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1

Ruan, Xiaogang, Yingxin Li, Jiangeng Li, Daoxiong Gong, and Jinlian Wang. "Tumor-specific gene expression patterns with gene expression profiles." Science in China Series C 49, no. 3 (June 2006): 293–304. http://dx.doi.org/10.1007/s11427-006-0293-1.

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2

Peterson, Carsten, and Markus Ringnér. "Analyzing tumor gene expression profiles." Artificial Intelligence in Medicine 28, no. 1 (May 2003): 59–74. http://dx.doi.org/10.1016/s0933-3657(03)00035-6.

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3

Chen, Xin, Siu Tim Cheung, Samuel So, Sheung Tat Fan, Christopher Barry, John Higgins, Kin-Man Lai, et al. "Gene Expression Patterns in Human Liver Cancers." Molecular Biology of the Cell 13, no. 6 (June 2002): 1929–39. http://dx.doi.org/10.1091/mbc.02-02-0023.

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Hepatocellular carcinoma (HCC) is a leading cause of death worldwide. Using cDNA microarrays to characterize patterns of gene expression in HCC, we found consistent differences between the expression patterns in HCC compared with those seen in nontumor liver tissues. The expression patterns in HCC were also readily distinguished from those associated with tumors metastatic to liver. The global gene expression patterns intrinsic to each tumor were sufficiently distinctive that multiple tumor nodules from the same patient could usually be recognized and distinguished from all the others in the large sample set on the basis of their gene expression patterns alone. The distinctive gene expression patterns are characteristic of the tumors and not the patient; the expression programs seen in clonally independent tumor nodules in the same patient were no more similar than those in tumors from different patients. Moreover, clonally related tumor masses that showed distinct expression profiles were also distinguished by genotypic differences. Some features of the gene expression patterns were associated with specific phenotypic and genotypic characteristics of the tumors, including growth rate, vascular invasion, and p53 overexpression.
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4

Greiner, Johannes, Janine Müller, Jörg Ebmeyer, and Holger Sudhoff. "Gene expression profiling reveals expression of tumor-relevant." Journal of Laryngology & Otology 130, S3 (May 2016): S114. http://dx.doi.org/10.1017/s0022215116004126.

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5

Lichtor, Terry, George J. Dohrmann, and Mark E. Gurney. "Cytokine Gene Expression by Human Gliomas." Neurosurgery 26, no. 5 (May 1, 1990): 788–93. http://dx.doi.org/10.1227/00006123-199005000-00009.

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Abstract Two glioma tumor lines and specimens from five patients with gliomas were analyzed to determine genic expression of four growth factors found in human brain. Messenger RNA encoding for interleukin-1β, interleukin-6, and basic fibroblast growth factor was found to be expressed in significant amounts in some of these tumors, while mRNA for interleukin-3 was found in small quantities in only the tumor lines. Multiple species of mRNA for basic fibroblast growth factor were found. Expression of growth factor genes may play a role in the growth of human gliomas.
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6

Granzow, M., D. Berrar, W. Dubitzky, A. Schuster, F. J. Azuaje, and R. Eils. "Tumor classification by gene expression profiling." ACM SIGBIO Newsletter 21, no. 1 (April 2001): 16–22. http://dx.doi.org/10.1145/381371.381384.

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7

Marx, J. "TUMOR ANGIOGENESIS: Gene Expression Patterns Identified." Science 289, no. 5482 (August 18, 2000): 1121a—1122. http://dx.doi.org/10.1126/science.289.5482.1121a.

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8

Iwamoto, Akemi, Masahide Ikeguchi, Sachico Matsumoto, Youji Hukumoto, Masashi Inoue, Tomohiro Ozaki, Masayuki Ataka, et al. "Tumor Cyclooxygenase-2 Gene Suppresses Local Immune Responses in Patients with Hepatocellular Carcinoma." Tumori Journal 92, no. 2 (March 2006): 130–33. http://dx.doi.org/10.1177/030089160609200208.

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Aims and Background In several neoplastic diseases including hepatocellular carcinoma (HCC) immunosuppression is correlated with disease stage, progression and outcome. Moreover, recent studies have demonstrated that cyclooxygenase-2 (COX-2) enhances tumor growth in HCCs. The present study analyzed the correlation between local immune responses and COX-2 gene expression levels in patients with primary HCCs. Methods Fresh tissues were obtained from 59 patients who underwent resection of an HCC. The COX-2 gene expression levels were quantified by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and compared with the CD8+ T cell densities detected by immunohistochemistry. Results COX-2 gene expression was detected in 35 of the 59 tumors. The CD8+ T cell density in COX-2-expressing tumors (6.1 cells/high-power field (HPF), x200 magnification) was suppressed compared with that in non-COX-2-expressing tumors (13.6 cells/HPF, P = 0.009). Tumor COX-2 gene expression was associated with a poorer disease-free survival rate. Conclusions Elevation of the tumor COX-2 level is correlated with the suppression of local immune responses in HCCs, suggesting that COX-2 plays a role in early tumor recurrence in the residual liver in patients after HCC resection.
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9

Xiong, Momiao, Wuju Li, Jinying Zhao, Li Jin, and Eric Boerwinkle. "Feature (Gene) Selection in Gene Expression-Based Tumor Classification." Molecular Genetics and Metabolism 73, no. 3 (July 2001): 239–47. http://dx.doi.org/10.1006/mgme.2001.3193.

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10

Bakary, Nermeen. "Calcitriol Revises Aromatase Gene Expression in Ehrlich Solid Tumor Bearing Mice Exposed to Low Dose Gamma Radiation." Cancer Research and Cellular Therapeutics 5, no. 1 (February 12, 2021): 01–09. http://dx.doi.org/10.31579/2640-1053/074.

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Background: Dysregulation of aromatase expression had been monitored in many types of cancer. Our study aimed to evaluate the possible role of calcitriol (Cal; Vit D3-OH) or/and low dose of gamma radiation in regulation of aromatase gene expression and the regression of tumor proliferation in murine model (EST; Ehrlich solid tumor bearing mice). Methods: Mice with ≈1 cm3 EST were received (i.p. injection) day after day repeated doses of Calcitriol (Cal) (0.05µg/mouse) for 14day or/and exposed to 0.5 Gy gamma radiation (low dose) delivered as one shot at dose rate 0.48 Gy/min. Results: Our results demonstrated that, mRNA expression of aromatase, levels of cyclooxygenase (COX2) and prostaglandin (PGE2) in addition to volume of the tumor are significantly decreased while caspase 3 level is significantly increased in EST mice treated with Cal or/and exposed to 0.5 Gy gamma ray compared to untreated EST bearing mice. However, the most pronounced improvements in all of the measured parameters were obviously indicated in EST mice group treated with Cal and exposed to gamma radiation. This was accomplished by suppression of inflammatory markers which cause down regulation in aromatase mRNA expression as well as augmenting apoptosis by inducing Caspase3 concentration. Conclusion: It could be concluded that the exposure to low dose gamma radiation potentiate the action of Calcitriol against tumor growth in the subjected murine model which represent a prospective policy for the management of solid tumor and decreasing the possibilities of tumor drug resistance.
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11

Hilal, N. R., D. V. Novikov, V. V. Novikov, and A. V. Karaulov. "Cancer-testis genes in colon cancer." Terapevticheskii arkhiv 89, no. 5 (May 15, 2017): 113–17. http://dx.doi.org/10.17116/terarkh2017895113-117.

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The expression of cancer-testis (CT) genes varies with tumor type. There are tumors with high, low, and intermediate gene expressions. Tumor cells of different origin are characterized by ST gene co-expression. The expression of ST genes increases in later stages of tumor development in the presence of metastases. In colon cancer, the tumor samples showed most frequently MAGE-A and SSX mRNA. The peripheral blood samples displayed most commonly XAGE, MAGE-C, and SSX mRNA. In patients with colon cancer, the expression of TSP50, MAGE-A(1-6), and SSX1,2,4 genes was associated with a poor prognosis, that of MAGE-C1 and XAGE1 was related to a favorable prognosis.
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12

Scian, Mariano J., Katherine E. R. Stagliano, Michelle A. E. Anderson, Sajida Hassan, Melissa Bowman, Mike F. Miles, Swati Palit Deb, and Sumitra Deb. "Tumor-Derived p53 Mutants Induce NF-κB2 Gene Expression." Molecular and Cellular Biology 25, no. 22 (November 15, 2005): 10097–110. http://dx.doi.org/10.1128/mcb.25.22.10097-10110.2005.

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ABSTRACT Overexpression of mutant p53 is a common theme in tumors, suggesting a selective pressure for p53 mutation in cancer development and progression. To determine how mutant p53 expression may lead to survival advantage in human cancer cells, we generated stable cell lines expressing p53 mutants p53-R175H, -R273H, and -D281G by use of p53-null human H1299 (lung carcinoma) cells. Compared to vector-transfected cells, H1299 cells expressing mutant p53 showed a survival advantage when treated with etoposide, a common chemotherapeutic agent; however, cells expressing the transactivation-deficient triple mutant p53-D281G (L22Q/W23S) had significantly lower resistance to etoposide. Gene expression profiling of cells expressing transcriptionally active mutant p53 proteins revealed the striking pattern that all three p53 mutants induced expression of approximately 100 genes involved in cell growth, survival, and adhesion. The gene NF-κB2 is a prominent member of this group, whose overexpression in H1299 cells also leads to chemoresistance. Treatment of H1299 cells expressing p53-R175H with small interfering RNA specific for NF-κB2 made these cells more sensitive to etoposide. We have also observed activation of the NF-κB2 pathway in mutant p53-expressing cells. Thus, one possible pathway through which mutants of p53 may induce loss of drug sensitivity is via the NF-κB2 pathway.
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13

Nabors, Michael W., Constance A. Griffin, Barbara A. Zehnbauer, Ralph H. Hruban, Peter C. Phillips, Stuart A. Grossman, Henry Brem, and O. Michael Colvin. "Multidrug resistance gene (MDR1) expression in human brain tumors." Journal of Neurosurgery 75, no. 6 (December 1991): 941–46. http://dx.doi.org/10.3171/jns.1991.75.6.0941.

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✓ Multidrug resistance for many types of cancer outside the central nervous system (CNS) has been found to be due to the overexpression of the multidrug resistance gene MDR1, of which the gene-product P-glycoprotein acts as a membrane-bound efflux pump for many anticancer drugs. To examine whether brain tumors overexpress the MDR1 gene, 25 brain-tumor specimens were subjected to Northern blot analysis: 10 gliomas, eight meningiomas, three schwannomas, one malignant lymphoma, and three tumors metastatic to the brain. Ten fresh-frozen autopsy specimens of various parts of normal brain were also analyzed. Blots were hybridized with 32P-labeled Chinese hamster complementary deoxyribonucleic acid (cDNA) and 32P-labeled human MDR1 cDNA. The MDR1 gene messenger ribonucleic acid (mRNA) was detected in two tumors using the Chinese hamster probe (one sphenoid wing meningioma and one metastatic prostate tumor) and in one CNS lymphoma using the human probe. Intact mRNA could not be extracted from the fresh-frozen autopsy specimens of normal brain. Seventeen tumors were examined for P-glycoprotein by immunohistochemical staining using murine monoclonal antibody C219: eight gliomas, eight meningiomas, and one craniopharyngioma. The neoplastic cells from two gliomas and three meningiomas and the blood vessels within six gliomas and two meningiomas stained positively for P-glycoprotein. Seven of 10 normal brain specimens stained positively for P-glycoprotein in blood vessels but no specimen demonstrated staining of parenchymal cells. This study demonstrates that the MDR1 gene can be detected in normal brain, and in malignant, benign, and metastatic lesions. P-glycoprotein can be present in tumor blood vessels even when it is not seen in neoplastic cells. Although the role of P-glycoprotein in tumor blood vessels needs to be further examined and more clearly defined, drug resistance in malignant primary brain tumors may result from characteristics not solely of neoplastic cells but also tumor vasculature.
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14

Shaw, Elisabeth J., Brian Haylock, David Husband, Daniel du Plessis, D. Ross Sibson, Peter C. Warnke, and Carol Walker. "Gene Expression in Oligodendroglial Tumors." Analytical Cellular Pathology 33, no. 2 (2010): 81–94. http://dx.doi.org/10.1155/2010/304806.

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Background: Oligodendroglial tumors with 1p/19q loss are more likely to be chemosensitive and have longer survival than those with intact 1p/19q, but not all respond to chemotherapy, warranting investigation of the biological basis of chemosensitivity.Methods: Gene expression profiling was performed using amplified antisense RNA from 28 oligodendroglial tumors treated with chemotherapy (26 serial stereotactic biopsy, 2 resection). Expression of differentially expressed genes was validated by real-time PCR.Results: Unsupervised hierarchical clustering showed clustering of multiple samples from the same case in 14/17 cases and identified subgroups associated with tumor grade and 1p/19q status. 176 genes were differentially expressed, 164 being associated with 1p/19q loss (86% not on 1p or 19q). 94 genes differed between responders and non-responders to chemotherapy; 12 were not associated with 1p/19q loss. Significant differential expression was confirmed in 11/13 selected genes. Novel genes associated with response to therapy includedSSBP2,GFRA1,FAPandRASD1.IQGAP1,INA,TGIF1,NR2F2andMYCBPwere differentially expressed in oligodendroglial tumors with 1p/19q loss.Conclusion: Gene expression profiling using serial stereotactic biopsies indicated greater homogeneity within tumors than between tumors. Genes associated with 1p/19q status or response were identified warranting further elucidation of their role in oligodendroglial tumors.
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15

Schug, Christina, Sarah Urnauer, Carsten Jaeckel, Kathrin A. Schmohl, Mariella Tutter, Katja Steiger, Nathalie Schwenk, et al. "TGFB1-driven mesenchymal stem cell-mediated NIS gene transfer." Endocrine-Related Cancer 26, no. 1 (January 2019): 89–101. http://dx.doi.org/10.1530/erc-18-0173.

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Based on their excellent tumor-homing capacity, genetically engineered mesenchymal stem cells (MSCs) are under investigation as tumor-selective gene delivery vehicles. Transgenic expression of the sodium iodide symporter (NIS) in genetically engineered MSCs allows noninvasive tracking of MSC homing by imaging of functional NIS expression as well as therapeutic application of 131I. The use of tumor stroma-activated promoters can improve tumor-specific MSC-mediated transgene delivery. The essential role of transforming growth factor B1 (TGFB1) and the SMAD downstream target in the signaling between tumor and the surrounding stroma makes the biology of this pathway a potential option to better control NIS expression within the tumor milieu. Bone marrow-derived MSCs were stably transfected with a NIS-expressing plasmid driven by a synthetic SMAD-responsive promoter (SMAD-NIS-MSCs). Radioiodide uptake assays revealed a 4.9-fold increase in NIS-mediated perchlorate-sensitive iodide uptake in SMAD-NIS-MSCs after TGFB1 stimulation compared to unstimulated cells demonstrating the successful establishment of MSCs, which induce NIS expression in response to activation of TGFB1 signaling using a SMAD-responsive promoter. 123I-scintigraphy revealed significant tumor-specific radioiodide accumulation and thus NIS expression after systemic application of SMAD-NIS-MSCs into mice harboring subcutaneous tumors derived from the human hepatocellular carcinoma (HCC) cell line HuH7, which express TGFB1. 131I therapy in SMAD-NIS-MSCs-treated mice demonstrated a significant delay in tumor growth and prolonged survival. Making use of the tumoral TGFB1 signaling network in the context of MSC-mediated NIS gene delivery is a promising approach to foster tumor stroma-selectivity of NIS transgene expression and tailor NIS-based gene therapy to TGFB1-rich tumor environments.
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Vulcani-Freitas, Tânia Maria, Nasjla Saba-Silva, Andréa Cappellano, Sérgio Cavalheiro, and Sílvia Regina Caminada de Toledo. "PRAME gene expression profile in medulloblastoma." Arquivos de Neuro-Psiquiatria 69, no. 1 (February 2011): 9–12. http://dx.doi.org/10.1590/s0004-282x2011000100003.

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Medulloblastoma is the most common malignant tumors of central nervous system in the childhood. The treatment is severe, harmful and, thus, has a dismal prognosis. As PRAME is present in various cancers, including meduloblastoma, and has limited expression in normal tissues, this antigen can be an ideal vaccine target for tumor immunotherapy. In order to find a potential molecular target, we investigated PRAME expression in medulloblastoma fragments and we compare the results with the clinical features of each patient. Analysis of gene expression was performed by real-time quantitative PCR from 37 tumor samples. The Mann-Whitney test was used to analysis the relationship between gene expression and clinical characteristics. Kaplan-Meier curves were used to evaluate survival. PRAME was overexpressed in 84% samples. But no statistical association was found between clinical features and PRAME overexpression. Despite that PRAME gene could be a strong candidate for immunotherapy since it is highly expressed in medulloblastomas.
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17

Lindskog, Elinor B., Yvonne Wettergren, Elisabeth Odin, Bengt Gustavsson, and Kristoffer Derwinger. "Thymidine Phosphorylase Gene Expression in Stage III Colorectal Cancer." Clinical Medicine Insights: Oncology 6 (January 2012): CMO.S10226. http://dx.doi.org/10.4137/cmo.s10226.

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Background The thymidine phosphorylase (TP) enzyme has several tumor-promoting functions. The aim of this study was to explore TP gene expression in relation to clinical and histopathological data obtained from patients with stage III colorectal cancer. Methods and Results TP gene expression was analyzed by real-time quantitative PCR in tumor and mucosa samples from 254 patients. TP gene expression in tumors correlated with lymph node staging, with higher expression relating to a higher number of positive nodes and a worse N-stage. Higher TP expression was also associated with a worse histological tumor grade. Patients with rectal cancer had significantly higher TP expression in mucosa and tumors compared with patients having colon cancer. Conclusion Higher intratumoral TP expression appears to be related to a worse N stage, and thus, with a worse prognosis. TP gene expression measured in a preoperative biopsy could be of interest in preoperative staging.
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18

Huang, C., D. Liu, J. Nakano, S. Ishikawa, H. Yokomise, and M. Ueno. "E2F1 overexpression associated with TS and survivin gene expressions in non-small cell lung cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 7669. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.7669.

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7669 Background: The thymidylate synthase (TS) expression is related to 5-FU sensitivity. The survivin expression is associated with tumor apoptosis, an indicator to predict the efficacy of chemotherapy. Recently, TS and Survivin have been reported to be E2F1 target genes. We investigate the clinical significance of the E2F1 gene expression in relation to gene expressions of TS and Survivin among non-small cell lung cancer (NSCLC). Methods: One hundred and twenty-seven NSCLC patients were investigated. Quantitative RT-PCR was performed to evaluate gene expressions of E2F1, TS, and survivin. The Ki-67 proliferation index and the apoptotic index using TUNEL method were also evaluated. Results: The E2F1 gene expression was significantly higher in stage II to III tumors than in stage I tumors (p=0.006). The E2F1 gene expression significantly correlated with the Ki-67 proliferation index (p<0.001), while no correlation was observed between the E2F1 gene expression and the apoptotic index. Regarding E2F1-target genes, the E2F1 gene expression significantly correlated with the TS gene expression (p<0.001). The E2F1 gene expression also significantly correlated with the survivin gene expression (p<0.001). The TS expression and the survivin expression significantly correlated with the Ki-67 proliferation index (p<0.001 and p<0.001, respectively). There was a significant inverse relationship between the survivin expression and the apoptotic index (p<0.001). The overall survival was significantly lower in patients with high-E2F1 tumors than in those with low-E2F1 tumors (p=0.002), especially among patients with stage II to III NSCLCs (p=0.018). The Cox regression analysis demonstrated that the E2F1 status was a significant prognostic factor for NSCLC patients (p=0.026). Conclusions: The present study revealed the E2F1 gene expression to correlate with TS and survivin gene expressions, and tumor proliferation. E2F1 overexpression could occur to produce more aggressive tumors with high proliferation rate and chemo-resistance during progression of NSCLCs. The suppression of E2F1 by RNA interference would be a useful strategy for cancer gene therapy. No significant financial relationships to disclose.
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19

Pauli, Urs. "Control of Tumor Necrosis Factor Gene Expression." Critical Reviews™ in Eukaryotic Gene Expression 4, no. 2-3 (1994): 323–44. http://dx.doi.org/10.1615/critreveukargeneexpr.v4.i2-3.20.

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20

Leo, Cornelia, Amato J. Giaccia, and Nicholas C. Denko. "The hypoxic tumor microenvironment and gene expression." Seminars in Radiation Oncology 14, no. 3 (July 2004): 207–14. http://dx.doi.org/10.1016/j.semradonc.2004.04.007.

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21

Dachs, Gabi U., Adam V. Patterson, John D. Firth, Peter J. Ratcliffe, K. M. Stuart Townsend, Ian J. Stratford, and Adrian L. Harris. "Targeting gene expression to hypoxic tumor cells." Nature Medicine 3, no. 5 (May 1997): 515–20. http://dx.doi.org/10.1038/nm0597-515.

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22

Baraz, L., Y. Haupt, M. Elkin, T. Peretz, and I. Vlodavsky. "Tumor suppressor p53 regulates heparanase gene expression." Oncogene 25, no. 28 (February 13, 2006): 3939–47. http://dx.doi.org/10.1038/sj.onc.1209425.

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23

Tagge, Edward P., Patricia Hanson, Gian G. Re, H. Biemann Othersen, Charles D. Smith, and A. Julian Garvin. "Paired box gene expression in Wilms' tumor." Journal of Pediatric Surgery 29, no. 2 (February 1994): 134–41. http://dx.doi.org/10.1016/0022-3468(94)90308-5.

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24

Rahmsdorf, Hans J., and Peter Herrlich. "Regulation of gene expression by tumor promoters." Pharmacology & Therapeutics 48, no. 2 (January 1990): 157–88. http://dx.doi.org/10.1016/0163-7258(90)90079-h.

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25

Sajib, Abdul Mohin, Maninder Sandey, Samantha Morici, Bradley Schuler, Payal Agarwal, and Bruce F. Smith. "Analysis of endogenous and exogenous tumor upregulated promoter expression in canine tumors." PLOS ONE 15, no. 11 (November 9, 2020): e0240807. http://dx.doi.org/10.1371/journal.pone.0240807.

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Gene therapy is a promising treatment option for cancer. However, its utility may be limited due to expression in off-target cells. Cancer-specific promoters such as telomerase reverse transcriptase (TERT), survivin, and chemokine receptor 4 (CXCR4) have enhanced activity in a variety of human and murine cancers, however, little has been published regarding these promoters in dogs. Given the utility of canine cancer models, the activity of these promoters along with adenoviral E2F enhanced E1a promoter (EEE) was evaluated in a variety of canine tumors, both from the endogenous gene and from exogenously administered constructs. Endogenous expression levels were measured for cTERT, cSurvivin, and cCXCR4 and were low for all three, with some non-malignant and some tumor cell lines and tissues expressing the gene. Expression levels from exogenously supplied promoters were measured by both the number of cells expressing the construct and the intensity of expression in individual cells. Exogenously supplied promoters were active in more cells in all tumor lines than in normal cells, with the EEE promoter being most active, followed by cTERT. The intensity of expression varied more with cell type than with specific promoters. Ultimately, no single promoter was identified that would result in reliable expression, regardless of the tumor type. Thus, these findings imply that identification of a pan-cancer promoter may be difficult. In addition, this data raises the concern that endogenous expression analysis may not accurately predict exogenous promoter activity.
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Nagaya, Takashi, Hisao Seo, Akio Kuwayama, Tsuyoshi Sakurai, Nobuhiro Tsukamoto, Kenichiro Sugita, and Nobuo Matsui. "Prolactin gene expression in human growth hormone-secreting pituitary adenomas." Journal of Neurosurgery 72, no. 6 (June 1990): 879–82. http://dx.doi.org/10.3171/jns.1990.72.6.0879.

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✓ To elucidate the mechanism of hyperprolactinemia often observed in patients with growth hormone (GH)-secreting pituitary adenomas, the presence of immunoreactive prolactin (ir-PRL) and prolactin (PRL) messenger ribonucleic acid (mRNA) in the tumor tissue was examined by immunohistochemistry and cytoplasmic dot hybridization. Hyperprolactinemia was observed in three of 18 patients with GH-secreting adenoma. The tumor tissue was demonstrated to contain ir-PRL in nine patients and PRL mRNA in 13. The presence of ir-PRL in the tumor tissue was always associated with positive PRL mRNA, indicating production of PRL in GH-secreting tumors. Among the three patients with hyperprolactinemia, both ir-PRL and PRL mRNA was revealed in the tumor tissue of one, PRL mRNA but not ir-PRL was detected in the adenoma tissue of another, and neither PRL mRNA nor ir-PRL was found in the tumor tissue of the third. The association of hyperprolactinemia with the presence of both ir-PRL and PRL mRNA or PRL mRNA alone is indicative of PRL production and secretion. However, the absence of ir-PRL and PRL mRNA in the tumor tissue may indicate that hyperprolactinemia is caused by the suppression of PRL inhibitory factor due to hypothalamic dysfunction by the tumor mass. Thus, the study of PRL gene expression and immunohistochemistry in GH-secreting adenomas is valuable to understanding the pathophysiology of pituitary tumors.
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Uchibori, Ryosuke, Takashi Okada, Takayuki Ito, Masashi Urabe, Hiroaki Mizukami, Akihiro Kume, and Keiya Ozawa. "Retroviral Vector-Producing Mesenchymal Stem Cells for Tumor Tracking and Therapeutic Gene Amplification in Suicide Cancer Gene Therapy." Blood 110, no. 11 (November 16, 2007): 1917. http://dx.doi.org/10.1182/blood.v110.11.1917.1917.

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Abstract Mesenchymal stem cells (MSCs) are known to have a tendency to accumulate at the site of tumors, and therefore can be utilized as a platform for targeted delivery of anti-cancer agents. The MSC-based targeted cancer gene therapy can enhance the therapeutic efficacy, because MSCs are considered to reach tumors including metastatic lesions and to deliver therapeutic molecules in a concentrated fashion. This targeted therapy can also reduce systemic adverse side effects, because the anti-cancer agents act locally at the site of tumors without elevating their systemic concentrations. In the present study, we developed genetically-modified MSCs that produce retroviral vectors encoding HSVtk, aiming at augmenting therapeutic efficacy of systemic suicide cancer gene therapy. The tumor tropism and anti-tumor effects of vector-producing MSCs (VP-MSCs) were examined by intravascular injection in tumor-bearing nude mice. MSCs isolated from the bone marrow of SD rats were transfected with plasmid DNA expressing luciferase alone (=non-VP-MSCs) or whole retroviral vector components (LTR-Luc or LTR-HSVtk with Gag-pol and VSV-G) (=VP-MSCs) by nucleofection. To assess tumor tropism of MSCs, nude mice were subcutaneously inoculated with 9L rat glioma cells or Rat-1 fibroblasts, and were subsequently injected with luciferase-expressing MSCs through the left ventricular cavity. The transgene expression was periodically traced by using an in vivo imaging system. As a result, the transgene expression accumulated at the site of subcutaneous 9L tumors, but undetectable at the site of Rat-1 fibroblasts. In addition, the injection of luciferase-expressing VP-MSCs caused much stronger signal of bioluminescence at the site of 9L tumors compared with luciferease-expressing non-VP-MSCs. Immunostaining study showed that luciferase-positive cells (injected MSCs and transduced glioma cells) were detected at the periphery of tumors. To evaluate the therapeutic efficacy, tumor-bearing nude mice were treated with non-VP-MSCs or VP-MSCs combined with HSVtk/GCV system and then the size of subcutaneous tumors was periodically measured. In this model experiments, tumor growth was more efficiently suppressed by injecting VP-MSCs compared with non-VP-MSCs. The present study suggests the effectiveness of VP-MSCs in suicide cancer gene therapy. The therapeutic benefit of this strategy should be further examined in orthotopic and metastatic tumor models.
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Zhou, Yunli, Xun Zhang, and Anne Klibanski. "MEG3 noncoding RNA: a tumor suppressor." Journal of Molecular Endocrinology 48, no. 3 (March 2, 2012): R45—R53. http://dx.doi.org/10.1530/jme-12-0008.

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Maternally expressed gene 3 (MEG3) is an imprinted gene belonging to the imprinted DLK1–MEG3 locus located at chromosome 14q32.3 in humans. Its mouse ortholog, Meg3, also known as gene trap locus 2 (Gtl2), is located at distal chromosome 12. The MEG3 gene encodes a long noncoding RNA (lncRNA) and is expressed in many normal tissues. MEG3 gene expression is lost in an expanding list of primary human tumors and tumor cell lines. Multiple mechanisms contribute to the loss of MEG3 expression in tumors, including gene deletion, promoter hypermethylation, and hypermethylation of the intergenic differentially methylated region. Re-expression of MEG3 inhibits tumor cell proliferation in culture and colony formation in soft agar. This growth inhibition is partly the result of apoptosis induced by MEG3. MEG3 induces accumulation of p53 (TP53) protein, stimulates transcription from a p53-dependent promoter, and selectively regulates p53 target gene expression. Maternal deletion of the Meg3 gene in mice results in skeletal muscle defects and perinatal death. Inactivation of Meg3 leads to a significant increase in expression of angiogenesis-promoting genes and microvessel formation in the brain. These lines of evidence strongly suggest that MEG3 functions as a novel lncRNA tumor suppressor.
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Edfeldt, Katarina, Peyman Björklund, Göran Åkerström, Gunnar Westin, Per Hellman, and Peter Stålberg. "Different gene expression profiles in metastasizing midgut carcinoid tumors." Endocrine-Related Cancer 18, no. 4 (June 2, 2011): 479–89. http://dx.doi.org/10.1530/erc-10-0256.

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The genetic events leading the progression of midgut carcinoid tumors are largely unknown. The disease course varies from patient to patient, and there is a lack of reliable prognostic markers. In order to identify genes involved in tumor progression, gene expression profiling was performed on tumor specimens. Samples comprised 18 primary tumors, 17 lymph node (LN) metastases, and seven liver metastases from a total of 19 patients. Patients were grouped according to clinical data and histopathology into indolent or progressive course. RNA was subjected to a spotted oligo microarray and B-statistics were performed. Differentially expressed genes were verified using quantitative real-time PCR. Self-organizing maps demonstrated three clusters: 11 primary tumors separated in one cluster, five LN metastases in another cluster, whereas all seven liver metastases, seven primary, and 12 LN metastases formed a third cluster. There was no correlation between indolent and progressive behavior. The primary tumors with Ki67 >5%, with low frequency of the carcinoid syndrome, and a tendency toward shorter survival grouped together. Primary tumors differed in expression profile from their associated LN metastases; thus, there is evidence for genetic changes from primary tumors to metastases.ACTG2, GREM2, REG3A, TUSC2, RUNX1, TPH1, TGFBR2, andCDH6were differentially expressed between clusters and subgroups of tumors. The expression profile that assembles tumors as being genetically similar on the RNA expression level may not be concordant with the clinical disease course. This study reveals differences in gene expression profiles and novel genes that may be of importance in midgut carcinoid tumor progression.
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Liu, Z., X. Yang, Z. Li, C. McMahon, C. Sizer, L. Barenboim-Stapleton, V. Bliskovsky, et al. "CASZ1, a candidate tumor-suppressor gene, suppresses neuroblastoma tumor growth through reprogramming gene expression." Cell Death & Differentiation 18, no. 7 (January 21, 2011): 1174–83. http://dx.doi.org/10.1038/cdd.2010.187.

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Milosavljevic, Tanja, Michael Anthony Hall, Luis Del Valle, Elise Juge, Jovanny Zabaleta, J. Philip Boudreaux, Yi-Zarn Wang, Catherine T. Anthony, and Eugene Woltering. "Angiogenic gene expression in primary neuroendocrine tumors and their metastases." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 200. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.200.

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200 Background: Neuroendocrine tumors (NETs) are neoplasms arising from the cells of the nervous, endocrine and hormonal systems. They most commonly originate in the small bowel (SB) and frequently metastasize to the lymph nodes (LNs) and/or liver (LV). Current treatment of metastatic NETs involves a variety of approaches including antiangiogenic therapies. Our group demonstrated that there are significant histologic and functional differences between the primary NETs and their nodal or organ metastases. We hypothesized that sampling of multiple tumor sites within the same individual will reveal differential expression profiles of angiogenesis-related genes. Methods: Tissue-matched normal and tumor tissue samples were obtained from patients with well differentiated NETs who underwent simultaneous removal of their primary tumor, nodal, and organ metastasis. High quality RNA was extracted from each tumor site using TRIzol and RNeasy Mini kit. Gene expression of 28 well-documented angiogenesis-related genes was assessed using Custom Quantitative RT-PCR array. These gene expression trends were validated by Illumina microarray and TaqMan analysis. Immunohistochemistry (IHC) staining was performed using Avidin-Biotin-Peroxidase complex, with the markers: SSTR2 and FGFR3. Results: Normal SB, LN, and LV gene expression of 28 genes was compared to that of the tumor sample at each tumor site [4-fold change, p ≤ 0.01]. A consistent up-regulation of SSTR2 and SSTR1 was seen in 18/24 (75%) samples. Up-regulation of FGFR3 and SSTR5 was observed in 13/24 (50%) of tumors. TGFA and IGF were consistently down-regulated in 12/24 (50%) and 10/24 (42%) of tumor samples, respectively. Six genes expression trends were validated by TaqMan analysis and Illumina microarray analysis. IHC staining revealed higher SSTR2 and FGFR3 protein expression in all three tumor sites compared to the control. Conclusions: Expression of angiogenesis-related genes varies between the primary tumor (SB) and metastatic sites (LV, LN) within the same individual. We found a positive correlation between SSTR2 and FGFR3 gene and protein expression levels in all three tumor sites.
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Azuma, Mizutomo, Akira Naruke, Myungchul Kim, Kenji Ishido, Chikatoshi Katada, Katsuhiko Higuchi, Tohru Sasaki, Satoshi Tanabe, and Wasaburo Koizumi. "Intratumoral gene expression profile of genes involved in 5-FU metabolism and angiogenesis, comparison with tumor invasion depth in patients with advanced gastric cancer." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 56. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.56.

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56 Background: The biopsy specimen by endoscopy can only show the surface of its gene profiles. We hypothesis whether the biopsy specimen can reflect all part of gene profile or not. We tested how 5-FU related genes and angiogenesis gene expressed in the invasion depth in the primary tumor of the Stage II or III advanced gastric cancer. Methods: Twenty-five patients with stage II or III advanced gastric cancer who underwent gastrectomy were analyzed.Formalin-fixed, paraffin-embedded tumor tissues were dissected from the surface section (mainly mucosa), the middle section (mainly submucossa) and the deep section (the part invaded most deeply) of the primary tumor and the normal gastric mucosa tissue by the laser-captured microdissection technique and were analyzed for target gene expressions using a quantitative real-time polymerase chain reaction.We analyzed for target genes as TS, TP, DPD, ERCC1, EGFR, VEGF and HIF1α. Results: In the primary tumor, TP and HIF1α gene expression in the surface section was significantly higher than in the deep section (p=0.021, p=0.012). These gene expression and the depth of the primary tumor had a correlation coefficient (TP; r=0.29, HIF1α; r=0.33). There was no significantly difference between surface and deep section in the primary tumor in TS, DPD, ERCC1, VEGF, EGFR except TP and HIF1α. There was no significantly difference between surface and middle section in the primary tumor in all gene expression. There was no significantly difference between middle and deep section in the primary tumor in all gene expression. Conclusions: Only TP and HIF1α had tendency that these gene expression became higher as invaded from the surface section to the deep section of primary tumor. These data suggested that biopsy specimens could be predicted gene expression profile from the surface of gastric cancer. But as you know, gastric cancer has a heterogeneity gene profile. We need at least few samples to say whole gene expression of its tumors. This is preliminary data, it will need further study to proof these result.
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Dean-Colomb, Windy Marie, Rachel Martini, Akanksha Verma, Jason White, Olivier Elemento, Melissa Davis, Lisa Newman, Upender Manne, and Clayton Yates. "Ancestry-specific gene expression profiles in TNBC tumors." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 1547. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.1547.

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1547 Background: Due to persistent disparities in breast cancer mortality, there has been a renewed focus on investigating tumor biology. Deeper exploration has exposed distinctions in tumor biology based upon self-reported race and ancestry. The disparities associated with Triple Negative Breast Cancer (TNBC) across the modern African Diaspora suggests that there is a genetic ancestry connection between its aggressive tumor biology and clinical outcomes. Understanding this connection could hold the key to improving clinical outcomes in this group. Methods: We investigated 75 TNBC primary tumors using Self-Reported Race (SRR) groups: African American (AA, n = 42) and European American (EA, n = 33). Using best practices established by TCGA, we analyzed bulk RNA sequencing to measure changes in genome-wide expression levels. We next quantified global ancestry in a novel manner using RNAseq variants using 1000 Genomes as the reference data. We then identified African and European ancestry-associated genes using a logistic regression (adjusted FDR p < 0.05) between quantified ancestry and gene expression levels. Results: We identified > 150 genes associated with quantified African ancestry. We also found using quantified ancestry was a more robust method to screen for differentially expressed genes than SRR. Using an updated TNBC subtyping method, we noted higher incidences of Basal-like 2 tumors in AAs. Pathway analyses indicated several canonical cancer pathways; including, TP53, NFKB1 and AKT, have altered functionality in patients of African descent. For example, TP53-associated genes were activated in TNBC tumors of AA versus EA. This upregulation, rather than loss of function, is suggestive of polymorphic and/or ancestry-specific expression regulation, likely driven by population-private genetic variants. Lastly, we used TCGA data to validate a subset of African ancestry-specific genes that were upregulated in AA patients in our cohort. Specifically, PIM3, ZBTB22 and PPP2R4 each retained significant upregulation, in our cohort, but also TNBC tumors from TCGA (p = 0.0018, 0.023 and 0.022, respectively). Conclusions: Our study has uncovered ancestry-specific gene expression profiles in TNBC tumors. The distinct distribution of TNBC subtypes and altered functional oncologic pathways are evidence that biological underpinnings in TNBC can be driven by shared genetic ancestry. These findings emphasize the need to investigate patient populations of various ancestral origins in order to fully appreciate the molecular diversity in tumor biology for precision of disease management.
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Rubenstein, James L., Jane Fridlyand, Arthur Shen, Ken Aldape, David Ginzinger, Tracy Batchelor, Patrick Treseler, et al. "Gene expression and angiotropism in primary CNS lymphoma." Blood 107, no. 9 (May 1, 2006): 3716–23. http://dx.doi.org/10.1182/blood-2005-03-0897.

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Primary CNS lymphoma is an aggressive form of non-Hodgkin lymphoma whose growth is restricted to the central nervous system. We used cDNA microarray analysis to compare the gene expression signature of primary CNS lymphomas with nodal large B-cell lymphomas. Here, we show that while individual cases of primary CNS lymphomas may be classified as germinal center B-cell, activated B-cell, or type 3 large B-cell lymphoma, brain lymphomas are distinguished from nodal large B-cell lymphomas by high expression of regulators of the unfolded protein response (UPR) signaling pathway, by the oncogenes c-Myc and Pim-1, and by distinct regulators of apoptosis. We demonstrate that interleukin-4 (IL-4) is expressed by tumor vasculature as well as by tumor cells in CNS lymphomas. We also identify high expression in CNS lymphomas of several IL-4-induced genes, including X-box binding protein 1 (XBP-1), a regulator of the UPR. In addition, we demonstrate expression of the activated form of STAT6, a mediator of IL-4 signaling, by tumor cells and tumor endothelia in CNS lymphomas. High expression of activated STAT6 in tumors was associated with short survival in an independent set of patients with primary CNS lymphoma who were treated with high-dose intravenous methotrexate therapy.
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Liu, Yan-Nian, Ying Liu, Han-Jung Lee, Yung-Hsiang Hsu, and Ji-Hshiung Chen. "Activated Androgen Receptor Downregulates E-Cadherin Gene Expression and Promotes Tumor Metastasis." Molecular and Cellular Biology 28, no. 23 (September 15, 2008): 7096–108. http://dx.doi.org/10.1128/mcb.00449-08.

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ABSTRACT The loss of E-cadherin gene expression can cause the dysfunction of the cell-cell junction to trigger tumor metastasis. Members of the Snail family of transcription factors are repressors of the expression of the E-cadherin gene. In this study, we showed that the activated androgen receptor (AR) is a novel repressor of E-cadherin gene expression and can promote metastasis. Our results demonstrated that the activated AR could bind to the E-cadherin promoter in vitro and in vivo. The activated AR and HDAC1 had synergistic effects in downregulating E-cadherin gene expression. Treating cells with the AR ligand, dihydrotestosterone (DHT), triggered the reduction of E-cadherin expression and induced changes in cell morphology from an epithelial-like to a mesenchymal-like appearance. When nonmetastatic breast cancer cells expressing cytoplasmic AR were transplanted into mice and the mice were treated with DHT, tumors were detected at metastatic sites, whereas no tumors were detected in transplanted mice without DHT treatment. Furthermore, clinical data from breast cancer patients with invasive ductal carcinomas showed high levels of AR expression in the nuclei and low levels of E-cadherin expression. These results suggest that, similarly to Snail and Twist, the activated AR can downregulate E-cadherin expression to promote the activation of epithelial-mesenchymal transition and tumor metastasis.
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Lee, Ju-Seog, Sun-Hee Leem, Sang-Yeop Lee, Sang-Cheol Kim, Eun-Sung Park, Sang-Bae Kim, Seon-Kyu Kim, Yong-June Kim, Wun-Jae Kim, and In-Sun Chu. "Expression Signature of E2F1 and Its Associated Genes Predict Superficial to Invasive Progression of Bladder Tumors." Journal of Clinical Oncology 28, no. 16 (June 1, 2010): 2660–67. http://dx.doi.org/10.1200/jco.2009.25.0977.

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Purpose In approximately 20% of patients with superficial bladder tumors, the tumors progress to invasive tumors after treatment. Current methods of predicting the clinical behavior of these tumors prospectively are unreliable. We aim to identify a molecular signature that can reliably identify patients with high-risk superficial tumors that are likely to progress to invasive tumors. Patients and Methods Gene expression data were collected from tumor specimens from 165 patients with bladder cancer. Various statistical methods, including leave-one-out cross-validation methods, were applied to identify a gene expression signature that could predict the likelihood of progression to invasive tumors and to test the robustness of the expression signature in an independent cohort. The robustness of the gene expression signature was validated in an independent (n = 353) cohort. Results Supervised analysis of gene expression data revealed a gene expression signature that is strongly associated with invasive bladder tumors. A molecular classifier based on this gene expression signature correctly predicted the likelihood of progression of superficial tumor to invasive tumor. Conclusion We present a molecular signature that can predict, at diagnosis, the likelihood of bladder cancer progression and, possibly, lead to improvements in patient therapy.
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Zhou, C., Y. Tong, K. Wawrowsky, S. Bannykh, I. Donangelo, and S. Melmed. "Oct-1 induces pituitary tumor transforming gene expression in endocrine tumors." Endocrine Related Cancer 15, no. 3 (May 22, 2008): 817–31. http://dx.doi.org/10.1677/erc-08-0060.

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38

Stålhammar, Gustav, and Hans E. Grossniklaus. "Intratumor Heterogeneity in Uveal Melanoma BAP-1 Expression." Cancers 13, no. 5 (March 7, 2021): 1143. http://dx.doi.org/10.3390/cancers13051143.

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Malignant tumors are rarely homogenous on the morphological, genome, transcriptome or proteome level. In this study, we investigate the intratumor heterogeneity of BAP-1 expression in uveal melanoma with digital image analysis of 40 tumors. The proportion of BAP-1 positive cells was measured in full tumor sections, hot spots, cold spots and in scleral margins. The mean difference between hot spots and cold spots was 41 percentage points (pp, SD 29). Tumors with gene expression class 1 (associated with low metastatic risk) and 2 (high metastatic risk) had similar intratumor heterogeneity. Similarly, the level of intratumor heterogeneity was comparable in tumors from patients that later developed metastases as in patients that did not. BAP-1 measured in any tumor region added significant prognostic information to both American Joint Committee on Cancer (AJCC) tumor size category (p ≤ 0.001) and gene expression class (p ≤ 0.04). We conclude that there is substantial intratumor heterogeneity in uveal melanoma BAP-1 expression. However, it is of limited prognostic importance. Regardless of region, analysis of BAP-1 expression adds significant prognostic information beyond tumor size and gene expression class.
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Costales-Carrera, Alba, Asunción Fernández-Barral, Pilar Bustamante-Madrid, Orlando Domínguez, Laura Guerra-Pastrián, Ramón Cantero, Luis del Peso, Aurora Burgos, Antonio Barbáchano, and Alberto Muñoz. "Comparative Study of Organoids from Patient-Derived Normal and Tumor Colon and Rectal Tissue." Cancers 12, no. 8 (August 15, 2020): 2302. http://dx.doi.org/10.3390/cancers12082302.

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Colon and rectal tumors, often referred to as colorectal cancer, show different gene expression patterns in studies that analyze whole tissue biopsies containing a mix of tumor and non-tumor cells. To better characterize colon and rectal tumors, we investigated the gene expression profile of organoids generated from endoscopic biopsies of rectal tumors and adjacent normal colon and rectum mucosa from therapy-naive rectal cancer patients. We also studied the effect of vitamin D on these organoid types. Gene profiling was performed by RNA-sequencing. Organoids from a normal colon and rectum had a shared gene expression profile that profoundly differed from that of rectal tumor organoids. We identified a group of genes of the biosynthetic machinery as rectal tumor organoid-specific, including those encoding the RNA polymerase II subunits POLR2H and POLR2J. The active vitamin D metabolite 1α,25-dihydroxyvitamin D3/calcitriol upregulated stemness-related genes (LGR5, LRIG1, SMOC2, and MSI1) in normal rectum organoids, while it downregulated differentiation marker genes (TFF2 and MUC2). Normal colon and rectum organoids share similar gene expression patterns and respond similarly to calcitriol. Rectal tumor organoids display distinct and heterogeneous gene expression profiles, with differences with respect to those of colon tumor organoids, and respond differently to calcitriol than normal rectum organoids.
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Maiti, Aparna, Ichiro Okano, Masanori Oshi, Maiko Okano, Wanqing Tian, Tsutomu Kawaguchi, Eriko Katsuta, et al. "Altered Expression of Secreted Mediator Genes That Mediate Aggressive Breast Cancer Metastasis to Distant Organs." Cancers 13, no. 11 (May 27, 2021): 2641. http://dx.doi.org/10.3390/cancers13112641.

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Heterogeneity is the characteristic of breast tumors, making it difficult to understand the molecular mechanism. Alteration of gene expression in the primary tumor versus the metastatic lesion remains challenging for getting any specific targeted therapy. To better understand how gene expression profile changes during metastasis, we compare the primary tumor and distant metastatic tumor gene expression using primary breast tumors compared with its metastatic variant in animal models. Our RNA sequencing data from cells revealed that parental cell and the metastatic variant cell are different in gene expression while gene signature significantly altered during metastasis to distant organs than primary breast tumors. We found that secreted mediators encoding genes (ANGPTL7, MMP3, LCN2, S100A8, and ESM1) are correlated with poor prognosis in the clinical setting as divulged from METABRIC and TCGA-BRCA cohort data analysis.
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41

Rehemtulla, Alnawaz, Daniel E. Hall, Lauren D. Stegman, Uttara Prasad, Grace Chen, Mahaveer Swaroop Bhojani, Thomas L. Chenevert, and Brian D. Ross. "Molecular Imaging of Gene Expression and Efficacy following Adenoviral-Mediated Brain Tumor Gene Therapy." Molecular Imaging 1, no. 1 (January 1, 2002): 153535002002000. http://dx.doi.org/10.1162/15353500200200005.

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Cancer gene therapy is an active area of research relying upon the transfer and subsequent expression of a therapeutic transgene into tumor cells in order to provide for therapeutic selectivity. Noninvasive assessment of therapeutic response and correlation of the location, magnitude, and duration of transgene expression in vivo would be particularly useful in the development of cancer gene therapy protocols by facilitating optimization of gene transfer protocols, vector development, and prodrug dosing schedules. In this study, we developed an adenoviral vector containing both the therapeutic transgene yeast cytosine deaminase (yCD) along with an optical reporter gene (luciferase). Following intratumoral injection of the vector into orthotopic 9L gliomas, anatomical and diffusion-weighted MR images were obtained over time in order to provide for quantitative assessment of overall therapeutic efficacy and spatial heterogeneity of cell kill, respectively. In addition, bioluminescence images were acquired to assess the duration and magnitude of gene expression. MR images revealed significant reduction in tumor growth rates associated with yCD/5-fluorocytosine (5FC) gene therapy. Significant increases in mean tumor diffusion values were also observed during treatment with 5FC. Moreover, spatial heterogeneity in tumor diffusion changes were also observed revealing that diffusion magnetic resonance imaging could detect regional therapeutic effects due to the nonuniform delivery and/or expression of the therapeutic yCD transgene within the tumor mass. In addition, in vivo bioluminescence imaging detected luciferase gene expression, which was found to decrease over time during administration of the prodrug providing a noninvasive surrogate marker for monitoring gene expression. These results demonstrate the efficacy of the yCD/5FC strategy for the treatment of brain tumors and reveal the feasibility of using multimodality molecular and functional imaging for assessment of gene expression and therapeutic efficacy.
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Wickstrom, Eric, Edward Sauter, Xianben Tian, Sampath Rao, Weyng Quin, and Mathew Thakur. "Radiolabeled PNAs for imaging gene expression." Brazilian Archives of Biology and Technology 45, spe (September 2002): 57–59. http://dx.doi.org/10.1590/s1516-89132002000500008.

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Scintigraphic imaging of gene expression in vivo by non-invasive means could precisely direct physicians to appropriate intervention at the onset of disease and could contribute extensively to the management of patients. However, no method is currently available to image specific overexpressed oncogene mRNAs in vivo by scintigraphic imaging. Nevertheless, we have observed that Tc-99m-peptides can delineate tumors, and that PNA-peptides are specific for receptors on malignant cells and are taken up specifically and concentrated in nuclei. We hypothesize that antisense Tc-99m-PNA-peptides will be taken up by human breast cancer cells, hybridize to complementary mRNA targets, and permit imaging of oncogene mRNAs in human breast cancer xenografts in a mouse model, providing a proof-of-principle for non-invasive detection of precancerous and invasive breast cancer. Oncogenes cyclin D1, erbB-2, c-MYC, and tumor suppressor p53 will be probed. If successful, this technique will be useful for diagnostic imaging of other solid tumors as well.
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Lee, Eunhye, Taeyun A. Lee, Hye Jin Yoo, Sungwook Lee, and Boyoun Park. "CNBP controls tumor cell biology by regulating tumor‐promoting gene expression." Molecular Carcinogenesis 58, no. 8 (May 13, 2019): 1492–501. http://dx.doi.org/10.1002/mc.23030.

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44

Hannemann, Juliane, Hendrika M. Oosterkamp, Cathy A. J. Bosch, Arno Velds, Lodewyk F. A. Wessels, Claudette Loo, Emiel J. Rutgers, Sjoerd Rodenhuis, and Marc J. van de Vijver. "Changes in Gene Expression Associated With Response to Neoadjuvant Chemotherapy in Breast Cancer." Journal of Clinical Oncology 23, no. 15 (May 20, 2005): 3331–42. http://dx.doi.org/10.1200/jco.2005.09.077.

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Purpose At present, clinically useful markers predicting response of primary breast carcinomas to either doxorubicin-cyclophosphamide (AC) or doxorubicin-docetaxel (AD) are lacking. We investigated whether gene expression profiles of the primary tumor could be used to predict treatment response to either of those chemotherapy regimens. Patients and Methods Within a single-institution, randomized, phase II trial, patients with locally advanced breast cancer received six courses of either AC (n = 24) or AD (n = 24) neoadjuvant chemotherapy. Gene expression profiles were generated from core-needle biopsies obtained before treatment and correlated with the response of the primary tumor to the chemotherapy administered. Additionally, pretreatment gene expression profiles were compared with those in tumors remaining after chemotherapy. Results Ten (20%) of 48 patients showed a (near) pathologic complete remission of the primary tumor after treatment. No gene expression pattern correlating with response could be identified for all patients or for the AC or AD groups separately. The comparison of the pretreatment biopsy and the tumor excised after chemotherapy revealed differences in gene expression in tumors that showed a partial remission but not in tumors that did not respond to chemotherapy. Conclusion No gene expression profile predicting the response of primary breast carcinomas to AC- or AD-based neoadjuvant chemotherapy could be detected in this interim analysis. More subtle differences in gene expression are likely to be present but can only be reliably identified by studying a larger group of patients. Response of a breast tumor to neoadjuvant chemotherapy results in alterations in gene expression.
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Timoshkina, Natalya N., Oleg I. Kit, Anton Pushkin, Anna V. Antonets, Eduard Evgenevich Rostorguev, David H. Porksheyan, Sergey E. Kavitskiy, and Natalya S. Kuznetsova. "Comparative gene expression analysis in gliomas with different IDH1/2 status." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e13008-e13008. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13008.

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e13008 Background: The new 2016 WHO classification of tumors of the central nervous system takes into consideration mutational status of IDH genes. Research of molecular changes in gliomas remain to be an actual issue. We analyzed the gene expression of some significant pathways in gliomas. Methods: 27 patients (12 females, 15 males) aged from 27 to 76 years with verified brain tumors (glioblastomas (G4) – 67%, anaplastic astrocytomas and oligoastrocytomas (G3) – 11%, astrocytomas (G2) – 22%) were investigated. 7 mutations in the IDH1 gene and 5 ones in IDH2 in fresh frozen tumor tissues were detected by RT-qPCR with Therascreen IDH1/2 RGQPCR kit (Qiagen). The expressions of EGFR, SMAD4, SMAD7, SMO, NOTCH1, NOTCH2, HBP1, HIF1A, EGLN1, EGLIN3, KDM1B, KDM1A, MSI1, MSI2, TET1 genes in tumor and normal brain tissue obtained while surgical access were assessed with RT-qPCR. PSMC, TBP and RPLO were used as reference genes. Results: Analysis of IDH1/2 status revealed only R132H mutation of IDH1 in 6 patients. The ratio of the relative expression of genes in tumor tissue with mutation and wild-type and the significance of the differences in the Mann-Whitney test are presented in the table below . Conclusions: Expression of SMAD7, EGLN1, EGLN3 as an activating factor of TGF-b-signaling pathway potentially may be used as an additional prognostic marker of gliomas progression.[Table: see text]
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Maxwell, Marius, Sarah D. Shih, Theofanis Galanopoulos, E. Tessa Hedley-Whyte, and G. Rees Cosgrove. "Familial meningioma: analysis of expression of neurofibromatosis 2 protein Merlin." Journal of Neurosurgery 88, no. 3 (March 1998): 562–69. http://dx.doi.org/10.3171/jns.1998.88.3.0562.

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✓ Meningiomas are primarily benign brain tumors thought to arise through multistep tumorigenesis, involving both the activation of oncogenes and the loss of tumor suppressor genes. The recently isolated neurofibromatosis 2 (NF2) tumor suppressor gene has been found to be mutated in a large proportion of meningiomas. Almost all cases of familial meningioma occur in association with NF2. Familial meningioma in isolation from NF2 (sporadic) is exceedingly rare, with only 14 reports since 1959. The authors report the existence of a family lacking any stigmata of NF2, in which two members had spinal meningiomas. Tumor specimens were subjected to immunocytochemical analysis for the NF2 protein product Merlin, which has been implicated in the tumorigenesis of meningioma. Merlin immunoreactivity was present in both tumor specimens, implying that the NF2 tumor suppressor gene was not deleted in these tumors. This supports the hypothesis that a second tumor suppressor gene locus, other than NF2, acts in the formation of familial sporadic meningioma. The results are discussed in the context of putative oncogenic mechanisms of familial meningiomas.
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Bai, Xiao-Hui, Hae-Ra Cho, Serisha Moodley, and Mingyao Liu. "XB130—A Novel Adaptor Protein: Gene, Function, and Roles in Tumorigenesis." Scientifica 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/903014.

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Several adaptor proteins have previously been shown to play an important role in the promotion of tumourigenesis. XB130 (AFAP1L2) is an adaptor protein involved in many cellular functions, such as cell survival, cell proliferation, migration, and gene and miRNA expression. XB130’s functional domains and motifs enable its interaction with a multitude of proteins involved in several different signaling pathways. As a tyrosine kinase substrate, tyrosine phosphorylated XB130 associates with the p85αregulatory subunit of phosphoinositol-3-kinase (PI3K) and subsequently affects Akt activity and its downstream signalling. Tumourigenesis studies show that downregulation of XB130 expression by RNAi inhibits tumor growth in mouse xenograft models. Furthermore, XB130 affects tumor oncogenicity by regulating the expression of specific tumour suppressing miRNAs. The expression level and pattern of XB130 has been studied in various human tumors, such as thyroid, esophageal, and gastric cancers, as well as, soft tissue tumors. Studies show the significant effects of XB130 in tumourigenesis and suggest its potential as a diagnostic biomarker and therapeutic target for cancer treatments.
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Peng, W., J. Chen, Y.-H. Huang, and J. A. Sawicki. "Tightly-regulated suicide gene expression kills PSA-expressing prostate tumor cells." Gene Therapy 12, no. 21 (June 30, 2005): 1573–80. http://dx.doi.org/10.1038/sj.gt.3302580.

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49

Barzon, Luisa, Roberta Bonaguro, Ignazio Castagliuolo, Marco Chilosi, Elisa Gnatta, Cristina Parolin, Marco Boscaro, and Giorgio Palù. "Transcriptionally Targeted Retroviral Vector for Combined Suicide and Immunomodulating Gene Therapy of Thyroid Cancer." Journal of Clinical Endocrinology & Metabolism 87, no. 11 (November 1, 2002): 5304–11. http://dx.doi.org/10.1210/jc.2002-020975.

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Abstract Gene therapy may be an effective approach to thyroid carcinoma refractory to conventional treatment. A transcriptionally targeted retroviral vector for gene therapy of thyroid carcinomas was generated replacing the viral enhancer with the enhancer sequence of the human thyroglobulin (TG) gene, yielding a chimeric long-terminal repeat. The TG enhancer was used to drive the expression of either a reporter gene (β-galactosidase) or two therapeutic genes, i.e. the prodrug-activating enzyme thymidine kinase of herpes simplex virus (HSV-TK) and human IL-2, separated by an internal ribosome entry site. The corresponding vector having an unmodified long-terminal repeat was used as control. The targeted vector allowed selective transgene expression and cell killing in differentiated thyroid tumor cells but not in anaplastic thyroid carcinoma cells and nonthyroid cells, as demonstrated by quantitative RT-PCR and cytotoxicity assays. Nude mice injected with tumor cells underwent near complete or complete regression of tumors transduced with the control vector after ganciclovir treatment. On the other hand, infection with the thyroid-specific vector led to regression only of TG-expressing tumors. In addition, tumors expressing human IL-2 showed significant growth retardation, compared with nontransduced tumors while exhibiting signs of necrosis and presence of an inflammatory infiltrate. However, HSV-TK/IL-2 plus ganciclovir was significantly more efficient than HSV-TK/IL-2 alone in eradicating tumor masses. Our results indicate that replacement of viral enhancer with TG enhancer confers selectivity of transgene expression in thyroid cells. Thus, the combined thyroid-specific expression of two therapeutic genes (cytokine and suicide genes), although a safe tumor-targeted treatment, would allow an increased anticancer effect.
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Tsuruta, Toshihisa, Hitoshi Kanno, Yasuo Aihara, Takako Hamada, Masako Sakauchi, Makiko Osawa, Emiko Wada, Osami Kubo, Tomokatsu Hori, and Hisaichi Fujii. "Target Marker Gene Expressions and the Possibility of Molecular Therapy for Children’s Brain Tumors." Blood 108, no. 11 (November 16, 2006): 5468. http://dx.doi.org/10.1182/blood.v108.11.5468.5468.

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Abstract ErbB2, c-Myc and p53 gene expressions are widely reported for the poor prognostic markers for medulloblastoma (MB) patients. Recently, Wnt pathway and Sonic Hedgehog (SHH) pathways are known to related to the oncogenesis of MB cells, and the PDGF receptor gene and some adhesion molecule gene expressions are also known to the markers of the dissemination or the metastasis of MB cells. For adult malignant brain tumors, the molecular targeted therapy of the antibody (trastuzumab, cetuximab), the tyrosine kinase inhibitor (imatinib, gefinitib) or other signal transduction inhibitor (cyclopamin) are clinically researched. We examined several important marker gene expressions of the molecular therapy in various children’s brain tumors and searched the possible molecular targeted therapy. [Materials and methods] Fifteen children’s brain tumor (five MB, seven glioma, three ependymoma) and four adult brain tumor (two glioma, two glioblastoma) were examind. The three MB cases were primary metaststic ones. The mRNA expressions of the marker genes (ErbB2, PDGF receptor, PCNA, SPARC, β-catenin, SUFU, c-Myc, p53, TrkC and so on) were examined by quantity polymerase chain (qPCR) reaction with fresh frozen tumor cells. For the normal control, we used the normal cerebellum total RNA samples of the Becton, Dikinson and Company. CYBR green coloring system was used for the qPCR and their primers were designed in the region between two exons. GAPDH gene expression was also examined as an internal control and all of the gene expression were normalized by GAPDH expression. [Results] ErbB2 gene expression in MB cells were various, but their expression were similar to clinical futures, such as, the higher expressed cases had some high risk factors. In glioma cells, ErbB2 gene expression were almost equal by lower levels. PDGF receptor gene expression were more than five to ten times elevated in all of the glioma cells, even if they were low grade malignancy glioma, and were higher than that in MB cells. PCNA was specially elevated in primary metastatic MB cells. [Conclusion] Our data shows that the molecular characteristics of the children’s brain tumors were thought to be different by cases, even if they had same histopathological characters. Some special gene tageting therapy, such as anti-ErbB2, PDGFR and/or PCNA therapy can be used for the various children’s brain tumors which are resistant for conventional therapies and are cured by adequate molecular therapy.
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