Prostaglandins, their inhibitors and cancer

Lupulescu, A.

doi:10.1016/s0952-3278(96)90064-2

Cited by 119 publications

(50 citation statements)

References 81 publications

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“…Experimental data are supportive of this hypothesis and also suggest that NSAIDs might provide protection against cancers of the mammary gland, skin and liver as well as the urinary bladder (Moon et al, 1992;Kelloff et al, 1994;Giardiello et al, 1995;Denda et al, 1997). The preventive mechanisms remain to be elucidated in detail but have been postulated to involve their inhibition of cyclooxygenase (COX), thereby inhibiting production of prostaglandins which influence tumour growth through both by stimulating cell proliferation and by disturbing immunological surveillance (Marnett, 1992;Giardiello et al, 1995;Lupulescu, 1996). There are two COX isoenzymes in humans, COX-1 and COX-2, and limited evidence suggests that COX-2 is the pivotal COX enzyme involved in carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…COX-2, in contrast to the constitutively expressed COX-1 which contributes to physiological functions in most tissues, is inducible and has proven involvement in inflammatory responses and cell proliferation (Herschman, 1994). It is known that COX-2 is highly expressed in colon, stomach, skin and mammary tumours (Kargman et al, 1995;Müller-Decker et al, 1995;DuBois et al, 1996;Liu et al, 1996;Ristimäki et al, 1997), in conjunction with increased levels of prostaglandins (Lupulescu, 1996).…”

Section: Discussionmentioning

confidence: 99%

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Non-steroidal anti-inflammatory drugs and bladder cancer prevention

et al. 2000

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Summary Inclusion of phenacetin among 'proven' human carcinogens by the IARC in 1987, raised concerns about the carcinogenic potential of acetaminophen, its major metabolite. Acetaminophen has been implicated as a possible causal agent in the development of cancer of the renal pelvis. The bladder and renal pelvis, which derive from the same embryological structure, share the same transitional type of epithelium. Past studies have been inconclusive on the possible relationship among these analgesics and bladder cancer but no large, highly detailed study of this association has been conducted. A population-based case-control study conducted in Los Angeles, California, involved 1514 incident bladder cancer cases and an equal number of controls who were matched to the index cases by sex, date of birth (within 5 years) and race. Detailed information on medication use and prior medical conditions was collected through in-person interviews. Regular use of analgesics was not associated with an increased risk of bladder cancer in either men or women. In fact, compared with non-or irregular users, regular analgesic users were at a decreased risk of bladder cancer overall (odds ratio (OR) = 0.81, 95% confidence interval (CI) = 0.68-0.96). However, there were clear differences in both the direction and strength of the associations between the different formulation classes of analgesics and bladder cancer risk. Intake of phenacetin was positively related to bladder cancer risk in a dose-dependent manner while intake of its major metabolite in humans, acetaminophen, was unrelated to risk. Intake of all classes of NSAIDs, except pyrazolon derivatives, were negatively associated with bladder cancer risk, with suggestive evidence that the protective effect varies in strength by subcategories of formulation. Acetic acids seemed to exhibit the strongest protective effect, whereas aspirin/other salicylic acids and oxicam showed the weakest protection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Non-steroidal anti-inflammatory drugs and bladder cancer prevention

et al. 2000

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“…PBMC were cultured with 10 −6 M JTE-522 (Fig. 2a), in 10 −6 M JTE-522 with KB cells (2×10 6 ) directly in contact with PBMC (Fig. 2b), in normal medium with KB cells separated with Biocoat Cell Culture Inserts (Becton Dickinson Labware; Fig.…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

“…The inhibition of COX and PGs has been postulated to be one of the chemopreventive mechanisms by directly intervening in the signal cascade for cell proliferation or by disturbing immunological surveillance. 2,5,6) However, prolonged use of the drugs frequently results in untoward gastrointestinal side effects, which has led to the development of more selective COX inhibitors. 7) Two isoforms of COX, COX-1 and COX-2, have been identified and they are rate-limiting enzymes involved in the conversion of arachidonic acid to prostanoids.…”

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confidence: 99%

A Selective Cyclooxygenase‐2 Inhibitor Suppresses Tumor Growth in Nude Mouse Xenografted with Human Head and Neck Squamous Carcinoma Cells

Nishimura

Yanoma

Mizuno

et al. 1999

Japanese Journal of Cancer Research

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The anti-tumor effect of a selective cyclooxygenase (COX)-2 inhibitor, JTE-522, was examined with the human head and neck squamous cell carcinoma cell line KB. KB cells do not produce prostaglandin (PG)-E2. In vitro, JTE-522 induced an increase of G1 phase-arrested cells, suppression of platelet-derived growth factor (PDGF) production and inhibition of telomerase activity. No cytotoxic effect was detected. In vivo, the growth of the tumor xenografted into nude mice was significantly suppressed by JTE-522. Suppression of angiogenesis at the periphery of the tumor, increase of G1-arrested cells and suppression of telomerase activity were observed, together with an increase of apoptotic cell death in the tumor. Immunological enhancement did not play a role. We concluded that the anti-tumor effect of JTE-522 was caused by anti-angiogenesis action, cell cycle arrest and inhibition of telomerase activity of the tumor cells. These combined effects might induce apoptosis.Key words: Head and neck squamous carcinoma cells -Selective cyclooxgenase-2 inhibitor -Cell cycle arrest -Anti-angiogenesis -Telomerase activity inhibition Nonsteroidal anti-inflammatory drugs (NSAIDs) are promising candidates for chemopreventive agents active against the development of cancers in the colon, the bladder, the mammary gland, the skin, and the liver.

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“…COX-2 and PGE 2 play important roles in the development and progression of malignancies. Levels of COX-2 and PGE 2 are increased in both intraepithelial neoplasia and multiple cancers (3)(4)(5)(6)8). The development and growth of experimental tumors are suppressed by treatment with selective COX-2 inhibitors (3, 9-11).…”

Section: Introductionmentioning

confidence: 99%

Elevated Levels of Urinary PGE-M Are Found in Tobacco Users and Indicate a Poor Prognosis for Oral Squamous Cell Carcinoma Patients

Kekatpure

Wang

et al. 2016

Cancer Prevention Research

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Cyclooxygenase-2 (COX-2)-derived prostaglandin E 2 (PGE 2 ) plays a role in the development and progression of epithelial malignancies. Measurements of urinary PGE-M, a stable metabolite of PGE 2 , reflect systemic PGE 2 levels. Here, we investigated whether urinary PGE-M levels were elevated in healthy tobacco users and in patients with oral squamous cell carcinoma (OSCC). Median urinary PGE-M levels were increased in healthy tobacco quid chewers [21.3 ng/mg creatinine (Cr); n ¼ 33; P ¼ 0.03] and smokers (32.1 ng/mg Cr; n ¼ 31; P < 0.001) compared with never tobacco quid chewers-never smokers (18.8 ng/mg Cr; n ¼ 30). Urinary PGE-M levels were also compared in OSCC patients versus healthy tobacco users. An approximately 1-fold increase in median urinary PGE-M level was found in OSCC patients (48.7 ng/mg Cr, n ¼ 78) versus healthy controls (24.5 ng/mg Cr, n ¼ 64; P < 0.001). We further determined whether baseline urinary PGE-M levels were prognostic in OSCC patients who underwent treatment with curative intent. A nearly 1-fold increase in baseline urinary PGE-M levels (64.7 vs. 33.8 ng/mg Cr, P < 0.001) was found in the group of OSCC patients who progressed (n ¼ 37) compared with the group that remained progression free (n ¼ 41). Patients with high baseline levels of urinary PGE-M had both worse disease-specific survival [HR, 1.01 per unit increase; 95% confidence interval (CI), 1.01-1.02; P < 0.001] and overall survival (HR, 1.01 per unit increase; 95% CI, 1.00-1.02; P ¼ 0.03). Taken together, our findings raise the possibility that NSAIDs, prototypic inhibitors of PGE 2 synthesis, may be beneficial for reducing the risk of tobacco-related aerodigestive malignancies or treating OSCC patients with high urinary PGE-M levels. Cancer Prev Res; 9(6); 428-36. Ó2016 AACR.

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Prostaglandins, their inhibitors and cancer

Cited by 119 publications

References 81 publications

Non-steroidal anti-inflammatory drugs and bladder cancer prevention

Non-steroidal anti-inflammatory drugs and bladder cancer prevention

A Selective Cyclooxygenase‐2 Inhibitor Suppresses Tumor Growth in Nude Mouse Xenografted with Human Head and Neck Squamous Carcinoma Cells

Elevated Levels of Urinary PGE-M Are Found in Tobacco Users and Indicate a Poor Prognosis for Oral Squamous Cell Carcinoma Patients

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