Reduction of tumor progression and paraneoplastic syndrome development in murine lung adenocarcinoma by nonsteroidal antiinflammatory drugs

Peluffo, Guillermo; Stillitani, Isabel; Rodríguez, Vanina; Diament, Miriam J.; Klein, Slobodanka

doi:10.1002/ijc.20226

Cited by 39 publications

(38 citation statements)

References 27 publications

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“…Kwak et al also showed that celecoxib reduced MMP-2 and MMP-9 in a squamous cell carcinoma and inhibited migration through a collagen matrix [87]. In a mouse model of lung adenocarcinoma both indomethacin and celecoxib significantly reduced MMP-9 activity and migration/invasion of malignant cells [88]. Since Cox-2 activity appears to have some control over MMP expression and invasion of tumor cells, it is hopeful that Cox inhibitors can curb metastasis of hematological malignancies.…”

Section: Cox-2/pge 2 Promotes Angiogenesis and Metastasismentioning

confidence: 99%

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Bernard¹,

Bancos²,

Sime³

et al. 2008

CPD

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There is much interest in the potential use of Cox-2 selective inhibitors in combination with other cancer therapeutics. Malignancies of hematopoietic and non-hematopoietic origin often have increased expression of cyclooxygenase-2 (Cox-2), a key modulator of inflammation. For example, hematological malignancies such as chronic lymphocytic leukemia, chronic myeloid leukemia, Hodgkin's lymphoma, non-Hodgkin's lymphoma and multiple myeloma often highly express Cox-2, which correlates with poor patient prognosis. Expression of Cox-2 enhances survival and proliferation of malignant cells, while negatively influencing anti-tumor immunity. Hematological malignancies expressing elevated levels of Cox-2 potentially avoid immune responses by producing factors that enhance angiogenesis and metastases. Cellular immune responses regulated by natural killer cells, cytotoxic T lymphocytes, and T regulatory cells are also influenced by Cox-2 expression. Therefore, Cox-2 selective inhibitors have promising therapeutic potential in patients suffering from certain hematological malignancies.

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Section: Cox-2/pge 2 Promotes Angiogenesis and Metastasismentioning

confidence: 99%

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Bernard¹,

Bancos²,

Sime³

et al. 2008

CPD

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show abstract

“…Other studies demonstrated that celecoxib and sulindac exerted antiangiogenic effects by inhibiting proliferation of human umbilical vein endothelial cells, 86 and by inhibiting activities of other proangiogenic factors, such as matrix metalloprotease 2 and 9, and the early growth response factor Egr-1. [87][88][89] Aspirin, at therapeutic concentrations, was found to inhibit tube formation in a 3-dimensional collagen angiogenesis model, via a COX-independent mechanism, which may contribute to its cancer chemoprotective effects. 90 The question of exactly how statins and NSAIDs work in a synergistic fashion to produce enhanced anticarcinogenic effects is largely unresolved.…”

Section: Mechanisms Of Actionsmentioning

confidence: 99%

Combination regimen with statins and NSAIDs: A promising strategy for cancer chemoprevention

Xiao

Yang

2008

Intl Journal of Cancer

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Statins and nonsteroidal antiinflammatory drugs (NSAIDs) are commonly prescribed for lowering cholesterol and antiinflammation, respectively. Recently, their potential roles as cancer chemopreventive agents have been subject to intensive studies. Human trials have not provided conclusive results on the protective effects of statins against different cancers, while more convincing results have been observed for cancer preventive effects of NSAIDs, especially on colorectal cancer. A promising strategy to enhance the cancer preventive efficacy of statins and NSAIDs is to use them in combination, which may produce synergy and lower the dose required for each agent. This strategy is of particular interest for potential use of low doses of statins and NSAIDs on a long-term basis for cancer chemoprevention; increased risks for gastrointestinal and cardiovascular side effects associated with the use of NSAIDs have been observed in colorectal cancer chemopreventive trials. This article reviews the evidence for the cancer preventive actions of statins and NSAIDs, as well as their possible synergistic action and the mechanisms involved. ' 2008 Wiley-Liss, Inc.Key words: statins; NSAIDs; cancer chemoprevention While the mortality from major chronic diseases, such as cardiovascular and cerebrovascular diseases, has decreased substantially during the past half century in the United States, the mortality from cancer has just begun to show a slight decrease. Cancer has become the number one killer of both men and women under age 85 years in the United States.1 A promising approach to controlling cancer is to prevent it before malignant events have occurred.2 Cancer chemoprevention refers to the use of natural or synthetic substances to inhibit, retard or reverse the carcinogenesis.3 A wealth of evidence from preclinical studies have convincingly demonstrated the cancer preventive efficacy of various agents in different animal models. However, the data from observational, case-control, cohort studies, and randomized trials in humans have overall demonstrated mixed results. Statins and nonsteroidal antiinflammatory drugs (NSAIDs) have been reported to be potential cancer chemopreventive agents. This review focuses on an attractive approach of chemoprevention using the combination of statins and NSAIDs. Statin and cancer chemopreventionStatins are small-molecule inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which are widely used as cholesterol-lowering drugs. Besides their use in the treatment of lipid disorders, statins have showed anticarcinogenic activities in many in vitro and in vivo preclinical studies, and attracted much attention in exploring their roles in cancer chemoprevention. Several observational human studies reported potential protective effects of statin use against overall risk of cancer, 4-6 whereas other studies did not 7,8 (Table I). In a case-control study in Quebec, Canada, statin use was found to be associated with a 28% reduction in the risk of developing cancer (RR 5 0.72, 95% ...

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“…PGE 2 also increases production of inducible nitric oxide synthetase, an enzyme involved in free radical generation (44). Further evidence for a role of COX-2 in cancer formation comes from the observation that carcinogenesis is inhibited in mice treated with COX-2-selective inhibitors and in COX-2 knockout mice (45,46). Hence, neoplastic transformation may be initiated by DNA damage incurred by cells as a result of free radical generation.…”

Section: The Inflammation-cancer Linkmentioning

confidence: 99%

Inflammation and Endometrial Cancer: A Hypothesis

Modugno

Ness

Chen

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

224

201

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Endometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E 2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk factors for endometrial cancer-unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early menarche, and late menopause-may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14 (12):2840 -7)

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Reduction of tumor progression and paraneoplastic syndrome development in murine lung adenocarcinoma by nonsteroidal antiinflammatory drugs

Cited by 39 publications

References 27 publications

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Targeting Cyclooxygenase-2 in Hematological Malignancies: Rationale and Promise

Combination regimen with statins and NSAIDs: A promising strategy for cancer chemoprevention

Inflammation and Endometrial Cancer: A Hypothesis

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