Cyclooxygenase-2 promotes tumor growth and suppresses tumor immunity Abstract. Cyclooxygenase-2 (COX-2), an inducible form of the enzyme that catalyzes the first step in the synthesis of... Background. Human malignancies generally arise as the culmination of a multistep process that involves various. An fast allen Prozessen der Kanzerogenese ist COX-2 beteiligt - von der Bildung von Tumoren, über deren Blutversorgung bis hin zur Metastasenbildung. Zur Entstehung von Tumoren trägt COX durch seine Peroxidase-Aktivität bei. Als bifunktionelles Enzym fungiert COX nicht nur als Cyclooxygenase sondern auch als Peroxidase. Mit dieser Aktivität kann es Prokanzerogene wie Benzpyren in Kanzerogene umwandeln und produziert somit Mutagene im Gewebe. Vor allem in Organen, die mit Tabak. COX-2 is released by cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and cancer cells to the tumor microenvironment (TME). COX-2 induces cancer stem cell (CSC)-like activity, and promotes apoptotic resistance, proliferation, angiogenesis, inflammation, invasion, and metastasis of cancer cells. COX-2 mediated hypoxia within the TME along with its positive interactions with YAP1 and antiapoptotic mediators are all in favor of cancer cell resistance to chemotherapeutic drugs.
We found no differences in COX-2 expression with respect to patient age, gender, tumour size, degree of tumour invasiveness, or whether tumours were immunopositive or immunonegative for pituitary hormones, nor have we found any relation between COX-2 expression and recurrence or progression of tumour size. CONCLUSIONS: COX-2 does not appear to be a predictive factor for recurrence or. Its clinical relevance is consistent with the striking distinct expression patterns of COX-2 (tumor), prolactin (stroma), and prolactin receptor (tumor) that are evident in a large number of human prostate, colorectal, and lung cancers. Together, these observations implicate a specific paracrine signaling pathway as contributing to the well-established tumor-suppressive effect of the COX-2 inhibitors in human cancer, which has traditionally been attributed to their general antiinflammatory. Cox-2-Hemmer gegen Krebs Da die Cyclooxygenase 2 (Cox-2) auch in die Krebsentstehung eingreift, versprechen Cox-2-Hemmer im Sinne einer Chemoprophylaxe Schutz vor Krebs. Eröffnen sich damit neue Behandlungshorizonte? Die Produktion von Cox-2 wird durch Zytokine, Wachstumsfaktoren und Tumorpromotoren induziert
Folgende COX-2-Funktionen, die für Krankheitsprozesse von besonderer Bedeutung sind, können durch COX-2-Hemmer unterdrückt werden: COX-2 wird in Entzündungen vermehrt gebildet; seine Stoffwechselprodukte führen zu akuten Entzündungsreaktionen... COX-2 findet sich in aussprossenden Gefäßen, wie sie. Sogenannte Cox-2 Hemmer (auch NSAID - nicht steroidale entzündungshemmende Substanzen) werden routinemäßig beim Menschen und beim Tier zur Behandlung von Entzündungszuständen eingesetzt: Während und nach Operationen zur Schmerzvorbeuge Bei Lahmheiten wegen der Wirkung auf den Gelenkstoffwechsel Bei.
COX‐2 specific inhibitors induce apoptosis by decreasing the expression of an apoptosis‐repressor gene, Bcl‐2. 12, 20, 21 Furthermore, COX and COX‐2 specific inhibitors suppress tumor growth in vitro and in vivo by reducing the production of angiogenic factors in endothelial cells and tumor cells. 11, 22, 23 Thus, COX or COX‐2 specific inhibitors may be useful for chemoprevention in. Die beiden COX-2-Hemmer Rofecoxib (Vioxx ® ) und Celecoxib (Celebra ® , noch nicht im Handel) werden als die Lösung für die gastrointestinalen Nebenwirkungen der bisher eingesetzten nicht. DKFZ Heidelberg, Core Facility Tumormodelle, COX-2-Tumormaus, Haut, Haarfollikel, Talgdrüsen, Dysplasie, Hyperplasie Die Keratin 5-Promoter-COX-2 transgene Maus bildet der Diagnose von Human-pathologen nach frühe (Hyperplasien/Dysplasien in Haut, Blase, Milchdrüse, Pankreas) und späte Stadien (Karzinome in Harnblase und Haut nach DMBA-Gabe) menschlicher Läsionen und Tumoren mit vergleichbaren Progressionsstadien nach The COX-2 enzyme was discovered in 1988 by Daniel Simmons, a Brigham Young Universityresearcher. The mouse COX-2 gene was cloned by UCLA scientist Harvey Herschman, a finding published in 1991. The basic research leading to the discovery of COX-2 inhibitors has been the subject of at least two lawsuits
Although previous studies have shown that COX-2 inhibitors affect cytokine expression profiles and tumor microenvironments ( 26), the effect of COX-2 inhibition on TAM phenotype remains unclear. To examine the effect of COX-2 inhibition on TAMs, we investigated the status of TAMs in Apc Min/+ mouse intestinal polyps and concomitant cytokine expression profiles with or without selective COX-2. Die bösartigen Tumore (siehe Fakt 1) werden umgangssprachlich als Krebs bezeichnet. Ein Tumor ist somit nicht immer gleich Krebs (Schwellungen, Zysten werden nicht als Krebs bezeichnet). Ungefähr die Hälfte aller Krebserkrankungen kann geheilt werden, wobei es zum Teil deutliche Unterschiede zwischen den verschiedenen Krebsarten geben kann. Dennoch sind in Industrieländern maligne Tumore ., 2005 ) from human cutaneous melanoma biopsies containing tumor cells, stroma, and infiltrate were analyzed for the association of PTGS2 expression with that of.
In contrast, COX‐2 is an inducible enzyme that is activated by extracellular stimuli, such as UV radiation. Enhanced expression of COX‐2 in skin exposed to UV radiation has been identified as a risk factor for the development of skin cancer.5, The principal COX-2 product in tumors is PGE 2, which acts through four G protein-coupled receptors designated EP1, EP2, EP3, and EP4.61, 62 In the present study, EP3 and EP4 receptor signaling was found to be crucial for tumor stromal formation and tumor growth. We previously considered the AP-1-dependent upregulation of VEGF to be important in tumor-associated angiogenesis mediated by. VVB ANNALENA MICHEL Prävalenz der Cyclooxygenase-2 bei intranasalen Tumoren des Hundes und klinische Untersuchungen zur palliativen Therapie intranasaler Neoplasien mit Meloxicam un
The expression of COX-2 is undetectable under physiological conditions but up-regulated in many malignant tumors. COX-2, which is a PKC-dependent gene, is important for the genesis of cancer. COX-2 promoter contains a cAMP response element and sites for AP-2 and NF-κB that are both PKC-responsive cis-elements. COX-2 promoter has been used to target gene expression in pancreatic [1. The revelation that aspirin and aspirin-like compounds have notableantineo plastic properties has revolutionized cancer research. COX-2 Blockade in Cancer Prevention and Therapy chronicles the evidence and presents exciting new op portunities for the use of cyclooxygenase-2 (COX-2) blockade in the prevention and treatment of cancer COX-2 inhibitors, which block the formation of prostaglandins, suppress tumor growth, whereas sEH inhibitors, which increase endogenous EETs, stimulate primary tumor growth and metastasis. However, the functional interactions of these two pathways in cancer are unknown. Using pharmacological inhibitors as probes, we show here that dual inhibition of COX-2 and sEH synergistically inhibits primary tumor growth and metastasis by suppressing tumor angiogenesis. COX-2/sEH dual pharmacological. Der COX-2-Expression wird aber auch eine Bedeutung in der Karzinogenese beigemessen, was sowohl durch Tierversuchsmodelle als auch durch klinische Untersuchungen belegt wird. Eine Überexpression von COX-2 wird in einer Reihe von Neoplasien, wie dem kolorektalen- und dem Prostata-Adenokarzinom sowie bei Plattenepithelkarzinomen der Luft- und obere In verschiedenen humanen Tumoren konnte eine COX-2-Expression nachgewiesen werden. COX-2 regt die Proliferation von Tumorzellen an und hemmt die Apoptose. Ein protektiver Effekt konnte beim.
The clinical application of immunotherapy is the milestone of cancer treatment. However, some patients have bad reaction. Cyclooxygenase-2 (COX-2) is frequently expressed in multiple cancer cells and is associated with poor prognosis. It is the key enzyme of prostaglandin E2 (PGE2) that has been proved to promote the development, proliferation and metastasis of tumor cells Cyclooxygenase 2 (COX-2)-positive human breast cancer carcinoma cells may be chemotherapy-resistant cancer stem cells (CSCs) Among the 815 cases of breast invasive carcinoma26 from The Cancer Genome Atlas (TCGA) database, 12% have COX-2 gene ampliﬁcation. A signiﬁcant difference between survival of the two groups is observed for patients wit
COX-2 suppresses NK cells, dendritic cells (DCs) and T cells leading to tumor escape from host immune detection. In fact, enhanced expression of PGE2 and COX-2 inhibits T cells and DC function in breast cancer patients . PGE2 mediates cancer growth via stimulation of a family of G-protein coupled receptors The role of cyclooxygenase-2 (COX-2) in tumor neovascularization of human colorectal carcinoma is yet to be delineated. One hundred colorectal carcinoma specimens were evaluated for COX-2 expression and CD34-stained microvessel density (MVD) by immunohistochemical methods. The relationships between COX-2 expression and clinicopathological feature of the patients, MVD, and survival time were. We also aim to determine whether a combinatorial inhibition of the ACSL4-LOX-COX-2 pathway affects tumor growth in vivo using a xenograft model based on MDA-MB-231 cells, a highly aggressive breast cancer cell line naturally overexpressing ACSL4. The first novel finding is that stable transfection of MCF-7 cells with ACSL4 using the tetracycline Tet-Off system of MCF-7 cells resulted in development of growing tumors when injected into nude mice. Tumor xenograft development.
Accurate identification of cancer from inflammation and normal tissue in a rapid, sensitive, and quantitative fashion is important for cancer diagnosis and resection during surgery. Here we report the use of cyclooxygenase-2 as a marker for identification of cancer from inflammation and the design of a novel smart COX-2-specific fluorogenic probe (NANQ-IMC6). The probe's fluorescence is. When investigating the mechanisms of COX-2 induction during spheroid formation, the typical tumor microenvironmental factors such as glucose deprivation, hypoxia or tumor cell apoptosis failed to enhance COX-2. Interestingly, when interfering with apoptosis in DU145 spheroids, the pan-caspase inhibitor Z-VAD-FMK triggered a Summary 12 shift towards necrosis, thus enhancing COX-2 expression. Targeted cyclooxygenase (COX)-2 inhibition in tumor, stromal and endothelial cells is an attractive antiangiogenic strategy; however, the associated cardiovascular side effects have led to the development of a new generation of nonsteroidal anti-inflammatory drugs (NSAIDs) acting downstream of COX COX-2 protein levels Tumor-associated macrophages in unperturbed TRAMP increase after irradiation in a dose-dependent manner (35), tumors expressed much higher mRNA levels of Arg-1 than and a 12-Gy dose was found to increase COX-2 mRNA in iNOS, suggesting an immunosuppressive, tumor growth- I407 epithelial cells biphasically, the first peak being within promoting phenotype. Depletion of. Regulating the Golgi apparatus by co-delivery of a COX-2 inhibitor and Brefeldin A for suppression of tumor metastasis regulating the Golgi apparatus of tumor cells is a viable strategy to inhibit tumor metastasis. Herein, celecoxib (CLX) and Brefeldin A (BFA) were encapsulated into the biocompatible polymer PLGA-PEG to form nanoparticles that act on the Golgi apparatus to treat metastatic.
Sie sollen der Vorbeugung eines Herzinfarkts und Schlaganfalls dienen, ohne die Nebenwirkung einer zusätzlichen COX-2-Hemmung aufzuweisen. Zudem erwartet man sich positive Wirkungen selektiver COX-1-Hemmer bei Demenzerkrankungen , wie dem Morbus Parkinson oder Morbus Alzheimer , und bei der Behandlung von eines Gewichtsverlusts bei Tumorkrankheiten COX-2 expression. Large difference in gene expression was observed when comparing tumor tissue with high COX-2 expression to normal colon mucosa tissue from the same patients (2557↑, 3182↓) (Table 3).A large number of genes with altered expression appeared also in colon cancer tissue of tumors with high COX-2 expression when compared to tumors with low COX-2 expression (3086↑, 3031. Indomethacin did not change overall COX-2 staining in tumor tissue, but altered its distribution towards increased staining in cell nuclei/nucleoli and decreased COX-2 staining heterogeneity in tumor tissue. P53 staining was decreased, while PCNA and TGFβ3 staining were increased by indomethacin in tumor areas with high presence of COX-2, which correlated to staining of BAX, TUNEL, Bcl-2, c. Increased COX‐2 expression and elevated PGE2 have been associated with a poor prognosis in lung cancer. Cannabinoids have been known to exert some of their biological effects via modulation of prostaglandin production. We evaluated the impact of methanandamide on COX‐2 expression, PGE2 production, and tumor growth in murine lung cancer Both COX-2 and PGE 2 have been implicated in tumor progression , mainly as mediators of angiogenesis and tumor cell proliferation and survival (56, 57). Importantly, elevated PTGS2 levels have been linked to unfavorable disease-free survival, larger tumor size, and higher metastatic incidence in breast, gastrointestinal, and colorectal cancers ( 58 - 62 )
Although we were unable to establish Cox-2 −/− glioma cells due to the lack of consistent tumor formation in these mice, Cox-2 +/+ and Cox-2 +/ − glioma cells proliferated at similar rates in vitro (Supplementary Fig. S3). Endogenous CCL2 promotes glioma development and tumor infiltration of MDSCs. These data led us to hypothesize that the ASA treatment would induce dynamic changes in. Meanwhile, it was found that tumor cell repopulation was significantly restrained by celecoxib, a COX-2 inhibitor that inhibited PGE2 synthesis, in a dose-dependent manner (Fig. 5e). Although PGE2 was found to accelerate the proliferation of tumor cells, addition of PGE2 to tumor cells immediately after radiation reversely inhibited cell viability (Fig. 5 f) Melittin (1) is a major polypeptide in honey bee venom that has been used traditionally against chronic inflammation and cancer. However, its molecular mechanism has not been determined. In this study, the antitumor effect of 1 was compared with that of NS398, a cyclooxygenase-2 (COX-2) inhibitor, in vivo and in vitro. Subcutaneous injection of 1 at 0.5 and 5 mg/kg suppressed significantly.
Purpose: The objectives of this study were to evaluate the effect of a cyclooxygenase (COX)-2 inhibitor, nimesulide, on the growth inhibition of s.c. human lung A549 adenocarcinoma tumors and to assess the effect of nimesulide on the expression of COX-2 and peroxisome proliferator-activated receptor (PPAR)-γ in lung tumors harvested from mice The COX-2 ARE is also bound by the RNA-binding protein HuR. In colorectal cancer tumors, HuR is overexpressed and localized within the cytoplasm, where it promotes ARE-mRNA stabilization. Under conditions of HuR overexpression, miR-16 was unable to promote rapid mRNA decay through the COX-2 ARE. Ribonucleoprotein immunoprecipitation of HuR showed direct association with miR-16 that was.
COX-2, PGE2 and NO levels depended on the tumor grade of the cells, being the highest in Duke's stage III colon carcinoma. Summing up, we showed that addition of L-arginine at doses which did not stimulate NO level caused a significant decrease in COX-2 and PGE2 amounts in co-cultures of colon tumor spheroids with normal epithelial cells and myofibroblasts. Any imbalances in NO level caused. COX-2, cyclooxygenase-2; DT(s), desmoid tumor(s); NSAID, non-steroidal anti-inflammatory drug. References. 1. Buitendijk S, van de Ven CP, Dumans TG, et al. Pediatric aggressive fibromatosis: a retrospective analysis of 13 patients and review of literature. Cancer. 2005;104(5):1090-9. Article PubMed Google Scholar 2. Latchford AR, Sturt NJH, Neale K, et al. A 10-year review of surgery for. COX-2 and nostic value of iNOS to that of COX-2 and therefore we PGE synthase have been well documented in the regula- examined their levels of expression as well as the presence tion of various aspects of tumor progression and metastasis. of activating BRAF/NRAS mutations in metastatic lymph Aberrant or increased expression of COX-2 has been impli- nodes from stage III cutaneous melanoma. Moreover, our data revealed that inhibition of tumor-derived PGE 2 by COX-2 siRNA suppressed uPA and VEGF expression, suggesting that PGE 2, both tumor-derived and exogenous, regulates this process in prostate cancer cells. Angiogenesis is one of the most crucial steps in the development of tumor. The proliferation and migration of endothelial cells play crucial roles in the regulation of. Elevated cyclooxygenase‐2 (COX‐2) expression is observed in a variety of premalignant neoplastic tissues, suggesting COX‐2 expression might serve as a potential indicator of subsequent tumor develo..
Overexpression of SphK1 in human colon cancer xenografts enhances tumor growth. SphK1 and COX-2 intensity tended to reduce overall survival of late stage colon cancer patients. Previously, our group discussed the role of SphK1 and S1P in dextran sulfate sodium (DSS)-induced colitis, AOM-induced aberrant crypt foci (ACF, colonic preneoplastic lesion) and AOM/DSS-induced inflammation-related. Cyclooxygenase (COX)-2-derived prostanoids can influence several processes that are linked to carcinogenesis. We aimed to address the hypothesis that platelets contribute to aberrant COX-2 expression in HT29 colon carcinoma cells and to reveal the role of platelet-induced COX-2 on the expression of proteins involved in malignancy and marker genes of epithelial-mesenchymal transition (EMT)
Purpose: Cyclooxygenase-2 (COX-2) and its enzymatic product prostaglandin E2 (PGE 2) possess tumor-promoting activity, and COX-2 is considered as a candidate for targeted cancer therapy. However, several randomized clinical trials using COX-2 inhibitors to treat advanced lung cancer have failed to improve survival indices. To employ a more effective therapeutic strategy to inhibit the COX-2. In preclinical studies, tumors that consitutively expressed the protein indoleamine 2,3-dioxygenase (IDO1) responded to the cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) and had improved. T1 - Tumor COX-2 expression and prognosis of patients with resectable pancreatic cancer. AU - Matsubayashi, Hiroyuki. AU - Infante, Jeffrey R. AU - Winter, Jordan. AU - Klein, Alison P. AU - Schulick, Richard. AU - Hruban, Ralph. AU - Visvanathan, Kala. AU - Goggins, Michael. N1 - Funding Information: This work was supported by the NCI grant (CA90709, CA62924) and the Michael Rolfe Foundation. Cyclooxygenase-2 (COX-2, PTGS2) is an enzyme involved in the synthesis of prostaglandins and thromboxanes, which are regulators of biologic processes such as inflammation, cell proliferation and angiogenesis. COX-2 over-expression was reported in many (pre) malignant tissues, but data strongly vary and seem to depend on the methodology used. Normal colorectal mucosa and paired cancerous tissue from 60 patients with colorectal cancer was investigated for the levels of COX-2 mRNA by.
Tumor onset, multiplicity and cell proliferation were suppressed inCOX-2 MEC KO tumors.COX-2 MEC KO tumors aredenoted as KO. (A) Percent of tumor free mice against weeks of age. Meantumor free time for COX-2 MEC KO mice was 29 weeks versus 23 weeks forWT (left graph, n = 13 to 19). The right graph shows tumormultiplicity as number of tumors per mice at necroscopy (n = 14 to18) However, we did not observe significant reduction of COX-2 expression in xenograft tumors by treatment of ZD1839 or celecoxib alone, or the combination treatment compared with the control using immunohistochemical analysis. One possible explanation is that the dosage for ZD1839 or celecoxib used in this study may not be high enough to reduce COX-2 expression levels in tumor cells. The.
Our study shows that COX-2 inhibition by CXB has no detectable consequences for various molecular and cellular markers of tumor growth in several glioblastoma and pancreatic carcinoma cell lines with variable levels of COX-2 expression. Inhibition of COX-2 per se is neither required nor sufficient to implement the acutely growth-inhibitory and cytotoxic effects of celecoxib, nor does it. COX-2 seems to be involved in the processes of malignant transformation and tumor progression by affecting cell proliferation, mitosis, cell adhesion, apoptosis, immune-surveillance, and angiogenesis. 73 COX-2 protein expression has been described in several canine tumors. 11,28,29,41,51 Even though the role of COX-2 and its derived metabolites in tumorigenesis appears clear, the prognostic. The COX-2 expression IHC scoring was performed based on the percentage of COX-2 positive tumor cells and intensity of staining. Sum of intensity score was categorized as follows; 1% - 5%: (1) indicating weak expression, 5% - 50%; (2) indicating moderate expression and > 50%; (3) indicating severe expression. Tumors with sum score ≥ 2 were considered positive . Figure 3. IHC study showing: A. In einer anderen Studie wurde die Wirksamkeit des COX-2-Hemmers Rofecoxib bei hepatocellulärem Karzinom geprüft. Dahinter steht der Gedanke, dass sehr viele Tumoren die Cyclooxygenase-2.
Our present results indicate that tissue 11βHSD2 activity contributes to increased COX-2 expression in colorectal tumors and that inhibition of 11βHSD2 activity in vivo suppresses COX-2-derived PGE 2 production and colorectal tumor growth as a result of increased intracellular active glucocorticoids (Figure (Figure7). 7) Our results indicate that COX-2 expression modulates the expression of many extracellular matrix components, including collagen, glycoproteins (e.g., THBS-1), hyaluronan, and proteoglycans (e.g., lumican). It is therefore possible that tumor-derived COX-2 modifies the extracellular matrix enabling tumors to successfully establish metastases. Modification of the extracellular matrix by microenvironment-derived COX-2 could also explain why tissues with active inflammatory processes, such as.
However, the role of primary tumor tissue, the metastasis, in the cultured tumor COX-2 expression in cervical lymph node metastases of cells by standard immunohistochemistry, as well as head and neck cancer has not been clarified yet. cytochemistry. Patient and methods We comment on a male patient aged Conclusions A simultaneous expression of COX-2 in head 53 who was admitted to an ENT. Most of the cardiovascular toxicities appear to be related to the effects of these agents on non-tumor COX-2 inhibitors (eg, aspirin, celecoxib) have a variety of effects on tumor and systemic vasculature. One mechanism whereby COX-2 overexpression might influence tumor biology is through effects on › Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations.
COX-2 in Murine Intestinal Tumors Dear Sir: Shattuck-Brandt et al.1 recently reported that cyclooxygenase (COX)-2 was localized to inﬂammatory cells and subepithelial myo-ﬁbroblasts within tumors from interleukin 10 knockout mice, mul-tiple intestinal neoplasia (Min) mice, and mice treated with azoxymethane. We showed previously that a population of tumor COX-2/PGE2 pathway is known to play pivotal role in inflammation-induced gastric tumorigenesis. The neutrophils and lymphocytes infiltration was suppressed significantly, and the mRNA levels of the proinflammatory cytokines COX-2, IL-1β and IL-12b were also downregulated in gastric mucosa. Additionally, immunohistochemical analysis showed that COX-2, EP2, Gαs and β-catenin, key factors involving in PGE2 signal transduction, were positive staining with higher H scores in Non. Tumors with PR and with degree III of pathomorphosis after the treatment and disease recurrence are characterized by high levels of the COX-2 and VEGF expression but of low intensity. In patients with complete tumor regression after the treatment and without cervical cancer recurrence for more than 5 years no COX -2 and VEGF expressions were found The present study showed that oral mushroom beta-glucan treatment significantly increased IFN- γ mRNA expression but significantly reduced COX-2 mRNA expression within the lung. For LLC tumor model, oral Ganoderma lucidum or Antrodia camphorata polysaccharides treatments significantly reduced TGF- β production in serum Das Enzym COX 2 wird nämlich hauptsächlich im Rahmen von Entzündungen gebildet. Durch die COX-2-Hemmung wird die Entzündung (und damit die Schmerzen) gedämpft. Die COX-2-Hemmer bewirken nahezu ausschließlich eine Hemmung des Enzyms COX-2. Dies hat zur Folge, dass Nebenwirkungen durch eine zusätzliche COX-1-Hemmung (wie bei den NSAR) kaum auftreten. Stufe 1: Nichtsaure Schmerzmedikamente.
Verfahren zur Identifizierung eines humanen Tumors, der unempfindlich oder empfindlich bezüglich Capecitabin, ggf. in Kombination mit Docetaxel oder Paclitaxel oder Herceptin oder einem COX-2 Hemmer, vorzugsweise Celebrex, ist, insbesondere eines metastasierenden Karzinoms des Dickdarms oder der Brust oder eines anderen soliden Tumors, dadurch gekennzeichnet, dass in dem Gewebe dieses Tumors. COX-2-Expression in Tumoren beim Kleintier; Antineoplastische Wirkung von NSAID; Einsatz von NSAID in der Kleintieronkologie; Wahl des NSAID; Retinoide; Kryochirurgie. Grundlagen; Technik ; Durchführung; Indikationen und Kontraindikationen. Kryochirurgie ausgewählter Tumoren. Tumoren der Haut; Tumoren der Augen und Augenadnexen ; Tumoren der Mundhöhle; Tumoren des äußeren Ohres; Tumoren. High expression of COX-2 gene in tumours is more related to tumour aggressive behaviour and a worse prognosis. Results: There are five mechanisms that the COX-2 enzyme applies to develop tumours and increase the malignant phenotype of tumour cells: 1- Apoptosis inhibition 2- Angiogenesis increase 3- Invasion rise 4- Inflammation modulation/weakened immunity, suppression 5- Procarcinogen. Depending on tumor type, initial analysis showed that IDO1 was constitutively expressed by 10% to 50% of human tumors. IDO1 expression and COX-2/PGE2 axis activation were found to be associated in. Both COX-2 and PGE 2 are highly expressed in extremely aggressive tumors and are associated with invasion and angiogenesis[13, 14]. Interestingly, in breast cancer, tumor cells that over-express COX-2 have the unique ability to form VM and their activity of signaling pathway COX-2/PGE 2 /EP 3 are activated. However, whether TAMs can directly induce VM formation in GBMs is still unknown. In this study, we evaluated the relationship between macrophages infiltration and VM expression in glioma. decreased COX-2 expression and activity in colonic adenomas and tumors and significantly suppressed adenoma and tumor growth. These findings suggest an important role for 11βHSD2 in regulation of COX-2 expression in colonic tumors and identify 11βHSD2 as a possible target for prevention and/or therapy of colorectal cancer. Result