• Title/Summary/Keyword: tumor development

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IMAGING IN RADIATION THERAPY

  • Kim Si-Yong;Suh Tae-Suk
    • Nuclear Engineering and Technology
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    • v.38 no.4
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    • pp.327-342
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    • 2006
  • Radiation therapy is an important part of cancer treatment in which cancer patients are treated using high-energy radiation such as x-rays, gamma rays, electrons, protons, and neutrons. Currently, about half of all cancer patients receive radiation treatment during their whole cancer care process. The goal of radiation therapy is to deliver the necessary radiation dose to cancer cells while minimizing dose to surrounding normal tissues. Success of radiation therapy highly relies on how accurately 1) identifies the target and 2) aim radiation beam to the target. Both tasks are strongly dependent of imaging technology and many imaging modalities have been applied for radiation therapy such as CT (Computed Tomography), MRI (Magnetic Resonant Image), and PET (Positron Emission Tomogaphy). Recently, many researchers have given significant amount of effort to develop and improve imaging techniques for radiation therapy to enhance the overall quality of patient care. For example, advances in medical imaging technology have initiated the development of the state of the art radiation therapy techniques such as intensity modulated radiation therapy (IMRT), gated radiation therapy, tomotherapy, and image guided radiation therapy (IGRT). Capability of determining the local tumor volume and location of the tumor has been significantly improved by applying single or multi-modality imaging fur static or dynamic target. The use of multi-modality imaging provides a more reliable tumor volume, eventually leading to a better definitive local control. Image registration technique is essential to fuse two different image modalities and has been In significant improvement. Imaging equipments and their common applications that are in active use and/or under development in radiation therapy are reviewed.

Regulatory Network of ARF in Cancer Development

  • Ko, Aram;Han, Su Yeon;Song, Jaewhan
    • Molecules and Cells
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    • v.41 no.5
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    • pp.381-389
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    • 2018
  • ARF is a tumor suppressor protein that has a pivotal role in the prevention of cancer development through regulating cell proliferation, senescence, and apoptosis. As a factor that induces senescence, the role of ARF as a tumor suppressor is closely linked to the p53-MDM2 axis, which is a key process that restrains tumor formation. Thus, many cancer cells either lack a functional ARF or p53, which enables them to evade cell oncogenic stress-mediated cycle arrest, senescence, or apoptosis. In particular, the ARF gene is a frequent target of genetic and epigenetic alterations including promoter hyper-methylation or gene deletion. However, as many cancer cells still express ARF, pathways that negatively modulate transcriptional or post-translational regulation of ARF could be potentially important means for cancer cells to induce cellular proliferation. These recent findings of regulators affecting ARF protein stability along with its low levels in numerous human cancers indicate the significance of an ARF post-translational mechanism in cancers. Novel findings of regulators stimulating or suppressing ARF function would provide new therapeutic targets to manage cancer- and senescence-related diseases. In this review, we present the current knowledge on the regulation and alterations of ARF expression in human cancers, and indicate the importance of regulators of ARF as a prognostic marker and in potential therapeutic strategies.

Microarray Analysis of the Gene Expression Profile in Diethylnitrosamine-induced Liver Tumors in Mice

  • Jung Eun-Soo;Park Jung-Duck;Ryu Doug-Young
    • Environmental Mutagens and Carcinogens
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    • v.25 no.4
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    • pp.134-142
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    • 2005
  • Liver cancer is a leading cause of tumor-related mortality, Diethylnitrosamine (DEN) is one of the most extensively studied hepatic carcinogens to date. In this study, the mRNA expression profile in DEN-induced liver tumors in mice was analyzed using DNA microarrays. We report increased expression of genes that participate in hypoxia response, including metallothionein 1 (Mt1), metallothionein 2 (Mt2), fatty acid synthase (Fasn), transferrin (Trf), adipose differentiation-related Protein (AdfP) and ceruloplasmin (CP), as well as those involved in predisposition and development of cancers, such as cytochrome P450 2A5 (Cyp2a5), alpha 2-HS-glycoprotein (Ahsg) and Jun-B oncogene (Junb). The hepatic iron regulatory peptide, hepcidin (Hampl), was downregulated in DEN-stimulated liver tumors. Expression of tumor suppressor genes, such as tripartite motif protein 13 (Trim13), was decreased under these conditions. The data collectively indicate that DEN-induced tumor development can be exploited as a possible model for liver cancer, since this process involves various genes with important functions in hepatic carcinogenesis.

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Elevated level of PLRG1 is critical for the proliferation and maintenance of genome stability of tumor cells

  • Hyunji Choi;Moonkyung Kang;Kee-Ho Lee;Yeon-Soo Kim
    • BMB Reports
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    • v.56 no.11
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    • pp.612-617
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    • 2023
  • Pleiotropic regulator 1 (PLRG1), a highly conserved element in the spliceosome, can form a NineTeen Complex (NTC) with Prp19, SPF27, and CDC5L. This complex plays crucial roles in both pre-mRNA splicing and DNA repair processes. Here, we provide evidence that PLRG1 has a multifaceted impact on cancer cell proliferation. Comparing its expression levels in cancer and normal cells, we observed that PLRG1 was upregulated in various tumor tissues and cell lines. Knockdown of PLRG1 resulted in tumor-specific cell death. Depletion of PLRG1 had notable effects, including mitotic arrest, microtubule instability, endoplasmic reticulum (ER) stress, and accumulation of autophagy, ultimately culminating in apoptosis. Our results also demonstrated that PLRG1 downregulation contributed to DNA damage in cancer cells, which we confirmed through experimental validation as DNA repair impairment. Interestingly, when PLRG1 was decreased in normal cells, it induced G1 arrest as a self-protective mechanism, distinguishing it from effects observed in cancer cells. These results highlight multifaceted impacts of PLRG1 in cancer and underscore its potential as a novel anti-cancer strategy by selectively targeting cancer cells.

ANXA2 Regulates the Behavior of SGC-7901 Cells

  • Sun, Meng-Yao;Xing, Rui-Huan;Gao, Xiao-Jie;Yu, Xiang;He, Hui-Min;Gao, Ning;Shi, Hong-Yan;Hu, Yan-Yan;Wang, Qi-Xuan;Xu, Jin-Hui;Hou, Ying-Chun
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.10
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    • pp.6007-6012
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    • 2013
  • ANXA2, a member of the annexin family, is overexpressed and plays important roles in tumor development. However, the significance of ANXA2 expression in gastric carcinoma has not been clarified.To elucidate its roles in growth of gastric cancer, ANXA2 expression in SGC-7901 cells was inhibited with a designated siRNA, then cell proliferation, cell cycling, apoptosis and motility were determined by MTT assay, flow cytometry, Hoechst 33342 staining and wound healing assay, respectively. To further assess the behavior of ANXA2 deleted SGC-7901 cells, changes of microstructures were observed under fluorescence microscopy, laser scanning confocal microscopy and electron microscopy. We found that inhibition of ANXA2 expression caused cell proliferation to decrease significantly with G1 arrest, motility to be reduced with changes in pseudopodia/filopodia structure and F-actin and ${\beta}$-tubulin expression, and apoptosis to be enhanced albeit without significance. At the same time, ANXA2 deletion resulted in fewer pseudopodia/filopodia, non-stained areas were increased, contact inhibition among cells reappeared, and expression of F-actin and ${\beta}$-tubulin was decreased, with induction of polymerized disassembled forms. Taken together, these data suggest that ANXA2 overexpression is important to maintain the malignancy of cancer cells, and this member of the annexin family has potential to be considered as a target for the gene therapy of gastric carcinoma.

Formation of Genetic Tumor and Characteristics of Teratoma Shoot from Tobacco Interspecific Reciprocal Hybrids (연초종간 상호교잡에 의한 Genetic Tumor의 유도 및 Teratoma Shoot의 특성)

  • 양덕춘;윤의수;최광태;이정명
    • Korean Journal of Plant Tissue Culture
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    • v.25 no.2
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    • pp.135-139
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    • 1998
  • Reciprocal interspecific hybrids between N. glauca(2n=24) and N. langsdorffii(2n=18) were obtained by intercrossing. One hundred percent of F$_1$ seeds was produced from intercrossing of N. glauca $\times$ N. langsdorffii, whereas the frequency of F$_1$ hybrid seed formation from N. langsdorffii $\times$ N. glauca was very low. However, all the hybrid seeds were germinated well and then grown to normal plantlets. All the plants of F$_1$ hybrids have chromosome number of interspecific hybrids (2n=21). From observation of morphological characteristic, the structure of petrol, leaf, flower, and the morphology of pollen have characteristics of F1 hybrid. Spontaneous tumors (genetic tumor) were formed from each F$_1$ hybrid; the genetic tumor arose at the reproductive phase when the maternal type of F$_1$ hybrid came from N. glauca, while the genetic tumor arose only after reproductive phase when the maternal type of F$_1$ hybrid came from N. langsdorffii. The genetic tumor actively proliferated on hormone-free medium and produced numerous teratoma shoots. In addition, normal leaf or stem explants of F$_1$ hybrid produced calli on hormone-free medium after 15 days of culture, the calli produced new numerous teratoma shoots after 30 days. The frequency of teratoma shoot formation from rnterspecific hybrid was higher in the N. glauca $\times$ N. langsdorffii than in the N. langsdorffii $\times$ N. glauca. Root development from the teratoma shoots was hardly obtained. Teratoma shoots without roots in vitro can form genetic tumor at the vegetative growth phase after tissue culture.

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Effect of Lymphangiogenic Factors on Survival in a Murine Model of Oral Squamous Cell Carcinoma (구강암 마우스모델에서 림프관형성 인자가 생존율에 미치는 영향)

  • Park, Young-Wook;Cho, Ju-Won
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.35 no.1
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    • pp.1-12
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    • 2013
  • Purpose: Vascular endothelial growth factor (VEGF)-C and its tyrosine kinase receptor, VEGF receptor (VEGFR)-3 are recently known to have lymphangiogenic activities in various tumor types. In this study, we determined whether the expression of lymphangiogenic factors correlate with nodal metastasis or survival in a nude mouse model of oral squamous cell carcinoma (OSCC). Methods: Three OSCC cells (KB, SCC4, SCC9) were xenografted into the right mandibular gland of athymic nude mice. The mice were followed for tumor development and growth, and the mice were sacrificed when they had lost more than 20% of their initial body weight, or the diameter of the induced tumor exceeds 20 mm. After necropsy, the murine tumors were examined histologically and radiologically (micro-positron emission tomography computed tomography) for regional or distant metastasis. We performed immunohistochemical assays with anti-VEGF-C, VEGFR-3, CD105, and D2-40 antibodies. Immunofluorescence double staining for LYVE-1/CD31 was also performed. To quantify the VEGF-C and VEGFR-3 level in the cancer tissue, Western blotting was performed. Finally, we determined the correlation between the degree of expression of VEGF-C/VEGFR-3 and the mean survival time. Results: OSCC tumor cells into the mandibular gland of the nude mice successfully resulted in the formation of recapitulating orthotopic tumor. Tumor cells of the induced tumor did not express VEGF-C. VEGF-C/VEGFR-3 expression was mainly distributed in the endothelial cells of the stromal area. There were no correlation between the degree of expression of VEGF-C/VEGFR-3 and the mean survival time of mice injected with different OSCC cell lines. Conclusion: An recapitulating orthotopic model of OSCC in nude mice was established, which copies the cervical nodal metastasis of human OSCC. Overexpression of lymphangiogenic factors seems to have no effect on survival of hosts in this in vivo experiment.

Seizures in Patients with Brain Tumors

  • Yang, Seung-Ho;Lee, Kwan-Sung;Lee, Tae-Kyu;Jeun, Sin-Soo;Park, Chun-Kun;Hong, Yong-Kil
    • Journal of Korean Neurosurgical Society
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    • v.41 no.6
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    • pp.387-390
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    • 2007
  • Objective : To determine the presentation, incidence, and risk factors of seizures in patients treated for brain tumors. Methods : One hundred patients who consecutively underwent a craniotomy for the treatment of supratentorial brain tumors were assessed. The pathologies of the patients enrolled in the study included glioma [n=56], meningioma [n=31], metastatic brain tumor [n=7], primary central nervous system lymphoma [n=4], and central neurocytoma [n=2]. Anti-epileptic drugs [AEDs] were administered to all patients for up to six months after the surgery. Pre-defined variables for outcome analysis included tumor grade and location, extent of tumor resection, number of seizures, age at tumor diagnosis, adjuvant therapy, medication and radiological abnormalities. Results : Thirty patients [30%] presented at least a single episode of seizure at the time of admission. Five of these patients [16.7%] developed the seizure during the follow-up period. Newly developed seizure was noticed in six out of seventy patients [8.6%] without prior seizure. Histopathology was malignant gliomas in 10 and supratentorial meningioma in one. Early seizure developed only in two patients. Conclusion : Compared with patients without seizure, patients with seizure at the time of admission showed younger age [p=0.003], a higher portion of low-grade glioma [p=0.001], tumor location in the frontal and temporal lobes [p=0.003] and cortical involvement [p=0.017]. Our study suggestes that tumor progression is considered a significant risk factor for seizure development in glioma patients.

Current Radiopharmaceuticals for Positron Emission Tomography of Brain Tumors

  • Jung, Ji-hoon;Ahn, Byeong-Cheol
    • Brain Tumor Research and Treatment
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    • v.6 no.2
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    • pp.47-53
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    • 2018
  • Brain tumors represent a diverse spectrum of histology, biology, prognosis, and treatment options. Although MRI remains the gold standard for morphological tumor characterization, positron emission tomography (PET) can play a critical role in evaluating disease status. This article focuses on the use of PET with radiolabeled glucose and amino acid analogs to aid in the diagnosis of tumors and differentiate between recurrent tumors and radiation necrosis. The most widely used tracer is $^{18}F$-fluorodeoxyglucose (FDG). Although the intensity of FDG uptake is clearly associated with tumor grade, the exact role of FDG PET imaging remains debatable. Additionally, high uptake of FDG in normal grey matter limits its use in some low-grade tumors that may not be visualized. Because of their potential to overcome the limitation of FDG PET of brain tumors, $^{11}C$-methionine and $^{18}F$-3,4-dihydroxyphenylalanine (FDOPA) have been proposed. Low accumulation of amino acid tracers in normal brains allows the detection of low-grade gliomas and facilitates more precise tumor delineation. These amino acid tracers have higher sensitivity and specificity for detecting brain tumors and differentiating recurrent tumors from post-therapeutic changes. FDG and amino acid tracers may be complementary, and both may be required for assessment of an individual patient. Additional tracers for brain tumor imaging are currently under development. Combinations of different tracers might provide more in-depth information about tumor characteristics, and current limitations may thus be overcome in the near future. PET with various tracers including FDG, $^{11}C$-methionine, and FDOPA has improved the management of patients with brain tumors. To evaluate the exact value of PET, however, additional prospective large sample studies are needed.