Administration of a Prostaglandin Synthetase Inhibitor Associated With an Increased Immune Cell Infiltrate in Squamous Cell Carcinoma of the Head and Neck

Cross, David S.; Platt, Jeffrey L.; Juhn, Steven K.; Bach, Fritz H.; Adams, George L.

doi:10.1001/archotol.1992.01880050080019

Cited by 30 publications

(19 citation statements)

References 18 publications

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“…Indomethacin administration is associated with an increased immune cell infiltration in squamous cell carci¬ noma of the head and neck, suggesting that the inhibition of prostaglandin E2 may contribute to the homing ofmononuclear cells to the tumor. 19 Use of sunscreens3,20 and adherence to a diet low in fatty acids21 can help prevent actinic kératoses. How¬ ever, for existing lesions, 3% diclofenac in a 2.5% hyal¬ uronic acid gel shows promise as another topical agent for the treatment of active keratosis, and our findings sug¬ gest that a double-blind randomized study is warranted.…”

Section: Provocative Use Testmentioning

confidence: 99%

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

Rivers

McLean²

1997

Arch Dermatol

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Section: Provocative Use Testmentioning

confidence: 99%

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

Rivers

McLean²

1997

Arch Dermatol

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“…In one study, esophageal squamous cancer cell lines were found to produce prostaglandins of both the E and F series, and the cells that produced the greater amounts of each were more metastatic in athymic mice. Cross et al 80 examined two tongue-derived squamous cell lines and found both to make PGE 2 and PGI 2 (prostacyclin). Both cell lines produced levels of PGE 2 that were high enough to cause immunosuppressive effects on leukocytes.…”

Section: Prostaglandin Metabolism In Cell Linesmentioning

confidence: 99%

“…Recently, Suen and Simonton-Atchley 93 reported on additional patients who experienced similar regres-sions with cyclooxygenase inhibition. Cross et al 80 demonstrated that treatment of patients for 2 weeks with indomethacin before head and neck cancer resection is associated with increased numbers of immune cell infiltrates in affected lymph nodes. Braun and Harris 55 have conducted several studies with NSAID and have been able to reverse many immune defects in patients with a variety of solid tumors.…”

Section: Clinical Studies With Prostaglandin Synthesis Inhibitorsmentioning

confidence: 99%

Arachidonic acid metabolism: A primer for head and neck surgeons

Ondrey

1998

Head & Neck

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“…The antitumor effect of indomethacin on tumors in cancer patients 1,2) and in animals 3,4) has been described. We previously showed that indomethacin suppresses the growth of Colon 26 tumor in mice by enhancing the cellular immune function and improving cancer cachexia.…”

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confidence: 99%

Indomethacin Suppresses the Growth of Colon 26, Meth‐A and FM3A Tumors in Mice by Reducing the Prostaglandin E₂ Content and Telomerase Activity in Tumor Tissues

Ogino

Higuchi

Murata³

et al. 1999

Japanese Journal of Cancer Research

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The antitumor effect of indomethacin on Colon 26, Meth-A and FM3A tumors was investigated in mice. The prostaglandin E 2 content in tumor tissues was assayed to find out if indomethacin acts on tumors, and the telomerase activity in tumors and somatic tissues (testis, liver, spleen and colon) was also monitored during indomethacin treatment. Growth of Colon 26, Meth-A and FM3A tumors was significantly (P< < < <0.001-0.05) suppressed by indomethacin compared to the untreated controls. The prostaglandin E 2 content in the three tumors was markedly (P< < < <0.001) reduced by indomethacin. Telomerase activity in Colon 26 and FM3A tumors was significantly (P< < < <0.001) lower than that of untreated tumors (80% and 45% decrease versus the controls, respectively), and the activity in Meth-A tumor was slightly decreased (10% decrease versus the control) by indomethacin. Telomerase activity in the somatic tissues was not significantly affected by indomethacin. In summary, this study shows the effectiveness of indomethacin as an antitumor agent against three types of tumors, and suggests that indomethacin affects telomerase activity in tumors in vivo.Key words: Indomethacin -Prostaglandin E 2 -Telomerase activity -Fluorescence-based telomeric repeat amplification protocolThe antitumor effect of indomethacin on tumors in cancer patients 1, 2) and in animals 3, 4) has been described. We previously showed that indomethacin suppresses the growth of Colon 26 tumor in mice by enhancing the cellular immune function and improving cancer cachexia. 5)Indomethacin does not have a cytotoxic effect on Colon 26 tumor cells in vitro, 5) but it may have an antitumor effect via immunological pathways. We previously reported that indomethacin treatment of tumors reduces tumor size less in nude mice (deficient in T-lymphocytes) than in normal mice, compared with untreated tumors. 6)Although these results indicate that the effectiveness of indomethacin as an antitumor agent is, at least in part, due to its modification of T-cell-mediated immune functions, the precise mechanism of tumor growth suppression by indomethacin remains unknown.Recent studies have shown that many proliferating tumor cells retain a certain level of telomerase activity. [7][8][9] We previously reported that tumor growth in Colon 26-bearing mice is significantly suppressed by indomethacin treatment compared with the untreated controls, and that the telomerase activity declines preferentially in tumor tissues, while telomerase activity in somatic tissues is not significantly affected by indomethacin treatment.10) More recently, Kido et al. 11) reported that tumor size reduction by cisplatin treatment correlates with a decline in telomerase activity in tumor tissues.In this study, we transplanted Colon 26, Meth-A and FM3A tumors into normal mice to assess if the effect of indomethacin is independent of tumor cell type. Prostaglandin E 2 synthesis is inhibited by indomethacin, and therefore we measured the prostaglandin E 2 content in tumors to confirm the effect of ind...

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Administration of a Prostaglandin Synthetase Inhibitor Associated With an Increased Immune Cell Infiltrate in Squamous Cell Carcinoma of the Head and Neck

Cited by 30 publications

References 18 publications

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

Arachidonic acid metabolism: A primer for head and neck surgeons

Indomethacin Suppresses the Growth of Colon 26, Meth‐A and FM3A Tumors in Mice by Reducing the Prostaglandin E₂ Content and Telomerase Activity in Tumor Tissues

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Administration of a Prostaglandin Synthetase Inhibitor Associated With an Increased Immune Cell Infiltrate in Squamous Cell Carcinoma of the Head and Neck

Cited by 30 publications

References 18 publications

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

An Open Study to Assess the Efficacy and Safety of Topical 3% Diclofenac in a 2.5% Hyaluronic Acid Gel for the Treatment of Actinic Keratoses

Arachidonic acid metabolism: A primer for head and neck surgeons

Indomethacin Suppresses the Growth of Colon 26, Meth‐A and FM3A Tumors in Mice by Reducing the Prostaglandin E2 Content and Telomerase Activity in Tumor Tissues

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Indomethacin Suppresses the Growth of Colon 26, Meth‐A and FM3A Tumors in Mice by Reducing the Prostaglandin E₂ Content and Telomerase Activity in Tumor Tissues