, radiological, and histopathological perspectives. The lesion in the oral cavity in this study was clinically and radiologically malignant. However, the lesion was histopathologically benign. Surgical intervention was not performed except biopsy. The lesion improved after about one month of supportive medication after the biopsy. The importance of decision making process was emphasized in this report.

Human malignant melanoma is an aggressive skin cancer which has been rising at a greater rate than any other cancers. Although various new therapeutic methods have been developed in previous studies, this disease has properties of high proliferation and metastasis rate which remain obstacles that have lead to a poor prognosis in patients. It has been reported that a specific Lactobacillus extract has anti-cancer and –metastasis effect in vitro and in vivo. However, previous research has not specified precisely what effect the Lactobacillus rhamnosus GG (LGG) extract has had on human malignant melanomas. In this study, we showed that the LGG extract has anti-cancer and –metastasis effects on the human malignant melanoma cell lines, A375P and A375SM. At first, it was found that, while the LGG extract affects human neonatal dermal fibroblasts slightly, it induced the dose-dependent anti-cancer effect on A375P and A375SM by a WST-1 proliferation assay. As a result of a real-time PCR analysis, the expression patterns of several genes related to cell cycle, proliferation, and apoptosis were modulating in a manner that inhibited the growth of both malignant melanoma cell lines after the treatment of the LGG extract. Furthermore, genes related to the epithelialmesenchymal transition were down-regulated, and migration rates were also decreased significantly by the LGG extract. Our study showed that the LGG extract could be used as a potential therapeutic source.

Malignant peripheral nerve sheath tumors (MPNSTs) are defined as malignant tumors arising from peripheral nerves or differentiating along the line of the elements of the nerve sheath. MPNSTs that originate from the brain parenchyma are exceptionally rare and are termed malignant intracerebral nerve sheath tumors. We experienced a case of the epithelioid variant of malignant intracerebral nerve sheath tumor (MINST) occurring in the right frontal lobe of a 50-year-old man. He underwent gross total resection of the tumor. Histologically, the tumor cells had round, polygonal, or ovoid nuclei and moderate amounts of eosinophilic cytoplasm, which was defined as epithelioid cells. The tumor cells were arranged in short cords or nests with vaguely nodular patterns embedded in the myxoid stroma. Regarding mitotic activity, 15 mitotic figures were noted per 10 high-power fields. Immunohistochemically, tumor cells were positive for S-100 protein and synaptophysin, but negative for glial fibrillary acidic protein, HMB-45, EMA, and AE1/ AE3. Furthermore, immunostaining for INI1 was negative. Loss of the tumor-suppressor gene product SMARCB1/ INI1 expression has been recognized in epithelioid MPNST, but not in conventional MPNST. Postoperatively, he underwent radiotherapy and was followed for almost 1 year without recurrence. The present case is the first report of the epithelioid MINST.

담관 협착의 원인을 양성인지 악성인지 구별하기가 어려운 경우가 종종 있어 많은 임상의사들을 곤혹스럽게 한다. 그러한 이유는 여러 가지 영상검사와 내시경적 역행성 담췌관 조영술에 의한 반복적인 세포검사와 조직검사를 시행함에도 불구하고 양성 담관 협착과 악성 담관 협착을 수술 전 정확히 감별하지 못하는 경우가 많기 때문이다. 저자들은 50 세 남자환자에게 원위부 담도 폐쇄 소견이 있어 세포 검사와 조직검사를 여러 차례 반복적으로 시행하였으나 악성세포는 나오지 않았고, 간흡충 충란이 다량 발견되어 간흡충증에 의한 양성 협착과 악성 협착의 감별이 어려운 상황에서 1개월 후 복부 전산화 단층촬영을 시행하였다. 그 결과 췌장실질의 위축과 췌관확장이 진행하여 악성종양을 강력히 의심하고 유문부 보존 췌십이지장 절제술을 시행하였다. 조직검사 결과에서 췌장 머리의 선암으로 진단하였다. 악성 담관 협착을 수술 전에 정확히 진단하기는 쉽지 않지만, 담관 협착은 악성이 의심되면 수술적 진단 등의 적극적 검사를 주저해서는 안될 것이다.

초기에 진단된 담낭암은 담낭 용종이나 담낭 결석 같은 다 른 양성 질환에 대한 치료 목적으로 담낭절제술을 시행한 이 후에 우연히 발견되는 경우가 대부분이다. 의료기술과 향상 에 따라 담낭 용종의 발생률이 증가했음에도 불구하고, 담낭 용종에서 악성을 시사하는 인자들에 대한 연구는 부족한 상 태이다. 본 연구에서는 437명의 환자 중, 담낭 용종으로 진단 된 첫 번째 군의 환자들은 359명이었고, 53명의 담낭선종, 25 명의 담낭암으로 진단된 환자들은 두번째 군에 분류하였다. 두번째 군의 환자들이 첫 번째 군의 환자들에 비해서 유의하 게 고령(50세 이상), 10 mm 이상의 크기, 담낭벽의 두께 증 가를 보였다. 담석 여부는 두 군간에 유의한 차이를 보이지 않았다. 50세 이상, 크기 증가, 담낭벽의 두께 증가 등은 담낭 용종에서 담낭암 또는 전구 병변의 가능성을 시사할 수 있 다. 이런 인자들을 가지고 있는 담낭 용종 환자에서 담낭절 제술을 고려해야 한다.

췌장의 낭종성 질환은 현재 영상기술의 발달로 인하여 우연히 발견되는 경우가 많다. 그리고 췌장 낭종성 질환은 다양한 질환으로 이루어져 있으며 그 종류에 따라 다양한 악성 도를 보인다 췌관의 편평세포낭종은 내층이 비각화 편평 상피로 이루어져 있는 췌관의 낭성 확장을 특징으로 한다. 현재까지 이 질환은 재발이나 악성 변화가 관찰되지 않는 양성 질환으로 알려져 있다. 그러나 저자들은 수술 전 영상검사에서 타 장기 침습 의심 소견을 보이며, 수술 후 경과에서 악성 형태를 보이는 췌관의 편평세포낭종 1예를 경험하였기에 문헌고찰과 함께 보고한다.

Development of squamous cell carcinoma around dental implants is an uncommon clinical manifestation with only a few cases described in the literature. Recently, we observed primary squamous cell carcinoma that developed from leukoplakia around dental implants. We report this case to emphasize the importance of careful oral examination, for implant surgery has to be preceded by thorough evaluation of oral mucosal conditions.

Malignant pleural effusion (MPE) and blood samples can be used as a practical source for detection of epidermal growth factor receptor (EGFR) mutations in patients with advanced non-small cell lung cancer. We compared EGFR mutation status of cell blocks, cell-free fluid of MPE, and plasma from patients with lung adenocarcinoma. We obtained paired samples of MPE and plasma from 14 pathologically-confirmed lung adenocarcinoma patients. Peptide nucleic acid (PNA)-mediated real-time polymerase chain reaction (RT-PCR) clamping was performed for determination of EGFR mutation status. EGFR mutations were detected in five (35.7%) cell blocks of MPE, which showed results identical to those of the corresponding cell-free fluid, whereas mutations were detected in the plasma of only two (40.0%) of the five patients. Of seven patients treated with EGFR tyrosine kinase inhibitors (TKIs), EGFR mutations were detected in cell blocks, cell-free fluid of MPE, and plasma for only one of the four patients who responded to EGFR TKIs, while mutations were detected only in cell blocks of MPE and cell-free fluid of the three remaining patients. Our results suggest that detection of EGFR mutations in cell-free pleural fluid from lung adenocarcinoma patients using highly sensitive methods may be feasible, but that analysis of free plasma may lead to undetected mutations and misdiagnosis.

Immunohistochemical localization of vimentin, glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), neuron-specific enolase (NSE) were performed to confirm the canine schwannoma diagnosed histologically. Biopsy samples from skin masses occurred on a 6 year old female dog and a 13 year old female dog were used for immunohistochemical analysis. Histologically, the tumor tissues showed the characteristics of schwannoma mainly composed of predominantly fusiform or spindle cells. The cells are arranged in small interwoven bundles with intervening fibrous and mucinous stroma that imitate a herringbone pattern. The cell nuclei have an elongated, wavy, buckled appearnce and closely bunched together. In high magnification, mitotic figure, nuclear hyperchromatism, pleomorphism and poorly defined cytoplasms were noted. the vimentin was highly expressed in the cytoplasm of all neoplastic cells. Positive reactions against NSE and GFAP, widely used to suggest a neural origin of cell types, are observed in cytoplasms of tumor cells. These results can be used as a reference data for definitive diagnosis of canine schwannoma.

Considering the great potential of iron chelators at inhibiting the proliferation of tumor cells, in order to determine the molecular and biological basis for the effects of iron chelator in oral cancer, we investigated the effects of iron chelator, desferrioxamine (DFO), on the gene profiling analysis of immortalized human oral keratinocytes (IHOK), and oral cancer cells (HN12), using the cDNA microarray. We identified 46 clones cDNA exhibiting more than 2 fold overexpression in DFO treated IHOK and HN12 cells, and 94 cDNA reveal more than 2 fold down-regulated expression. Examination of gene expression that differs between DFO treated vs. control IHOK and HN12 cells apprear to be related to : cell cycle regulator, cell growth and apoptosis, signal transduction and stress. p21 for cell cell cycle factor was upregualted, and cyclin-cdk gene was decreased expression, so we observed cell cycle arrest in DFO treated IHOK and HN12 cells. In tumor growth, we have identified downregulation of hemidesmosomal protein (bullous pemphigoid antigen 1) and epiregulin expression in DFO treated IHOK and oral cancer cells. Signal transducers including mitogen-activated protein kinase-activated protein kinase 5, serine/thereonine kinase 6 were downregulated with DFO treated cells, suggesting the DFO regulates the p38 MAP kianse pathway in immortalized and maignant oral keratincytes. In conclusion, we have demonstrated the high-throughput utility of cDNA array hybridization in parallel to the gene expression analysis to identify genes that are expressed differentially in DFO treated with immortalized and malignant oral keratinocytes. The differentially expressed genes identified here should be informative in DFO-induced anti-cancer effects.

A 13-year-old, male mixed breed dog was presented to Veterinary Medical Center, Chungbuk National University for diagnosis and treatment of enlarged mass in right inguinal region. On hematological test, monocytes and neutrophils were slight increased, but other hematological values were normal. On radiological finding, opacity and size of mass in right inguinal region were increased. The mass and testis were removed surgically. Removed mass was oval-shpae and bulky with 5.6×7.6×5.2 cm. Histopathological finding of the mass revealed large and round to polyhedral cells and it was diagnosed as malignant seminoma. That was diffuse type seminoma near to malignant tumor without metastasis. During the follow-up for 13 months, patient showed normal contition without recurrence.

Oral malignant melanoma of the oral cavity is rare. Although the Asian population has a relatively high incidence of oral malignant melanoma in contrast to Caucasians, the clinical information in Korean has been rarely known. In addition, the clinical and histological classification of oral malignant melanoma has not been established up to now. So we investigated 26 cases of oral malignant melanomas on the basis of clinicopathological and immunohistochemical findings and reclassified the clinical and histological type. The results of this study are as followed. Oral malignant melanomas occurred at any age from 28 years to 73 years and their mean age was 58.6 years. Of 26 cases, 14 occurred in male and 12 in female. Oral malignant melanomas occurred almost in palate and/or maxillary gingiva (25 cases; 96.2%). Only one case occurred in mandibular gigiva. Oral malignant melanomas were clinically divided into macular(9 cases) and nodular type(17 cases), showing that the nodular type occurred more frequently. Oral malignant melanomas were histologically divided into in situ spreading(5 cases), invasive(13 cases), and combined type(8 cases), showing that the invasive type occurred most frequently. All cases showed positivity for S-100 and 15 cases(57.7%) for HMB-45 in immunohistochemical analysis. It was thought these results could provide basic data for the research on oral malignant melanoma in Korean and additional prospective and retrospective studies would be needed in order to find the relations with the prognosis of the patients

Macrophage inflammatory prote in -3α (M1P-3a 01' CCL20) is an intr땅uing molecule in CanCel‘ irrununotherapy‘ but M1P-3 a expr ession and signaling are not well under s tood in oral cancer cell s. We investigated CCL20 expression a nd signal trans duction by treating immortal ized hllman oral keratinocyte (IHO찌 and oral ca ncer (뻐 4) cells with defe roxa llline (DFO) and examined the mRNA express ion 01' CCL20 using RT- PCR and ELI8A. lHOK and HN4 cells treated with DFO sbowed increased mRNA and protein expression 01' CCL20. and the upregulation 01' DFO-induced CCL20 expression was higher in IHOK cells than in HN4 cells 8elective inhibitors of p38 and ERKl/2 abol ished DF'O- induced CCL20 expression in both lHOK and HN12 cells. and p38 and ERKl/2 inhibitors prevented DFO- induceddegradati on 01' 1 -κ B and NF'-K B activation. Activation 01' c-fos and c-jun also occmred fo l lowing DFO treatment in IHOK and HN4 cells Collectively, these results suggest that DFO-indllced M1 P- 3a. which is involved in the MAP kinase‘ c-fos, c-jun, and NF-K B pathways, may be an important mediator of the a ntitumor immune response in oral keratinocytes ancl warrants con sideration as a target molecule for oral cancer t reatment

Heme oxygenase-l (HO-l) exhibits cyt oprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts‘ However‘ therole of HO- l in cancer cells exposed to nicotine has not previously been descnbed We investigated the effects of nicotine on HO-l protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human ora l keratinocyte cells using the MTT assay and Western blotting. We al so examined the involvement of t he phosphoinosit ide-3-0H- kinase (PI3K), mitogen-acti vated protein kinase (MAPK) , and nucJear factor-κ B (NF-κ B) signaling pathways in nicotine-induced cytotoxicity and HO- l levels in IHOK and HN12 cell s‘ Nicotine induced HO- l pro ducti on and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotox icity and accumulation of HO- l were greater in JJ-IOK cells than in HN12 cells Molecular inhibitors of the ERK, p38 MAP kinase, PI3K, and NF-κ B signaling pathways blocked the cytotoxic effects and induction of J-IO-l expression by nicotine. Treatmen t with an t ioxida nts (bil irubin, N-acetyl cysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregula tion of J-IO- l, the effects of which were more pronounced in II-IOK cells than in HN12 cells Collecti vely, these results suggest that J-IO- l plays a principal role in the protective response to nicotine in oral cancel and immortalized keratinocytes. Moreover, the addition of exogenous antioxidants may help to protect oral epithelial cells as chemopreventive agents against nicotine-induced oxidative stress.

Heme oxygenase-l (HO-l) exhibits cyt oprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts‘ However‘ therole of HO- l in cancer cells exposed to nicotine has not previously been descnbed We investigated the effects of nicotine on HO-l protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human ora l keratinocyte cells using the MTT assay and Western blotting. We al so examined the involvement of t he phosphoinosit ide-3-0H- kinase (PI3K), mitogen-acti vated protein kinase (MAPK) , and nucJear factor-κ B (NF-κ B) signaling pathways in nicotine-induced cytotoxicity and HO- l levels in IHOK and HN12 cell s‘ Nicotine induced HO- l pro ducti on and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotox icity and accumulation of HO- l were greater in JJ-IOK cells than in HN12 cells Molecular inhibitors of the ERK, p38 MAP kinase, PI3K, and NF-κ B signaling pathways blocked the cytotoxic effects and induction of J-IO-l expression by nicotine. Treatmen t with an t ioxida nts (bil irubin, N-acetyl cysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregula tion of J-IO- l, the effects of which were more pronounced in II-IOK cells than in HN12 cells Collecti vely, these results suggest that J-IO- l plays a principal role in the protective response to nicotine in oral cancel and immortalized keratinocytes. Moreover, the addition of exogenous antioxidants may help to protect oral epithelial cells as chemopreventive agents against nicotine-induced oxidative stress.

Sulfur is commonly used in Asia as a n herba l medicine to treat infl ammation and cancel‘. and potent chemopreventive effects have been demonstrated in various in vivo and in vitromodels for sulfur-containing compounds found in naturally occun‘ ing products. Here, we report the growth inhibitory and apoptosis-related effects of a newly developedhigh- purity eclible sulfur (ES) on immortali zecl human oral keratinocytes (IHOKs) and on oral cancer cells representing two stages of oral can cer (HN4‘ HN12) basecl on an 3-(4. 5-Dimethylt hiazol-2-yl)-2.5-cliphenyl tetrazolium bromide (MTT) a ssay, Western blotting, cell cycle analysis, ancl nuclear staining. The puri ty of the ES used in th is s tucly was verified by high performance liquid chromat ography (HPLC) , amino acid analysis and energy di spersive spectroscopy (EDS). ES inhibitecl the proliferation of immor talized and malignant oral kerati nocytes in a dose- and time-dependent manner FITC-Annexin V staining. DNA fragmentation testing. and Hoechst 33258 staining revealed that ES inhibits cell growth via apoptosis . ES blocked cell-cycle progression at the sub- Gl phase, with decreased expression 0 1' cyclins Dl, D2, and E, and t heir activating partners cdk2, cdk4, and cdk6‘ and a concomitant induction of p53 and p21/WAF1. Furthermore, ES treatment increased the cytosolic level of cytochrome c a nd resulted in caspase-3 activation‘ and thi s effect was correlated wi th Bax up- regulation and Bcl-2 down- regulation Taken together, these clata suggest that ES is a potential chemopreventive and chemotherapeutic agent for oral cancel

Cytokines play a vital role in the host immune response by regulating the development and function of im munocompetent ce11s One immunomodulatory agent that has received attention in oncology research recently is interleukin - lO(IL-lO). IL-IO inhibi ted tumor antigen presenta tion and induced energy in T lymphocytes that had been s timu lated by autologous MHC class II positive tumor ce11s Patients with head and neck cancer have been shown to exhibit profound irnmunosuppression. The mechani sm by which tumor ce11s alter immunological function in the host is poorly understood. Recently. production of biological active IL- IO was confirmed in ovar‘ian cancer, melanoma, skin cancel‘ & head and neck cancer, suggesting that IL- lO reduces the function of tumor infiltrating lymphocytes and contributes to the tumor growth. IL-IO expression has not been examined extensively in human oral cancer and has not yet been cla rified. The purpose of t his study were to investigate IL-IO mRNA and protein expression in NHOK, IHOK and oral squamous ce11 carcinoma(OSCC) ce11 line by RT-PCR and irnmunoslot blotting, and to apply its results to examine its thera peutic significance for oraJ cancers. Cultured NHOK showed a lower level of IL-IO mRNA and protein expression than cultured IHOK and HN 22 OSCC cell line under pre and postconfluency. HN 22 OSCC cell line under pre and postconfl u ency. showed the highest level of IL-I0 Cul tured IHOK showing a intermediate expression of IL- IO could be as a vaJ u a bJe marker for oral carci nogenesis ste p. During the terminal differentiation of a11 the ce11 lines, IL- IO ex pression was significantly unchangeabl e. IL- IO mRNA expression of a11 the ce11 lines was consistent with IL-10 protein expression. It suggested that IL- lO expression might play an important role in oral carcinogenesis and IHOK could be a valuable marker for oral carcinogenesis step. And aJso IL- 10 related gene may be future targets for gene discovery and possi bJy therapeutic intervention