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At least 37 records · Page 2Linked to original sources
PubMed1989

Inhibitory effects of non-steroidal anti-inflammatory drugs, piroxicam and indomethacin on 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in male ACI/N rats.

The effects of the non-steroidal anti-inflammatory drugs (NSAIDs), piroxicam and indomethacin on 4-nitroquinoline 1-oxide-(4-NQO)-induced tongue carcinogenesis in male ACI/N rats were examined. Rats were given 4-NQO (10 ppm) in the drinking water for 12 weeks and followed by either diet containing 150 ppm piroxicam or the drinking water containing 10 ppm indomethacin for 24 weeks. The incidence of tongue neoplasms (squamous cell papilloma and carcinoma) in rats given 4-NQO plus piroxicam (4/13, 31%) and those given 4-NQO plus indomethacin (3/13, 23%) were significantly lower than that of animals given 4-NQO alone (12/17, 71%) (P less than 0.05 and P less than 0.005). Rats given piroxicam or indomethacin alone had no neoplasms in the tongue. Thus, piroxicam and indomethacin significantly inhibited the development of tongue neoplasms in male ACI/N rats.

4-Nitroquinoline-1-oxide↗
PubMed1994

Chemoprevention of 4-nitroquinoline 1-oxide-induced oral carcinogenesis by dietary protocatechuic acid during initiation and postinitiation phases.

The modifying effects of three doses of dietary protocatechuic acid (PCA) given the initiation and postinitiation phases of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. At 6 weeks of age, rats were divided into experimental and control groups and fed the diet containing PCA at various doses of 0 g/kg diet (basal diet alone), 0.5 g/kg diet (500 ppm), 1 g/kg diet (1000 ppm), and 2 g/kg diet (2000 ppm). At 7 weeks of age, all animals except PCA alone and control groups were given 4-NQO (20 ppm) in the drinking water for 8 weeks to induce oral cancer. Seven days after the 4-NQO exposure, groups of animals fed the PCA diets were switched to the basal diet and continued on this diet until the end of the study. Starting 1 week after the end of 4-NQO exposure, the groups given 4-NQO and a basal diet were switched to the diets containing PCA and maintained on these diets for 22 weeks. The other groups consisted of rats given 2000 ppm PCA alone or untreated rats. All animals were necropsied at the termination of the experiment (week 32). The incidences of tongue neoplasms and preneoplastic lesions, polyamine levels in the tongue tissue, and cell proliferation activity estimated by bromodeoxyuridine-labeling index and by morphometric analysis of silver-stained nucleolar organizer regions' protein were compared among the groups. Feeding of PCA at all doses during initiation or postinitiation phase significantly decreased the development of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplasia (hyperplasia and dysplasia) (P < 0.05). There were no such lesions in rats treated with 2000 ppm PCA alone or those in an untreated control group. Dietary administration of PCA also caused significant decreases in the labeling index of bromodeoxyuridine and the number and area of silver-stained nucleolar organizer regions per cell nucleus, known as cell proliferation indices, of the tongue squamous epithelium (P < 0.05). In addition, PCA exposure during either initiation or postinitiation phase decreased polyamine levels in the oral mucosa (P < 0.05). These results clearly indicated that PCA inhibited rat oral carcinogenesis in both initiation and postinitiation phases, when administered in these respective phases together with or following treatment with 4-NQO, and such inhibition might be related to suppression of cell proliferation by PCA.

4-Nitroquinoline-1-oxide↗
PubMed2005

Dietary garcinol inhibits 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in rats.

The effects of dietary feeding with a polyisoprenylated benzophenone, garcinol, isolated from Garcinia indica fruit rind on the development of 4-nitroquinoline 1-oxide (4-NQO)-induced oral carcinogenesis were investigated in male F344 rats. At 7 weeks of age, animals were given 4-NQO at 20 ppm in the drinking water for 8 weeks to induce tongue neoplasms. They also received the diets containing 100 or 500 ppm garcinol either during (for 10 weeks) or after (for 22 weeks) the carcinogen exposure. The other rats were given tap water without 4-NQO throughout the experiment, and fed garcinol (500 ppm)-containing diet or basal diet alone. At the end of the study (week 32), incidences of tongue neoplasms and preneoplastic lesions, cell proliferation activity in the normal-like tongue epithelium estimated by 5-bromodeoxyurideine (BrdU)-labeling index and cyclin D1-positive cell ratio, and immunohistochemical expression of cyclooxygenase-2 (COX-2) in the tongue lesions were determined. Dietary garcinol significantly decreased the incidence and multiplicity of 4-NQO-induced tongue neoplasms and/or preneoplasms as compared to the control diet. Dietary administration of garcinol also significantly reduced the BrdU-labeling index and cyclin D1-positive cell ratio, suggesting reduction in cell proliferation activity in the tongue by garcinol. The COX-2 expression in the tongue lesions was also suppressed by feeding with garcinol. These results indicate that dietary administration of garcinol inhibited 4-NQO-induced tongue carcinogenesis through suppression of increased cell proliferation activity in the target tissues and/or COX-2 expression in the tongue lesions.

4-Nitroquinoline-1-oxide↗
PubMed1993

Inhibition of 4-nitroquinoline-1-oxide-induced rat tongue carcinogenesis by the naturally occurring plant phenolics caffeic, ellagic, chlorogenic and ferulic acids.

The modifying effects of dietary administration of the plant phenolic antioxidants caffeic acid (CA), ellagic acid (EA), chlorogenic acid (CGA) and ferulic acid (FA) during the initiation phase on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and on the number and area of silver-stained nucleolar organizer region proteins (AgNORs), a new cell proliferation marker, of the tongue squamous epithelium were investigated in male F344 rats. Rats were fed the diet containing 500 p.p.m. CA, 400 p.p.m. EA, 250 p.p.m. CGA or 500 p.p.m. FA for 7 weeks. One week after the commencement of the diets, 4-NQO (20 p.p.m.) was administered in the drinking water for 5 weeks. Feeding of four phenolic compounds significantly reduced the incidences of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplastic lesions (hyperplasia and dysplasia) by 32 weeks, and rats fed CA or EA had no tongue neoplasms. The number and area of AgNORs per nucleus were decreased significantly by dietary treatment with these four phenolics. Thus, CA, EA, CGA and FA inhibited the tongue carcinogenesis induced by 4-NQO when they were administered concurrently with the carcinogen. These results might suggest possible application of these natural substances for cancer chemoprevention in tongue in addition to other tissues (skin, lung, liver and esophagus).

4-Nitroquinoline-1-oxide↗
PubMed2003

Inhibitory effects of troglitazone, a peroxisome proliferator-activated receptor gamma ligand, in rat tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide.

Ligands for peroxisome proliferator-activated receptor (PPAR) gamma have been implicated in growth inhibition and cell differentiation in certain malignancies. In this study, the effects of troglitazone, a PPAR gamma ligand, given during the postinitiation phase of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. Rats aged 6 weeks were given 4-NQO at 20 ppm for 8 weeks to induce tongue neoplasms. Starting 1 week after the cessation of 4-NQO exposure, animals were fed diets containing 0, 30 or 100 ppm troglitazone for 22 weeks. At the end of the study (week 32), the incidences of 4-NQO-induced tongue neoplasms and preneoplasms were determined histopathologically and cell proliferation activity was estimated by counting bromodeoxyuridine (BrdU)-labeling indices and cyclin D1-positive cell ratios. In addition, immunohistochemical expression of cyclooxygenase (COX)-2 and PPAR gamma was assessed in the tongue lesions. Feeding with 100 ppm troglitazone significantly decreased the incidence of squamous cell carcinoma when compared to the group without troglitazone treatment (5.0% vs. 45.8%, P < 0.005). Interestingly, the BrdU-labeling index and cyclin D1-positive cell ratio assessed in the non-lesional tongue squamous epithelium were reduced by dietary administration of troglitazone (P < 0.0001-0.005). Additionally, the immunoreactivity of COX-2 in the tongue lesions was also decreased by the treatment (P < 0.01-0.05). These results clearly showed that dietary troglitazone inhibits 4-NQO-induced tongue carcinogenesis and such inhibition is related to suppression of increased cell proliferation and/or COX-2 expression. This study warrants further investigation on the use of PPAR gamma ligands as a novel preventive approach for oral malignancy.

4-Nitroquinoline-1-oxide↗
PubMed1992

Inhibitory effects of the natural products indole-3-carbinol and sinigrin during initiation and promotion phases of 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis.

The modifying effects of indole-3-carbinol (I3C) and sinigrin (SIN) on the initiation and post-initiation phases of tongue carcinogenesis induced by 4-nitroquinoline 1-oxide (4-NQO) were investigated in male ACI/N rats. Rats were divided into eight groups: group 1 was given 4-NQO (10 ppm) in the drinking water for 12 weeks, starting at 7 weeks of age; groups 2 and 3 were given 4-NQO and fed the diets containing I3C (1,000 ppm) and SIN (1,200 ppm) for 14 weeks, respectively, starting at 6 weeks of age; groups 4 and 5 were given 4-NQO and then they were fed I3C and SIN containing diets for 23 weeks, respectively, starting one week after 4-NQO exposure; groups 6 and 7 were given I3C and SIN alone, respectively, during the experiment; group 8 served as an untreated control. At the termination of the experiment (week 37), the incidence of tongue neoplasms (squamous cell papilloma and carcinoma) in group 2 (1/15, 7%), group 3 (1/15, 7%), group 4 (3/15, 20%) or group 5 (2/15, 13%) was significantly smaller than that in group 1 (12/17, 71%) (P = 0.0003, P = 0.005 or P = 0.002). No tongue carcinomas developed in rats of groups 2, 3, and 5. Similarly, the incidence of preneoplastic lesions (hyperplasia and dysplasia) of the tongue in group 2 (11/15, 73%), group 3 (10/15, 67%), group 4 (11/15, 73%) or group 5 (10/15, 67%) was significantly lower than that in group 1 (17/17, 100%) (P = 0.04 or P = 0.02). There were no tongue neoplasms in rats of groups 6, 7, and 8. Administration of I3C and SIN also caused significant decreases in the number and area of silver-stained nucleolar organizer regions protein (AgNORs), a new cell proliferation index, of tongue squamous epithelium. Thus, I3C and SIN inhibited rat tongue carcinogenesis in both the initiation and post-initiation phases, when administered in these respective phases together with, or following treatment with, 4-NQO.

4-Nitroquinoline-1-oxide↗
PubMed2000

Chemopreventive effect of bovine lactoferrin on 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in male F344 rats.

The modifying effects of dietary feeding of bovine lactoferrin (bLF) on tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. The activities of phase II detoxifying enzymes, glutathione S-transferase (GST) and quinone reductase (QR), polyamine content and ornithine decarboxylase (ODC) activity in the tongue were also examined for mechanistic analysis of possible modifying effects of bLF on carcinogenesis. At 7 weeks of age, all animals except those treated with bLF alone and untreated rats were given 20 ppm 4-NQO in drinking water for 8 weeks to induce tongue neoplasms. Starting 7 days before 4-NQO exposure, experimental groups were fed experimental diets containing bLF (0.2% and 2%) for 10 weeks ("initiation feeding"). Starting 1 week after the cessation of exposure to 4-NQO, the other experimental groups given 4-NQO and a basal diet were fed the experimental diets for 22 weeks ("postinitiation feeding"). At week 32, the incidence and multiplicity of tongue neoplasms in the "initiation feeding" groups of 0.2% and 2% bLF and the "post-initiation feeding" group of 0.2% bLF were lower than those of the 4-NQO alone group, but without statistical significance. However, "post-initiation feeding" of 2% bLF caused a significant reduction in the incidence (20% vs. 55%, P=0.02418) and multiplicity (0.25+/-0.54 vs. 0.70+/-0.71, P<0.05) of tongue squamous cell carcinoma (by 64%, P=0.02418). bLF treatment elevated liver and tongue GST activities and liver QR activity. The "post-initiation feeding" with 2% bLF significantly decreased QR activity, proliferating cell nulcear antigen-positive index and ODC activity in the tongue. In addition, feeding with bLF decreased tongue polyamine content. These results suggest that bLF, when given at the 2% dose level during the post-initiation phase, exerts chemopreventive action against tongue tumorigenesis through modification of cell proliferation activity and/or the activities of detoxifying enzymes.

4-Nitroquinoline-1-oxide↗
PubMed1986

Sonography of the tongue and floor of mouth. Part II: Neoplasms of the tongue.

Frequently, correct evaluation of space-occupying lesions in the tongue is not possible with clinical methods only. In an attempt to assess the value of sonography in the detection of tongue lesions, we used submental sonography to examine 62 patients with suspicious palpatory findings upon physical examination of the tongue. Ultrasound detected 45 out of 47 tumours that were eventually confirmed either by surgery or by biopsy. Inadequate technique was the only factor that affected the detection rate. Sonography appears to be a reasonable guide in determining size and site of a tumour of the tongue. Thus, more precision in therapy planning may be achieved.

Aged↗
PubMed1989

Tongue metastasis from carcinoma of the rectum.

A case report of a patient with carcinoma of the rectum with metastasis to the tongue clinically mimicking a primary tongue neoplasm is described. The patient presented with an ulcer in the tongue three years after undergoing an anterior resection for a Dukes C carcinoma of the rectum. Other asymptomatic metastatic lesions were discovered only after the histology report suggested that the tongue ulcer biopsy was metastatic in origin. Metastatic tumour to the tongue is extremely rare and often occurs at a late stage, when there is disseminated disease. We are not aware of any reported case of tongue metastasis from carcinoma of the rectum.

Adenocarcinoma, Mucinous↗