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1. Sells DM, Brix AE, Nyska A, Jokinen MP, Orzech DP, Walker NJ: Respiratory tract lesions in noninhalation studies. Toxicol Pathol; 2007 Jan;35(1):170-7
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  • Changes included respiratory epithelial hyperplasia, degeneration and necrosis of olfactory epithelium, olfactory epithelial metaplasia, adenoma, adenocarcinoma, squamous cell carcinoma, and neuroblastoma.
  • In the lung, compound-related lesions included alveolar histiocytosis, alveolar epithelial hyperplasia, bronchiolar metaplasia of the alveolar epithelium, squamous metaplasia, alveolar/bronchial adenoma and carcinoma, and squamous tumors.
  • The presence of respiratory tract lesions in noninhalation studies emphasizes the need for a thorough examination of the respiratory tract including nasal passages, regardless of the route of administration.
  • [MeSH-major] Respiratory System / drug effects. Xenobiotics / administration & dosage. Xenobiotics / toxicity
  • [MeSH-minor] Administration, Oral. Injections. Lung / drug effects. Nasal Cavity / drug effects. Nasal Cavity / pathology. Nasal Mucosa / drug effects. Nasal Mucosa / pathology. Toxicity Tests / methods

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  • (PMID = 17325986.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Xenobiotics
  • [Number-of-references] 24
  • [Other-IDs] NLM/ NIHMS33525; NLM/ PMC3433271
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2. Paiva I, Ribeiro C, Gomes L, Baptista C, Gomes F, Rito M, Rebelo O, Marnoto D, Moura C, Leitão F, Carvalheiro M: [ACTH-dependent Cushing's syndrome: a revision of 43 cases]. Acta Med Port; 2004 Sep-Oct;17(5):367-74
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  • [Title] [ACTH-dependent Cushing's syndrome: a revision of 43 cases].
  • [Transliterated title] Síndroma de cushing ACTH-dependente: estudo retrospectivo de 43 casos.
  • AIM: To evaluate the characteristics and outcomes of the patients diagnosed as ACTH-dependent Cushing syndrome, registered in the department.
  • The more reliable diagnostic tests were: 11 pm cortisol, day curve of ACTH and cortisol, and dexamethasone suppression tests.
  • In thirty-seven patients a pituitary adenoma was diagnosed.
  • The three patients diagnosed before 1985 went for bilateral adrenalectomy (Nelson's syndrome in two); the others were submitted to transsphenoidal pituitary adenomectomy, obtaining remission in twenty six at the first operation and in two others at the second.
  • Four patients had a bronchial carcinoid, successfully removed in three.
  • More effective technical methods and drugs, as well as a multidisciplinary and dedicated medical team, lead to long lasting remissions in most of the patients.

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  • (PMID = 16197843.001).
  • [ISSN] 1646-0758
  • [Journal-full-title] Acta médica portuguesa
  • [ISO-abbreviation] Acta Med Port
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Portugal
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3. Lee YY, Wong KT, King AD, Ahuja AT: Imaging of salivary gland tumours. Eur J Radiol; 2008 Jun;66(3):419-36
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  • Most of them are benign and parotid gland is the commonest site.
  • As a general rule, the smaller the involved salivary gland, the higher is the possibility of the tumor being malignant.
  • Minor salivary gland lesions in the mucosa of oral cavity, pharynx and tracheo-bronchial tree, are also not accessible by conventional ultrasound.
  • Recent study suggests that MR spectroscopy may differentiate malignant and benign salivary gland tumours as well as distinguishing Warthin's tumor from pleomorphic adenoma.
  • Similarly, the role of nuclear medicine and PET scan, in imaging of parotid masses is limited.
  • [MeSH-major] Diagnostic Imaging. Salivary Gland Neoplasms / diagnosis

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  • (PMID = 18337041.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 44
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4. Gollini P, Cataldi A, Fava C: [MEN 1 and 2: the role of diagnostic imaging]. Radiol Med; 2004 Jan-Feb;107(1-2):78-87
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  • [Title] [MEN 1 and 2: the role of diagnostic imaging].
  • PURPOSE: To report the results of a retrospective study on the use of the different imaging methods in the diagnosis of type 1 and type 2 multiple endocrine neoplasias, and to provide an overall evaluation of the diagnostic yield of the various examinations performed correlating the results with the surgical findings.
  • In the patients with MEN1 the examinations revealed 4 parathyroid hyperplasias, 4 gastro-pancreatic endocrine-secreting lesions, one hypophyseal adenoma, one bronchial carcinoid and two bilateral adrenal hyperplasias.
  • In only one patient with MEN1 did the chest X-ray detect a bronchial carcinoma, confirmed by CT.
  • CT also enabled identification of a single hypophyseal adenoma.
  • DISCUSSION AND CONCLUSIONS: Given the rarity of this condition we believe that the only statistically important finding in our series concerns the sensitivity of the imaging examinations performed in that, with adequate clinical and laboratory data, the possible problem of false positive results is exceptional.
  • The role of diagnostic imaging in the management of patients with MEN1 and 2 is twofold: identification of the target organs of lesions suspected on the basis of clinical and laboratory findings to enable adequate medical and/or surgical treatment; staging of malignant lesions to enable correct surgical planning.
  • In particular, our study once again highlights the diagnostic efficacy of CT for the diagnosis of pheochromocytomas and of the combination of biopsy plus ultrasound and ultrasound plus scintigraphy for the diagnosis of MTC in MEN 2.
  • As for MEN1 spiral CT was found to have good sensitivity (66%) in localising endocrine neoplasias of the gastrointestinal tract; endoscopic ultrasound on the other hand revealed good diagnostic efficacy, showing constantly positive findings.
  • Finally, in both pathologies we believe that the assessment of parathyroid conditions to be mainly a matter for nuclear medicine.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Carcinoma, Medullary / diagnosis. Gastrinoma / diagnosis. Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 2a / diagnosis. Pancreatic Neoplasms / diagnosis. Pheochromocytoma / diagnosis. Pituitary Neoplasms / diagnosis. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biopsy. Bronchial Neoplasms / diagnosis. Bronchial Neoplasms / radiography. Bronchial Neoplasms / radionuclide imaging. Bronchial Neoplasms / ultrasonography. Carcinoid Tumor / diagnosis. Carcinoid Tumor / radiography. Carcinoid Tumor / radionuclide imaging. Carcinoid Tumor / ultrasonography. Endosonography. Female. Humans. Male. Middle Aged. Retrospective Studies. Sensitivity and Specificity. Thyroid Gland / pathology. Tomography, Spiral Computed. Tomography, X-Ray Computed


5. Gautschi O, Ratschiller D, Gugger M, Betticher DC, Heighway J: Cyclin D1 in non-small cell lung cancer: a key driver of malignant transformation. Lung Cancer; 2007 Jan;55(1):1-14
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  • [Title] Cyclin D1 in non-small cell lung cancer: a key driver of malignant transformation.
  • PURPOSE: To review the evidence implicating the deregulation of cyclin D1 in the pathogenesis of non-small cell lung cancer (NSCLC), and to discuss the opportunities for targeted clinical intervention.
  • CCND1 is amplified in NSCLC and cyclin D1 is frequently overexpressed in tumours and pre-invasive bronchial lesions, generally from one parental allele.
  • Genotype has been correlated with the risk and/or severity of disease or drug response across a range of malignancies, including lung cancer.
  • Together, these findings suggest a strong pathological role for cyclin D1 deregulation in bronchial neoplasia.
  • CONCLUSION: Current data indicate that cyclin D1 overexpression is not a consequence of, but rather a pivotal element in the process of malignant transformation in the lung and other tissues.
  • This understanding may open new avenues for lung cancer diagnosis, treatment and prevention.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Non-Small-Cell Lung / physiopathology. Cyclin D1 / genetics. Lung Neoplasms / pathology. Lung Neoplasms / physiopathology
  • [MeSH-minor] Adenoma / pathology. Adenoma / physiopathology. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glioblastoma / pathology. Glioblastoma / physiopathology. Humans. Polymorphism, Genetic


6. Biermasz NR, Smit JW, Pereira AM, Frölich M, Romijn JA, Roelfsema F: Acromegaly caused by growth hormone-releasing hormone-producing tumors: long-term observational studies in three patients. Pituitary; 2007;10(3):237-49
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  • We report on three newly diagnosed patients with extracranial ectopic GHRH-associated acromegaly with long-term follow-up after surgery of the primary tumor.
  • One patient with a pancreatic tumor and two parathyroid adenomas was the index case of a large kindred of MEN-I syndrome.
  • The other two patients had a large bronchial carcinoid.
  • We did not observe development of tachyphylaxis towards the drug or radiological evidence of (growing) metastases.
  • We propose life-long suppressive therapy with somatostatin analogs in cases with persisting elevated serum GHRH concentrations after removal of the primary tumor.
  • [MeSH-major] Acromegaly / etiology. Adenoma / secretion. Carcinoid Tumor / secretion. Human Growth Hormone / secretion. Lung Neoplasms / secretion. Pancreatic Neoplasms / secretion. Paraneoplastic Endocrine Syndromes / metabolism. Parathyroid Neoplasms / secretion

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  • (PMID = 17541749.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC2045692
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7. Sun W, Iijima T, Kano J, Kobayashi H, Li D, Morishita Y, Okubo C, Anami Y, Noguchi M: Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma. Cancer Sci; 2008 Nov;99(11):2177-84
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  • Aberrant methylation of promoter CpG islands is known to be a major inactivation mechanism of tumor-suppressor and tumor-related genes.
  • In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma.
  • Two of them showed downregulation of their expression in human lung adenocarcinoma.
  • Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14.
  • The expression of SAMD14 in A549 was rescued by treatment with the demethylation agent 5-aza-2'-deoxycytidine.
  • Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%).
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Lung Neoplasms / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. CpG Islands. DNA, Neoplasm / metabolism. Female. Humans. Kinesin / genetics. Kinesin / metabolism. Male. Mice. Mice, Inbred Strains. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 18823374.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / KIF21A protein, human; 0 / Kif21a protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.6.1.- / Kinesin
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8. Pereira MA, Li Y, Gunning WT, Kramer PM, Al-Yaqoub F, Lubet RA, Steele VE, Szabo E, Tao L: Prevention of mouse lung tumors by budesonide and its modulation of biomarkers. Carcinogenesis; 2002 Jul;23(7):1185-92
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  • [Title] Prevention of mouse lung tumors by budesonide and its modulation of biomarkers.
  • Chemopreventive drugs have the potential to decrease the morbidity and mortality of lung cancer.
  • The development of these drugs could be expedited by the application of surrogate end-point biomarkers that demonstrate chemopreventive efficacy.
  • In this study, the ability of budesonide to prevent lung tumors in mice was characterized further and its effects on biomarkers were determined.
  • Lung tumors were induced in female strain A mice by vinyl carbamate (16 mg/kg) administered once weekly for 2 consecutive weeks.
  • Budesonide caused a dose-dependent decrease in the multiplicity of lung tumors of 25, 58 and 82%, respectively.
  • Budesonide (2.4 mg/kg diet) administered starting at weeks 4, 10 or 16, decreased tumor multiplicity by 82, 66 and 30% at week 20.
  • Administering 2.4 mg/kg budesonide at weeks 4-20 or 20-35 and killing the mice at week 35 did not significantly decrease the yield of tumors, although both treatment regimens did decrease the size of the tumors and the progression of adenomas to carcinomas.
  • Thus, budesonide delayed the appearance of lung tumors and decreased their growth and progression to carcinomas.
  • Budesonide decreased the proliferating cell nuclear antigen labeling in lung adenomas, carcinomas, parenchyma and bronchial airways by 87.6, 59.0, 41.1 and 25.4%, respectively.
  • Thus, short-term treatment with budesonide modulated biological and molecular end-points in lung tumors that might be developed further as biomarkers for its clinical chemopreventive efficacy in the lung.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Budesonide / therapeutic use. Lung Neoplasms / prevention & control. Muscle Proteins. Urethane / analogs & derivatives
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Division / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / genetics. Cyclins / metabolism. DNA Primers / chemistry. Dose-Response Relationship, Drug. Female. Mice. Mice, Inbred A. Microfilament Proteins / genetics. Microfilament Proteins / metabolism. Polymerase Chain Reaction. RNA, Messenger / metabolism

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  • (PMID = 12117777.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01 CN 95107
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA Primers; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / RNA, Messenger; 0 / Tagln protein, mouse; 3IN71E75Z5 / Urethane; 51333-22-3 / Budesonide; 7Y2431GOM5 / vinyl carbamate
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9. National Toxicology Program: NTP toxicology and carcinogensis studies of vanadium pentoxide (CAS No. 1314-62-1) in F344/N rats and B6C3F1 mice (inhalation). Natl Toxicol Program Tech Rep Ser; 2002 Dec;(507):1-343
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  • Genetic toxicology studies were conducted in Salmonella typhimurium and mouse peripheral blood.
  • Relative lung weights of 4 mg/m(3) or greater males and 2 mg/m(3) or greater females were significantly greater than those of the chamber controls.
  • Lavage fluid analysis indicated an inflammatory response in the lung that was either directly mediated by vanadium pentoxide or was secondary to lung damage induced by vanadium pentoxide exposure.
  • Absolute and relative lung weights of 4 mg/m(3) or greater males and all exposed groups of females and liver weights of 16 mg/m(3) males were significantly greater than those of the chamber controls.
  • Lavage fluid analysis indicated an inflammatory response in the lung that was either directly mediated by vanadium pentoxide or was secondary to lung damage induced by vanadium pentoxide exposure.
  • Absolute and relative lung weights were significantly greater for 4 mg/m(3) or greater males and females than for the chamber controls as were the relative lung weights of 2 mg/m(3) males.
  • The incidences of several nonneoplastic lesions of the lung and nose were significantly increased in males and females exposed to 2 mg/m(3) or greater.
  • Data from pulmonary function analyses indicated that a restrictive lung disease was present in male and female rats exposed to 4 mg/m(3) or greater, while an obstructive lung disease was present only in the 16 mg/m(3) groups.
  • Absolute and relative lung weights of males and females exposed to 4 mg/m(3) or greater were significantly greater than those of the chamber controls.
  • Some mice exposed to 2 or 4 mg/m(3) had inflammation of the lung, and all mice exposed to 8 or 16 mg/m(3) had inflammation and epithelial hyperplasia of the lung.
  • Assessment of lung vanadium concentrations suggested deposition and clearance exhibited linear kinetics over the exposure range studied.
  • Lung clearance half-times ranged from 4.42 to 4.96 days.
  • Assessment of lung vanadium concentrations suggested deposition and clearance exhibited linear kinetics over the exposure range studied.
  • Lung clearance half-times ranged from 2.40 to 2.55 days.
  • Alveolar/bronchiolar adenomas were present in 0.5 and 1 mg/m(3) females; one 2 mg/m(3) female also had an alveolar/bronchiolar carcinoma.
  • The incidence of alveolar/bronchiolar adenoma in the 0.5 mg/m(3) group was at the upper end of the historical control ranges.
  • Nonneoplastic lesions related to vanadium pentoxide exposure occurred in the respiratory system (lung, larynx, and nose) of male and female rats, and the severities of these lesions generally increased with increasing exposure concentration.
  • Nonneoplastic lesions related to vanadium pentoxide exposure occurred in the respiratory system (lung, larynx, and nose) of male and female mice, and the severities of these lesions generally increased with increasing exposure concentration.
  • Bronchial lymph node hyperplasia was present in many exposed females.
  • [MeSH-major] Lung Neoplasms / chemically induced. Vanadium Compounds / toxicity
  • [MeSH-minor] Animals. Body Burden. Body Weight / drug effects. Dose-Response Relationship, Drug. Female. Humans. Inhalation Exposure. Lung / drug effects. Lung / pathology. Lung / physiology. Male. Mice. Pulmonary Alveoli / drug effects. Rats. Rats, Inbred F344

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  • (PMID = 12533744.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vanadium Compounds; BVG363OH7A / vanadium pentoxide
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10. D'Agostini F, Mastracci L, Izzotti A, Balansky R, Pennisi TM, Steele VE, De Flora S: Modulation by phenethyl isothiocyanate and budesonide of molecular and histopathologic alterations induced by environmental cigarette smoke in mice. Cancer Prev Res (Phila); 2009 Jun;2(6):546-56
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  • Our discovery that the perinatal period involves nucleotide modifications and gene overexpression in mouse lung prompted us to evaluate whether mice may become more susceptible to cigarette smoke when exposure starts immediately after birth.
  • Further on, we showed that exposure of mice to environmental cigarette smoke (ECS), starting at birth, results in alterations of a variety of intermediate biomarkers.
  • However, after 4 months of exposure to ECS followed by 7 months of recovery in filtered air, the lung tumor yield was rather low.
  • In the present study, we evaluated the protective effects of the glucocorticoid budesonide and of the dietary agent phenethyl isothiocyanate in mice exposed to ECS for 9 months followed by 2 months of recovery.
  • After weanling, the mice exposed to ECS since birth underwent a variety of alterations of molecular and cytogenetical end points, and 11 months after birth, they exhibited significant histopathologic changes, such as pulmonary anthracosis, emphysema, hemorrhagic areas, alveolar bronchiolarization, bronchial hyperplasia, and tumors, both benign and malignant.
  • Thus, although not as efficiently as the bioassay in mainstream cigarette smoke-exposed mice, the model in neonatal mice is suitable to evaluate both ECS carcinogenicity and its modulation by chemopreventive agents.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Budesonide / therapeutic use. Isothiocyanates / therapeutic use. Lung Neoplasms / prevention & control. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adenoma / etiology. Adenoma / prevention & control. Age Factors. Animals. Animals, Newborn. Apoptosis / drug effects. Bone Marrow Cells / drug effects. Bone Marrow Cells / pathology. Carcinoma / etiology. Carcinoma / prevention & control. DNA Adducts / analysis. Drug Screening Assays, Antitumor. Epithelial Cells / drug effects. Epithelial Cells / pathology. Female. Lung / chemistry. Lung / drug effects. Lung Diseases / drug therapy. Lung Diseases / pathology. Male. Mice. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Pregnancy. Time Factors

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  • (PMID = 19491290.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN53301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / DNA Adducts; 0 / Isothiocyanates; 0 / Tobacco Smoke Pollution; 51333-22-3 / Budesonide; 6U7TFK75KV / phenethyl isothiocyanate
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11. Hahn FF, Gigliotti AP, Hutt JA, March TH, Mauderly JL: A review of the histopathology of cigarette smoke-induced lung cancer in rats and mice. Int J Toxicol; 2007 Jul-Aug;26(4):307-13
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  • [Title] A review of the histopathology of cigarette smoke-induced lung cancer in rats and mice.
  • In the past several years an increased number of lung tumors has been reported in laboratory studies of rats and mice after lifetime exposure to mainstream cigarette smoke.
  • Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors.
  • Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas.
  • In addition, mice also have bronchiolar epithelial hyperplasia and bronchial papillomas not found in rats.
  • Lung tumors in rats and mice are found at the end of the life span and rarely metastasize.
  • The characteristics of the lung tumors, and the proliferative changes associated with the tumors, are important in helping understand the mechanisms of lung cancer induction.
  • These studies in rats and mice allow new approaches to the study of cigarette smoke-induced changes in the lung.
  • [MeSH-major] Adenocarcinoma / etiology. Adenoma / etiology. Lung Neoplasms / etiology. Precancerous Conditions / etiology. Pulmonary Alveoli / drug effects. Smoking / adverse effects
  • [MeSH-minor] Administration, Inhalation. Animals. Bronchi / drug effects. Bronchi / pathology. Bronchial Neoplasms / etiology. Bronchial Neoplasms / pathology. Disease Models, Animal. Female. Male. Mice. Mice, Inbred Strains. Papilloma / etiology. Papilloma / pathology. Rats. Rats, Inbred F344. Respiratory Mucosa / drug effects. Respiratory Mucosa / pathology. Species Specificity


12. Stinn W, Teredesai A, Anskeit E, Rustemeier K, Schepers G, Schnell P, Haussmann HJ, Carchman RA, Coggins CR, Reininghaus W: Chronic nose-only inhalation study in rats, comparing room-aged sidestream cigarette smoke and diesel engine exhaust. Inhal Toxicol; 2005 Oct;17(11):549-76
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  • Lung weights were increased markedly in the DEE (but not RASS) groups and did not decrease during the 6-month post-exposure period.
  • Bulky lung DNA adducts increased in the RASS groups, but not in the DEE groups.
  • Histopathological responses in the RASS groups were minimal and almost completely reversible; lung tumors were similar in number to those seen in the sham-exposed groups.
  • Malignant and multiple tumors were seen only in the DEE groups; after 30 months, the tumor incidence (predominantly bronchiolo-alveolar adenomas) was 2% in the sham-exposed groups, 5%in the high RASS groups, and 46% in the high DEE groups (sexes combined).
  • Our results suggest that in rats exposed to DEE, but not to RASS, the following series of events occurs: particle deposition in lungs --> lung "overload" --> pulmonary inflammation --> tumorigenesis, without a significant modifying role of cell proliferation or DNA adduct formation.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Aerosols / chemistry. Animals. Body Weight / drug effects. Bronchial Neoplasms / chemically induced. Bronchial Neoplasms / pathology. Carbon / analysis. Carboxyhemoglobin / metabolism. Carcinogenicity Tests / instrumentation. Carcinogenicity Tests / methods. Eating / drug effects. Female. Inhalation Exposure / analysis. Inhalation Exposure / statistics & numerical data. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / metabolism. Male. Nicotine / metabolism. Nicotine / urine. Particle Size. Rats. Rats, Wistar. Respiratory System / drug effects. Respiratory System / pathology. Respiratory Tract Neoplasms / chemically induced. Respiratory Tract Neoplasms / pathology. Time Factors

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  • (PMID = 16033752.001).
  • [ISSN] 0895-8378
  • [Journal-full-title] Inhalation toxicology
  • [ISO-abbreviation] Inhal Toxicol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 0 / Air Pollutants; 0 / Tobacco Smoke Pollution; 0 / Vehicle Emissions; 6M3C89ZY6R / Nicotine; 7440-44-0 / Carbon; 9061-29-4 / Carboxyhemoglobin
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13. Goralczyk R, Wertz K, Lenz B, Riss G, Buchwald Hunziker P, Geatrix B, Aebischer CP, Bachmann H: Beta-carotene interaction with NNK in the AJ-mouse model: effects on cell proliferation, tumor formation and retinoic acid responsive genes. Biochim Biophys Acta; 2005 May 30;1740(2):179-88
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  • [Title] Beta-carotene interaction with NNK in the AJ-mouse model: effects on cell proliferation, tumor formation and retinoic acid responsive genes.
  • We studied the influence of beta-carotene on the tobacco smoke carcinogen 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumor development in the A/J-mouse model.
  • The normally low beta-carotene absorption was facilitated with a diet enriched in fat and bile salt, resulting in plasma and lung tissue levels similar to humans. beta-Carotene enhanced NNK-induced early bronchial cell proliferation, however, this effect was not predictive for later tumor development.
  • Tumor multiplicity was not significantly affected by beta-carotene, neither in carcinogen-initiated nor in uninitiated mice, and regardless of dose and time point of supplementation during tumor development.
  • However, this interaction did not translate into enhanced tumor multiplicity.
  • These results indicate that impaired retinoid signaling is not likely a key factor in lung tumorigenesis in this mouse model.
  • [MeSH-major] Adenoma / pathology. Carcinogens. Lung / drug effects. Lung Neoplasms / pathology. Nitrosamines. beta Carotene / pharmacology
  • [MeSH-minor] Animals. Bronchi / drug effects. Cytochrome P-450 Enzyme System / biosynthesis. Cytochrome P-450 Enzyme System / genetics. Disease Models, Animal. Down-Regulation. Drug Interactions. Epithelial Cells / drug effects. Gene Expression Regulation / drug effects. Male. Mice. Protein Isoforms / biosynthesis. Receptors, Retinoic Acid / biosynthesis. Receptors, Retinoic Acid / genetics

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  • (PMID = 15949685.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Protein Isoforms; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 01YAE03M7J / beta Carotene; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / retinoic acid 4-hydroxylase
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14. Souici AC, Fitzhugh AL, Keefer LK, Felley-Bosco E: L-tyrosine and nitric oxide synergize to prevent cytotoxic effects of superoxide. Toxicology; 2001 Aug 28;165(2-3):163-70
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  • We found previously that the nitric oxide donor DEA/NO enhanced lipid peroxidation, DNA fragmentation, and cytotoxicity in human bronchial epithelial cells (BEAS-2B) when they were cultured in LHC-8 medium containing the superoxide-generating system hypoxanthine/xanthine oxidase (HX/XO).
  • We have now discovered that DEA/NO's prooxidant action can be reversed by raising the L-tyrosine concentration from 30 to 400 microM.
  • DEA/NO also protected the cells when they were cultured in Dulbecco's Modified Eagle's Medium (DMEM), whose standard concentration of L-tyrosine is 400 microM.
  • Similar trends were seen with the colon adenoma cell line CaCo-2.
  • Since HPLC analysis of cell-free DMEM or LHC-8 containing 400 microM L-tyrosine, DEA/NO, and HX/XO revealed no evidence of L-tyrosine nitration, our data suggest the existence of an as-yet uncharacterized mechanism by which L-tyrosine can influence the biochemical and toxicological effects of reactive nitrogen species.
  • [MeSH-minor] Bronchi / cytology. Bronchi / drug effects. Caco-2 Cells / drug effects. Cell Line. Cell Survival / drug effects. DNA Damage. Drug Synergism. Humans. Hypoxanthine / metabolism. Lipid Peroxidation / drug effects. Nitrogen Oxides. Reactive Oxygen Species / metabolism. Xanthine Oxidase / metabolism

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  • (PMID = 11522374.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-56000
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Nitric Oxide Donors; 0 / Nitrogen Oxides; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 2TN51YD919 / Hypoxanthine; 31C4KY9ESH / Nitric Oxide; 42HK56048U / Tyrosine; 86831-65-4 / 1,1-diethyl-2-hydroxy-2-nitrosohydrazine; EC 1.17.3.2 / Xanthine Oxidase
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15. Moody TW, Leyton J, Zia F, Tuthill C, Badamchian M, Goldstein AL: Thymosinalpha1 is chemopreventive for lung adenoma formation in A/J mice. Cancer Lett; 2000 Jul 31;155(2):121-7
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  • [Title] Thymosinalpha1 is chemopreventive for lung adenoma formation in A/J mice.
  • Lung adenomas were observed 2.5, 3, and 4 months after urethane injection (400 mg/kg i.p.) into female A/J mice.
  • Daily administration of THNalpha1 (0.4 mg/kg, s.c.) reduced lung adenoma multiplicity significantly, by approximately 45, 40, and 17%, respectively, 2.5, 3, and 4 months after urethane injection.
  • Animals treated with THNalpha1 had a significantly greater white cell density than control A/J mice.
  • Endogenous THNalpha1-like peptides were detected in the mouse lung.
  • By radioimmunoassay and by Western blot, prothymosin alpha was detected in the mouse lung.
  • By immunocytochemistry, THNalpha1-like peptides were detected in all lung compartments including the bronchus, adenoma, bronchioles, and alveoli.
  • These results indicate that exogenous THNalpha1 prevents lung carcinogenesis in A/J mice.
  • [MeSH-major] Adenoma / prevention & control. Lung Neoplasms / prevention & control. Thymosin / analogs & derivatives
  • [MeSH-minor] Animals. Blood / drug effects. Blotting, Western. Bronchi / metabolism. Carcinogens. Female. Immunohistochemistry. Lung / drug effects. Mice. Pulmonary Alveoli / metabolism. Radioimmunoassay. Time Factors. Tissue Distribution. Urethane

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  • (PMID = 10822126.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Carcinogens; 0 / thymalfasin; 3IN71E75Z5 / Urethane; 61512-21-8 / Thymosin
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