• Title/Summary/Keyword: tumor tissues

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Deep benign fibrous histiocytoma in the oral cavity: a case report

  • Jo, Eun;Cho, Eunae Sandra;Kim, Hyun Sil;Nam, Woong
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.41 no.5
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    • pp.270-272
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    • 2015
  • Benign fibrous histiocytoma (FH) is a benign tumor composed of fibroblasts and histiocytes in varying proportions. This tumor is usually found in adult extremities but rarely occurs in deep soft tissues of the oral cavity. As it is difficult to diagnose with physical and radiologic exams, deep benign FH can only be diagnosed by histopathology. We report a case of a 36-year-old female patient who came to our department with painless swelling in the right buccal mucosa. This case report reviews the clinical, radiological, and histological aspects of this tumor.

Overexpression of tumor necrosis factor receptor-associated protein 1 (TRAP1), leads to mitochondrial aberrations in mouse fibroblast NIH/3T3 cells

  • Im, Chang-Nim;Seo, Jeong-Sun
    • BMB Reports
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    • v.47 no.5
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    • pp.280-285
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    • 2014
  • Cancer cells undergo uncontrolled proliferation, and aberrant mitochondrial alterations. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein. TRAP1 mRNA is highly expressed in some cancer cell lines and tumor tissues. However, the effects of its overexpression on mitochondria are unclear. In this study, we assessed mitochondrial changes accompanying TRAP1 overexpression, in a mouse cell line, NIH/3T3. We found that overexpression of TRAP1 leads to a series of mitochondrial aberrations, including increase in basal ROS levels, and decrease in mitochondrial biogenesis, together with a decrease in peroxisome proliferator-activated receptor gamma coactivator-$1{\alpha}$ (PGC-$1{\alpha}$) mRNA levels. We also observed increased extracellular signal-regulated kinase (ERK) phosphorylation, and enhanced proliferation of TRAP1 overexpressing cells. This study suggests that overexpression of TRAP1 might be a critical link between mitochondrial disturbances and carcinogenesis.

Electron microscope study on Agrobacterium tumefaciens in tomato tumor (도마도 암종내 Agrobacterium tumefaciens의 동태에 대하여)

  • 윤권상;이민재;하영칠
    • Korean Journal of Microbiology
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    • v.10 no.1
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    • pp.41-50
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    • 1972
  • The tomato plant, Lycopersicon esculentum Mill, was inoculated with tumor inducing strain, $A_6K_1$, of Agrobacterium tumefaciens and its produced tumors were examined with the electron microscope. A number of bacteria are usually detected in the intercellular region of the host plant, and it is observed that the host cytoplasm is readily destroyed in the region where the bacterial invasion occurred. Some of the bacteria in the host tissues are enclosed with the single unit membranes, in other locations lots of bacteroids were examined and the bacterial lysis is generally observed in those bacteroids. The bacterial movement in the tumor tissue and some peculiar relationships between the pathogens and the host plant are discussed.

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Intraosseous Malignant Peripheral Nerve Sheath Tumor of Multiple Bones of the Midfoot: A Case Report (중족부에 발생한 다발성 악성 말초 신경초 종양 1예: 증례 보고)

  • Lee, Hyobeom;Kim, Gab-Lae;Kim, Donghyeon
    • Journal of Korean Foot and Ankle Society
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    • v.24 no.4
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    • pp.156-160
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    • 2020
  • Malignant peripheral nerve sheath tumors (MPNSTs) usually arise in soft tissues; they are rarely found in the bone. This paper reports a case of MPNST in the foot and ankle joint involving the distal tibia, talus, calcaneus, navicular, medial intermediate, and lateral cuneiform, cuboid, and 2nd to 4th metatarsal bone. Palliative treatment was performed. The authors encountered a patient with intraosseous MPNST of the midfoot who presented with nonspecific clinical and radiologic findings. This case shows that a high index of suspicion and a histopathology examination, including immunohistochemistry, will be necessary for an accurate diagnosis.

Mechanisms of radiation-induced normal tissue toxicity and implications for future clinical trials

  • Kim, Jae Ho;Jenrow, Kenneth A.;Brown, Stephen L.
    • Radiation Oncology Journal
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    • v.32 no.3
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    • pp.103-115
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    • 2014
  • To summarize current knowledge regarding mechanisms of radiation-induced normal tissue injury and medical countermeasures available to reduce its severity. Advances in radiation delivery using megavoltage and intensity-modulated radiation therapy have permitted delivery of higher doses of radiation to well-defined tumor target tissues. Injury to critical normal tissues and organs, however, poses substantial risks in the curative treatment of cancers, especially when radiation is administered in combination with chemotherapy. The principal pathogenesis is initiated by depletion of tissue stem cells and progenitor cells and damage to vascular endothelial microvessels. Emerging concepts of radiation-induced normal tissue toxicity suggest that the recovery and repopulation of stromal stem cells remain chronically impaired by long-lived free radicals, reactive oxygen species, and pro-inflammatory cytokines/chemokines resulting in progressive damage after radiation exposure. Better understanding the mechanisms mediating interactions among excessive generation of reactive oxygen species, production of pro-inflammatory cytokines and activated macrophages, and role of bone marrow-derived progenitor and stem cells may provide novel insight on the pathogenesis of radiation-induced injury of tissues. Further understanding the molecular signaling pathways of cytokines and chemokines would reveal novel targets for protecting or mitigating radiation injury of tissues and organs.

AN EXPERIMENTAL STUDY FOR ESTABLISHMENT OF ORTHOTOPIC SALIVARY TUMOR MODELS IN MICE (마우스에서 타액선암 동위종양 모델 제작을 위한 실험적 연구)

  • Park, Young-Wook;Chung, Seong-Hoon
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.33 no.2
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    • pp.81-93
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    • 2007
  • Purpose: Adenoid cystic carcinoma (ACC) is a relatively rare tumor that arises in glandular tissues of the head and neck region and sometimes has a protracted clinical course with perineural invasion and delayed onset of distant lung metastasis. Treatment failure of salivary ACC is most often associated with perineural and hematogenous tumor spread. However, very little has been known about the cellular and molecular mechanisms of perineural invasion and hematogenous distant metastasis of parotid ACC. This study was designed to develop an orthotopic tumor model of parotid adenoid cystic carcinoma in athymic nude mice. Experimental Design: A melanoma cell line was injected into the parotid gland of athymic mice to determine whether such implantation was technically feasible. A parotid ACC cell line was then injected into the parotid gland or the subcutaneous tissue of athymic mice at various concentrations of tumor cells, and the mice were thereafter followed for development of tumor nodule. The tumors were examined histopathologically for perineural invasion or regional or distant lung metastasis. We used an oral squmous cell carcinoma cell line as control. Results: Implantation of tumor(melanoma) cell suspension into the parotid gland of nude mice was technically feasible and resulted in the formation of parotid tumors. A parotid ACC cell line, ACC3 showed no significantly higher tumorigenicity, but showed significantly higher lung metastatic potential in the parotid gland than in the subcutis. In contrast, mucosal squmous cell carcinoma cell line doesn’t show significantly higher lung metastatic potential in the parotid gland than in the subcutis. The ACC tumor established in the parotid gland seemed to demonstrate perineural invasion of facial nerve, needs further study. Conclusion: An orthotopic tumor model of salivary ACC in athymic nude mice was successfully developed that closely recapitulates the clinical situations of human salivary ACC. This model should facilitate the understanding of the cellular and molecular mechanisms of tumorigenisis and metastasis of salivary ACC and aid in the development of targeted molecular therapies of salivary ACC.

S100A16 is a Prognostic Marker for Lung Adenocarcinomas

  • Saito, Keita;Kobayashi, Makoto;Nagashio, Ryo;Ryuge, Shinichiro;Katono, Ken;Nakashima, Hiroyasu;Tsuchiya, Benio;Jiang, Shi-Xu;Saegusa, Makoto;Satoh, Yukitoshi;Masuda, Noriyuki;Sato, Yuichi
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.16
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    • pp.7039-7044
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    • 2015
  • Background: Many functional molecules controlling diverse cellular function are included in low-molecular weight proteins and peptides. Materials and Methods: To identify proteins controlling function in lung adenocarcinomas (AC), we performed two-dimensional gel electrophoresis employing tricine-SDS polyacrylamide in the second dimension (tricine 2-DE). This system was able to detect proteins under 1 kDa even with post-translational modifications. To confirm the utility of detected proteins as novel tumor markers for AC, we performed immunohistochemical analysis using 170 formalin-fixed and paraffin-embedded lung AC tissues. Results: Tricine 2-DE revealed that five proteins including S100A16 were overexpressed in lung AC-derived cells compared with lung squamous cell carcinoma, small cell carcinoma, and large cell neuroendocrine carcinoma-derived cells. Immunohistochemically, S100A16 showed various subcellular localization in lung cancer tissues and a membranous staining status was correlated with the T-factor (P=0.0008), pathological stage (P=0.0015), differentiation extent (P=0.0001), lymphatic invasion (P=0.0007), vascular invasion (P=0.0001), pleural invasion (P=0.0087), and gender (P=0.039), but not with the age or smoking history. More importantly, membranous staining of S100A16 was significantly correlated with a poorer overall survival of either stage I (P=0.0088) or stage II / III (P=0.0003) lung AC patients, and multivariate analysis confirmed that membranous expression of S100A16 was an independent adverse prognostic indicator (P=0.0001). Conclusions: The present results suggest that S100A16 protein is a novel prognostic marker for lung AC.

Effect of dietary changes from high-fat diet to normal diet on breast cancer growth and metastasis (고지방식이에서 일반식이로의 전환이 유방암의 성장 및 전이에 미치는 영향)

  • Park, Seung hwa;Jung, InKyung;Kim, Jung-Hyun
    • Journal of Nutrition and Health
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    • v.53 no.4
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    • pp.369-380
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    • 2020
  • Purpose: It has been previously reported that breast tumor incidence, growth, and metastasis are stimulated by high-fat diet but reduced by caloric restriction. However, few studies have elucidated the effects of dietary change from a high-fat diet after breast cancer initiation. Therefore, in this study, we attempted to provide practical assistance to breast cancer prevention and management by investigating the effects of dietary change from a high-fat diet to normal diet on breast cancer growth and metastasis. Methods: The experimental animals were divided into 2 groups (high-fat diet control [HFC] group and diet restriction [DR] group) and consumed a high-fat diet for 8 weeks. 4T1 cells were transplanted into subcutaneous fat or tail vein to measure the growth and metastasis of breast cancer. The HFC and DR groups continuously ingested either high-fat diet or AIG-93G diet for 5 weeks or 3 weeks, respectively. Cell proliferation and apoptosis markers from tumor tissues were analyzed by Western blot analysis. The data were analyzed using the SPSS 25.0 package program. Results: The results show that the DR group significantly reduced breast tumor initiation, growth, and tumor tissue weight compared to the HFC group. The DR group suppressed tumor growth by decreasing proliferation and inducing apoptosis through down-regulation of Bcl-xL and up-regulation of caspase-3 activity. Furthermore, the DR group significantly reduced numbers of metastasized tumors in lung tissues. Conclusion: These results suggest that dietary change from a high-fat diet to normal diet decreased breast growth by reducing cell proliferation and inducing apoptosis and metastasis. Taken together, these results indicate that dietary change to a low-fat and balanced diet might suppress breast tumor growth and metastasis even after tumor diagnosis.

Pak1/LIMK1/Cofilin Pathway Contributes to Tumor Migration and Invasion in Human Non-Small Cell Lung Carcinomas and Cell Lines

  • Jang, In-Seok;Jeon, Byeong-Tak;Jeong, Eun-Ae;Kim, Eun-Jin;Kang, Da-Won;Lee, Jong-Sil;Jeong, Baek-Geun;Kim, Jin-Hyun;Choi, Bong-Hoi;Lee, Jung-Eun;Kim, Jong-Woo;Choi, Jun-Young;Roh, Gu-Seob
    • The Korean Journal of Physiology and Pharmacology
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    • v.16 no.3
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    • pp.159-165
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    • 2012
  • Squamous cell carcinoma (SCC) and adenocarcinoma (AC) are the major histological types of non-small cell lung carcinoma (NSCLC). Although both SCCs and ACs have been characterized histologically and clinically, the precise mechanisms underlying their migration and invasion are not yet known. Here, we address the involvement in NSCLC of the p21-associated kinase1 (Pak1)/LIM kinase1 (LIMK1)/cofilin pathway, which recently has been reported to play a critical role in tumor migration and invasion. The Pak1/LIMK1/cofilin pathway was evaluated in tumors from SCC (n=35) and AC (n=35) patients and in SCC- and AC-type cell lines by western blotting, immunohistochemistry, and in vitro migration and invasion assays. The levels of phosphorylated Pak1, LIMK1, and cofilin in lung tumor tissues from SCC patients were increased as compared to normal tissues. In addition, immunohistochemistry showed greater expression of phosphorylated cofilin in SCC tissues. Expression of phosphorylated Pak1 and LIMK1 proteins was also significantly higher in SCC-type cells than in AC-type cells. Moreover, migration and invasion assays revealed that a higher percentage of SCC type cells exhibited migration and invasion compared to AC type cells. Migration was also decreased in LIMK1 knockdown SK-MES-1 cells. These findings suggest that the activation of the Pak1/LIMK1/cofilin pathway could preferentially contribute to greater tumor migration and invasion in SCC, relative to that in AC.

Pathologic observations on the canine mammary gland tumors and immunohistochemical study on the origin of chondroid tissue in mammary gland mixed tumors (개 유선종양의 병리학적 관찰 및 유선 혼합종양의 연골기원에 관한 면역조직화학적 연구)

  • Kim, Yong-baek;Seo, Il-bok;Kim, Jae-hoon;Bak, Eun-jung;Kim, Dae-yong;Han, Jeong-hee
    • Korean Journal of Veterinary Research
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    • v.37 no.4
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    • pp.843-854
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    • 1997
  • Sixteen mammary gland tumors were collected from Seoul National University and Kangwon National University. The average age of the bitches with mammary gland tumor was 10 years. Total 17(60.7%) out of 28 tumor masses observed in 4th and 5th glands. Classification of these tumors according to Hampe and Misdorp were simple adenoma, complex adenoma, benign mixed tumor, papillary adenocarcinoma, solid adenocarcinoma and malignant mixed tumor. Immunohistochemical reaction of the intermediate filaments against normal canine mammary gland showed as followed; anti-cytokeratin 18 was strong and anti-cytokeratin 14 was moderate to the luminal epithelium. Anti-cytokeratin 14 and anti-pancytokeratin to the myoepithelium were showed strong, but anti-vimentin was weak in reactivity. Anti-vimentin to the interstitial cells was represented strong reactivity. The origin of cartilage in mixed tumor of canine mammary gland was studied immunohistochemically with antibodies against intermediate filament. In mammary gland mixed tumors, cartilage tumor tissues were surrounded with the irregularly demarcated three zones composed of adjacent star shaped cells in myxoid areas, proliferative spindle shaped cells and basal located proliferated cells. From basal proliferated cells to star shaped cells, the immunohistochemical reactivity of myoepithelium specific anti-pancytokeratin was decreased gradually and the reactivity of interstitial cell specific anti-vimentin was increased gradually. Based on these immunohistochemical staining patterns, we suggested that the origin of cartilagenous components in canine mammary gland mixed tumor is most likely to the proliferation and metaplsia of myoepithelium.

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