[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 20 of about 20
1. Aframian DJ, Redman RS, Yamano S, Nikolovski J, Cukierman E, Yamada KM, Kriete MF, Swaim WD, Mooney DJ, Baum BJ: Tissue compatibility of two biodegradable tubular scaffolds implanted adjacent to skin or buccal mucosa in mice. Tissue Eng; 2002 Aug;8(4):649-59
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue compatibility of two biodegradable tubular scaffolds implanted adjacent to skin or buccal mucosa in mice.
  • Radiation therapy for cancer in the head and neck region leads to a marked loss of salivary gland parenchyma, resulting in a severe reduction of salivary secretions.
  • To address this problem, we are using both tissue engineering and gene transfer principles to develop an orally implantable, artificial fluid-secreting device.
  • We implanted in Balb/c mice tubular scaffolds of poly-L-lactic acid (PLLA), poly-glycolic acid coated with PLLA (PGA/PLLA), or nothing (sham-operated controls) either beneath the skin on the back, a site widely used in earlier toxicity and biocompatibility studies, or adjacent to the buccal mucosa, a site quite different functionally and immunologically.
  • Inflammatory responses in the connective tissue were similar regardless of site or type of polymer implant used.
  • These results indicate that the tissue responses to PLLA and PGA/PLLA scaffolds are generally similar in areas subjacent to skin in the back and oral cavity.
  • [MeSH-minor] Animals. Drug Implants. Female. Inflammation / metabolism. Mice. Mice, Inbred BALB C

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LACTIC ACID .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12202004.001).
  • [ISSN] 1076-3279
  • [Journal-full-title] Tissue engineering
  • [ISO-abbreviation] Tissue Eng.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Drug Implants; 0 / Polymers; 26009-03-0 / Polyglycolic Acid; 26100-51-6 / poly(lactic acid); 33X04XA5AT / Lactic Acid
  •  go-up   go-down


2. Rauck R, North J, Gever LN, Tagarro I, Finn AL: Fentanyl buccal soluble film (FBSF) for breakthrough pain in patients with cancer: a randomized, double-blind, placebo-controlled study. Ann Oncol; 2010 Jun;21(6):1308-14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fentanyl buccal soluble film (FBSF) for breakthrough pain in patients with cancer: a randomized, double-blind, placebo-controlled study.
  • BACKGROUND: Fentanyl buccal soluble film (FBSF) has been developed as a treatment of breakthrough pain in opioid-tolerant patients with cancer.
  • The objective of this study was to evaluate the efficacy of FBSF at doses of 200-1200 microg in the management of breakthrough pain in patients with cancer receiving ongoing opioid therapy.
  • PATIENTS AND METHODS: This was a multicenter, randomized, double-blind, placebo-controlled, multiple-crossover study that included opioid-tolerant adult patients with chronic cancer pain who experienced one to four daily episodes of breakthrough pain.
  • In this study, FBSF was well tolerated in the oral cavity, with no reports of treatment-related oral AEs.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Pain.
  • Hazardous Substances Data Bank. FENTANYL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pain. 2001 Mar;91(1-2):123-30 [11240084.001]
  • [Cites] Clin Pharmacokinet. 2002;41(9):661-80 [12126458.001]
  • [Cites] Palliat Med. 2004 Apr;18(3):177-83 [15198130.001]
  • [Cites] Pain. 1990 Jun;41(3):273-81 [1697056.001]
  • [Cites] J Clin Oncol. 1996 Oct;14(10):2836-42 [8874346.001]
  • [Cites] J Natl Cancer Inst. 1998 Apr 15;90(8):611-6 [9554444.001]
  • [Cites] Clin Drug Investig. 2009;29(10):647-54 [19715381.001]
  • [Cites] Pain. 2005 Mar;114(1-2):3-6 [15733625.001]
  • [Cites] Clin J Pain. 2006 Nov-Dec;22(9):805-11 [17057563.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2008;48:33-60 [17666008.001]
  • [Cites] Drugs. 2008;68(7):913-24 [18457459.001]
  • [Cites] Neuron. 2008 Jul 31;59(2):195-206 [18667148.001]
  • [Cites] Ann Oncol. 2009 Aug;20(8):1420-33 [19244085.001]
  • [Cites] J Am Med Assoc. 1955 Dec 24;159(17):1602-6 [13271123.001]
  • (PMID = 19940014.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 0 / Dosage Forms; 0 / Placebos; UF599785JZ / Fentanyl
  • [Other-IDs] NLM/ PMC2875549
  •  go-up   go-down


3. Saran R, Tiwari RK, Reddy PP, Ahuja YR: Risk assessment of oral cancer in patients with pre-cancerous states of the oral cavity using micronucleus test and challenge assay. Oral Oncol; 2008 Apr;44(4):354-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk assessment of oral cancer in patients with pre-cancerous states of the oral cavity using micronucleus test and challenge assay.
  • Oral cancer is a common malignancy, ranking first among all cancers in Western and Asian countries.
  • Oral cancer is preceded by some benign lesions or conditions, which are termed pre-cancerous.
  • Only one-third of people at the pre-cancerous stage of disease succumb to cancer.
  • No biomarker is available to identify people with pre-cancerous lesions or conditions at high risk of developing cancer.
  • The study included 129 untreated people with cancer, 138 untreated people at the pre-cancerous stage and 176 control participants.
  • MNT and comet assay were carried out on buccal epithelial cells.
  • A significant stepwise increase in the DNA damage (basal/MNNG-treated/post-repair) was observed in buccal epithelial cells and peripheral blood leucocytes from control to pre-cancer patients and from pre-cancer to cancer patients.
  • Considerable inter-individual and inter-cellular variability in DNA damage was observed, which increased from control to pre-cancer patients and from pre-cancer to cancer patients.
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosome Aberrations. Comet Assay / methods. DNA Damage. DNA Repair. DNA, Neoplasm / genetics. Disease Progression. Female. Humans. Leukocytes / drug effects. Leukocytes / pathology. Male. Methylnitronitrosoguanidine / pharmacology. Micronucleus Tests / methods. Middle Aged. Mouth Mucosa / pathology. Risk Assessment / methods

  • Genetic Alliance. consumer health - Oral cancer.
  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • Hazardous Substances Data Bank. N-METHYL-N'-NITRO-N-NITROSOGUANIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Oral Oncol. 2008 Jul;44(7):716-7 [18381248.001]
  • (PMID = 17936677.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 12H3O2UGSF / Methylnitronitrosoguanidine
  •  go-up   go-down


Advertisement
4. Fujiki H, Takeuchi H, Nishitani N, Yamanaka H, Suzuki K, Kurusu M, Suganuma M: Carcinogenic potential of tobacco tar-resistant Staphylococcus aureus in buccal cavity. J Cancer Res Clin Oncol; 2004 May;130(5):301-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinogenic potential of tobacco tar-resistant Staphylococcus aureus in buccal cavity.
  • PURPOSE: The effects of cigarette smoking on the association between inflammation and cancer were studied, since some bacteria induce the production of tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine and endogenous tumor promoter, in cells.
  • METHODS: Bacteria from a gargled solution from the buccal cavity of 20 individuals were cultured in the presence of 4 mg/ml cigarette-smoke condensates.
  • RESULTS: One tobacco tar-resistant S. aureus strain (Sa-TA10) induced expression of the TNF-alpha gene in both Bhas 42 cells (v-Ha-ras transfected BALB/3T3 cells) and human lung cancer cell line H226B, while one tobacco tar-resistant S. warneri (Sw-TA75) did not induce it significantly.
  • CONCLUSION: These data suggest that tobacco tar-resistant S. aureus, with carcinogenic potential, is present in the buccal cavity of some individuals, and that cigarette smoking simultaneously inhibits growth of most of the bacteria and selects carcinogenic bacteria.
  • [MeSH-major] Carcinogens / adverse effects. Drug Resistance, Bacterial. Mouth Mucosa / microbiology. Staphylococcus aureus / growth & development. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] 3T3 Cells / pathology. Adult. Animals. Cell Transformation, Neoplastic / drug effects. Cells, Cultured. Gene Expression. Humans. Lung Neoplasms / pathology. Mice. Mice, Inbred BALB C. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

  • MedlinePlus Health Information. consumer health - Antibiotic Resistance.
  • MedlinePlus Health Information. consumer health - Secondhand Smoke.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2004 Springer-Verlag
  • [Cites] Jpn J Cancer Res. 1995 Aug;86(8):749-55 [7559098.001]
  • [Cites] Cancer Res. 1996 Aug 15;56(16):3711-5 [8706012.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1404-7 [10197602.001]
  • [Cites] Cancer Res. 1993 May 1;53(9):1982-5 [8481899.001]
  • [Cites] Jpn J Cancer Res. 1999 Nov;90(11):1187-95 [10622527.001]
  • [Cites] Infect Immun. 1999 Jan;67(1):286-93 [9864228.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6356-9 [11522625.001]
  • [Cites] Mech Ageing Dev. 2002 Nov;123(12):1655-63 [12470903.001]
  • [Cites] J Natl Cancer Inst. 2000 Jun 21;92(12):959-60 [10861300.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4516-8 [10493498.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):11-22 [14708024.001]
  • [Cites] Jpn J Cancer Res. 1988 Aug;79(8):921-30 [3141328.001]
  • [Cites] N Engl J Med. 1997 Apr 10;336(15):1066-71 [9091804.001]
  • [Cites] J Natl Cancer Inst. 1996 Nov 6;88(21):1550-9 [8901853.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Infect Immun. 2002 Jul;70(7):3649-55 [12065506.001]
  • [Cites] J Clin Microbiol. 2001 Oct;39(10):3578-82 [11574575.001]
  • [Cites] Infect Immun. 2003 Feb;71(2):614-20 [12540537.001]
  • (PMID = 15014984.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / RNA, Messenger; 0 / Tobacco Smoke Pollution; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


5. Johnson ES, Ndetan H, Lo KM: Cancer mortality in poultry slaughtering/processing plant workers belonging to a union pension fund. Environ Res; 2010 Aug;110(6):588-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer mortality in poultry slaughtering/processing plant workers belonging to a union pension fund.
  • BACKGROUND: The role of zoonotic biological agents in human cancer occurrence has been little studied.
  • Humans are commonly exposed to viruses that naturally infect and cause cancer in food animals such as poultry that constitute part of the biological environment.
  • It is not known if these viruses cause cancer in humans.
  • OBJECTIVE: To study cancer mortality in the largest cohort to date, of 20,132 workers in poultry slaughtering and processing plants, a group with the highest human exposures to these viruses.
  • METHODS: Mortality in poultry workers was compared with that in the US general population through the estimation of standardized mortality ratios.
  • RESULTS: Significantly increased risks were observed in the cohort as a whole or in subgroups, for several cancer sites, viz: cancers of the buccal cavity and pharynx; pancreas; trachea/bronchus/lung; brain; cervix; lymphoid leukemia; monocytic leukemia; and tumors of the hemopoietic and lymphatic systems.
  • These findings may have implications for public health amongst persons in the general population who may also be exposed to these viruses.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Food Packaging / statistics & numerical data. Humans. Inhalation Exposure / analysis. Labor Unions. Middle Aged. Oncogenic Viruses / pathogenicity. Pensions. Risk Factors

  • MedlinePlus Health Information. consumer health - Occupational Health.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Environ Res. 2011 Jan;111(1):188-90
  • (PMID = 20541185.001).
  • [ISSN] 1096-0953
  • [Journal-full-title] Environmental research
  • [ISO-abbreviation] Environ. Res.
  • [Language] eng
  • [Grant] United States / NIOSH CDC HHS / OH / 1R01OH008071; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  •  go-up   go-down


6. Maruoka Y, Ando T, Hoshino M, Ogiuchi Y, Nishihara N, Okamoto T, Fukada K, Kuwazawa T, Ogiuchi H: [Combination chemotherapy with nedaplatin (CDGP) and 5-FU for oral cancer]. Gan To Kagaku Ryoho; 2002 Mar;29(3):421-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Combination chemotherapy with nedaplatin (CDGP) and 5-FU for oral cancer].
  • Chemotherapy using CDGP plus 5-FU was evaluated in patients with oral cancer.
  • The subjects were patients with squamous cell carcinoma of the oral cavity who had not received any therapy, comprising 7 patients with carcinoma of the tongue, 2 with buccal carcinoma, 2 with maxillary gingival carcinoma, and 1 with carcinoma of the oral floor.
  • There were 4 patients in Stage II, 3 patients in Stage III and 5 patients in Stage IV.
  • Since CDGP + 5-FU therapy achieved a good response rate (75%) in the treatment of squamous cell carcinoma of the oral cavity, we plan to use this therapy in the future and assess its benefit in a larger number of patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Mouth Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Leukopenia / chemically induced. Male. Middle Aged. Nausea / chemically induced. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Vomiting, Anticipatory / etiology

  • Genetic Alliance. consumer health - Oral cancer.
  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11915732.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 8UQ3W6JXAN / nedaplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


7. Brady G, Crean SJ, Lorenzon A, Kapas S: IGF-I protects human oral buccal mucosal epithelial cells from sodium nitroprusside-induced apoptosis via PI3-kinase. Growth Horm IGF Res; 2008 Aug;18(4):298-306
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IGF-I protects human oral buccal mucosal epithelial cells from sodium nitroprusside-induced apoptosis via PI3-kinase.
  • OBJECTIVE: Cancers of the head and neck account for the vast majority of all malignancies of the oral cavity.
  • The insulin-like growth factor (IGF) family of proteins is well documented to have an important role in rescuing cells from apoptosis.
  • While it is known the IGF proteins are present in normal oral epithelial and cancer cells its role is not fully understood.
  • Our aim was to study the ability of IGFs to rescue sodium nitroprusside (SNP)-induced apoptotic normal oral epithelial cells in vitro.
  • DESIGN: Cultured normal human oral keratinocytes (NOKs) or epithelial cells were used.
  • Exposing cells to IGF proteins prevented their apoptosis.
  • It lends further evidence to the significance of IGF proteins in the possible development of oral cancer.
  • [MeSH-major] Apoptosis / drug effects. Cytoprotection / drug effects. Epithelial Cells / drug effects. Insulin-Like Growth Factor I / pharmacology. Mouth Mucosa / drug effects. Nitroprusside / pharmacology. Phosphatidylinositol 3-Kinases / physiology
  • [MeSH-minor] Animals. Butadienes / pharmacology. Cells, Cultured. Chromones / pharmacology. DNA Fragmentation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Insulin-Like Growth Factor II / pharmacology. Keratinocytes / drug effects. Mice. Morpholines / pharmacology. Nitriles / pharmacology. Swiss 3T3 Cells

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18269934.001).
  • [ISSN] 1096-6374
  • [Journal-full-title] Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
  • [ISO-abbreviation] Growth Horm. IGF Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Butadienes; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 169D1260KM / Nitroprusside; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  •  go-up   go-down


8. Lee VH: Mucosal drug delivery. J Natl Cancer Inst Monogr; 2001;(29):41-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mucosal drug delivery.
  • This review focuses on epithelial drug transport mechanisms in mucosal drug delivery: the final step of a four-part process.
  • Reference is made to the mucosae lining the oral cavity and the gastrointestinal tract, the two mucosae most often succumbing to the side effects of cytotoxic chemotherapeutic drugs.
  • This transporter protein appears to be enriched in tumor epithelial cells, to be rather robust to the cytotoxic effects of chemotherapeutic drugs, and to lend itself to the molecular engineering of drugs that target this transporter in tumor epithelial cells.
  • In contrast to the gastrointestinal tract, much less is known about the type and capacity of drug transport processes in the buccal epithelial cells and about how these processes may be altered in disease state (including cancer) and be manipulated pharmaceutically to optimize drug absorption.
  • [MeSH-major] Drug Delivery Systems. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Symporters
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Biological Transport. Carrier Proteins / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Epithelial Cells / metabolism. Humans. Models, Biological. Models, Chemical. Neoplasms / metabolism. Neoplasms / pathology. Time Factors

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11694565.001).
  • [ISSN] 1052-6773
  • [Journal-full-title] Journal of the National Cancer Institute. Monographs
  • [ISO-abbreviation] J. Natl. Cancer Inst. Monographs
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM59297
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / PepT1 protein; 0 / SLC15A1 protein, human; 0 / Symporters
  • [Number-of-references] 33
  •  go-up   go-down


9. Trivedy CR, Craig G, Warnakulasuriya S: The oral health consequences of chewing areca nut. Addict Biol; 2002 Jan;7(1):115-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The oral health consequences of chewing areca nut.
  • Deleterious effects of areca nut on oral soft tissues are published extensively in the dental literature.
  • Its effects on dental caries and periodontal tissues, two major oral diseases, are less well researched.
  • Areca-induced lichenoid lesions mainly on buccal mucosa or tongue are reported at quid retained sites.
  • Areca nut chewing is implicated in oral leukoplakia and submucous fibrosis, both of which are potentially malignant in the oral cavity.
  • Oral cancer often arises from such precancerous changes in Asian populations.
  • In 1985 the International Agency for Research on Cancer concluded that there is limited evidence to conclude that areca chewing may directly lead to oral cancer.
  • There is, however, new information linking oral cancer to pan chewing without tobacco, suggesting a strong cancer risk associated with this habit.
  • Public health measures to quit areca use are recommended to control disabling conditions such as submucous fibrosis and oral cancer among Asian populations.
  • [MeSH-major] Areca / adverse effects. Carcinoma, Squamous Cell / chemically induced. Leukoplakia, Oral / chemically induced. Mouth Neoplasms / chemically induced. Precancerous Conditions / chemically induced. Substance-Related Disorders / complications
  • [MeSH-minor] Dental Caries / prevention & control. Humans. Mouth Mucosa / drug effects. Mouth Mucosa / pathology. Periodontitis / chemically induced. Periodontitis / pathology. Risk Factors


10. Nakamoto T, Wagner M, Melvin JE, Bogdanffy MS: Vinyl acetate induces intracellular acidification in mouse oral buccal epithelial cells. Toxicol Lett; 2005 Aug 14;158(2):116-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vinyl acetate induces intracellular acidification in mouse oral buccal epithelial cells.
  • Prolonged intracellular acidification is thought to produce cytotoxic and/or mitogenic responses that are the sentinel pharmacodynamic steps toward cancer.
  • To determine whether exposure to vinyl acetate affects the intracellular pH of intact oral cavity tissue, isolated mouse oral buccal epithelium was loaded with the pH-sensitive dye BCECF, and then exposed to vinyl acetate concentrations ranging from 10 to 1000 microM for up to 4 min.
  • These results are consistent with the hypothesis that vinyl acetate contributes to the generation and progression of oral cavity tumors via a process of intracellular acidification.
  • [MeSH-major] Acids. Carcinogens / toxicity. Epithelial Cells / drug effects. Intracellular Space / drug effects. Mouth Mucosa / drug effects. Vinyl Compounds / toxicity
  • [MeSH-minor] Animals. Cells, Cultured. Dose-Response Relationship, Drug. Hydrogen-Ion Concentration. Mice

  • Hazardous Substances Data Bank. VINYL ACETATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16039400.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acids; 0 / Carcinogens; 0 / Vinyl Compounds; L9MK238N77 / vinyl acetate
  •  go-up   go-down


11. Besaratinia A, Van Straaten HW, Godschalk RW, Van Zandwijk N, Balm AJ, Kleinjans JC, Van Schooten FJ: Immunoperoxidase detection of polycyclic aromatic hydrocarbon-DNA adducts in mouth floor and buccal mucosa cells of smokers and nonsmokers. Environ Mol Mutagen; 2000;36(2):127-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoperoxidase detection of polycyclic aromatic hydrocarbon-DNA adducts in mouth floor and buccal mucosa cells of smokers and nonsmokers.
  • Tobacco smoking is a major risk factor for oral cancer; mouth floor and buccal mucosa are among the most and least cancer-prone subsites, respectively, in the oral cavity.
  • We investigated the applicability of immunohistochemistry of smoking-induced DNA adducts in oral cells for assessing the exposure to carcinogens, and estimating the risk for oral cancer.
  • Polycyclic aromatic hydrocarbon (PAH)-DNA adducts were measured in mouth floor and buccal mucosa cells of smokers (n = 26) and nonsmokers (n = 22) by means of a semiquantitative immunoperoxidase assay.
  • Smokers had elevated levels of PAH-DNA adducts compared to nonsmokers in their mouth floor cells (0.045 +/- 0.022 versus 0.022 +/- 0.016, P = 0.0008 arbitrary units of immunohistochemistry) as well as in their buccal mucosa cells (0.058 +/- 0.028 versus 0.028 +/- 0.012, P = 0.001).
  • Also, there was a correlation between the levels of PAH-DNA adducts in mouth floor cells and those in buccal mucosa cells (r = 0.4, P = 0.01).
  • Furthermore, PAH-DNA adduct levels in both mouth floor and buccal mucosa cells were significantly related to current smoking indices (amount of tar and number of cigarettes consumed per day).
  • Expectedly, the levels of PAH-DNA adducts neither in mouth floor cells nor in buccal mucosa cells, both being short-lived cells, were related to smoking history index (pack years).
  • The levels of PAH-DNA adducts, however, in mouth floor cells as the cancer prone cells were lower than those in buccal mucosa cells (0.037 +/- 0.023 versus 0.044 +/- 0.026, P = 0.04).
  • We conclude that immunohistochemistry of PAH-DNA adducts in oral cells can be used for exposure assessment of tobacco-related carcinogens, however, it cannot be used for oral cancer risk estimation.
  • [MeSH-minor] Adult. Cheek. Disease Susceptibility. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Mouth Mucosa / chemistry. Mouth Mucosa / cytology. Mouth Neoplasms / diagnosis. Mouth Neoplasms / etiology. Peroxidase / chemistry. Peroxidase / immunology

  • MedlinePlus Health Information. consumer health - Smoking.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • [ErratumIn] Environ Mol Mutagen. 2005 Aug;46(2):140. Besarati Nia, A [corrected to Besaratinia, A]
  • (PMID = 11013411.001).
  • [ISSN] 0893-6692
  • [Journal-full-title] Environmental and molecular mutagenesis
  • [ISO-abbreviation] Environ. Mol. Mutagen.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / DNA Adducts; 0 / Polycyclic Hydrocarbons, Aromatic; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


12. Camidge DR, Pemberton MN, Growcott JW, Johnstone D, Laud PJ, Foster JR, Randall KJ, Hughes AM: Assessing proliferation, cell-cycle arrest and apoptotic end points in human buccal punch biopsies for use as pharmacodynamic biomarkers in drug development. Br J Cancer; 2005 Jul 25;93(2):208-15
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessing proliferation, cell-cycle arrest and apoptotic end points in human buccal punch biopsies for use as pharmacodynamic biomarkers in drug development.
  • Easily accessible normal tissues expressing the same molecular site(s) of drug action as malignant tissue offer an enhanced potential for early proof of anticancer drug mechanism and estimation of the biologically effective dose.
  • Studies were undertaken in healthy male volunteers to assess the tolerability of single and multiple (four in 24 h) 3 mm punch biopsies of the buccal mucosa, and to determine the feasibility of detecting and quantifying a range of proliferation, cell-cycle arrest and apoptosis markers by immunohistochemistry (IHC) for use as potential pharmacodynamic (PD) end points.
  • Neither site of biopsy within the oral cavity, nor the nominal time of biopsy had any significant impact on any of the four markers expression levels.
  • In conclusion, quantitation of such markers in 3 mm buccal punch biopsies would be suitable to explore as PD end points within intervention studies of drugs acting on these pathways.
  • [MeSH-minor] Adult. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / pharmacology. Biopsy / methods. Endpoint Determination. Humans. Immunohistochemistry. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2000 Mar 20;89(2):160-6 [10754494.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):110-24 [11773160.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3689-95 [10919634.001]
  • [Cites] Oncologist. 2000;5(6):510-3 [11110604.001]
  • [Cites] J Oral Pathol Med. 2002 Apr;31(4):204-12 [12076323.001]
  • [Cites] Oral Oncol. 2002 Oct;38(7):691-8 [12167422.001]
  • [Cites] J Can Dent Assoc. 2002 Nov;68(10):617-21 [12410942.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1301-6 [12663718.001]
  • [Cites] J Clin Oncol. 2003 May 1;21(9):1760-6 [12721252.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2389-90 [12855608.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2457-64 [12855618.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2478-86 [12855621.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2887-92 [12912932.001]
  • [Cites] J Oral Pathol Med. 2003 Oct;32(9):513-21 [12969225.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):175-84 [14701780.001]
  • [Cites] Br Dent J. 2004 Mar 27;196(6):329-33; quiz 362 [15044984.001]
  • [Cites] J Pathol. 2004 Oct;204(2):175-82 [15376256.001]
  • [Cites] Cell. 1989 Sep 22;58(6):1097-105 [2673543.001]
  • [Cites] Toxicol Pathol. 1990;18(1 Pt 1):24-31 [2194274.001]
  • [Cites] J Am Dent Assoc. 1990 Jul;121(1):145-9 [2196297.001]
  • [Cites] EMBO J. 1997 Sep 1;16(17):5334-44 [9311993.001]
  • [Cites] Am J Pathol. 1998 Feb;152(2):585-90 [9466585.001]
  • [Cites] Am J Pathol. 1999 Feb;154(2):613-22 [10027418.001]
  • [Cites] Cancer Res. 2000 May 15;60(10):2737-44 [10825149.001]
  • (PMID = 15999099.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2361555
  •  go-up   go-down


13. Dussor GO, Leong AS, Gracia NB, Kilo S, Price TJ, Hargreaves KM, Flores CM: Potentiation of evoked calcitonin gene-related peptide release from oral mucosa: a potential basis for the pro-inflammatory effects of nicotine. Eur J Neurosci; 2003 Nov;18(9):2515-26
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potentiation of evoked calcitonin gene-related peptide release from oral mucosa: a potential basis for the pro-inflammatory effects of nicotine.
  • Inflammation of the buccal mucosa, gingiva and periodontal tissues is a significant problem in users of nicotine-containing tobacco products; however, the potential role of nicotine in the development of this inflammation is unclear.
  • The purpose of the present studies was to determine the effects of nicotine and other nAChR agonists on capsaicin-evoked immunoreactive CGRP (iCGRP) release from rat buccal mucosa and to identify a potential cellular basis for these effects.
  • These data support the hypothesis that nicotinic agents, acting at nAChRs contained on primary sensory neurons, are capable of directly modulating the stimulated release of iCGRP.
  • In the case of users of nicotine-containing tobacco products, this modulation could contribute to inflammatory processes within the oral cavity.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CAPSAICIN .
  • Hazardous Substances Data Bank. CYTISINE .
  • Hazardous Substances Data Bank. NICOTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pharmacol Exp Ther. 2003 Jan;304(1):217-22 [12490594.001]
  • [Cites] J Neurosci. 2002 Feb 15;22(4):1208-17 [11850448.001]
  • [Cites] Toxicon. 1978;16(3):245-51 [653752.001]
  • [Cites] Brain Res. 1980 Jun 9;191(2):443-57 [6155172.001]
  • [Cites] Cancer Res. 1981 Nov;41(11 Pt 1):4305-8 [7198005.001]
  • [Cites] J Am Dent Assoc. 1983 May;106(5):617-21 [6575080.001]
  • [Cites] Brain Res. 1983 Aug 1;272(1):57-69 [6193836.001]
  • [Cites] Nature. 1985 Jan 3-9;313(5997):54-6 [3917554.001]
  • [Cites] J Physiol. 1985 Feb;359:31-46 [3999040.001]
  • [Cites] Eur J Pharmacol. 1985 Aug 7;114(1):61-6 [2412851.001]
  • [Cites] Br J Pharmacol. 1985 Dec;86(4):855-60 [2416378.001]
  • [Cites] Brain Res. 1987 Jan 27;402(1):197-200 [2881599.001]
  • [Cites] Acta Physiol Scand. 1987 May;130(1):33-40 [2438899.001]
  • [Cites] Trends Pharmacol Sci. 1988 Jan;9(1):16-20 [2907694.001]
  • [Cites] Br J Pharmacol. 1989 May;97(1):65-70 [2720313.001]
  • [Cites] J Comp Neurol. 1989 Jun 8;284(2):314-35 [2754038.001]
  • [Cites] J Neurosci. 1989 Nov;9(11):3796-802 [2479725.001]
  • [Cites] Trends Pharmacol Sci. 1989 Mar;10(3):110-4 [2574510.001]
  • [Cites] Trends Pharmacol Sci. 1990 Aug;11(8):330-3 [2203194.001]
  • [Cites] J Neurosci. 1991 Mar;11(3):837-45 [1705971.001]
  • [Cites] Nature. 1991 Mar 21;350(6315):235-8 [2005979.001]
  • [Cites] Brain Res. 1990 Aug 27;526(1):45-53 [2078817.001]
  • [Cites] J Biol Chem. 1991 Jun 15;266(17):11192-8 [2040627.001]
  • [Cites] Acta Physiol Scand. 1991 Jun;142(2):191-9 [1715114.001]
  • [Cites] Histochem J. 1991 Apr;23(4):171-9 [1684179.001]
  • [Cites] Exp Brain Res. 1991;86(2):414-20 [1756814.001]
  • [Cites] Br J Pharmacol. 1991 Oct;104(2):305-10 [1724624.001]
  • [Cites] Neurosci Lett. 1992 Mar 16;137(1):72-4 [1378220.001]
  • [Cites] Br J Pharmacol. 1992 Sep;107(1):116-9 [1384904.001]
  • [Cites] Acta Physiol Scand. 1992 Sep;146(1):119-27 [1279940.001]
  • [Cites] J Clin Periodontol. 1992 Nov;19(10):731-6 [1280655.001]
  • [Cites] J Periodontol. 1993 Jan;64(1):16-23 [8426285.001]
  • [Cites] Brain Res Bull. 1993;30(3-4):239-43 [7681350.001]
  • [Cites] J Endod. 1992 Dec;18(12):597-600 [1284348.001]
  • [Cites] J Neurophysiol. 1993 Jul;70(1):397-405 [8103089.001]
  • [Cites] Neurosci Lett. 1994 Jan 17;166(1):39-42 [8190355.001]
  • [Cites] J Appl Physiol (1985). 1994 Apr;76(4):1651-6 [8045845.001]
  • [Cites] Neuropharmacology. 1994 Oct;33(10):1147-54 [7862250.001]
  • [Cites] Brain Res. 1995 Jan 9;669(1):93-9 [7536103.001]
  • [Cites] Mol Pharmacol. 1995 Oct;48(4):774-82 [7476906.001]
  • [Cites] J Invest Dermatol. 1995 Dec;105(6):774-81 [7490471.001]
  • [Cites] J Invest Dermatol. 1996 Sep;107(3):412-8 [8751979.001]
  • [Cites] J Neurosci. 1996 Dec 15;16(24):7892-901 [8987817.001]
  • [Cites] Mol Pharmacol. 1997 Feb;51(2):320-7 [9203638.001]
  • [Cites] Nature. 1997 Oct 23;389(6653):816-24 [9349813.001]
  • [Cites] Neurochem Int. 1997 Dec;31(6):739-57 [9413835.001]
  • [Cites] Pain. 1997 Nov;73(2):201-7 [9415506.001]
  • [Cites] Neurosci Lett. 1998 Jul 10;250(3):177-80 [9708861.001]
  • [Cites] Neuron. 1998 Sep;21(3):531-43 [9768840.001]
  • [Cites] Brain Res. 1998 Nov 2;809(2):238-45 [9853116.001]
  • [Cites] Mol Pharmacol. 1999 Jul;56(1):11-9 [10385679.001]
  • [Cites] Arch Physiol Biochem. 1998 Dec;106(5):362-9 [10441058.001]
  • [Cites] Arch Neurol. 1961 Jun;4:617-50 [13692408.001]
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):233-40 [10609551.001]
  • [Cites] J Comp Neurol. 2000 Mar 13;418(3):299-309 [10701828.001]
  • [Cites] Neuropharmacology. 2000 Oct;39(13):2561-9 [11044727.001]
  • [Cites] Neuropharmacology. 2000 Oct;39(13):2570-90 [11044728.001]
  • [Cites] J Neurophysiol. 2001 Oct;86(4):1773-82 [11600638.001]
  • [Cites] Eur J Neurosci. 2001 Oct;14(7):1113-20 [11683903.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Feb 15;291(1):124-9 [11829471.001]
  • [Cites] Br J Pharmacol Chemother. 1967 Sep;31(1):138-51 [6055248.001]
  • (PMID = 14622152.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / F31 DA006085-02; United States / NIDA NIH HHS / DA / DA05982; United States / NIDA NIH HHS / DA / DA10510; United States / NIDA NIH HHS / DA / R01 DA010510; United States / NIDA NIH HHS / DA / F31 DA005982; United States / NIDA NIH HHS / DA / F31 DA006085; United States / NIDA NIH HHS / DA / DA006085-02
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Azocines; 0 / Bicyclo Compounds, Heterocyclic; 0 / Nicotinic Agonists; 0 / Nicotinic Antagonists; 0 / Pyridines; 0 / Quinolizines; 0 / Receptors, Drug; 0 / Receptors, Nicotinic; 140111-52-0 / epibatidine; 53S5U404NU / cytisine; 6EE945D3OK / Mecamylamine; 6M3C89ZY6R / Nicotine; 83652-28-2 / Calcitonin Gene-Related Peptide; S07O44R1ZM / Capsaicin
  • [Other-IDs] NLM/ NIHMS222095; NLM/ PMC2914552
  •  go-up   go-down


14. Nagao T, Ikeda N, Fukano H, Hashimoto S, Shimozato K, Warnakulasuriya S: Incidence rates for oral leukoplakia and lichen planus in a Japanese population. J Oral Pathol Med; 2005 Oct;34(9):532-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence rates for oral leukoplakia and lichen planus in a Japanese population.
  • BACKGROUND: Data on the incidence rates of potentially malignant diseases of the oral cavity in different populations is meagre.
  • This is the first study to report on the age-specific incidence of oral leukoplakia and oral lichen planus from an industrialized country.
  • METHODS: Annual screening for oral cancer and pre-cancer was undertaken in Municipal Health Centres in Tokoname city, Japan from 1995 to 1998.
  • RESULTS: Over a 4-year follow-up period, 18 new oral leukoplakias (all homogenous; 11 idiopathic and seven tobacco-associated) and 24 oral lichen planus (22 reticular, one erythematous and one ulcerative) were detected at screening and confirmed by re-examination at specialist units.
  • Age-specific incidence rates for oral leukoplakia varied by age groups.
  • New oral leukoplakias were more prevalent on gingival/alveolar ridge (33.3%) than in other oral sites, and lichen planus at buccal site (33.3%).
  • Regular drinking was not related to occurrence of either oral leukoplakia or oral lichen planus.
  • In cases with diabetes mellitus, relative risk for oral lichen planus adjusted by logistic regression was 6.4 (95% CI: 2.4-17.6), suggesting an association.
  • CONCLUSIONS: The reported incidence rates for oral leukoplakia in this Japanese population are somewhat higher to those reported from India, the risk habits of the two groups being markedly different.
  • The reported rates for oral leukoplakia and lichen planus allow estimation of service needs in specialist oral medicine clinics and for the training of primary care dentists.
  • [MeSH-major] Leukoplakia, Oral / epidemiology. Lichen Planus, Oral / epidemiology

  • Genetic Alliance. consumer health - Leukoplakia.
  • Genetic Alliance. consumer health - Oral leukoplakia.
  • Genetic Alliance. consumer health - Oral lichen planus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16138891.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  •  go-up   go-down


15. Cabrerizo-Merino Mdel C, Oñate-Sánchez RE: Some odontostomatological aspects in childhood oncology. Med Oral Patol Oral Cir Bucal; 2005 Jan-Feb;10(1):44-7; 41-4
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Childhood neoplasias have become increasingly important in recent years in the ambit of paediatric medicine.
  • This phenomenon has been accompanied by a spectacular improvement in the treatment of childhood cancer, long-term survival rates reaching 90% in the case of some tumours.
  • A corollary of this success is the obligation to provide new and improved medical assistance both as regards the possible prevention of any alterations and, if possible, the avoidance of complications derived from the neoplasm itself and its treatment.
  • Among possible secondary effects are oral manifestations of a chronic or acute nature, which may cause great discomfort, act as foci of systemic infections or have long-term after effects, all of which will depend on the exact moment of the child s development that treatment is undertaken.
  • The incidence and severity of most oral complications is associated with pre-existent factors, such as caries, gingivitis or generally poor hygiene, which strongly affect the beginning, increase and persistence of the same.
  • It is to be decried that a problem in the buccal cavity is allowed to develop, which a simple preventative measure, simple hygiene or dental conservation treatment could prevent or reduce.

  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • MedlinePlus Health Information. consumer health - Mouth Disorders.
  • MedlinePlus Health Information. consumer health - Tooth Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15627907.001).
  • [ISSN] 1698-4447
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng; spa
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 25
  •  go-up   go-down


16. Neagu I, Tabarcea IC, Vataman R: [Associated risk factors in developing oral manifestations in patients with blood dyscrasia]. Rev Med Chir Soc Med Nat Iasi; 2010 Apr-Jun;114(2):555-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Associated risk factors in developing oral manifestations in patients with blood dyscrasia].
  • [Transliterated title] Factori de risc asociaţi în apariţia manifestărilor orale la pacienţii cu discrazii sanguine.
  • The oral and dental complications arising in cancer patients can be attributable to the malignant disease itself and to the various modalities of cancer therapy.
  • Up to 37.2% of all patients receiving cancer chemotherapy develop acute oral complications and up to 31.1% of all patients receiving cancer radiotherapy develop acute oral manifestations.
  • Oral complications may result in significant morbidity, impaired nutrition, treatment delays, and dose reductions which are affecting the prognosis of the primary disease.
  • MATERIAL AND METHOD: We investigated 312 cases of blood dyscrasia which 296 cases had oral manifestations (86.2%).
  • RESULTS: Oral complications are frequently encountered in patients receiving anticancer therapy and these complications may result in significant morbidity, treatment delays, dose reductions, and nutritional deficiencies.
  • The acute effects of anticancer chemotherapy upon the oral cavity include mucositis, infection, hemorrhage, xerostomia and nutritional deficiencies.
  • Patients which undergo radiotherapy, specific in head and neck carcinomas, display a 30-60% incidence of the oral manifestations.
  • The antineoplastic therapy will interfere with the turnover of the epithelial cells, followed by mucosal injury, later by infections, due to indirect invasion of Gram-negative bacteria and fungal species, as most of the anti-cancer drugs cause immunological changes.
  • CONCLUSIONS: The mucosal surface that is the oral cavity may provide insight into the immune function of the patient.
  • Differential diagnosis is important as many disorders may manifest themselves similarly in the buccal area.
  • [MeSH-major] Leukemia / complications. Mouth Diseases / diagnosis. Mouth Diseases / etiology. Mouth Mucosa / drug effects. Mouth Mucosa / radiation effects. Neoplasms / drug therapy. Neoplasms / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant / adverse effects. Child. Diagnosis, Differential. Female. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / radiotherapy. Hematologic Diseases / complications. Humans. Incidence. Male. Middle Aged. Radiotherapy, Adjuvant / adverse effects. Retrospective Studies. Risk Factors. Romania / epidemiology. Statistics, Nonparametric. Stomatitis / diagnosis. Stomatitis / etiology. Xerostomia / diagnosis. Xerostomia / etiology


17. Myers R, Harvey M, Kaufmann TJ, Greiner SM, Krempski JW, Raffel C, Shelton SE, Soeffker D, Zollman P, Federspiel MJ, Blanco M, Galanis E: Toxicology study of repeat intracerebral administration of a measles virus derivative producing carcinoembryonic antigen in rhesus macaques in support of a phase I/II clinical trial for patients with recurrent gliomas. Hum Gene Ther; 2008 Jul;19(7):690-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Development of novel therapeutic agents is urgently needed.
  • We have previously demonstrated that oncolytic measles virus strains derived from the Edmonston vaccine lineage have significant antitumor activity against gliomas [Phuong, L.K., Allen, C., Peng, K.W., Giannini, C., Greiner, S., Teneyck, C.J., Mishra, P.K., Macura, S.I., Russell, S.J., Galanis, E.C. (2003). Cancer. Res.
  • MV-CEA is an Edmonston vaccine lineage measles virus strain engineered to express the marker peptide carcinoembryonic antigen (CEA): CEA levels can serve as a correlate of viral gene expression.
  • In support of a phase I clinical trial of intratumoral and resection cavity administration of MV-CEA to patients with recurrent gliomas, we assessed the neurotoxicity of MV-CEA in adult immune male rhesus macaques (Macaca mulatta).
  • The animals ' immune status and administration schedule mimicked the trial population and proposed administration schema.
  • The animals were stereotactically administered either vehicle (n = 1) or MV-CEA at 2 x 10(5)or 2 x 10(6) TCID(50) (each, n = 2) in the right frontal lobe in two injections on days 1 and 5.
  • Body weight, temperature, complete blood count, CEA, clinical chemistries, coagulation, complement levels, immunoglobulin, measles antibody titers, viremia, and shedding (buccal swabs) were tested at multiple time points.
  • Quantitative RT-PCR analysis of blood, buccal swabs, and cerebrospinal fluid (CSF) was negative for MV-CEA at all time points, with the exception of viral genome deletion in the blood of one asymptomatic animal at the 2 x 10(6) TCID(50) dose level on day 85.
  • A clinical trial of intratumoral and resection cavity administration of MV-CEA in patients with recurrent glioblastoma multiforme is currently ongoing.

  • Genetic Alliance. consumer health - Measles.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 1971 Sep 15;8(2):298-303 [5002518.001]
  • [Cites] J Neurosurg. 2000 May;92(5):804-11 [10794295.001]
  • [Cites] Cancer Lett. 1985 Jan;25(3):283-95 [2578868.001]
  • [Cites] Gan No Rinsho. 1987 Feb;33(2):188-92 [3560451.001]
  • [Cites] Acta Virol. 1987 Aug;31(4):346-51 [2892384.001]
  • [Cites] Epidemiol Rev. 1993;15(2):265-302 [8174658.001]
  • [Cites] J Infect Dis. 1994 Nov;170 Suppl 1:S32-41 [7930752.001]
  • [Cites] J Virol. 1998 Sep;72(9):7420-7 [9696838.001]
  • [Cites] N Engl J Med. 1960 Jul 28;263:153-9 [13820246.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Breast Cancer Res Treat. 2006 Sep;99(2):177-84 [16642271.001]
  • [Cites] Hepatology. 2006 Dec;44(6):1465-77 [17133484.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11840-50 [17178881.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Mol Ther. 2007 Apr;15(4):677-86 [17299404.001]
  • [Cites] Expert Opin Biol Ther. 2008 Feb;8(2):213-20 [18194077.001]
  • [Cites] J Infect Dis. 1972 Aug;126(2):154-61 [4626543.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4656-62 [12183422.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2462-9 [12750267.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2508-18 [12839017.001]
  • [Cites] Nat Med. 2002 May;8(5):527-31 [11984600.001]
  • (PMID = 18576918.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108961-030002; United States / NCI NIH HHS / CA / P50 CA108961; United States / PHS HHS / / P50 108961; United States / NCI NIH HHS / CA / P50 CA108961-030002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Carcinoembryonic Antigen
  • [Other-IDs] NLM/ NIHMS130695; NLM/ PMC2748764
  •  go-up   go-down


18. Delgado-Guay MO: Efficacy and safety of fentanyl buccal for cancer pain management by administration through a soluble film: an update. Cancer Manag Res; 2010;2:303-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy and safety of fentanyl buccal for cancer pain management by administration through a soluble film: an update.
  • More than half of patients receiving prescription medicine for cancer pain have been reported to experience inadequate pain relief or breakthrough pain.
  • Buccal administration can deliver lipophilic opioids rapidly to the systemic circulation through the buccal mucosa, limiting gastrointestinal motility and first-pass metabolism.
  • This review updates the safety and efficacy of fentanyl buccal soluble film (FBSF) in patients with cancer pain.
  • Search terms included combinations of the following: cancer pain, fentanyl, fentanyl buccal soluble film, pharmacology, kinetics, safety, efficacy and toxicity.
  • FBSF is an oral transmucosal form of fentanyl citrate developed as a treatment of breakthrough pain in opioid-tolerant patients with cancer.
  • Studies have shown that it is well tolerated in the oral cavity, with adequate bioavailability and safety in cancer patients.
  • Further studies are warranted to evaluate, in comparison with other short-acting opioids, its efficacy in the management of breakthrough cancer pain, its addictive potential and its economic impact in cancer patients.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anesthesiology. 1999 Sep;91(3):681-5 [10485779.001]
  • [Cites] Pain. 2000 Mar;85(1-2):239-45 [10692624.001]
  • [Cites] Anesthesiology. 2000 Mar;92(3):739-53 [10719953.001]
  • [Cites] Palliat Med. 2004 Apr;18(3):177-83 [15198130.001]
  • [Cites] Clin Geriatr Med. 2005 Feb;21(1):93-119, viii [15639040.001]
  • [Cites] Ann Pharmacother. 2005 Dec;39(12):2139-40 [16288064.001]
  • [Cites] Clin Pharmacokinet. 2005;44(12):1279-86 [16372825.001]
  • [Cites] Bioorg Med Chem. 2006 May 1;14(9):2887-95 [16376082.001]
  • [Cites] J Palliat Med. 2006 Apr;9(2):391-408 [16629570.001]
  • [Cites] Acta Oncol. 2007;46(4):417-32 [17497308.001]
  • [Cites] Drugs Aging. 2007;24(9):761-76 [17727305.001]
  • [Cites] J Pain Palliat Care Pharmacother. 2007;21(2):5-16 [17844723.001]
  • [Cites] Oncology (Williston Park). 2008 Jan;22(1):56-61 [18251283.001]
  • [Cites] Clin J Pain. 2008 May;24 Suppl 10:S3-7 [18418225.001]
  • [Cites] Drugs. 2008;68(7):913-24 [18457459.001]
  • [Cites] Ann Oncol. 2009 Aug;20(8):1420-33 [19244085.001]
  • [Cites] Cancer. 2009 Jun 1;115(11):2571-9 [19373888.001]
  • [Cites] J Palliat Med. 2009 Oct;12(10):947-54 [19807240.001]
  • [Cites] Ann Oncol. 2010 Jun;21(6):1308-14 [19940014.001]
  • [Cites] Drugs. 2010;70(1):57-72 [20030425.001]
  • [Cites] J Clin Pharmacol. 2010 Jul;50(7):785-91 [20150521.001]
  • [Cites] Pain Pract. 2010 Jul-Aug;10(4):287-93 [20230447.001]
  • [Cites] Pain Med. 2010 Jul;11(7):1017-23 [20492573.001]
  • [Cites] J Pain Symptom Manage. 2004 Nov;28(5):497-504 [15504625.001]
  • [Cites] Clin Pharmacokinet. 2002;41(9):661-80 [12126458.001]
  • (PMID = 21301590.001).
  • [ISSN] 1179-1322
  • [Journal-full-title] Cancer management and research
  • [ISO-abbreviation] Cancer Manag Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3033036
  • [Keywords] NOTNLM ; cancer pain / fentanyl buccal soluble film
  •  go-up   go-down


19. Nishimura M, Matsuura K, Tsukioka T, Yamashita H, Inagaki N, Sugiyama T, Itoh Y: In vitro and in vivo characteristics of prochlorperazine oral disintegrating film. Int J Pharm; 2009 Feb 23;368(1-2):98-102
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo characteristics of prochlorperazine oral disintegrating film.
  • Oral disintegrating film containing prochlorperazine, a dopamine D(2) receptor antagonist with anti-emetic property, was newly developed using microcrystalline cellulose, polyethlene glycol and hydroxypropylmethyl cellulose as the base materials.
  • The uniformity of dosage units of the preparation was acceptable according to the criteria of JP15 or USP27.
  • Subsequently, rats were used to compare pharmacokinetic properties of the film preparation applied topically into the oral cavity with those of oral administration of prochlorperazine solution.
  • None of the parameters, including T(max), C(max), area under curves, clearance and steady-state distribution volume was significantly different between oral disintegrating film and oral solution.
  • These findings suggest that the present prochlorperazine-containing oral film is potentially useful to control emesis induced by anti-cancer agents or opioid analgesics in patients who limit the oral intake.
  • [MeSH-major] Antiemetics / administration & dosage. Antiemetics / pharmacokinetics. Drug Delivery Systems. Prochlorperazine / administration & dosage. Prochlorperazine / pharmacokinetics
  • [MeSH-minor] Administration, Buccal. Animals. Area Under Curve. Biological Availability. Cellulose / chemistry. Chemistry, Pharmaceutical. Chromatography, High Pressure Liquid. Dosage Forms. Drug Compounding. Drug Stability. Excipients / chemistry. Hypromellose Derivatives. Male. Mass Spectrometry. Methylcellulose / analogs & derivatives. Methylcellulose / chemistry. Polyethylene Glycols / chemistry. Rats. Rats, Sprague-Dawley. Solubility. Time Factors

  • Hazardous Substances Data Bank. Prochlorperazine .
  • Hazardous Substances Data Bank. METHYL CELLULOSE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18992311.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiemetics; 0 / Dosage Forms; 0 / Excipients; 0 / microcrystalline cellulose; 30IQX730WE / Polyethylene Glycols; 3NXW29V3WO / Hypromellose Derivatives; 9004-34-6 / Cellulose; 9004-67-5 / Methylcellulose; YHP6YLT61T / Prochlorperazine
  •  go-up   go-down


20. Colt JS, Stallones L, Cameron LL, Dosemeci M, Zahm SH: Proportionate mortality among US migrant and seasonal farmworkers in twenty-four states. Am J Ind Med; 2001 Nov;40(5):604-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: US migrant and seasonal farmworkers may be exposed to potentially carcinogenic pesticides and other agents.
  • Proportionate cancer mortality analyses found excess cancers of the buccal cavity, larynx, esophagus, stomach, skin (NW), and cervix, and deficits for cancers of the colon, breast, kidney, pancreas (NW), and lymphohematopoietic system.
  • CONCLUSIONS: The excess deaths from injuries, respiratory disease, and stomach cancer, and the deficits of colon cancer and arteriosclerotic heart disease among farmworkers, are consistent with typical mortality patterns previously observed among farm owner/operators.
  • The excess buccal, laryngeal, esophageal, and cervical cancers, and the deficits of breast cancer and lymphohematopoietic cancers have not generally been observed in studies of farm owner/operators.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Published 2001 Wiley-Liss, Inc.
  • (PMID = 11675631.001).
  • [ISSN] 0271-3586
  • [Journal-full-title] American journal of industrial medicine
  • [ISO-abbreviation] Am. J. Ind. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down






Advertisement