• Asian Pacific Journal of Cancer Prevention
• /
• 제16권13호
• /
• pp.5187-5190
• /
• 2015

This study aimed to investigate the correlation between ${\beta}$-catenin immunoexpression and histopathological grades of lower lip squamous cell carcinoma (LSCC). $\beta$-Catenin abnormal expression was found in 29% of the squamous cells of well differentiated LSCC, 63% of moderately differentiated and 86% of poorly differentiated, and therefor was significantly associated with histological grade (p=0.000). Nuclear $\beta$-catenin expression appeared in 5% of the cells and was also correlated with the histological grades (p=0.000). In 14.7% of the cells it was localized in the cytoplasm, again correlating with histology (p=0.002). According to this study the expression of $\beta$-catenin is an independent prognostic factor for histological grade and to the tumor differentiation. This appears to reflect a structural association and the role of $\beta$-catenin in tumor progression.

• Molecules and Cells
• /
• 제28권1호
• /
• pp.7-12
• /
• 2009

Gliomas, much like other cancers, are composed of a heterogeneous mix of neoplastic and non-neoplastic cells that include both native and recruited cells. There is extensive diversity among the tumor cells, with differing capacity for In vitro and in vivo growth, a property intimately linked to the cell's differentiation status. Those cells that are undifferentiated, self-renewing, with the capacity for developing tumors (tumorigenic) cells are designated by some as cancer stem cells, because of the stem-like properties. These cells may be a critical therapeutic target. However the exact identity and cell(s) of origin of the socalled glioma cancer stem cell remain elusive. Here we review the current understanding of glioma cancer stem cell biology.

• Molecules and Cells
• /
• 제22권2호
• /
• pp.228-232
• /
• 2006

The Drosophila protein, Rbp9, is homologous to human Hu, which is reported to be involved in small cell lung cancer. Rbp9 functions in cystocyte differentiation, and mutations in Rbp9 cause ovarian tumors. Here we show that the antimicrobial peptide, Attacin, is upregulated in Rbp9 mutants, especially in ovaries where tumors form. Upregulation seems to result from activation of the NF-${\kappa}B$ pathway since we detected nuclear localization of Relish in Rbp9 mutant ovaries but not in wild type ovaries. Inactivation of NF-${\kappa}B$ in the Rbp9 mutant allows prolonged survival of malformed egg chambers. We conclude that Drosophila initiates an anti-tumor defense response via activation of NF-${\kappa}B$.

• Journal of Digestive Cancer Research
• /
• 제3권1호
• /
• pp.21-25
• /
• 2015

Gastric neuroendocrine tumors (GNETs, also known as gastric carcinoids) are rare form of hormone-secreting neoplasms that present with varied clinical syndromes. There are four types of GNETs based on size, proliferation, localization, differentiation, and hormone production. Type I GNET is related to autoimmune atrophic gastritis and hypergastrinemia. Type II GNETs are related to multiple endocrine neoplasia (MEN)-1, Zollinger-Ellison syndrome and hypergastrinemia. Type 3 GNETs are not associated with any background pathology, and type 4 GNETs are poorly differentiated tumors. The most useful diagnostic and prognostic marker for gastrointestinal NETs is plasma chromogranin A (CgA) levels. Endoscopic ultrasound is the method of choice to determine tumor size and depth of infiltration. For optimal management, the type, biology, and stage of the tumor must be considered. Here, we provide a comprehensive and up-to-date review of GNETs.

• Journal of Korean Neurosurgical Society
• /
• 제50권3호
• /
• pp.244-247
• /
• 2011

Two-thirds of ependymomas arise in the infratentorial or intraventricles, whereas one-third are located supratentorially. But supratentorial "cortical" ependymomas are very rare. We report a case of a cortical ependymoma in a 21-month-old boy. The patient presented with simple partial seizures. This tumor was located in the postcentral gyrus and he had gross total excision. Microscopy and immunohistochemistry showed grade II differentiation ependymoma.

• 대한약학회:학술대회논문집
• /
• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
• /
• pp.184.3-185
• /
• 2003

Inosine 5'-monophosphate dehydrogenase (IMPDH) is a critical enzyme in the regulation of cell proliferation and differentiation. This enzyme catalyzes the $NAD^+$-dependent oxidation of IMP to XMP, the rate limiting step in de novo biosynthesis of guanine nucleotides. Therefore, the biochemical effect of IMPDH inhibition in sensitive cell types is decrease in intracellular guanine nucleotide levels, and the decrease in cellular GTP and deoxy GTP pool levels blocks DNA and RNA synthesis in rapidly proliferating tumor cells. (omitted)

• Korean Journal of Radiology
• /
• 제22권7호
• /
• pp.1185-1193
• /
• 2021

Objective: Clear cell sarcoma of the kidney (CCSK) is the second-most common but extremely rare primary renal malignancy in children after Wilms' tumor. The aims of this study were to evaluate the imaging features that could distinguish between CCSK and Wilms' tumor and to assess the features with diagnostic value for identifying CCSK. Materials and Methods: We reviewed the initial contrast-enhanced abdominal-pelvic CT scans of children with CCSK and Wilms' tumor between 2010 to 2019. Fifty-eight children (32 males and 26 females; age, 0.3-10 years), 7 with CCSK, and 51 with Wilms' tumor, were included. The maximum tumor diameter, presence of engorged perinephric vessels, maximum density of the tumor (Tmax) of the enhancing solid portion, paraspinal muscle, contralateral renal vein density, and density ratios (Tmax/muscle and Tmax/vein) were analyzed on the renal parenchymal phase of contrast-enhanced CT. Fisher's exact tests and Mann-Whitney U tests were conducted to analyze the categorical and continuous variables, respectively. Logistic regression and receiver operating characteristic curve analyses were also performed. Results: The age, sex, and tumor diameter did not differ between the two groups. Engorged perinephric vessels were more common in patients in the CCSK group (71% [5/7] vs. 16% [8/51], p = 0.005). Tmax (median, 148.0 vs. 111.0 Hounsfield unit, p = 0.004), Tmax/muscle (median, 2.64 vs. 1.67, p = 0.002), and Tmax/vein (median, 0.94 vs. 0.59, p = 0.002) were higher in the CCSK compared to the Wilms' group. Multiple logistic regression revealed that engorged vessels (odds ratio 13.615; 95% confidence interval [CI], 1.770-104.730) and Tmax/muscle (odds ratio 5.881; 95% CI, 1.337-25.871) were significant predictors of CCSK. The cutoff values of Tmax/muscle (86% sensitivity, 77% specificity) and Tmax/vein (71% sensitivity, 86% specificity) for the diagnosis of CCSK were 1.97 and 0.76, respectively. Conclusion: Perinephric vessel engorgement and greater tumor enhancement (Tmax/muscle > 1.97 or Tmax/vein > 0.76) are helpful for differentiating between CCSK and Wilms' tumor in children aged below 10 years.

• Asian Pacific Journal of Cancer Prevention
• /
• 제13권9호
• /
• pp.4739-4743
• /
• 2012

Background: Predictive biomarkers for lung cancer recurrence after curative tumor resection remain unclear. This study set out to assess the role of FoxM1 in the recurrence of non-small cell lung cancer. Methods: Immunohistochemistry for FoxM1 expression was performed on paraffin-embedded tumor tissues from 165 NSCLC patients. Association of FoxM1 expression with clinicopathological parameters and disease free survival were evaluated. Results: Our results indicated FoxM1 expression to be significantly associated with poorer tissue differentiation (P =0.03), higher TNM stage (P <0.01), lymph node metastasis (P <0.01), advanced tumor stage (P <0.01), and poorer disease free survival (P <0.01). Multivariable analysis showed that FoxM1 expression increased the hazard of recurrence (hazard ratio= 1.96, 95% CI, 1.04-3.17, P <0.05), indicating that FoxM1 is an independent and significant predictor of lung cancer recurrence. Conclusion: Therefore, FoxM1 is an independent risk factor for recurrence of NSCLC. Elevated FoxM1 expression could be used as an indicator of poor disease free survival.

• Nutrition Research and Practice
• /
• 제4권6호
• /
• pp.455-461
• /
• 2010

The tumor microenvironment, particularly sufficient nutrition and oxygen supply, is important for tumor cell survival. Nutrition deprivation causes cancer cell death. Since apoptosis is a major mechanism of neuronal loss, we explored neuronal apoptosis in various microenvironment conditions employing neuroblastoma (NB) cells. To investigate the effects of tumor malignancy and differentiation on apoptosis, the cells were exposed to poor microenvironments characterized as serum-free, low-glucose, and hypoxia. Incubation of the cells in serum-free and low-glucose environments significantly increased apoptosis in less malignant and more differentiated N-type IMR32 cells, whereas more malignant and less differentiated I-type BE(2)C cells were not affected by those treatments. In contrast, hypoxia (1 % $O_2$) did not affect apoptosis despite cell malignancy. It is suggested that DLK1 constitutes an important stem cell pathway for regulating self-renewal, clonogenicity, and tumorigenicity. This raises questions about the role of DLK1 in the cellular resistance of cancer cells under poor microenvironments, which cancer cells normally encounter. In the present study, DLK1 overexpression resulted in marked protection from apoptosis induced by nutrient deprivation. This in vitro model demonstrated that increasing severity of nutrition deprivation and knock-down of DLK1 caused greater apoptotic death, which could be a useful strategy for targeted therapies in fighting NB as well as for evaluating how nutrient deprived cells respond to therapeutic manipulation.

• BMB Reports
• /
• 제51권5호
• /
• pp.207-208
• /
• 2018

Chitinase-Like Proteins (CLPs) are an evolutionarily conserved protein which lose their enzymatic activity for degrading chitin macromolecules. Chitinase-3-like-1 (Chi3l1) is a type of CLP that is highly expressed in epithelial cells, macrophages, etc., and is known to have correlations with type 2 inflammation and cancer. Although the increased level of Chi3l1 in the blood was reported in various disease patients, the function of Chi3l1 in adaptive immunity has been totally unknown. Recently, we found that Chi3l1 is expressed in T cells and has a negative regulatory role in T-cell activation and proliferation. A genetic ablation study of Chi3l1 in T cells showed hyperresponsiveness to TcR stimulation, which increased proliferation and Th1 differentiation. A significant increase of $IFN{\gamma}$ signaling in Chi3l1-deficient T cells synergistically increased Th1 and CTL functions against melanoma cells in vitro and in vivo. In addition, targeted knockdown by Chi3l1 siRNA complexed with the cell-penetrating peptide dNP2, which showed decreased pulmonary melanoma metastasis with increased infiltration of Th1 and CTL in the lung. This study first suggests that Chi3l1 is a novel regulator of Th1/CTL responses and could be a target for treating cancer to increase tumor immunity.