• Archives of Pharmacal Research
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• v.20 no.2
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• pp.128-137
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• 1997

The effects of cylindan, a polysaccharide isolated from the basidiocarps of Agrocybe cylindracea, on murine sarcoma 180 tumor and murine immune cells were examined after intraperitoneal administration. Cylindan exhibited a marked life extension effect in mice against ascite forms of sarcoma 180 and Lewis lung carcinoma at a dose of 50 mg/kg/day, although it did not show any direct cytotoxicity against sarcoma 180, X5563, and MM46 murine tumor cells. Cylindan increased numbers of bone marrow stem cells as well as peritoneal exudate cells in flow cytometry using monoclonal antibodies. The tumor bearing mice group apparently showed the increase of macrophages and cytotoxic T lymphocytes in mouse spleen cells during the early stage of tumor growth. But during the later stage, the control group decreased immune cells and cylindan restored the decreased immune cells in the tumor bearing mice to the normal level. In non-specific immune response, cylindan stimulated the bacterial phagocytosis and acid phosphatase production in macrophages. It also activated components of the alternative complement pathway and natural killer activity against YAC-1 lymphoma. In number of plasma cells as token of stimulation of the differentiation of B lymphocytes. In cellular immunity, cylindan restored the depressed response of delayed type hypersensitivity in the tumor bearing mice to 60% of the normal level and increased the interleukin-2 (IL-2) responsiveness in the IL-2 dependent CTLL-2 cells. These results suggest that cylindan did not show direct cytotoxic effects on tumor cells but restored the decreased immune response of the tumor bearing mice.

• Journal of Veterinary Clinics
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• v.17 no.2
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• pp.305-314
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• 2000

Recombinant inteileukin-2 (IL-2) is a potent inductive stimulus for nitric oxide synthesis (NO.) and has been demonstrated as an antineoplastic agent in mice and human. But it is not let clear whether NO. can contribute to IL-2-induced therapeutic responses. Therefore, the current experiment was undertaken to clarify the effect of IL-2 on antitumor response against subcutaneous Meth-A tumor in mice. At the beginning of each experiment, normal BALB/c mice were injected subcuta-neously with $5{\times}10^6 Meth-A$ tumor cells. Some mice were implanted with osmotic minipumps con- taining 225 $\mu$l of 3.38 M $N^{\gamma}$ -monomethyl-L-arginine (MLA. an NOS inhibitor). Beginning on day 7, experimental groups were treated with a f-day course of IL-2 (50,000 lU,75,000 nJ,100,0007, 50,000 IU+MLA, 75,000 IU+MLA, 100,000 IU+MLA intraperitoneal injection every 12 hours for 5 days). The result of this experiment revealed that Meth-A tumor grew progressively in control mice. Intraperitoneal IL-2 treatment decreased tumor growth and prolonged survival. compared with con-trol mice. But no significant differences among 50.000 lU.75.000 lU and 100,000 lU of 7-2 treat-ment were observed. MLA administration prevented partially the decrease tumor growth and prolong survival of IL-2 treated mice compared with mice receiving IL-2 alone.

• Current Optics and Photonics
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• v.3 no.6
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• pp.555-565
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• 2019

Development of a biomarker for predicting tumor-treatment efficacy is a matter of great concern, to reduce time, medical expense, and effort in oncology therapy. In a preclinical study, we hypothesized that the blood-flow parameter based on laser speckle flowmetry (LSF) could be a potential indicator to estimate the efficacy of breast-cancer treatment. To verify this hypothesis, a 13762-MAT-B-III rat breast tumor was grown in a dorsal skinfold window chamber applied to a nude mouse, and the change in blood flow rate (BFR) - or the speckle flow index (SFI) is used together as the same meaning in this manuscript - was longitudinally monitored during tumor growth and metronomic cyclophosphamide treatment. Based on the daily LSF angiogram, several BFR parameters (baseline SFI, normalized SFI, and △rBFR) were compared to tumor size in the normal, treated, and untreated tumor groups. Despite the incomplete tumor treatment, we found that the daily changes in all BFR parameters tended to have partially positive correlation with tumor size. Moreover, we observed that the changes in baseline SFI and normalized SFI responded one day earlier than the tumor shrinkage during chemotherapy. However, daily variations in the hypercapnia-induced △rBFR lagged tumor shrinkage by one day. This study would contribute not only to evaluating tumor vascular response to treatment, but also to monitoring blood-flow-mediated diseases (in brain, skin, and retina) by using LSF in preclinical settings.

• Korean Journal of Plant Tissue Culture
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• v.26 no.1
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• pp.31-35
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• 1999

Morphological characteristic during formation of tobacco crown gall tumor and genetic tumor, and their differential response to growth regulator were investigated in in vitro culture. Crown gall tumor was induced from tumor tissue transformed by infecting Agrobacterium tumefaciens C58. Genetic tumor was induced from tumor tissue which was induced spontaneously from reciprocal interspecific hybrids between Nicotiana glauca (2n=24) and Nicotiana langsdorffii (2n=18). Morphological characteristic of crown gall tumor, genetic tumor, and teratoma shoot was very similar, and they were actively proliferated on hormone-free medium. Typical tumor callus and teratoma shoot formed from crown gall tumor on the hormone-free medium. On the contrary, tumor callus derived from genetic tumor formed as a crown gall tumor callus on the medium supplemented with 0.5 mg/L of 2,4-D, and lots of teratoma shoots without any root formed on the hormone-free medium. Root development from the teratoma shoots was hardly obtained on the medium with IAA, GA and active carbon. However, teratoma shoots with roots, as normal shoots, were initiated occasionally on the hormone-free medium. These shoots also formed new genetic tumor on the stem, which leaves formed lots of teratoma shoot on the hormone-free medium in in vitro culture.

• Korean Journal of Veterinary Research
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• v.51 no.4
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• pp.319-323
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• 2011

A 12-year-old spayed female Yorkshire terrier dog was presented with two-weeks history of lethargy, mental dullness and polydipsia. Neurologic examination revealed proprioceptive defect of all limbs and loss of swallowing gag reflex. The dog revealed persistent dehydration, hypernatremia, hyperosmolarity and hyposthenuria. On magnetic resornance imaging (MRI), the mass were heterogeneous signality on T1 weighted images, hyperintense signality on T2 weighted image with contrast enhancement on hypothalamohypophyseal lesion. Based on these findings, the dog was suspected as having pituitary gland tumor. Through water deprivation test and response to desmopressin acetate (1-deamino-8-D-arginine, DDAVP), this case was diagnosed by central diabetes insipidus (CDI). This paper reports the clinical sign, MRI, response to the exogenous antidiuretic hormone of CDI due to suspected pituitary tumor in a dog and DDAVP administration was evaluated effective therapy to correct hypernatremia induced by CDI.

• Journal of Breast Cancer
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• v.21 no.4
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• pp.354-362
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• 2018

Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, selfprotecting signal transduction pathway called the unfolded protein response. Notably, ERS signaling is involved in the development of a variety of diseases and is closely related to tumor development, particularly in breast cancer. This review discusses recent research regarding associations between ERS and tumor metastasis. The information presented here will help researchers elucidate the precise mechanisms underlying ERS-mediated tumor metastasis and provide new directions for tumor therapies.

• Radiation Oncology Journal
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• v.36 no.3
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• pp.172-181
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• 2018

Successful anticancer strategies require a differential response between tumor and normal tissue (i.e., a therapeutic ratio). In fact, improving the effectiveness of a cancer therapeutic is of no clinical value in the absence of a significant increase in the differential response between tumor and normal tissue. Although radiation dose escalation with the use of intensity modulated radiation therapy has permitted the maximum tolerable dose for most locally advanced cancers, improvements in tumor control without damaging normal adjacent tissues are needed. As a means of increasing the therapeutic ratio, several new approaches are under development. Drugs targeting signal transduction pathways in cancer progression and more recently, immunotherapeutics targeting specific immune cell subsets have entered the clinic with promising early results. Radiobiological research is underway to address pressing questions as to the dose per fraction, irradiated tumor volume and time sequence of the drug administration. To exploit these exciting novel strategies, a better understanding is needed of the cellular and molecular pathways responsible for both cancer and normal tissue and organ response, including the role of radiation-induced accelerated senescence. This review will highlight the current understanding of promising biologically targeted therapies to enhance the radiation therapeutic ratio.

• Korean Journal of Head & Neck Oncology
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• v.18 no.2
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• pp.219-222
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• 2002

Malignant glomus tumor is a very rare disease originating from the paraganglia system through the body. Glomus tumor, also known as paraganglioma, usually are considered benign, and arises in a variety of head and neck locations, most of which include the carotid body, the vagus nerve, and the jugulotympanic area. The most widely accepted management of benign glomus tumor is surgical extiration. Here, we report a case of recurrent laryngeal glomus tumor which is proven malignant and metastatic to the brain and the lungs. We have treated the patient with combination chemotherapy and radiation to the brain, the result of which is partial response in terms of decreased size of metastatic lung lesions.

• Current Optics and Photonics
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• v.2 no.1
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• pp.1-6
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• 2018

Our previous study showed that switching the inhaled gas from hypoxic gas to hyperoxic gas for 10 minutes increased tumor oxygenation and that the magnitude of oxyhemoglobin increase responded earlier than tumor volume change after chemotherapy. During 10 minutes of inhaled-oxygen modulation, oxyhemoglobin concentration first shows a rapid increase and then a slow but gradual increase, which has been fitted with a double-exponential equation in this study. Two amplitude values, amplitudes 1 and 2, respectively represent the magnitudes of rapid and slow increase of oxyhemoglobin. The trends of changes in amplitudes 1 and 2 were different, depending on tumor volume when chemotherapy started. However, both amplitudes 1 and 2 changed earlier than tumor volume, regardless of when chemotherapy was initiated. These results imply that by observing amplitude 1 changes post chemotherapy, we can reduce the time of a respiratory challenge from 10 minutes to less than 2 minutes, to see the chemotherapy response. We believe that by reducing the time of the respiratory challenge, we have taken a step forward to translating our previous study into clinical application.

• IMMUNE NETWORK
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• v.16 no.2
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• pp.134-139
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• 2016

Programmed death-1 (PD-1) is a strong negative regulator of T lymphocytes in tumor-microenvironment. By engaging PD-1 ligand (PD-L1) on tumor cells, PD-1 on T cell surface inhibits anti-tumor reactivity of tumor-infiltrating T cells. Systemic blockade of PD-1 function using blocking antibodies has shown significant therapeutic efficacy in clinical trials. However, approximately 10 to 15% of treated patients exhibited serious autoimmune responses due to the activation of self-reactive lymphocytes. To achieve selective activation of tumor-specific T cells, we generated T cells expressing a dominant-negative deletion mutant of PD-1 (PD-1 decoy) via retroviral transduction. PD-1 decoy increased IFN-γ secretion of antigen-specific T cells in response to tumor cells expressing the cognate antigen. Adoptive transfer of PD-1 decoy-expressing T cells into tumor-bearing mice potentiated T cell-mediated tumor regression. Thus, T cell-specific blockade of PD-1 could be a useful strategy for enhancing both efficacy and safety of anti-tumor T cell therapy.