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1. Morishita C, Jin E, Kikuchi M, Egawa S, Fujiwara M, Ohaki Y, Ghazizadeh M, Takemura T, Kawanami O: Angiogenic switching in the alveolar capillaries in primary lung adenocarcinoma and squamous cell carcinoma. J Nippon Med Sch; 2007 Oct;74(5):344-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenic switching in the alveolar capillaries in primary lung adenocarcinoma and squamous cell carcinoma.
  • The status of angiogenic switching was examined in alveolar capillaries of primary lung adenocarcinoma (ADC) from 10 patients and primary squamous cell carcinoma (SCC) from 11 patients, using immunostaining for CD31, thrombomodulin, von Willebrand factor (vWF), collagen types IV and VII, and alpha-smooth muscle actin (alpha-SMA).
  • In bronchioloalveolar and papillary subtypes of ADC, the neoplastic cells, replacing the normal alveolar epithelial cells, had spread over alveolar walls and adhered firmly to alveolar interstitium as shown by the development of type IV collagen.
  • Neoplastic cells of SCC were characterized by local proliferation in alveolar sacs without firm attachment to alveolar walls.
  • In ADC and SCC, alveolar capillary endothelial cells newly obtained reactivity to vWF.
  • CD31 was consistently expressed in normal and ADC tissues, but each endothelial cell marker was often attenuated or even lost in SCC, suggesting degeneration or necrosis of the alveolar capillaries.
  • In ADC, apoptosis occurred in cells of alveolar capillaries more frequently in the peripheral zone than in the deeper zone of the tumor, whereas the frequency was not consistent in SCC.
  • In microdissected alveolar wall tissues, mRNA expression patterns of VEGF isoforms and VEGFRs were similar in both ADC and SCC.
  • In ADC, de novo angiogenic switching took place in cytoplasm as a unit of cells segments in alveolar capillary endothelium.
  • Suppression of angiogenic switching in SCC implies that factors other than VEGF-VEGFR interaction, such as physical contact and compression of tumor cells, might play a critical role in alveolar capillaries.
  • [MeSH-major] Adenocarcinoma / blood supply. Carcinoma, Squamous Cell / blood supply. Lung Neoplasms / blood supply. Pulmonary Alveoli / blood supply

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  • (PMID = 17965528.001).
  • [ISSN] 1345-4676
  • [Journal-full-title] Journal of Nippon Medical School = Nippon Ika Daigaku zasshi
  • [ISO-abbreviation] J Nippon Med Sch
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Thrombomodulin; 0 / Vascular Endothelial Growth Factor A; 0 / von Willebrand Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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2. Tajiri M, Kameda Y, Nakayama H, Sakamoto K: Prognosis and morphometrical features of non-bronchioloalveolar cell adenocarcinoma: an assessment of the non-alveolar replacing area and high grade atypical area. J Clin Pathol; 2006 Mar;59(3):269-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognosis and morphometrical features of non-bronchioloalveolar cell adenocarcinoma: an assessment of the non-alveolar replacing area and high grade atypical area.
  • AIM: It has become obvious that the prognosis of bronchioloalveolar cell carcinoma (BAC) in small peripheral adenocarcinoma of the lung is good, but most cases actually treated as pulmonary adenocarcinoma in hospitals tend to be non-bronchioloalveolar cell carcinoma (non-BAC).
  • We considered that the non-alveolar replacing area and the high grade atypical area were related to the prognosis, and therefore defined the ratio of both areas to the total area at the maximum face of the tumours as the non-alveolar replacing area ratio (NAAR) and the high grade atypical area ratio (HAAR), respectively.
  • [MeSH-major] Adenocarcinoma / pathology. Bronchial Neoplasms / pathology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Aged. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Proportional Hazards Models. Survival Rate

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  • (PMID = 16505277.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860342
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3. Pouniotis DS, Plebanski M, Apostolopoulos V, McDonald CF: Alveolar macrophage function is altered in patients with lung cancer. Clin Exp Immunol; 2006 Feb;143(2):363-72
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  • [Title] Alveolar macrophage function is altered in patients with lung cancer.
  • The alveolar macrophage (AM) is believed to be of central importance in the immune response against infection and tumour.
  • We examined patients with lung cancer in order to evaluate the immuno-stimulatory potential of AM in lung cancer.
  • Bronchoalveolar lavage fluid samples were obtained from patients with adenocarcinoma, squamous cell carcinoma, large cell undifferentiated lung carcinoma, small cell carcinoma and control subjects.
  • AM from adenocarcinoma patients showed similar levels of IL-10, IL-6, IL-1 and TNF-alpha compared to controls.
  • Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma.
  • Mannose receptor levels were only decreased on AM from patients with squamous and small cell carcinoma but not adenocarcinoma and large cell undifferentiated carcinoma.
  • We conclude that there are type-specific alterations in uptake ability, cytokine secretion and phenotype of AM from lung cancer patients, which may result in an inability to stimulate anti-tumour immunity.
  • The observed differences between lung cancer subgroups may explain previously reported inconsistencies in descriptions of AM characteristics in lung cancer.
  • [MeSH-major] Lung Neoplasms / immunology. Macrophages / immunology. Pulmonary Alveoli / immunology
  • [MeSH-minor] Adenocarcinoma / immunology. Aged. Antigens, CD / analysis. Biomarkers / analysis. Bronchoalveolar Lavage Fluid / immunology. Carcinoma, Large Cell / immunology. Carcinoma, Small Cell / immunology. Carcinoma, Squamous Cell / immunology. Cytokines / immunology. HLA-DR Antigens / analysis. Humans. Immunoglobulins / analysis. Intercellular Adhesion Molecule-1 / analysis. Lectins, C-Type / analysis. Mannose-Binding Lectins / analysis. Membrane Glycoproteins / analysis. Microspheres. Middle Aged. Phenotype. Polystyrenes / pharmacokinetics. Receptors, Cell Surface / analysis

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  • (PMID = 16412062.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / CD83 antigen; 0 / Cytokines; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Lectins, C-Type; 0 / Mannose-Binding Lectins; 0 / Membrane Glycoproteins; 0 / Polystyrenes; 0 / Receptors, Cell Surface; 0 / mannose receptor; 126547-89-5 / Intercellular Adhesion Molecule-1
  • [Other-IDs] NLM/ PMC1809587
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4. Wang GF, Lai MD, Chen PH: [Correlation of multiple primary lung cancer with bronchial and alveolar epithelial dysplasia]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2005 Sep;34(5):427-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Correlation of multiple primary lung cancer with bronchial and alveolar epithelial dysplasia].
  • OBJECTIVE: To investigate the correlation of multiple primary lung cancer with bronchial epithelial dysplasia and atypical adenomatous hyperplasia of bronchiolo-alveolar epithelium.
  • METHODS: Careful pathological examinations were performed on 114 surgical specimens of primary lung carcinoma.
  • The correlation of multiple primary lung cancer with bronchial epithelial dysplasia and atypical adenomatous hyperplasia of bronchiolo-alveolar epithelium was analyzed.
  • RESULTS: Of 114 cases of primary lung cancer,13 cases of multiple primary lung cancer (11.4 %) was identifiedìwhich consisted of 6 cases containing two primary bronchogenic carcinoma and 7 containing one bronchogenic carcinoma and one bronchiolo-alveolar carcinoma.
  • The rate of multiple primary lung cancers was significantly higher in individuals with high grade bronchial epithelial dysplasia than in those with low grade dysplasia (r=0.238, P<0.05).
  • CONCLUSION: Bronchial and alveolar epithelial cells may develop malignancy synchronously or metachronously.
  • The probability of developing multiple primary lung cancer will increase in the lungs with extensive and severe bronchial epithelial dysplasia.
  • [MeSH-major] Bronchi / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Pulmonary Alveoli / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Small Cell / pathology. Cell Proliferation. Female. Humans. Hyperplasia. Male. Middle Aged. Precancerous Conditions / pathology. Respiratory Mucosa / pathology

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  • (PMID = 16216054.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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5. Ioachimescu OC, Mehta AC: From cystic pulmonary airway malformation, to bronchioloalveolar carcinoma and adenocarcinoma of the lung. Eur Respir J; 2005 Dec;26(6):1181-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] From cystic pulmonary airway malformation, to bronchioloalveolar carcinoma and adenocarcinoma of the lung.
  • The authors present an unusual case of BAC developed in an area of CPAM, with subsequent progression to metastatic adenocarcinoma (AC).
  • The case is unique due to the combination of: early age of presentation; neoplastic transformation of a CPAM; unaltered course over 15 yrs; and its particular pattern of slow morphogenesis and degeneration into an invasive AC of the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Cell Transformation, Neoplastic / pathology. Cystic Adenomatoid Malformation of Lung, Congenital / pathology. Lung Neoplasms / pathology

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  • (PMID = 16319347.001).
  • [ISSN] 0903-1936
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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6. Fujita A, Kameda Y, Goya T: Clinicopathology of stromal invasion in lung adenocarcinoma. Pathol Int; 2009 Jan;59(1):1-6
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  • [Title] Clinicopathology of stromal invasion in lung adenocarcinoma.
  • In the World Health Organization classification, lung adenocarcinoma with mixed subtypes is defined as invasive carcinoma with evidence of vascular, pleural, or stromal invasion.
  • A total of 157 peripheral pure bronchioloalveolar carcinoma (BAC) or lung adenocarcinoma with mixed BAC and others were reviewed.
  • Destruction of alveolar framework (DAF) was defined as distortion or discontinuity of the alveolar framework by tumor growth.
  • The extra-alveolar area involvement (EAAI) was defined as tumor growth outside the alveolar framework, which includes the following areas: bronchial wall, perivascular connective tissue and/or the vascular wall, interlobular septum and the visceral pleura.
  • Survival of patients with adenocarcinoma without DAF (n = 41) was 100%.
  • Even when adenocarcinoma involved DAF and lacked EAAI (n = 21), survival was 100%.
  • Tumor growth outside the alveolar framework is the hallmark of stromal invasion.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology

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  • (PMID = 19121086.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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7. Wislez M, Antoine M, Rabbe N, Gounant V, Poulot V, Lavolé A, Fleury-Feith J, Cadranel J: Neutrophils promote aerogenous spread of lung adenocarcinoma with bronchioloalveolar carcinoma features. Clin Cancer Res; 2007 Jun 15;13(12):3518-27
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutrophils promote aerogenous spread of lung adenocarcinoma with bronchioloalveolar carcinoma features.
  • PURPOSE: Adenocarcinoma with bronchioloalveolar carcinoma (BAC) features is a subtype of non-small cell lung cancers characterized by an intense inflammatory reaction composed of macrophages and neutrophils and by a distinct natural history with intrapulmonary spread leading to death due to respiratory failure.
  • We hypothesized that neutrophils could promote aerogenous spread of lung adenocarcinoma with BAC features.
  • EXPERIMENTAL DESIGN: We examined the effect of neutrophils on A549 cell line detachment in vitro and we quantified desquamation of tumor cells on tumor tissue (n = 25) and on matched bronchioloalveolar lavage (n = 17) in vivo in a series of patients with adenocarcinoma with BAC features.
  • It is a significant factor of shorter survival and may be an important event in adenocarcinoma progression.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology. Neoplasm Invasiveness / pathology. Neutrophils / metabolism

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  • (PMID = 17575214.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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8. Jain D, Joshi K, Jindal SK: Precursor lesions of adenocarcinoma lung--two case reports. Indian J Pathol Microbiol; 2005 Jul;48(3):399-402
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  • [Title] Precursor lesions of adenocarcinoma lung--two case reports.
  • Although precursor lesions of bronchogenic squamous cell carcinoma are well documented, the preinvasive lesions of pulmonary adenocarcinoma are seen very rarely.
  • It has been hypothesized that there is a stepwise progression of alveolar epithelial hyperplasia to atypical alveolar hyperplasia and subsequently to malignancy in the pathogenesis of peripheral adenocarcinoma of the lung.
  • In the present paper we would like to share our experience of two cases of pulmonary adenocarcinoma with their precursor lesions in the form of atypical alveolar hyperplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Diseases, Interstitial / pathology. Lung Neoplasms / pathology. Precancerous Conditions / pathology. Pulmonary Alveoli / pathology

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  • (PMID = 16761769.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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9. Wang C, Yang R, Yue D, Zhang Z: Expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma. Lung; 2009 Mar-Apr;187(2):104-9
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  • [Title] Expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma.
  • Bronchioloalveolar carcinoma (BAC) is classified as a subset of lung adenocarcinoma but has a distinct clinical presentation, tumor biology, response to therapy, and prognosis compared with other subtypes of lung adenocarcinoma.
  • This study was designed to investigate the clinicopathological differences between BAC and adenocarcinoma and the expression of focal adhesion kinase (FAK) and phosphatase and tensin homologue (PTEN) and their clinical significance in BAC and adenocarcinoma.
  • A retrospective analysis was performed on 77 patients with BAC and 172 patients with pure adenocarcinoma seen during the period from January 1998 to December 2000.
  • Clinicopathological characteristics and survival outcome were reviewed and compared between patients with BAC and adenocarcinoma.
  • Lymph node status, clinical symptoms, CT appearance and expression of FAK were different between BAC and adenocarcinoma.
  • The overall survival of BAC was better than that of adenocarcinoma.
  • In patients with FAK(-), the overall survival was not different between BAC and adenocarcinoma.
  • In patients with adenocarcinoma, the overall survival was better for FAK(-) compared with FAK(+).
  • Expression of PTEN had a prognostic significance in patients with BAC and adenocarcinoma.
  • BAC and adenocarcinoma have different clinicopathological presentations.
  • Expression of FAK has some effect on such differences and affects survival of lung adenocarcinoma.
  • Expression of PTEN can predict outcome of resected lung adenocarcinoma and BAC.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma, Bronchiolo-Alveolar / enzymology. Biomarkers, Tumor / analysis. Focal Adhesion Kinase 1 / analysis. Lung Neoplasms / enzymology. PTEN Phosphohydrolase / analysis

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  • [CommentIn] Lung. 2009 May-Jun;187(3):207-8 [19408043.001]
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  • (PMID = 19242756.001).
  • [ISSN] 1432-1750
  • [Journal-full-title] Lung
  • [ISO-abbreviation] Lung
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.1.3.67 / PTEN protein, human
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10. Su KC, Lay SL, Perng RP, Chang SC, Chen YM: Lung cancer may develop subsequently or coincidently with pulmonary alveolar proteinosis. Lung Cancer; 2007 Oct;58(1):144-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer may develop subsequently or coincidently with pulmonary alveolar proteinosis.
  • Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by an accumulation of periodic acid-Schiff (PAS) positive lipoproteinaceous material in the alveolar space.
  • We herein report two cases of PAP associated with lung cancer: one, a case of idiopathic PAP with subsequent development of lung cancer, and the other, a case of coexisting lung cancer and PAP.
  • In conclusion, PAP can occur prior to or coincidently with lung cancer.
  • [MeSH-major] Adenocarcinoma / etiology. Lung Neoplasms / etiology. Pulmonary Alveolar Proteinosis / complications

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  • (PMID = 17566600.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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11. Morandi L, Asioli S, Cavazza A, Pession A, Damiani S: Genetic relationship among atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and adenocarcinoma of the lung. Lung Cancer; 2007 Apr;56(1):35-42
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  • [Title] Genetic relationship among atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and adenocarcinoma of the lung.
  • Atypical adenomatous hyperplasia (AAH) has been recently defined by WHO as a small lesion, not exceeding 5mm in major axis, composed of slightly enlarged alveolar septa lined by pneumocytes with plump, atypical nuclei.
  • AAH is frequently found in tissue surrounding lung adenocarcinoma and is considered a precursor of this subtype of lung cancer by many Authors.
  • However, the genetic relationship between adenocarcinoma and the associated foci of AAH is not well defined.
  • In particular, it is not clear whether multiple foci of AAH and of adenocarcinoma in the same patients are clonally related to each other or represent independent neoplastic foci.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenomatosis, Pulmonary / genetics. Lung Neoplasms / genetics. Precancerous Conditions / genetics

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  • (PMID = 17241687.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Mitochondrial
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12. Jian Z, Tomizawa Y, Yanagitani N, Iijima H, Sano T, Nakajima T: Papillary adenocarcinoma of the lung is a more advanced adenocarcinoma than bronchioloalveolar carcinoma that is composed of two distinct histological subtypes. Pathol Int; 2005 Oct;55(10):619-25
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  • [Title] Papillary adenocarcinoma of the lung is a more advanced adenocarcinoma than bronchioloalveolar carcinoma that is composed of two distinct histological subtypes.
  • To clarify the clinicopathological nature of papillary adenocarcinoma (PA) of the lung, 20 cases of PA were collected consecutively from resected adenocarcinoma of the lung, studied immunohistochemically and, using molecular techniques, compared with bronchioloalveolar carcinoma (BAC).
  • Morphologically, PA was divided into two subtypes according to the presence of residual alveolar structures, detected by elastica van Gieson stain.
  • One of these subtypes was closely related to the morphology of BAC and might be diagnosed as adenocarcinoma with mixed subtypes.
  • The other PA subtype was composed of tall columnar cells and grew compressively, which was similar to type F adenocarcinoma previously reported by Noguchi et al.
  • Immunohistochemical studies using lung tissue-specific antigens, progression markers and tumor suppressor products found that PA seemed a more advanced adenocarcinoma than BAC, but no differences were observed among PA subtypes.
  • These findings suggest that PA is a more advanced adenocarcinoma subtype than BAC.
  • Further investigations are needed to clarify true PA as clinicopathologically and biologically independent from other histological subtypes of adenocarcinoma of the lung.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Lung Neoplasms / pathology

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  • (PMID = 16185291.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Genetic Markers
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13. Shen HT, Zhang XH, Huang XH, Li YH, Wang J, Yan X, Wang F: [Histogenesis of lung adenocarcinoma induced by oral adminstration of mycotoxins in mice]. Wei Sheng Yan Jiu; 2005 May;34(3):341-4
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  • [Title] [Histogenesis of lung adenocarcinoma induced by oral adminstration of mycotoxins in mice].
  • OBJECTIVE: To study the histogenesis and the putative mechanisms of adenocarcinoma induced by AFG1 and ST in NIH mice.
  • METHODS: Thirty-four cases of lung adenocarcinomas induced by AFG1 and ST in NIH mice were included in this study and 12 cases of normal lung tissues were used as control.
  • The phenotype of the lung adenocarcinomas was determined by immunohistochemical expression of SP-C and CC-10 at protein level.
  • RESULT: The positive expression of SP-C was found in all the lung adenocarcinomas, while no expression of CC-10 could be seen.
  • CONCLUSION: The lung adenocarcinomas induced by the two mycotoxins in NIH mice arise from alveolar type II cells and no expression of mutant P53 and Ras at protein level was found in the lung adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / etiology. Aflatoxin B1 / toxicity. Lung Neoplasms / etiology. Sterigmatocystin / toxicity

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  • (PMID = 16111048.001).
  • [ISSN] 1000-8020
  • [Journal-full-title] Wei sheng yan jiu = Journal of hygiene research
  • [ISO-abbreviation] Wei Sheng Yan Jiu
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 10048-13-2 / Sterigmatocystin; 9N2N2Y55MH / Aflatoxin B1
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14. Quesenberry PJ, Del Tatto M, Berz D, Miner T, Ng T, Winer ES, Aliotta J, Colvin G, Dooner M, Dooner G, Fontaine JP: Marrow cell genetic phenotype change induced by human lung cancer cells. J Clin Oncol; 2009 May 20;27(15_suppl):11108

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Marrow cell genetic phenotype change induced by human lung cancer cells.
  • : 11108 Background: Murine lung-derived microvesicles are capable of inducing lung-specific mRNA in marrow cells, when co-cultured across from these cells, but separated from them by a cell-impermeable (0.4 micron) membrane.
  • These converted murine marrow cells showed mRNA elevations, lung-specific protein production and enhanced capacity to convert to lung epithelial cells after in vivo transplantation into irradiated mice.
  • We examine here whether fresh tissue from lung cancer patients would have the same capacity to genetically alter co-cultured human marrow cells.
  • METHODS: Lung cancer samples were collected from 5 patients undergoing surgery.
  • Marrow cell RNA was analyzed for lung specific mRNA using real time RT-PCR.
  • RESULTS: Lung cancers studied were adenocarcinoma, endobronchial alveolar carcinoma, bronchioloalveolar carcinoma, non-small cell carcinoma and squamous cell carcinoma. mRNAs for aquaporin 1-5, specific for type I pneumocytes and surfactant A-D, specific for type II pneumocytes, were measured.
  • Aquaporin I was elevated in marrow cells from co culture with all lung cancers; elevations ranging from 2.15 to 56.7 fold (mean 23 fold).
  • Similarly surfactant B mRNA was induced in marrow cells by all lung cancers with fold elevations ranging from 7.9 to 2164 (mean fold elevation 668).
  • CONCLUSIONS: These observations indicate that the genetic phenotype of cells in the vicinity of lung cancer cells can be altered and that these alterations might be mediated by microvesicle transfer of genetic information.

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  • (PMID = 27963460.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Lin DM, Ma Y, Zheng S, Liu XY, Zou SM, Wei WQ: Prognostic value of bronchioloalveolar carcinoma component in lung adenocarcinoma. Histol Histopathol; 2006 06;21(6):627-32
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  • [Title] Prognostic value of bronchioloalveolar carcinoma component in lung adenocarcinoma.
  • BAC is a common pattern in conventional lung adenocarcinoma.
  • As a result, it was difficult to evaluate the prognosis on this type of lung adenocarcinoma.
  • Though the 1999 WHO classification of BAC provides a useful framework, it does not provide detailed enough information to predict prognosis in lung adenocarcinomas with BAC feature.
  • The aim of this study was to address the prognostic value of bronchioloalveolar carcinoma (BAC) component in lung adenocarcinoma.
  • Ninety-one consecutive surgically treated patients with adenocarcinoma exhibiting various degrees of BAC features and complete follow-up records were retrospectively studied.
  • In lung adenocarcinoma, the BAC component may prove to be useful to predict the outcome of the patients, and the percentage of BAC pattern and pathological stage appear to be two independent prognostic factors.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology

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  • (PMID = 16528673.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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16. Mazziotti S, Celona A, Gaeta M: Usefulness of heavily T2-weighted magnetic resonance imaging in the diagnosis of alveolar lung metastases from pancreas mucinous adenocarcinoma. J Thorac Imaging; 2008 Feb;23(1):44-6
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  • [Title] Usefulness of heavily T2-weighted magnetic resonance imaging in the diagnosis of alveolar lung metastases from pancreas mucinous adenocarcinoma.
  • We report the case of a patient with pancreatic adenocarcinoma and mucinous air-space metastases, in which the diagnosis was suspected at magnetic resonance using heavily T2-weighted images obtained with magnetic resonance hydrographic sequences.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / secondary. Magnetic Resonance Imaging / methods. Pancreatic Neoplasms / pathology. Pulmonary Alveoli / pathology
  • [MeSH-minor] Contrast Media / administration & dosage. Diagnosis, Differential. Female. Humans. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 18347520.001).
  • [ISSN] 0883-5993
  • [Journal-full-title] Journal of thoracic imaging
  • [ISO-abbreviation] J Thorac Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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17. Chen J, Zhang J, Zheng XW, Guo YY, Fu X, Li B, Ran PX: [Effect of adenoviral E1A-involved apoptosis of rat alveolar epithelial cells and human lung adenocarcinoma epithelial cell line]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2010 May;26(5):423-6
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  • [Title] [Effect of adenoviral E1A-involved apoptosis of rat alveolar epithelial cells and human lung adenocarcinoma epithelial cell line].
  • AIM: The relationship between latent adenovirus infection and apoptosis of airway epithelial cell have not been well documented.We want to illustrating the roles of adenovirus E1A protein on the apoptotic alveolar epithelial in response to TNF-alpha.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoviridae / genetics. Adenovirus E1A Proteins / metabolism. Apoptosis. Epithelial Cells / pathology. Lung Neoplasms / pathology. Pulmonary Alveoli / pathology

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  • (PMID = 20423646.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / Tumor Necrosis Factor-alpha
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18. Findeis-Hosey JJ, Yang Q, Spaulding BO, Wang HL, Xu H: IMP3 expression is correlated with histologic grade of lung adenocarcinoma. Hum Pathol; 2010 Apr;41(4):477-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IMP3 expression is correlated with histologic grade of lung adenocarcinoma.
  • This study aimed to determine the correlation of insulin-like growth factor II mRNA binding protein 3 expression with histologic grade of lung adenocarcinoma.
  • These findings show that insulin-like growth factor II mRNA binding protein 3 is strongly and diffusely expressed in a large proportion of moderately/poorly differentiated lung adenocarcinomas, in particular in the solid component of mixed subtype adenocarcinomas, less frequently expressed in well-differentiated adenocarcinomas and bronchioloalveolar carcinomas, and negative in atypical adenomatous hyperplasias.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Proteins / biosynthesis. RNA-Binding Proteins / biosynthesis
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Humans. Hyperplasia. Immunohistochemistry. Lung / metabolism. Lung / pathology. Neoplasm Invasiveness. Neoplasm Staging. Precancerous Conditions / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc.
  • (PMID = 20004948.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IMP3 protein, human; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins
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19. Manson GV, Ma PC: Response to pemetrexed chemotherapy in lung adenocarcinoma-bronchioloalveolar carcinoma insensitive to erlotinib. Clin Lung Cancer; 2010 Jan;11(1):57-60
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  • [Title] Response to pemetrexed chemotherapy in lung adenocarcinoma-bronchioloalveolar carcinoma insensitive to erlotinib.
  • Targeted therapy against epidermal growth factor receptor (EGFR) in non-small-cell lung cancer has heralded an era of mutationally targeted inhibition of this receptor and its oncogenic signal transduction using the tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib.
  • Herein, we report a case of a patient with recurrent metastatic lung adenocarcinoma-bronchioloalveolar carcinoma that showed primary insensitivity to erlotinib therapy who later demonstrated substantial durable response to single-agent pemetrexed.
  • We also present discussion on the evolving paradigm of the use of erlotinib in lung cancer and the current status of determinants of sensitivity in pemetrexed chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Glutamates / therapeutic use. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Drug Resistance, Neoplasm. Erlotinib Hydrochloride. Female. Humans. Middle Aged. Neoplasm Metastasis. Neoplasm Recurrence, Local. Pemetrexed. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Quinazolines / pharmacology. Quinazolines / therapeutic use. Treatment Outcome

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  • (PMID = 20085869.001).
  • [ISSN] 1938-0690
  • [Journal-full-title] Clinical lung cancer
  • [ISO-abbreviation] Clin Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glutamates; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; DA87705X9K / Erlotinib Hydrochloride
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20. Garfield DH, Cadranel JL, Wislez M, Franklin WA, Hirsch FR: The bronchioloalveolar carcinoma and peripheral adenocarcinoma spectrum of diseases. J Thorac Oncol; 2006 May;1(4):344-59
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  • [Title] The bronchioloalveolar carcinoma and peripheral adenocarcinoma spectrum of diseases.
  • Bronchioloalveolar carcinoma (BAC) develops from terminal bronchiolar and acinar epithelia, growing along alveolar septa but without evidence of vascular or pleural involvement.
  • A final diagnosis of BAC can only be achieved from a surgical specimen.
  • The recent interest and potential importance of BAC and the related peripheral adenocarcinoma (ADC), mixed subtype, is attributable to mounting evidence that some, perhaps many, of what are called peripheral ADCs have arisen from and often contain BAC.
  • Clinical characteristics often differ from other types of non-small cell lung cancers.
  • Because of frequent lung-only recurrences, lung transplantation, although performed rarely, may hold promise.
  • [MeSH-major] Adenocarcinoma / therapy. Adenocarcinoma, Bronchiolo-Alveolar / therapy. Lung Neoplasms / therapy
  • [MeSH-minor] Female. Humans. Lung Transplantation. Male. Neoplasm Invasiveness. Neoplasm Staging. Positron-Emission Tomography. Prognosis. Tomography, X-Ray Computed

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  • [ErratumIn] J Thorac Oncol. 2006 Jun;1(5):405
  • (PMID = 17409882.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA 058187
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 207
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21. Kamiya K, Hayashi Y, Douguchi J, Hashiguchi A, Yamada T, Izumi Y, Watanabe M, Kawamura M, Horinouchi H, Shimada N, Kobayashi K, Sakamoto M: Histopathological features and prognostic significance of the micropapillary pattern in lung adenocarcinoma. Mod Pathol; 2008 Aug;21(8):992-1001
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  • [Title] Histopathological features and prognostic significance of the micropapillary pattern in lung adenocarcinoma.
  • We investigated the histopathobiological properties of the micropapillary pattern with immunohistochemistry, serial sections, and electron microscopy in lung adenocarcinoma.
  • The subjects included 383 adenocarcinoma cases, of which 184 (48%) were micropapillary pattern-positive and 199 (52%) were micropapillary pattern-negative.
  • On histology, micropapillary tufts seemed to float in the alveolar space or spaces encased by connective tissues, whereas serial sections revealed that most tufts had continuity with other tufts and even with the main tumor.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Lung Neoplasms / pathology

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  • (PMID = 18516041.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Ki-67 Antigen; 0 / Laminin; 0 / beta Catenin
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22. Kubo T, Yamamoto H, Ichimura K, Jida M, Hayashi T, Otani H, Tsukuda K, Sano Y, Kiura K, Toyooka S: DNA methylation in small lung adenocarcinoma with bronchioloalveolar carcinoma components. Lung Cancer; 2009 Sep;65(3):328-32
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  • [Title] DNA methylation in small lung adenocarcinoma with bronchioloalveolar carcinoma components.
  • We examined the methylation status in 100 specimens of lung adenocarcinomas measuring 2cm or less and with bronchioloalveolar carcinoma (BAC) components (Noguchi types A-C) and then compared the methylation status between noninvasive tumors (Noguchi type A or B) and invasive tumors (Noguchi type C).
  • Our results indicate the involvement of epigenetic alterations in the progression of adenocarcinoma with BAC components.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. DNA Methylation. Genes, p16. Lung Neoplasms / genetics

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  • (PMID = 19144441.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cadherins; 0 / Cyclin D2; 0 / DNA, Neoplasm; 0 / H-cadherin; 0 / RASSF1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor beta
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23. Tsutsumida H, Goto M, Kitajima S, Kubota I, Hirotsu Y, Wakimoto J, Batra SK, Imai K, Yonezawa S: MUC4 expression correlates with poor prognosis in small-sized lung adenocarcinoma. Lung Cancer; 2007 Feb;55(2):195-203
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  • [Title] MUC4 expression correlates with poor prognosis in small-sized lung adenocarcinoma.
  • The mortality of lung cancer remains high, despite improved diagnostic techniques that allow small lung tumors to be detected.
  • In this study, we evaluated the prognostic significance of the tracheal mucin MUC4 by immunohistochemical investigation of the expression profiles of MUC4, ErbB2, p27 and MUC1 in lung adenocarcinoma specimens (non-bronchiolo-alveolar type, < or =3cm) from 185 patients.
  • However, MUC4 expression was found to be unrelated to expression of MUC1, ErbB2 and p27 in small-sized lung adenocarcinomas.
  • In conclusion, high MUC4 expression in small-sized lung adenocarcinomas correlates with a short DFI and a poor survival rate.
  • Therefore, MUC4 expression might be a new independent factor for prediction of outcome and indication of poor prognosis in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Mucins / metabolism

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  • (PMID = 17126950.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 78590
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / MUC4 protein, human; 0 / Mucin-4; 0 / Mucins; 0 / Proliferating Cell Nuclear Antigen; 0 / p27 antigen; EC 2.7.10.1 / Receptor, ErbB-2
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24. Zheng B, Zhou J, Geng Q, Dong Q: [A preliminary study on the origin of human lung adenocarcinoma stem cells from lung bonchioalveolar stem cells.]. Zhongguo Fei Ai Za Zhi; 2008 Dec 20;11(6):759-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A preliminary study on the origin of human lung adenocarcinoma stem cells from lung bonchioalveolar stem cells.].
  • BACKGROUND: Lung adenocarcinomas are proposed to originate from the malignant transformation of bronchioalveolar stem cells (BASC).
  • In the present study, we determined to analyze the BASC properties in human lung adenocarcinoma stem cells.
  • METHODS: The human lung adenocarcinoma stem cells were obtained by flow cytometry (FCM) and induced with the sphereforming assay.
  • RESULTS: The majority of A549 and SPC-A1 human lung adenocarcinoma cells expressed the type II alveolar cell-specific marker SP-C.
  • The CD24(+)CD221(+) human lung adenocarcinoma stem cells were purified by FCM and then subjected to the immunofluorescent staining.
  • CONCLUSIONS: The human lung adenocarcinoma stem cells may originate from the transformation of BASC, as their mouse counterparts.

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  • (PMID = 20797324.001).
  • [ISSN] 1999-6187
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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25. Kuroda N, Hamaguchi N, Takeuchi E, Ohara M, Hirouchi T, Mizuno K: Lung adenocarcinoma with a micropapillary pattern: a clinicopathological study of 25 cases. APMIS; 2006 May;114(5):381-5
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  • [Title] Lung adenocarcinoma with a micropapillary pattern: a clinicopathological study of 25 cases.
  • Lung adenocarcinoma with a micropapillary pattern has recently been described, but its biological behavior is as yet uncertain.
  • In this article we present a clinicopathological study of lung adenocarcinoma with micropapillary morphology.
  • We selected 25 patients with lung adenocarcinoma with micropapillary morphology from the 2001-2004 pathology files (age range 54 to 81 years; mean 64.5 years).
  • Micropapillary carcinoma is predominantly located at the periphery of the tumor nodule or mass and occurs irrespective of the subtype of the adenocarcinoma.
  • Four cases showed intensive invasive growth such as micropapillary adenocarcinoma of the breast and 21 showed alveolar type morphology with piling-up of the neoplastic cells with or without stromal invasion.
  • Regarding clinical outcome, 14 patients were alive without disease, 5 were alive with disease, and 5 died of the lung adenocarcinoma.
  • However, the carcinoma seen in the five patients who died showed breast type histology with intensive invasive growth in three cases and alveolar type histology with intensive stromal invasion in two.
  • Lung micropapillary carcinoma of breast type may behave more aggressively than the alveolar type.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Aged. Aged, 80 and over. Calcinosis / pathology. Carcinoma, Acinar Cell / pathology. Female. Humans. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Pleura / pathology. Survival Analysis

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  • (PMID = 16725015.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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26. Suau F, Cottin V, Archer F, Croze S, Chastang J, Cordier G, Thivolet-Béjui F, Mornex JF, Leroux C: Telomerase activation in a model of lung adenocarcinoma. Eur Respir J; 2006 Jun;27(6):1175-82
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  • [Title] Telomerase activation in a model of lung adenocarcinoma.
  • Ovine pulmonary adenocarcinoma (OPA) is a lung cancer strikingly similar to the pneumonic-type mixed invasive adenocarcinoma with a predominant bronchioloalveolar component in humans.
  • Lung tissues were collected from sheep with a histopathological diagnosis of OPA or controls.
  • Epithelial cell cultures were derived in vitro from lung tissues.
  • Telomerase activity was significantly higher in OPA lung tissues compared to control lung tissues.
  • Telomerase activation takes place in ovine pulmonary adenocarcinoma tumour cells and may be partly attributable to Akt activation.
  • Telomerase may inhibit cellular senescence and contribute to the accumulation of tumour cells in mixed adenocarcinoma with a bronchioloalveolar component.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Disease Models, Animal. Jaagsiekte sheep retrovirus / genetics. Lung Neoplasms / genetics. Pulmonary Adenomatosis, Ovine / genetics. Telomerase / genetics
  • [MeSH-minor] Animals. Cell Aging / genetics. Cell Division / genetics. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Enzyme Activation / genetics. Gene Expression Regulation / genetics. Humans. Lung / pathology. Proto-Oncogene Proteins c-akt / genetics. Pulmonary Alveoli / pathology. Sheep. Signal Transduction / genetics. Tumor Cells, Cultured / pathology

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  • [CommentIn] Eur Respir J. 2006 Jun;27(6):1079-81 [16772385.001]
  • (PMID = 16455826.001).
  • [ISSN] 0903-1936
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.7.49 / Telomerase
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27. Sawachi K, Shimada Y, Taniguchi H, Hirota K, Inagawa H, Kohchi C, Soma G, Makino K, Terada H: Cytotoxic effects of activated alveolar macrophages on lung carcinoma cells via cell-to-cell contact and nitric oxide. Anticancer Res; 2010 Aug;30(8):3135-41
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  • [Title] Cytotoxic effects of activated alveolar macrophages on lung carcinoma cells via cell-to-cell contact and nitric oxide.
  • AIM: It is possible that macrophages may be effective for cancer treatment because once activated, lung macrophages have enhanced contact with lung tumor cells and have a cytotoxic effect.
  • In this paper, we report that nitric oxide (NO) produced by lung macrophages activated with lipopolysaccharide (LPS) suppressed cell growth of human lung adenocarcinoma cells.
  • MATERIALS AND METHODS: A549, a lung adenocarcinoma cell line, was cultured with NR8383, a rat alveolar macrophage cell line, in the presence and absence of LPS.
  • CONCLUSION: Activation of alveolar macrophages by LPS suppresses the growth of lung carcinoma cells via NO production under cell-to-cell contact conditions.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Communication. Lung Neoplasms / pathology. Macrophage Activation. Macrophages, Alveolar / immunology. Nitric Oxide / biosynthesis

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  • (PMID = 20871032.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 31C4KY9ESH / Nitric Oxide
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28. Ding L, Getz G, Wheeler DA, Mardis ER, McLellan MD, Cibulskis K, Sougnez C, Greulich H, Muzny DM, Morgan MB, Fulton L, Fulton RS, Zhang Q, Wendl MC, Lawrence MS, Larson DE, Chen K, Dooling DJ, Sabo A, Hawes AC, Shen H, Jhangiani SN, Lewis LR, Hall O, Zhu Y, Mathew T, Ren Y, Yao J, Scherer SE, Clerc K, Metcalf GA, Ng B, Milosavljevic A, Gonzalez-Garay ML, Osborne JR, Meyer R, Shi X, Tang Y, Koboldt DC, Lin L, Abbott R, Miner TL, Pohl C, Fewell G, Haipek C, Schmidt H, Dunford-Shore BH, Kraja A, Crosby SD, Sawyer CS, Vickery T, Sander S, Robinson J, Winckler W, Baldwin J, Chirieac LR, Dutt A, Fennell T, Hanna M, Johnson BE, Onofrio RC, Thomas RK, Tonon G, Weir BA, Zhao X, Ziaugra L, Zody MC, Giordano T, Orringer MB, Roth JA, Spitz MR, Wistuba II, Ozenberger B, Good PJ, Chang AC, Beer DG, Watson MA, Ladanyi M, Broderick S, Yoshizawa A, Travis WD, Pao W, Province MA, Weinstock GM, Varmus HE, Gabriel SB, Lander ES, Gibbs RA, Meyerson M, Wilson RK: Somatic mutations affect key pathways in lung adenocarcinoma. Nature; 2008 Oct 23;455(7216):1069-75
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  • [Title] Somatic mutations affect key pathways in lung adenocarcinoma.
  • Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas.
  • These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B.
  • Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.


29. Tsuta K, Ishii G, Nitadori J, Murata Y, Kodama T, Nagai K, Ochiai A: Comparison of the immunophenotypes of signet-ring cell carcinoma, solid adenocarcinoma with mucin production, and mucinous bronchioloalveolar carcinoma of the lung characterized by the presence of cytoplasmic mucin. J Pathol; 2006 May;209(1):78-87
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  • [Title] Comparison of the immunophenotypes of signet-ring cell carcinoma, solid adenocarcinoma with mucin production, and mucinous bronchioloalveolar carcinoma of the lung characterized by the presence of cytoplasmic mucin.
  • The latest World Health Organization (WHO) classification divides adenocarcinoma mainly into adenocarcinoma mixed subtypes, acinar adenocarcinoma, papillary adenocarcinoma, bronchioloalveolar carcinoma, and solid adenocarcinoma with mucin production, and it mentions several variants, including fetal adenocarcinoma, mucinous ("colloid") adenocarcinoma, mucinous cystadenocarcinoma, signet-ring adenocarcinoma, and clear cell adenocarcinoma.
  • In general, the mucin-producing adenocarcinoma of the lung comprises signet-ring cell carcinoma (SRCC), solid adenocarcinoma with mucin production (SA), and mucinous bronchioloalveolar carcinoma (m-BAC), mucinous ("colloid") adenocarcinomas and/or mucinous cystadenocarcinoma, and mucoepidermoid carcinoma.
  • In this study we analysed SRCC, SA, m-BAC, normal lung, and foregut-related secretory tissue for immunohistochemical differences using tissue microarrays.
  • Hierarchical clustering showed that the immunophenotypes of SRCC and SA belong to the same category as alveolar lining cells, whereas m-BAC clustered onto another branch with gastric foveolar cells and bronchial goblet cells.
  • These immunohistochemical findings support the results of our previous clinicopathological analysis of SRCC of the lung showing that SRCC occurs anatomically in the peripheral portion of the lung rather than in the bronchial gland-bearing portion.
  • [MeSH-major] Adenocarcinoma / immunology. Lung Neoplasms / immunology. Mucins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / immunology. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Mucinous / immunology. Adenocarcinoma, Mucinous / metabolism. Carcinoma, Signet Ring Cell / immunology. Carcinoma, Signet Ring Cell / metabolism. Humans. Immunoenzyme Techniques. Immunophenotyping. Protein Array Analysis / methods

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16463270.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mucins; 0 / Neoplasm Proteins
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30. Abecasis F, Gomes Ferreira M, Oliveira A, Vaz Velho H: [Bronchioloalveolar carcinoma associated with congenital pulmonary airway malformation in an asymptomatic adolescent]. Rev Port Pneumol; 2008 Mar-Apr;14(2):285-90
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  • [Transliterated title] Carcinoma bronquíolo-alveolar associado a malformação congénita das vias aéreas pulmonares em adolescente assintomático.
  • We describe the case of a fourteen-year-old boy evaluated for the presence of a nodular image on the right lung on the chest x-ray.
  • Computerized Tomography (CT) showed a round lesion of medium density with cavitation on the right lung.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / complications. Lung / abnormalities. Lung Neoplasms / complications

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  • (PMID = 18363023.001).
  • [ISSN] 0873-2159
  • [Journal-full-title] Revista portuguesa de pneumologia
  • [ISO-abbreviation] Rev Port Pneumol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Portugal
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31. Kinoshita Y, Kishi K, Takaya H, Miyamoto A, Sakamoto S, Kurosaki A, Fujii T, Yoshimura K: [A case of desquamative interstitial pneumonia with adenocarcinoma of the lung]. Nihon Kokyuki Gakkai Zasshi; 2007 Nov;45(11):861-5
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  • [Title] [A case of desquamative interstitial pneumonia with adenocarcinoma of the lung].
  • A 73-year-old woman was admitted to our hospital because of dyspnea on effort and diffuse ground-glass opacities in bilateral lower lung fields on a chest radiograph.
  • Right upper lobectomy and lung biopsy of the right lower lobe were performed using video-assisted thoracoscopic surgery.
  • Histological examination revealed adenocarcinoma in the right S3 and an accumulation of pigmented macrophages in the alveolar spaces of the lower lobe, which was compatible with desquamative interstitial pneumonia (DIP).
  • It is unlikely that the lung cancer and DIP were closely associated etiologically, because the adenocarcinoma was located far from the area of DIP.
  • [MeSH-major] Adenocarcinoma / complications. Lung Diseases, Interstitial / complications. Lung Neoplasms / complications

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  • (PMID = 18051788.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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32. Archer F, Jacquier E, Lyon M, Chastang J, Cottin V, Mornex JF, Leroux C: Alveolar type II cells isolated from pulmonary adenocarcinoma: a model for JSRV expression in vitro. Am J Respir Cell Mol Biol; 2007 May;36(5):534-40
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  • [Title] Alveolar type II cells isolated from pulmonary adenocarcinoma: a model for JSRV expression in vitro.
  • Ovine pulmonary adenocarcinoma (OPA) is a naturally occurring cancer in sheep, with clinical, radiologic, and histopathologic features similar to that of human pneumonic-type bronchioloalveolar carcinoma.
  • JSRV (Jaagsiekte Sheep RetroVirus) is the etiologic agent of this contagious lung cancer in sheep.
  • Cells involved in the tumor derive from alveolar type II cells and Clara cells, epithelial cells of the distal respiratory tract.
  • In order to investigate the specific interactions between JSRV and alveolar type II cells, we developed an in vitro experimental model in which lung epithelial cells were isolated from OPA and control lungs.
  • Cells in culture expressed alveolar type II cell specific markers such as surfactant protein (SP)-A, SP-C, and a high alkaline phosphatase activity.
  • Alveolar Type II cells derived from tumoral lungs showed a proliferative advantage and expressed the JSRV virus.
  • We thus report on the first in vitro system whereby alveolar type II cells from OPA were efficiently maintained in culture and stably expressed JSRV.
  • This novel experimental model will set up the stage for elucidating lung epithelial transformation in the JSRV-induced tumor.
  • [MeSH-major] Jaagsiekte sheep retrovirus / genetics. Lung Neoplasms / veterinary. Pulmonary Adenomatosis, Ovine / virology. Pulmonary Alveoli / pathology. Pulmonary Alveoli / virology

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  • (PMID = 17158359.001).
  • [ISSN] 1044-1549
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DNA, Viral; 0 / Pulmonary Surfactant-Associated Protein A; 0 / Pulmonary Surfactant-Associated Protein C; EC 2.7.7.49 / RNA-Directed DNA Polymerase
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33. Li Y, Du H, Qin Y, Roberts J, Cummings OW, Yan C: Activation of the signal transducers and activators of the transcription 3 pathway in alveolar epithelial cells induces inflammation and adenocarcinomas in mouse lung. Cancer Res; 2007 Sep 15;67(18):8494-503
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  • [Title] Activation of the signal transducers and activators of the transcription 3 pathway in alveolar epithelial cells induces inflammation and adenocarcinomas in mouse lung.
  • The lung is an organ for host defense to clear up pathogens through innate and adaptive immunity.
  • Overexpression of Stat3C in alveolar type II epithelial cells of CCSP-rtTA/(tetO)(7)-Stat3C bitransgenic mice leads to severe pulmonary inflammation, including immune cell infiltration and up-regulation of proinflammatory cytokines and chemokines in the lung.
  • As a consequence, spontaneous lung bronchoalveolar adenocarcinoma was observed in bitransgenic mice.
  • Aberrantly expressed genes in the bitransgenic model were identified and served as biomarkers for human bronchoalveolar adenocarcinoma.
  • During tumorigenesis, genes that are critical to epithelial cell proliferation in lung development were reactivated.
  • Therefore, Stat3 is a potent proinflammatory molecule that directly causes spontaneous lung cancer in vivo.

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  • (PMID = 17875688.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL061803; United States / NHLBI NIH HHS / HL / R01 HL067862; United States / NHLBI NIH HHS / HL / HL-061803; United States / NHLBI NIH HHS / HL / HL-067862
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 0 / Cytokines; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse
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34. Taniguchi H, Shimada Y, Sawachi K, Hirota K, Inagawa H, Kohchi C, Soma G, Makino K, Terada H: Lipopolysaccharide-activated alveolar macrophages having cytotoxicity toward lung tumor cells through cell-to-cell binding-dependent mechanism. Anticancer Res; 2010 Aug;30(8):3159-65
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  • [Title] Lipopolysaccharide-activated alveolar macrophages having cytotoxicity toward lung tumor cells through cell-to-cell binding-dependent mechanism.
  • BACKGROUND: In lung tumor biotherapy, local macrophages such as alveolar macrophages and tumor-associated macrophages (TAMs) which normally exist in contact with tumor cells are thought to be hopeful target.
  • It is advantageous to clarify the potential for and mechanism by which lung tumor cells are killed by the neighboring macrophages in order to establish new lung cancer therapy using a drug delivery system to lung tissue.
  • MATERIALS AND METHODS: A549, a human lung adenocarcinoma cell line, and Lewis lung carcinoma LLC1, a mouse lung cancer cell line, were co-cultured with NR8383, a rat alveolar macrophage cell line, and AMJ2-C11, a mouse alveolar macrophage cell line, at a ratio of 1:10 and 1:5, respectively.
  • CONCLUSION: The LPS-activated alveolar macrophages demonstrated an increased cell-to-cell contact with lung tumor cells and inducing cytotoxicity with production of NO and cytokines TNF-α and IL-1β.
  • These results suggest that moderate activation of local macrophages in lung (alveolar macrophages and TAMs) is thought to be a hopeful means of establishing new immunotherapy for lung cancer.
  • [MeSH-major] Adenocarcinoma / immunology. Cell Fusion. Lipopolysaccharides / pharmacology. Lung Neoplasms / immunology. Macrophage Activation / drug effects. Macrophages, Alveolar / drug effects

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  • (PMID = 20871035.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
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35. Travis WD, Garg K, Franklin WA, Wistuba II, Sabloff B, Noguchi M, Kakinuma R, Zakowski M, Ginsberg M, Padera R, Jacobson F, Johnson BE, Hirsch F, Brambilla E, Flieder DB, Geisinger KR, Thunnisen F, Kerr K, Yankelevitz D, Franks TJ, Galvin JR, Henderson DW, Nicholson AG, Hasleton PS, Roggli V, Tsao MS, Cappuzzo F, Vazquez M: Evolving concepts in the pathology and computed tomography imaging of lung adenocarcinoma and bronchioloalveolar carcinoma. J Clin Oncol; 2005 May 10;23(14):3279-87
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  • [Title] Evolving concepts in the pathology and computed tomography imaging of lung adenocarcinoma and bronchioloalveolar carcinoma.
  • PURPOSE: To review recent advances in pathology and computed tomography (CT) of lung adenocarcinoma and bronchioloalveolar carcinoma (BAC).
  • METHODS: A pathology/CT review panel of pathologists and radiologists met during a November 2004 International Association for the Study of Lung Cancer/American Society of Clinical Oncology consensus workshop in New York.
  • The purpose was to determine if existing data was sufficient to propose modification of criteria for adenocarcinoma and BAC as newly published in the 2004 WHO Classification of Lung Tumors, and to address the pathologic/radiologic concept of diffuse/multicentric BAC.
  • Most lung adenocarcinomas with a BAC pattern are not pure BAC, but rather adenocarcinoma, mixed subtype with invasive patterns.
  • The percent of BAC versus invasive components in lung adenocarcinomas appears to be prognostically important.
  • While recognition of a BAC component is possible, the diagnosis of BAC with exclusion of invasive adenocarcinoma cannot be made by small biopsy or cytology specimens.
  • CONCLUSION: There is a need to work toward a mutual understanding and consensus between pathologists, clinicians, and researchers with the use of the term BAC versus adenocarcinoma.
  • Hopefully, this work will allow definition of a category of adenocarcinoma, mixed subtype with predominant BAC/minimal invasion and a favorable prognosis.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / radiography. Humans. Neoplasm Staging. Tomography, X-Ray Computed

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  • (PMID = 15886315.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 67
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36. Uji M, Matsushita H, Watanabe T, Suzumura T: [A case of primary Sjögren's syndrome complicated with lung adenocarcinoma]. Nihon Kokyuki Gakkai Zasshi; 2007 May;45(5):409-12
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  • [Title] [A case of primary Sjögren's syndrome complicated with lung adenocarcinoma].
  • The serum value of carcinoembryonic antigen was highly elevated, so we made a presumed diagnosis of primary non-small lung cancer.
  • The elevated values of serum antibodies against SS-A and SS-B and further examinations resulted in a definitive diagnosis of primary Sjögren's syndrome.
  • Autopsy revealed that the mass shadow was a primary lung adenocarcinoma.
  • Those lesions had bullae, emphysema, and alveolar septae thickened by infiltration of lymphoplasmacytic cells.
  • We raise a possibility that lung cancer might derive from cystic lesions associated with Sjögren's syndrome.
  • [MeSH-major] Adenocarcinoma / complications. Lung Neoplasms / complications. Sjogren's Syndrome / complications

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  • (PMID = 17554985.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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37. Toonkel RL, Borczuk AC, Powell CA: Tgf-beta signaling pathway in lung adenocarcinoma invasion. J Thorac Oncol; 2010 Feb;5(2):153-7
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  • [Title] Tgf-beta signaling pathway in lung adenocarcinoma invasion.
  • The clinical importance of lung adenocarcinoma invasion is supported by several recent studies indicating that the risk of death in nonmucinous bronchioloalveolar carcinoma is significantly lower than that of pure invasive tumors and in tumors with greater than 0.5 cm of fibrosis or linear invasion.

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  • (PMID = 20101143.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120174-04; United States / NCI NIH HHS / CA / R01 CA120174; United States / NCI NIH HHS / CA / R01 CA120174-04
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL5; 0 / Transforming Growth Factor beta
  • [Number-of-references] 81
  • [Other-IDs] NLM/ NIHMS251531; NLM/ PMC2992959
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38. Duruisseaux M, Cadranel J, Pérol M, Arpin D: The role of pemetrexed in lung adenocarcinoma, mixed subtype with bronchioloalveolar carcinoma features. Curr Drug Targets; 2010 Jan;11(1):74-7
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  • [Title] The role of pemetrexed in lung adenocarcinoma, mixed subtype with bronchioloalveolar carcinoma features.
  • Bronchioloalveolar carcinoma (BAC) and adenocarcinoma with bronchioloalveolar features (ADC-WBF) belong to the same anatomo-clinical entity and show very similar epidemiologic, clinical and biological characteristics.
  • Pemetrexed has proved to be particularly effective in advanced lung adenocarcinomas and unresectable mesotheliomas, and cases of major and sustained responses of ADC-WBF to pemetrexed have been reported.
  • BAC tumors overexpress FR-alpha, a protein involved in pemetrexed intracellular transport, at rates higher than those observed in lung adenocarcinomas and mesotheliomas and it would seem that pemetrexed efficacy is correlated to FR-alpha expression.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Glutamates / therapeutic use. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy

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  • (PMID = 19839924.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine
  • [Number-of-references] 38
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39. Riquet M, Foucault C, Berna P, Assouad J, Dujon A, Danel C: Prognostic value of histology in resected lung cancer with emphasis on the relevance of the adenocarcinoma subtyping. Ann Thorac Surg; 2006 Jun;81(6):1988-95
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  • [Title] Prognostic value of histology in resected lung cancer with emphasis on the relevance of the adenocarcinoma subtyping.
  • BACKGROUND: Adenocarcinoma (AC) is the most common lung cancer, followed by squamous cell carcinoma (SCC).
  • Therefore, we compared subgroups according to presence or not of bronchioloalveolar carcinoma or solid adenocarcinoma with mucin component, or both.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / mortality. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / surgery. Adenocarcinoma, Bronchiolo-Alveolar / therapy. Adenocarcinoma, Mucinous / mortality. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Mucinous / surgery. Adenocarcinoma, Mucinous / therapy. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant / statistics & numerical data. Combined Modality Therapy. Female. Humans. Life Tables. Male. Middle Aged. Neoplasm Staging. Pneumonectomy / methods. Pneumonectomy / statistics & numerical data. Prognosis. Radiotherapy, Adjuvant / statistics & numerical data. Survival Rate. Treatment Outcome

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  • (PMID = 16731118.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
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40. Matsubara D, Morikawa T, Goto A, Nakajima J, Fukayama M, Niki T: Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis. Mod Pathol; 2009 Jun;22(6):776-85
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  • [Title] Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis.
  • We report here the presence of subepithelial myofibroblasts in pure bronchioloalveolar carcinoma and a subset of invasive lung adenocarcinoma.
  • The subepithelial myofibroblasts we describe were observed in a peculiar location beneath the cancer cells in the alveolar septa.
  • To gain insight into their biological significance, we examined 116 surgically resected lung adenocarcinomas.
  • Analysis of subepithelial myofibroblasts may be helpful in identifying a subset of lung adenocarcinoma with excellent prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Fibroblasts / pathology. Lung Neoplasms / pathology. Myocytes, Smooth Muscle / pathology

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  • (PMID = 19329939.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. Duruisseaux M, Cadranel J, Biron E, Pérol M, Guérin JC, Arpin D: Major and prolonged response to pemetrexed in two cases of lung adenocarcinoma with bronchioloalveolar carcinoma features. Lung Cancer; 2009 Sep;65(3):385-7
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  • [Title] Major and prolonged response to pemetrexed in two cases of lung adenocarcinoma with bronchioloalveolar carcinoma features.
  • Bronchioloalveolar carcinoma (BAC) and adenocarcinoma mixed subtype with bronchioloalveolar features (ADC-WBF) represent a unique anatomo-clinical entity accounting for some 20% of non-small cell lung cancers (NSCLC).
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Antimetabolites, Antineoplastic / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Glutamates / therapeutic use. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology

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  • (PMID = 19346028.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; 935E97BOY8 / Folic Acid; P6YC3EG204 / Vitamin B 12
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42. Goto A, Niki T, Chi-Pin L, Matsubara D, Murakami Y, Funata N, Fukayama M: Loss of TSLC1 expression in lung adenocarcinoma: relationships with histological subtypes, sex and prognostic significance. Cancer Sci; 2005 Aug;96(8):480-6
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  • [Title] Loss of TSLC1 expression in lung adenocarcinoma: relationships with histological subtypes, sex and prognostic significance.
  • The TSLC1 (tumor suppressor in lung cancer 1) gene is a tumor suppressor recently identified through functional complementation in a lung adenocarcinoma cell line A549.
  • In this study we immunohistochemically examined the loss of TSLC1 expression in 93 cases of surgically resected lung adenocarcinoma, and investigated its correlation with clinicopathological parameters, including histological subtypes of tumors.
  • In non-cancerous lung tissue, TSLC1 was weakly positive in bronchial and bronchiolar epithelial cells, type II pneumocytes and bronchial glands.
  • Overall, TSLC1 was negative in 60 of 93 lung adenocarcinomas.
  • Notably, TSLC1 expression was preserved in a non-invasive, bronchiolo-alveolar histological pattern of tumor cells (P < 0.0001).
  • We conclude that TSLC1 is expressed in a subset of lung adenocarcinomas, especially in those with bronchiolo-alveolar spread pattern.
  • [MeSH-major] Adenocarcinoma / genetics. Immunoglobulins / genetics. Lung Neoplasms / genetics. Membrane Proteins / genetics

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  • (PMID = 16108829.001).
  • [ISSN] 1347-9032
  • [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 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / Tumor Suppressor Proteins
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43. Moran CA: Pulmonary adenocarcinoma: the expanding spectrum of histologic variants. Arch Pathol Lab Med; 2006 Jul;130(7):958-62
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  • [Title] Pulmonary adenocarcinoma: the expanding spectrum of histologic variants.
  • Pulmonary adenocarcinoma is one of the most common types of lung cancer.
  • In the majority of cases, this schema is sufficient to categorize these lung tumors.
  • Thus, although the terminology of adenocarcinoma is applied in such cases, the histopathologic features are different from those of the more conventional variants.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / chemistry. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Mucinous / chemistry. Adenocarcinoma, Mucinous / pathology. Biomarkers, Tumor / analysis. Carcinoma, Endometrioid / chemistry. Carcinoma, Endometrioid / pathology. Carcinoma, Non-Small-Cell Lung / chemistry. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Papillary / chemistry. Carcinoma, Papillary / pathology. Carcinoma, Signet Ring Cell / chemistry. Carcinoma, Signet Ring Cell / pathology. Carcinoma, Squamous Cell / chemistry. Carcinoma, Squamous Cell / pathology. Humans. Male

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  • (PMID = 16831050.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 33
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44. Izquierdo-Garcia FM, Moreno-Mata N, Herranz-Aladro ML, Cañizares MA, Alvarez-Fernandez E: Lung carcinoma with rhabdoid component. A series of seven cases associated with uncommon types of non-small cell lung carcinomas and alveolar entrapment. Histol Histopathol; 2010 10;25(10):1287-95
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  • [Title] Lung carcinoma with rhabdoid component. A series of seven cases associated with uncommon types of non-small cell lung carcinomas and alveolar entrapment.
  • Rhabdoid tumor, included in the WHO classification among large cell carcinomas of the lung, is an uncommon type of lung carcinoma with poor prognosis.
  • We report a series of 7 cases of lung carcinomas with rhabdoid component in 10% and 80% of the tumor.
  • The associated tumor was adenocarcinoma in 3 cases--one of them with focal micropapillary pattern--large cell carcinoma in 2 cases, squamous cell carcinoma in 1 case and pleomorphic carcinoma in 1 case.
  • Alveolar trapping inside the tumor was present in 3 cases--a phenomenon not well studied in lung carcinomas and also not reported in tumors with rhabdoid component.
  • Five patients died because of the tumor within 2 to 31 months after diagnosis, one of myocardial infarction and only one is alive and disease free 123 months after the diagnosis.
  • In summary, we describe 7 new cases of this uncommon lung tumor with aggressive clinical course, associated with infrequent histological types in nonrhabdoid component and with alveolar trapping, a nondescribed finding.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Large Cell / pathology. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Pulmonary Alveoli / pathology. Rhabdoid Tumor / pathology

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  • (PMID = 20712013.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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45. Noguchi M, Minami Y, Iijima T, Matsuno Y: Reproducibility of the diagnosis of small adenocarcinoma of the lung and usefulness of an educational program for the diagnostic criteria. Pathol Int; 2005 Jan;55(1):8-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reproducibility of the diagnosis of small adenocarcinoma of the lung and usefulness of an educational program for the diagnostic criteria.
  • Using 32 small adenocarcinomas of the lung including bronchioloalveolar carcinoma (BAC), the reproducibility of diagnosis by the modified diagnostic criteria for small adenocarcinoma (Cancer 75; 2844, 1995) and the effectiveness of an educational program for 27 volunteer general pathologists were examined.
  • The average coincidence rate of the diagnosis before and after the program was 42.4% and 56.6%, respectively.
  • In contrast, the average coincidence rate of six lung cancer specialists was 71.4%, and this was significantly higher than that for general pathologists after the program (P < 0.05).
  • When the cases were divided into two groups (in situ adenocarcinoma (BAC and BAC with alveolar collapse) and early invasive adenocarcinoma), the average coincidence rate for the general pathologists after the program increased to 85.3%, which was significantly higher than that before the program (80.3%; P < 0.05).
  • This trial was thought to provide a theoretical background for the histological diagnosis of peripheral type adenocarcinoma of the lung and to justify the existing diagnostic criteria.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma in Situ / diagnosis. Lung Neoplasms / diagnosis. Pathology, Surgical / education
  • [MeSH-minor] Diagnosis, Differential. Humans. Reproducibility of Results

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  • (PMID = 15660697.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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46. Pasqualini ME, Berra MA, Calderón RO, Cremonezzi DC, Giraudo C, Eynard AR: Dietary lipids modulate eicosanoid release and apoptosis of cells of a murine lung alveolar carcinoma. Prostaglandins Leukot Essent Fatty Acids; 2005 Apr;72(4):235-40
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  • [Title] Dietary lipids modulate eicosanoid release and apoptosis of cells of a murine lung alveolar carcinoma.
  • Plasma membrane fatty acid and cyclooxygenase (COX) and lipoxygenase (LOX) products were investigated in lung alveolar carcinoma cells from mice fed on different diets.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / secretion. Apoptosis / drug effects. Dietary Fats / pharmacology. Eicosanoids / secretion

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  • (PMID = 15763434.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Eicosanoids; 0 / Fatty Acids; EC 1.13.11.12 / Lipoxygenase; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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47. Nakamura N, Kobayashi K, Nakamoto M, Kohno T, Sasaki H, Matsuno Y, Yokota J: Identification of tumor markers and differentiation markers for molecular diagnosis of lung adenocarcinoma. Oncogene; 2006 Jul 13;25(30):4245-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of tumor markers and differentiation markers for molecular diagnosis of lung adenocarcinoma.
  • To identify tumor markers and differentiation markers for lung adenocarcinoma (AdC), we analysed expression profiles of 14,500 genes against three cases of type II alveolar epithelial cells, bronchiolar epithelial cells, and bronchial epithelial cells, respectively, and 10 cases of AdC cells isolated by laser capture microdissection.
  • Hierarchical clustering analysis indicated that AdC cells and noncancerous lung epithelial cells are significantly different in their expression profiles, and that different sets of differentiation markers are expressed among alveolar, bronchiolar and bronchial epithelial cells.
  • Nine genes were identified as being highly expressed in AdC cells, but not expressed in noncancerous lung epithelial cells.
  • Sixteen genes were identified as differentiation markers for lung epithelial cells.
  • Real-time RT-PCR analysis of 45 lung AdC cases further revealed that expression of four tumor markers in AdC cells was significantly higher than that in noncancerous lung cells and that expression of ten differentiation markers was retained in a considerable fraction of lung AdC cases.
  • Similarities and differences in expression profiles between normal epithelial cells from different lung respiratory compartments and AdC cells demonstrated in this study will be informative for the molecular diagnosis of lung AdC.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biomarkers, Tumor. Cell Differentiation. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology

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  • (PMID = 16491115.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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48. Matsushima H, Oda T, Hasejima N, Kou E, Kadoyama C, Takezawa S: [Pulmonary adenocarcinoma with multiloculated cystic change]. Nihon Kokyuki Gakkai Zasshi; 2007 Jul;45(7):556-9
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  • [Title] [Pulmonary adenocarcinoma with multiloculated cystic change].
  • There were no cystic lesions in the other lung fields except a ground-glass attenuation in the left lower lobe.
  • The pathological examination of trans-bronchial lung biopsy specimen revealed adenocarcinoma.
  • Therefore, primary lung cancer was diagnosed, and he underwent left lower lobectomy and mediastinal lymph node resection.
  • Macroscopic examination of the resected lung specimen revealed multiloculated cystic lesions associated with a poorly demarcated white-gray tumor.
  • The histological examination showed that papillary adenocarcinoma proliferated along the alveolar walls and that the walls of the multiloculated cystic lesions were composed of cancer cells.
  • We speculated that adenocarcinoma cells extended along the alveolar walls and destroyed the alveoli without disrupting the overall lung architecture, resulting in enlarged multiloculated cystic lesions.
  • [MeSH-major] Adenocarcinoma / pathology. Cysts / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Humans. Lung / pathology. Male. Middle Aged

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  • (PMID = 17682467.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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49. Hanada S, Maeshima A, Matsuno Y, Ohta T, Ohki M, Yoshida T, Hayashi Y, Yoshizawa Y, Hirohashi S, Sakamoto M: Expression profile of early lung adenocarcinoma: identification of MRP3 as a molecular marker for early progression. J Pathol; 2008 Sep;216(1):75-82
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  • [Title] Expression profile of early lung adenocarcinoma: identification of MRP3 as a molecular marker for early progression.
  • Early lung adenocarcinoma is well-recognized as a small-sized non-invasive adenocarcinoma or localized non-mucinous bronchioloalveolar carcinoma (LNMBAC); however, the molecular events associated with these early lesions are not clear.
  • To determine the genes involved in tumorigenesis at the early stage of lung adenocarcinoma, we compared the mRNA expression profiles of LNMBAC and normal lungs with an oligonucleotide array.
  • Among them, most up-regulated genes, such as AQP3 and Claudin-4, were expressed in both adenocarcinoma cells and type II alveolar pneumocytes, corresponding to the histological similarity between these cell types.
  • However, multidrug resistant protein 3 (MRP3) was only expressed on tumour cell membranes and not in type II alveolar pneumocytes, as confirmed by immunohistochemistry.
  • Moreover, the number of MRP3-positive cells significantly increased from AAH (the precursor lesion of lung adenocarcinoma) to LNMBAC.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / analysis. Lung Neoplasms / genetics. Multidrug Resistance-Associated Proteins / genetics

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  • (PMID = 18604784.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Neoplasm; 0 / multidrug resistance-associated protein 3
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50. Shinmura K, Suzuki M, Yamada H, Tao H, Goto M, Kamo T, Nagura K, Kageyama S, Kato M, Ogawa S, Maekawa M, Takamochi K, Suzuki K, Nakamura T, Sugimura H: Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient. Pathol Int; 2008 Nov;58(11):706-12
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  • [Title] Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient.
  • The incidence of several extracolonic tumors, such as duodenal carcinoma, is higher in familial adenomatous polyposis (FAP) patients than in the general population, but there is little information about lung carcinoma in FAP.
  • A 43-year-old woman presented with a lung tumor 17 years after total colectomy for FAP.
  • Pathohistological analysis of the lung tumor demonstrated mixed adenocarcinoma consisting of a papillary adenocarcinoma component and a bronchioloalveolar carcinoma component.
  • The other APC allele in the lung carcinoma was not inactivated by somatic mutations, promoter methylation, or chromosomal deletion.
  • The present results suggest that the chromosomal copy number alterations detected on SNP microarray were involved in the carcinogenesis of the adenocarcinoma of the lung in the present FAP patient.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Adenomatous Polyposis Coli / pathology. Lung Neoplasms / pathology


51. Ou SH, Ziogas A, Zell JA: Primary signet-ring carcinoma (SRC) of the lung: a population-based epidemiologic study of 262 cases with comparison to adenocarcinoma of the lung. J Thorac Oncol; 2010 Apr;5(4):420-7
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  • [Title] Primary signet-ring carcinoma (SRC) of the lung: a population-based epidemiologic study of 262 cases with comparison to adenocarcinoma of the lung.
  • BACKGROUND: The presence of signet-ring cell component has been described as a prominent feature of EML4-ALK positive non-small cell lung cancer.
  • We investigated the clinicopathologic features and survival outcome of primary signet-ring carcinoma (SRC) of the lung with comparison to adenocarcinoma of the lung.
  • METHODS: Retrospective population-based analysis of histologically diagnosed primary SRC of the lung in the California Cancer Registry between 1989 and 2006 with comparison with adenocarcinoma of the lung.
  • RESULTS: Two hundred sixty-two histologically diagnosed primary SRC of the lung were compared to 50,089 patients with lung adenocarcinoma.
  • Patients with primary SRC of the lung were significantly younger than patients with adenocarcinoma, with a significantly higher proportion of poorly differentiated tumor and stage IV disease.
  • There was no difference in the distribution of gender and ethnicity among patients with SRC when compared to patients with adenocarcinoma.
  • Subset analysis of patients with available smoking status revealed never smokers comprised a significantly higher proportion of patients with SRC (30.8%) when compared to patients with adenocarcinoma (11.0%; p = 0.0013).
  • Patients with SRC had decreased OS (versus adenocarcinoma; unadjusted hazard ratio = 1.507; 95% confidence interval: 1.326-1.714; p < 0.0001) and was an independent unfavorable prognostic factor by multivariate analysis (versus adenocarcinoma, hazard ratio 1.214, 95% confidence interval: 1.068-1.381; p = 0.0030).
  • CONCLUSIONS: Primary SRC of the lung is a rare subtype of adenocarcinoma, carries a worse prognosis when compared to adenocarcinoma and shares many of the recently identified clinicopathologic characteristics ascribed to EML4-ALK positive non-small cell lung cancer.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / epidemiology. Adenocarcinoma, Papillary / epidemiology. Carcinoma, Acinar Cell / epidemiology. Carcinoma, Signet Ring Cell / epidemiology. Lung Neoplasms / epidemiology

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  • (PMID = 20130484.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / PC / N01-PC-35136; United States / NCI NIH HHS / PC / N01-PC-35139; United States / NCI NIH HHS / PC / N01-PC-54404
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
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52. Cadranel J, Lavolé A, Gounant V, Wislez M: [Clinical types of thoracic cancer. Bronchiolo-alveolar carcinoma and adenocarcinoma with bronchioloalveolar features: a clinico-pathological spectrum]. Rev Mal Respir; 2006 Nov;23(5 Pt 3):16S158-16S163
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  • [Title] [Clinical types of thoracic cancer. Bronchiolo-alveolar carcinoma and adenocarcinoma with bronchioloalveolar features: a clinico-pathological spectrum].
  • Bronchioloalveolar carcinoma (BAC) is a primary pulmonary adenocarcinoma (ADC) arising in the cells of the terminal respiratory unit.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology

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  • (PMID = 17268353.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 30
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53. Griffiths DJ, Martineau HM, Cousens C: Pathology and pathogenesis of ovine pulmonary adenocarcinoma. J Comp Pathol; 2010 May;142(4):260-83

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  • [Title] Pathology and pathogenesis of ovine pulmonary adenocarcinoma.
  • Ovine pulmonary adenocarcinoma (OPA), also known as jaagsiekte, is a transmissible lung tumour of sheep caused by jaagsiekte sheep retrovirus (JSRV).
  • JSRV induces neoplastic transformation of alveolar and bronchiolar secretory epithelial cells and the resulting tumours can grow to occupy a significant portion of the lung.
  • Tumour growth is frequently accompanied by the overproduction of fluid in the lung, which further compromises normal respiration.
  • In addition to its veterinary importance, OPA is regarded as a potential large animal model for human lung adenocarcinoma and this has stimulated research into the pathogenesis of the ovine disease.
  • The recent advances in understanding JSRV and the pathogenesis of OPA should lead to novel strategies for diagnosis and control of this disease and for its exploitation as a comparative model for human lung cancer.
  • [MeSH-major] Adenocarcinoma / virology. Jaagsiekte sheep retrovirus / physiology. Pulmonary Adenomatosis, Ovine. Sheep Diseases / virology
  • [MeSH-minor] Animals. Body Fluids / virology. Epithelial Cells / pathology. Epithelial Cells / virology. Humans. Lung / pathology. Lung / virology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Lung Neoplasms / virology. Models, Animal. Sheep / genetics. Sheep / virology. Sheep, Domestic / genetics. Sheep, Domestic / virology

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20163805.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 171
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54. Weydert JA, Cohen MB: Small peripheral pulmonary adenocarcinoma: morphologic and molecular update. Adv Anat Pathol; 2007 Mar;14(2):120-8
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  • [Title] Small peripheral pulmonary adenocarcinoma: morphologic and molecular update.
  • The dichotomous histopathologic separation of lung carcinoma into "small cell" and "nonsmall cell" categories is validated by marked clinical and biologic differences between these groups of tumors.
  • However, nonsmall cell carcinoma represents a heterogenous group of tumors, and the subclassification of nonsmall cell lung carcinoma at the molecular, morphologic, and epidemiologic levels has led to the promise of precise treatment and better prognostication.
  • Activating mutations and increased gene copy number of the epidermal growth factor receptor protein and locus, respectively, have been shown to help predict responsiveness to small molecule receptor tyrosine kinase inhibitors in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar. Lung Neoplasms

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  • (PMID = 17471118.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 65
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55. Lin DM, Ma Y, Liu XY, Zheng S, Xue LY, Liu XY, Zou SM, Lü N, He ZG, Liu FS: [Prognostic significance of micropapillary pattern in pulmonary adenocarcinoma]. Zhonghua Bing Li Xue Za Zhi; 2006 Mar;35(3):151-4
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  • [Title] [Prognostic significance of micropapillary pattern in pulmonary adenocarcinoma].
  • OBJECTIVE: To evaluate the prognostic significance of micropapillary pattern (MPP) in adenocarcinoma of lung.
  • METHODS: Ninety-one consecutively excised cases of pulmonary adenocarcinoma, including follow-up data, were retrospectively studied.
  • In pulmonary adenocarcinoma, this characteristic histology correlated with tumor stage and size, but not with patient's gender and smoking history.
  • CONCLUSIONS: MPP in primary pulmonary adenocarcinoma, even when only constituting a minor component, predicts an aggressive clinical behavior and is associated with poor prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Papillary / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Bronchiolo-Alveolar / surgery. Adult. Aged. Female. Follow-Up Studies. Humans. Lung / pathology. Lung / surgery. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16630503.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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56. Wislez M, Fujimoto N, Izzo JG, Hanna AE, Cody DD, Langley RR, Tang H, Burdick MD, Sato M, Minna JD, Mao L, Wistuba I, Strieter RM, Kurie JM: High expression of ligands for chemokine receptor CXCR2 in alveolar epithelial neoplasia induced by oncogenic kras. Cancer Res; 2006 Apr 15;66(8):4198-207
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  • [Title] High expression of ligands for chemokine receptor CXCR2 in alveolar epithelial neoplasia induced by oncogenic kras.
  • Here, we investigated the role of KC and MIP-2, the murine homologues of CXCL8, in Kras(LA1) mice, which develop lung adenocarcinoma owing to somatic activation of the KRAS oncogene.
  • Malignant progression of normal alveolar epithelial cells to adenocarcinoma in Kras(LA1) mice was associated with enhanced intralesional vascularity and neutrophilic inflammation, which are hallmarks of chemoattraction by CXCR2 ligands.
  • In in vitro migration assays, supernatants of bronchoalveolar lavage samples from Kras(LA1) mice chemoattracted murine endothelial cells, alveolar inflammatory cells, and the LKR-13 lung adenocarcinoma cell line derived from Kras(LA1) mice, an effect that was abrogated by pretreatment of the cells with a CXCR2-neutralizing antibody.
  • CXCR2 and its ligands were highly expressed in LKR-13 cells and premalignant alveolar lesions in Kras(LA1) mice.
  • Treatment of Kras(LA1) mice with a CXCR2-neutralizing antibody inhibited the progression of premalignant alveolar lesions and induced apoptosis of vascular endothelial cells within alveolar lesions.
  • Thus, high expression of CXCR2 ligands may contribute to the expansion of early alveolar neoplastic lesions induced by oncogenic KRAS.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Genes, ras. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptors, Interleukin-8B / metabolism

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  • (PMID = 16618742.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA87879; United States / NCI NIH HHS / CA / P30 CA16672; United States / NCI NIH HHS / CA / P50 CA70907; United States / NCI NIH HHS / CA / P50 CA90388; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL1; 0 / Chemokine CXCL2; 0 / Chemokines; 0 / Chemokines, CXC; 0 / Cxcl1 protein, mouse; 0 / Cxcl2 protein, mouse; 0 / Cytokines; 0 / Ligands; 0 / Receptors, Interleukin-8B; 147037-79-4 / keratinocyte-derived chemokines
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57. Travis WD, Garg K, Franklin WA, Wistuba II, Sabloff B, Noguchi M, Kakinuma R, Zakowski M, Ginsberg M, Padera R, Jacobson F, Johnson BE, Hirsch F, Brambilla E, Flieder DB, Geisinger KR, Thunnissen F, Kerr K, Yankelevitz D, Franks TJ, Galvin JR, Henderson DW, Nicholson AG, Hasleton PS, Roggli V, Tsao MS, Cappuzzo F, Vazquez M: Bronchioloalveolar carcinoma and lung adenocarcinoma: the clinical importance and research relevance of the 2004 World Health Organization pathologic criteria. J Thorac Oncol; 2006 Nov;1(9 Suppl):S13-9
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  • [Title] Bronchioloalveolar carcinoma and lung adenocarcinoma: the clinical importance and research relevance of the 2004 World Health Organization pathologic criteria.
  • INTRODUCTION: Advances in the pathology and computed tomography (CT) of lung adenocarcinoma and bronchioloalveolar carcinoma (BAC) have demonstrated important new prognostic features that have led to changes in classification and diagnostic criteria.
  • METHODS: The literature and a set of cases were reviewed by a pathology/CT review panel of pathologists and radiologists who met during a November 2004 International Association for the Study of Lung Cancer/American Society of Clinical Oncology consensus workshop in New York.
  • The group addressed the question of whether sufficient data exist to modify the 2004 World Health Organization (WHO) classification of adenocarcinoma and BAC to define a "minimally invasive" adenocarcinoma with BAC.
  • The problems of diffuse and/or multicentric BAC and adenocarcinoma were evaluated.
  • Most lung adenocarcinomas, including those with a BAC component, are invasive and consist of a mixture of histologic patterns.
  • Therefore, they are best classified as adenocarcinoma, mixed subtype.
  • The percentage of BAC versus invasive components in lung adenocarcinomas seems to be prognostically important.
  • The diagnosis of BAC requires thorough histologic sampling of the tumor.
  • CONCLUSION: Advances in understanding of the pathology and CT features of BAC and adenocarcinoma have led to important changes in diagnostic criteria and classification of BAC and adenocarcinoma.
  • The 2004 WHO classification of adenocarcinoma is readily applicable to research studies, but attention needs to be placed on the relative proportion of the adenocarcinoma subtypes.
  • More work is needed to determine the most important prognostic pathologic features in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / classification. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / classification. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / classification. Adenocarcinoma / pathology. Adenocarcinoma / radiography. Biopsy, Needle. Cytodiagnosis / methods. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Risk Factors. Sensitivity and Specificity. Tomography, X-Ray Computed. World Health Organization

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  • (PMID = 17409995.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Consensus Development Conference; Journal Article
  • [Publication-country] United States
  • [Number-of-references] 43
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58. Kodama K, Ishii G, Miyamoto S, Goya M, Zhang SC, Sangai T, Yoshikawa T, Hasebe T, Hitomi Y, Izumi K, Ochiai A: Laminin 5 expression protects against anoikis at aerogenous spread and lepidic growth of human lung adenocarcinoma. Int J Cancer; 2005 Oct 10;116(6):876-84
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  • [Title] Laminin 5 expression protects against anoikis at aerogenous spread and lepidic growth of human lung adenocarcinoma.
  • Adenocarcinoma of the lung is characterized by frequent aerogenous spread (AE) and advancement along the alveolar wall (BAC growth).
  • To elucidate the mechanism of AE metastasis and BAC growth in human lung adenocarcinoma, we established an in vivo orthotopic animal model and an in vitro culture.
  • BAC growth ratio and AE was confirmed to be significantly correlated with LN5 expression in surgically resected human lung adenocarcinomas by immunohistochemistry.
  • Our results indicate that the activation of the EGF receptor by overexpressing LN5-integrin-FAK signaling pathway may play a crucial role in BAC growth and AE metastasis in human lung adenocarcinoma.
  • [MeSH-major] Anoikis / physiology. Gene Expression Regulation, Neoplastic. Laminin / genetics. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Division. Cell Line, Tumor. DNA Primers. Disease Models, Animal. Flow Cytometry. Humans. Immunohistochemistry. Integrins / genetics. Male. Mice. Mice, SCID. Polymerase Chain Reaction. RNA, Messenger / genetics. Retroviridae / genetics. Transplantation, Heterologous

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  • (PMID = 15856467.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Integrins; 0 / LAMB1 protein, human; 0 / Lamb1-1 protein, mouse; 0 / Laminin; 0 / RNA, Messenger; 170834-93-2 / laminin alpha 3
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59. Yamaguchi Y, Ishii G, Kojima M, Yoh K, Otsuka H, Otaki Y, Aokage K, Yanagi S, Nagai K, Nishiwaki Y, Ochiai A: Histopathologic features of the tumor budding in adenocarcinoma of the lung: tumor budding as an index to predict the potential aggressiveness. J Thorac Oncol; 2010 Sep;5(9):1361-8
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  • [Title] Histopathologic features of the tumor budding in adenocarcinoma of the lung: tumor budding as an index to predict the potential aggressiveness.
  • The purpose of this study was to evaluate the clinicopathologic significance of tumor budding in adenocarcinomas of the lung.
  • METHODS: We investigated the relationship between tumor budding and clinicopathologic parameters of adenocarcinomas of the lung and the prognostic significance of tumor budding by reviewing the cases of 201 consecutive patients who had undergone complete resection of adenocarcinoma of the lung measuring 30 mm or less in diameter.
  • RESULTS: Tumor budding was observed in 78 (43.1%) of the 181 cases with invasive adenocarcinoma.
  • Multivariate analysis revealed that tumor budding was significant independent prognostic factor of the small-sized adenocarcinoma of the lung.
  • CONCLUSIONS: Our data showed that tumor budding in adenocarcinoma of the lung is a distinct morphologic feature that has biologic and prognostic significance.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Papillary / pathology. Lung Neoplasms / pathology. Pleural Neoplasms / pathology

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  • (PMID = 20631633.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Cell Adhesion Molecules; 0 / beta Catenin; 0 / kalinin
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60. Amatya VJ, Takeshima Y, Kohno H, Kushitani K, Yamada T, Morimoto C, Inai K: Caveolin-1 is a novel immunohistochemical marker to differentiate epithelioid mesothelioma from lung adenocarcinoma. Histopathology; 2009 Jul;55(1):10-9
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  • [Title] Caveolin-1 is a novel immunohistochemical marker to differentiate epithelioid mesothelioma from lung adenocarcinoma.
  • There is difficulty in the accurate diagnosis of mesothelioma and its differentiation from lung adenocarcinoma.
  • Therefore, the use of a immunohistochemical panel that includes both positive and negative mesothelial markers has become a general rule for its accurate diagnosis.
  • The aim was to assess the diagnostic utility of caveolin-1 (Cav-1), which is expressed in endothelial cells, alveolar type I pneumocytes and mesothelial cells, as a novel positive marker of mesothelioma.
  • METHODS AND RESULTS: An immunohistochemical study of 80 cases of epithelioid mesothelioma and 80 cases of lung adenocarcinoma was performed for the analysis of the expression of Cav-1 and other markers.
  • In contrast, only six cases (7.5%) of lung adenocarcinoma showed focal Cav-1 expression in the cytoplasm of the tumour cells.
  • The sensitivity and specificity of Cav-1 expression for the differentiation of epithelioid mesothelioma from lung adenocarcinoma were 100 and 92.5%, respectively.
  • CONCLUSIONS: Cav-1 is a novel immunohistochemical marker for the differentiation of epithelioid mesothelioma from lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / metabolism. Caveolin 1 / metabolism. Lung Neoplasms / diagnosis. Mesothelioma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Epithelioid Cells / pathology. Humans. Sensitivity and Specificity

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  • (PMID = 19614762.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Caveolin 1
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61. Yamaguchi E, Nakayama T, Nanashima A, Matsumoto K, Yasutake T, Sekine I, Nagayasu T: Ets-1 proto-oncogene as a potential predictor for poor prognosis of lung adenocarcinoma. Tohoku J Exp Med; 2007 Sep;213(1):41-50
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  • [Title] Ets-1 proto-oncogene as a potential predictor for poor prognosis of lung adenocarcinoma.
  • We hypothesized that Ets-1 expression is also associated with tumor progression and a worse prognosis in lung carcinoma patients.
  • To clarify the role of the Ets-1 proto-oncogene, the expression of Ets-1 in non-small cell lung carcinomas using 156 paraffin-embedded specimens was determined in surgically resected tissue samples.
  • In adenocarcinomas, a higher proportion of acinar type expressed Ets-1 compared to papillary or alveolar type (p < 0.05).
  • The proportion of adenocarcinoma that expressed Ets-1 increased with poorer histologic differentiation of the adenocarcinoma (p < 0.05).
  • In adenocarcinoma patients, expression of Ets-1 was associated with disease-free (p = 0.09) and overall survivals (p < 0.05) after lung resection.
  • Our findings indicate that Ets-1 expression is related to histopathological differentiation, morphogenesis, and tumor progression of lung adenocarcinomas.
  • Ets-1 appears to be a useful predictor of poor prognosis after surgical resection in lung adenocarcinoma patients.
  • Ets-1 expression could be used to evaluate the malignant behaviors of lung adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Proto-Oncogene Protein c-ets-1 / metabolism

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  • (PMID = 17785952.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proto-Oncogene Protein c-ets-1
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62. Hata A, Katakami N, Fujita S, Kaji R, Imai Y, Takahashi Y, Nishimura T, Tomii K, Ishihara K: Frequency of EGFR and KRAS mutations in Japanese patients with lung adenocarcinoma with features of the mucinous subtype of bronchioloalveolar carcinoma. J Thorac Oncol; 2010 Aug;5(8):1197-200
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  • [Title] Frequency of EGFR and KRAS mutations in Japanese patients with lung adenocarcinoma with features of the mucinous subtype of bronchioloalveolar carcinoma.
  • INTRODUCTION: Adenocarcinoma of the lung, especially bronchioloalveolar carcinoma (BAC) and adenocarcinoma with BAC features (AWBF), is potentially sensitive to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs); however, the efficacy seems to differ between the histologic subtypes.
  • METHODS: One hundred ninety-one patients with adenocarcinoma of the lung underwent surgery at our institution.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Mucinous / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Mutation / genetics. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Incidence. Male. Middle Aged. Polymerase Chain Reaction. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Survival Rate. Treatment Outcome

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  • (PMID = 20661086.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins; S65743JHBS / gefitinib
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63. Sakao Y, Miyamoto H, Sakuraba M, Oh T, Shiomi K, Sonobe S, Izumi H: Prognostic significance of a histologic subtype in small adenocarcinoma of the lung: the impact of nonbronchioloalveolar carcinoma components. Ann Thorac Surg; 2007 Jan;83(1):209-14
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  • [Title] Prognostic significance of a histologic subtype in small adenocarcinoma of the lung: the impact of nonbronchioloalveolar carcinoma components.
  • BACKGROUND: We tried to clarify whether the histologic subtypes and the size of the solid component of an adenocarcinoma are more important predictive factors for invasiveness or prognosis than is total tumor size, even in lung adenocarcinomas that were 2 cm or smaller.
  • METHODS: Between 1996 and December 2005, after standard surgical treatment, 82 patients were diagnosed as having adenocarcinoma with a maximum diameter of 2 cm or less.
  • Histologic subtype was classified into two groups: mixed BAC (mixed adenocarcinoma with BAC) and minimal or non-BAC (tumors with little or no BAC component).
  • The first category is a minimal or non-BAC adenocarcinoma that shows aggressive biological behavior.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma, Bronchiolo-Alveolar / classification. Lung Neoplasms / classification

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  • [CommentIn] Ann Thorac Surg. 2007 Jan;83(1):214-5 [17184665.001]
  • (PMID = 17184664.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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64. Howroyd P, Allison N, Foley JF, Hardisty J: Apparent alveolar bronchiolar tumors arising in the mediastinum of F344 rats. Toxicol Pathol; 2009 Apr;37(3):351-8
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  • [Title] Apparent alveolar bronchiolar tumors arising in the mediastinum of F344 rats.
  • Rare tumors were observed in chronic studies in F-344 rats that were purely or largely free in the mediastinal cavity, yet had the histological architecture of alveolar bronchiolar tumors.
  • They had originally been diagnosed as either pulmonary alveolar bronchiolar tumors, mediastinal mesotheliomas, or thymomas.
  • Sections of 715 thoracic tumors originally diagnosed as alveolar bronchiolar tumors, mesotheliomas, or thymomas from control or treated F-344 rats in NTP two-year studies were reviewed.
  • Thirty (4%) were found to be purely or largely mediastinal, yet to have an alveolar bronchiolar histological pattern.
  • A subset of these tumors and some typical intrapulmonary alveolar bronchiolar carcinomas and pleural mesotheliomas were immunostained for Clara cell secretory protein (CCSP), beta-tubulin IV, and Wilm's tumor 1 susceptibility gene products (WT1).
  • The tumors with the histological architecture of alveolar bronchiolar tumors immunostained positive for CCSP and negative for WT1, implying they might have been of alveolar bronchiolar origin, despite their predominantly mediastinal location, although more certain identification would require the use of a larger panel of antibodies.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / secondary. Lung Neoplasms / pathology. Mediastinal Neoplasms / secondary

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  • (PMID = 19380845.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tubulin; 9060-09-7 / Uteroglobin
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65. Takeuchi A, Tsuchida M, Hashimoto T, Shinohara H, Hayashi J: Segmentectomy for multiple adenocarcinoma presenting as ground-glass opacities after lung cancer surgery. Gen Thorac Cardiovasc Surg; 2008 Aug;56(8):410-2
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  • [Title] Segmentectomy for multiple adenocarcinoma presenting as ground-glass opacities after lung cancer surgery.
  • During follow-up of patients after primary lung cancer resections, small nodules or ground-glass opacities (GGOs) are sometimes detected on chest computed tomography.
  • We report a case with multiple GGOs that were noted after primary lung cancer resection.
  • On histology, one adenocarcinoma and four bronchioloalveolar carcinomas (BACs), as well as two additional BACs that had not been detected preoperatively, were identified.
  • Given the high possibility of malignancy, the appearance of new GGOs in patients with a history of lung cancer requires appropriate investigation.
  • [MeSH-major] Adenocarcinoma / surgery. Adenocarcinoma, Bronchiolo-Alveolar / surgery. Lung Neoplasms / surgery. Neoplasms, Second Primary / surgery. Pneumonectomy / methods

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  • (PMID = 18696207.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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66. Shibata T, Hanada S, Kokubu A, Matsuno Y, Asamura H, Ohta T, Sakamoto M, Hirohashi S: Gene expression profiling of epidermal growth factor receptor/KRAS pathway activation in lung adenocarcinoma. Cancer Sci; 2007 Jul;98(7):985-91
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  • [Title] Gene expression profiling of epidermal growth factor receptor/KRAS pathway activation in lung adenocarcinoma.
  • We examined the genome-wide expression profiles of 86 primary lung adenocarcinomas and compared them with the mutation status of the four key molecules (EGFR, ERBB2, KRAS and BRAF) in the EGFR/KRAS/BRAF pathway.
  • Unsupervised classification revealed two subtypes (the bronchial type and the alveolar type) of lung adenocarcinoma.
  • KRAS mutations were observed significantly frequently in bronchial-type tumors, whereas the frequencies of EGFR mutations were similar in both the alveolar and bronchial types.
  • In particular, expression of BCR, which is required for EGFR protein degradation, was induced by EGF stimulation, suggesting a negative feedback loop in lung cancer.
  • A subgroup of the alveolar type tumors showed significantly better prognosis than other tumors.
  • [MeSH-major] Adenocarcinoma / genetics. Gene Expression Profiling. Lung Neoplasms / genetics. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics


67. Nakano H, Soda H, Takasu M, Tomonaga N, Yamaguchi H, Nakatomi K, Fujino S, Hayashi T, Nakamura Y, Tsukamoto K, Kohno S: Heterogeneity of epidermal growth factor receptor mutations within a mixed adenocarcinoma lung nodule. Lung Cancer; 2008 Apr;60(1):136-40
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  • [Title] Heterogeneity of epidermal growth factor receptor mutations within a mixed adenocarcinoma lung nodule.
  • It has been proposed that stepwise progression occurs from atypical adenomatous hyperplasia (AAH) through bronchioloalveolar carcinoma (BAC) to invasive lung adenocarcinoma.
  • We report a patient with a mixed adenocarcinoma of the lung that had different EGFR mutations in the papillary subtype, the acinar subtype, and the surrounding AAH and BAC areas.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics. Solitary Pulmonary Nodule / genetics

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  • (PMID = 17889960.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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68. Yoneda M, Suzuki T, Nakamura T, Ajima R, Yoshida Y, Kakuta S, Katsuko S, Iwakura Y, Shibutani M, Mitsumori K, Yokota J, Yamamoto T: Deficiency of antiproliferative family protein Ana correlates with development of lung adenocarcinoma. Cancer Sci; 2009 Feb;100(2):225-32
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  • [Title] Deficiency of antiproliferative family protein Ana correlates with development of lung adenocarcinoma.
  • Here, we show that expression of ana is relatively high in the lung, the expression being restricted in type II alveolar epithelial cells.
  • We further show that ana expression is reduced in 97% of the human lung cancer cell lines examined (61/63) and 86% of clinical samples from lung adenocarcinoma patients (36/42).
  • Long-term observation of ana-deficient (ana−/–) mice reveals that 8% of them develop lung tumors (5/66) by 21 months after birth, while 0% of wild-type mice (0/35) develop the same type of tumors.
  • We also show that exogenously expressed ana gene product suppresses the levels of matrix metalloproteinase-2 (MMP-2) and plasminogen activator inhibitor-1 (PAI-1) expression in lung cancer cells.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Proteins / metabolism. Proteins / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Proliferation. Female. Humans. Lung / metabolism. Lung / pathology. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. Middle Aged. NIH 3T3 Cells. Plasminogen Activator Inhibitor 1 / genetics. Plasminogen Activator Inhibitor 1 / metabolism. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19068083.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BTG3 protein, human; 0 / Btg3 protein, mouse; 0 / Plasminogen Activator Inhibitor 1; 0 / Proteins; 0 / RNA, Messenger; EC 3.4.24.24 / Matrix Metalloproteinase 2
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69. Wislez M, Spencer ML, Izzo JG, Juroske DM, Balhara K, Cody DD, Price RE, Hittelman WN, Wistuba II, Kurie JM: Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras. Cancer Res; 2005 Apr 15;65(8):3226-35
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  • [Title] Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras.
  • The serine/threonine kinase AKT and its downstream mediator mammalian target of rapamycin (mTOR) are activated in lung adenocarcinoma, and clinical trials are under way to test whether inhibition of mTOR is useful in treating lung cancer.
  • Here, we report that mTOR inhibition blocked malignant progression in K-ras(LA1) mice, which undergo somatic activation of the K-ras oncogene and display morphologic changes in alveolar epithelial cells that recapitulate those of precursors of human lung adenocarcinoma.
  • Levels of phospho-S6(Ser236/235), a downstream mediator of mTOR, increased with malignant progression (normal alveolar epithelial cells to adenocarcinoma) in K-ras(LA1) mice and in patients with lung adenocarcinoma.
  • Atypical alveolar hyperplasia, an early neoplastic change, was prominently associated with macrophages and expressed high levels of phospho-S6(Ser236/235).
  • mTOR inhibition in K-ras(LA1) mice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial neoplastic lesions (atypical alveolar hyperplasia and adenomas) and induced apoptosis of intraepithelial macrophages.
  • LKR-13, a lung adenocarcinoma cell line derived from K-ras(LA1) mice, was resistant to treatment with CCI-779 in vitro.
  • Lastly, conditioned medium from primary cultures of alveolar macrophages stimulated the proliferation of LKR-13 cells.
  • These findings provide evidence that the expansion of lung adenocarcinoma precursors induced by oncogenic K-ras requires mTOR-dependent signaling and that host factors derived from macrophages play a critical role in adenocarcinoma progression.
  • [MeSH-major] Adenocarcinoma / enzymology. Genes, ras / genetics. Lung Neoplasms / enzymology. Precancerous Conditions / enzymology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / metabolism. Pulmonary Alveoli / pathology. Sirolimus / analogs & derivatives. Sirolimus / pharmacology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Adenoma / pathology. Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Disease Progression. Enzyme Activation. Hyperplasia. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. Macrophages, Alveolar / pathology. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Ribosomal Protein S6 Kinases / biosynthesis. TOR Serine-Threonine Kinases

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  • (PMID = 15833854.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; W36ZG6FT64 / Sirolimus
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70. Yoo SB, Chung JH, Lee HJ, Lee CT, Jheon S, Sung SW: Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung. J Thorac Oncol; 2010 Jul;5(7):964-9
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  • [Title] Epidermal growth factor receptor mutation and p53 overexpression during the multistage progression of small adenocarcinoma of the lung.
  • INTRODUCTION: A progression model of atypical adenomatous hyperplasia (AAH) to bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma (ADC) has been proposed.
  • CONCLUSIONS: High frequency and similar incidence of EGFR mutation in AAH, BAC, and ADC support that EGFR gene mutation occurs in the early stage of pulmonary ADC development and tumor initiation from the preneoplastic lung parenchyma to neoplastic conditions.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenomatosis, Pulmonary / genetics. Adenomatosis, Pulmonary / metabolism. Adenomatosis, Pulmonary / pathology. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Polymerase Chain Reaction. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prognosis

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  • (PMID = 20512074.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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71. Land SC, Rae C: iNOS initiates and sustains metabolic arrest in hypoxic lung adenocarcinoma cells: mechanism of cell survival in solid tumor core. Am J Physiol Cell Physiol; 2005 Oct;289(4):C918-33
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  • [Title] iNOS initiates and sustains metabolic arrest in hypoxic lung adenocarcinoma cells: mechanism of cell survival in solid tumor core.
  • Mitochondria from human alveolar type II-like adenocarcinoma (A549) cells showed a fourfold increase in NO-sensitive 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM) fluorescence and sixfold increase in Ca2+-insensitive NO synthase (NOS) activity during equilibration from Po2s of 100-->23 mmHg, which was abolished by N(omega)-nitro-L-arginine methyl ester-HCl (L-NAME) and the inducible NOS (iNOS) inhibitor, N6-(1-iminoethyl)-L-lysine dihydrochloride (L-NIL).
  • Comparison with other cancer-derived (H441) or native tissue-derived (human bronchial epithelial; alveolar type II) lung epithelial cells revealed that the hypoxic suppression of deltapsi(m) was common to cells that expressed iNOS.
  • [MeSH-major] Adenocarcinoma / enzymology. Lung Neoplasms / enzymology. Nitric Oxide Synthase / metabolism

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  • (PMID = 15901597.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 8L70Q75FXE / Adenosine Triphosphate; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; IY9XDZ35W2 / Glucose
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72. Nakanishi K, Matsuo H, Kanai Y, Endou H, Hiroi S, Tominaga S, Mukai M, Ikeda E, Ozeki Y, Aida S, Kawai T: LAT1 expression in normal lung and in atypical adenomatous hyperplasia and adenocarcinoma of the lung. Virchows Arch; 2006 Feb;448(2):142-50
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  • [Title] LAT1 expression in normal lung and in atypical adenomatous hyperplasia and adenocarcinoma of the lung.
  • No previous study has investigated neutral large amino acid transporter type 1 (LAT1) in normal lung cells, or in atypical adenomatous hyperplasia(s) (AAH) and nonmucinous bronchioloalveolar carcinoma(s) (NMBAC) of the lung.
  • (1) the levels of LAT1 mRNA/glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA in 41 normal lung tissues and 34 NMBAC using semiquantitative reverse transcription-polymerase chain reaction;.
  • (2) LAT1 mRNA and protein expressions in 35 normal lung tissues, 34 AAH (11 lesions were interpreted as low-grade AAH and 23 as high-grade AAH), and 43 NMBAC using in situ hybridization and immunohistochemistry; and (2) the association of the incidences of LAT1 mRNA and protein expressions with cell proliferation in these lesions.
  • The level of LAT1 mRNA/GAPDH mRNA (1) tended to be higher in NMBAC (12.0+/-8.1) than in normal lung tissues (1.0+/-0.2), and (2) covered a much wider range (from 0 to 276) in NMBAC than in normal lung tissues (from 0 to 5.8), with six NMBAC having values higher than 7.0, while 5.8 was the highest value detected in normal lung tissues.
  • In peripheral normal lung tissues, LAT1 mRNA and protein were detected in bronchial surface epithelial cells and alveolar macrophages (but not in nonciliated bronchiolar epithelial cells, or in alveolar type I or type II cells).
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenomatosis, Pulmonary / pathology. Large Neutral Amino Acid-Transporter 1 / genetics. Lung / metabolism. Lung Neoplasms / pathology

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  • [Cites] J Biol Chem. 2001 May 18;276(20):16877-84 [11278397.001]
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  • (PMID = 16175382.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Large Neutral Amino Acid-Transporter 1; 0 / RNA, Messenger
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73. Chatterji B, Borlak J: Serum proteomics of lung adenocarcinomas induced by targeted overexpression of c-raf in alveolar epithelium identifies candidate biomarkers. Proteomics; 2007 Nov;7(21):3980-91
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  • [Title] Serum proteomics of lung adenocarcinomas induced by targeted overexpression of c-raf in alveolar epithelium identifies candidate biomarkers.
  • We previously reported a proteome map of lung adenocarcinomas in serine-threonine kinase of the Raf family (c-raf) transgenic mice.
  • Notably, we demonstrate significant regulation of alpha-1-antitrypsin, alpha-2-macroglobulin, hemoglobin subunit alpha, vitamin D-binding protein, major urinary proteins, and transthyretin (up to eight-fold) in serum of lung tumor bearing mice.
  • Thus, an identification of regulated serum proteins in this lung cancer disease model provides excellent opportunities for the search of novel biomarkers.
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / genetics. Biomarkers, Tumor / blood. Lung Neoplasms / blood. Lung Neoplasms / genetics. Proto-Oncogene Proteins c-raf / genetics


74. Qu P, Du H, Wang X, Yan C: Matrix metalloproteinase 12 overexpression in lung epithelial cells plays a key role in emphysema to lung bronchioalveolar adenocarcinoma transition. Cancer Res; 2009 Sep 15;69(18):7252-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Matrix metalloproteinase 12 overexpression in lung epithelial cells plays a key role in emphysema to lung bronchioalveolar adenocarcinoma transition.
  • Chronic obstructive pulmonary disease (COPD) and lung cancer are two diseases that are related to smoking in humans.
  • Because MMP12 overexpression in epithelial cells has been reported in inflammation-triggered lung remodeling, a murine CCSP-rtTA/(tetO)(7)-MMP12 bitransgenic model was created.
  • In this model, MMP12-Flag fusion protein overexpression and its increased enzymatic activity were observed in the lung in an inducible manner, which led to inflammatory cell infiltration and increased epithelial growth.
  • In sequential events, spontaneous emphysema and bronchioalveolar adenocarcinoma were developed as a result of MMP12 overexpression.
  • During this process, the concentration of interleukin-6 was steadily increased in bronchioalveolar lavage fluid, which activated the oncogenic signal transducer and activator of transcription 3 (Stat3) in alveolar type II epithelial cells.
  • Expression of Stat3 downstream genes that are known to stimulate inflammation and tumor formation was significantly increased in the lung.
  • When tested in humans, MMP12 up-regulation was highly associated with COPD and lung cancer in patients.
  • MMP12 up-regulation plays a critical role in emphysema to lung cancer transition that is facilitated by inflammation.

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  • (PMID = 19706765.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL-061803; United States / NHLBI NIH HHS / HL / R01 HL067862-04; United States / NHLBI NIH HHS / HL / HL067862-05; United States / NHLBI NIH HHS / HL / R01 HL067862-05; United States / NHLBI NIH HHS / HL / R01 HL087001-02; United States / NHLBI NIH HHS / HL / HL087001; United States / NHLBI NIH HHS / HL / R01 HL067862; United States / NHLBI NIH HHS / HL / R01 HL061803-08; United States / NHLBI NIH HHS / HL / R01 HL087001; United States / NHLBI NIH HHS / HL / HL-067862; United States / NHLBI NIH HHS / HL / HL061803-08; United States / NHLBI NIH HHS / HL / HL061803-09; United States / NHLBI NIH HHS / HL / R01 HL061803; United States / NCI NIH HHS / CA / CA138759; United States / NHLBI NIH HHS / HL / HL067862-04; United States / NHLBI NIH HHS / HL / R01 HL061803-09; United States / NHLBI NIH HHS / HL / HL087001-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.65 / Matrix Metalloproteinase 12
  • [Other-IDs] NLM/ NIHMS134473; NLM/ PMC2753283
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75. Luo DL, Liu YH, Zhuang HG, Liao RQ, Luo XL, Xu FP, Zhang F: [Clinicopathologic study of pulmonary adenocarcinoma with features of bronchioloalveolar carcinoma]. Zhonghua Bing Li Xue Za Zhi; 2008 Nov;37(11):737-42
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  • [Title] [Clinicopathologic study of pulmonary adenocarcinoma with features of bronchioloalveolar carcinoma].
  • (1) BAC of strictly defined, (2) adenocarcinoma with bronchioloalveolar features, (3) other different histologic subtypes of lung adenocarcinomas.
  • METHODS: Surgical specimens from 348 lung adenocarcinoma patients admitted in that hospital between 1998 - 2005 were included.
  • RESULTS: The resected lung adenocarcinomas consisted of different histologic subtypes.
  • The most frequent one was adenocarcinoma of mixed subtypes (78.2%, 272/348), followed by the acinar type (8.1%, 28/348), the papillary type (4.0%, 14/348), the BAC (3.7%, 13/348), the mucinous (colloid) type (3.4%, 12/348) and the solid types (2.3%, 8/348).
  • The fetal adenocarcinoma was the least component detected.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Kaplan-Meier Estimate. Lung Neoplasms / pathology. Survival Rate
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Lung / pathology. Male. Middle Aged. Neoplasm Staging / methods. Prognosis

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  • (PMID = 19094707.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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76. Zell JA, Ou SH, Ziogas A, Anton-Culver H: Long-term survival differences for bronchiolo-alveolar carcinoma patients with ipsilateral intrapulmonary metastasis at diagnosis. Ann Oncol; 2006 Aug;17(8):1255-62
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  • [Title] Long-term survival differences for bronchiolo-alveolar carcinoma patients with ipsilateral intrapulmonary metastasis at diagnosis.
  • BACKGROUND: It has been suggested that the current staging system does not accurately reflect survival outcomes for advanced bronchiolo-alveolar carcinoma (BAC) patients.
  • Overall survival (OS) and lung cancer-specific survival (LCSS) univariate analyses were conducted using the Kaplan-Meier method.

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  • (PMID = 16766595.001).
  • [ISSN] 0923-7534
  • [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
  • [Publication-country] England
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77. Rapa I, Volante M, Cappia S, Rosas R, Scagliotti GV, Papotti M: Cathepsin K is selectively expressed in the stroma of lung adenocarcinoma but not in bronchioloalveolar carcinoma. A useful marker of invasive growth. Am J Clin Pathol; 2006 Jun;125(6):847-54
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  • [Title] Cathepsin K is selectively expressed in the stroma of lung adenocarcinoma but not in bronchioloalveolar carcinoma. A useful marker of invasive growth.
  • Lung bronchioalveolar carcinomas (BACs) are noninvasive tumors showing lepidic growth and excellent prognosis, whereas all the other variants of adenocarcinoma are invasive tumors with a worse prognosis.
  • The identification of minimal invasive foci in adenocarcinoma, therefore, is of prognostic relevance.
  • Our findings suggest pathogenetic implications of cathepsin K in the mechanisms of tumor invasiveness in lung carcinoma; in addition, cathepsin K immunodetection may be a valuable adjunct in the correct classification of pulmonary adenocarcinomas, especially in small sclerosing BACs and mixed adenocarcinoma subtypes with minimal infiltrative growth.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma, Bronchiolo-Alveolar / enzymology. Cathepsins / metabolism. Lung Neoplasms / enzymology

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  • (PMID = 16690483.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.- / Cathepsins; EC 3.4.22.38 / CTSK protein, human; EC 3.4.22.38 / Cathepsin K
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78. Wu M, Orta L, Gil J, Li G, Hu A, Burstein DE: Immunohistochemical detection of XIAP and p63 in adenomatous hyperplasia, atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and well-differentiated adenocarcinoma. Mod Pathol; 2008 May;21(5):553-8
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  • [Title] Immunohistochemical detection of XIAP and p63 in adenomatous hyperplasia, atypical adenomatous hyperplasia, bronchioloalveolar carcinoma and well-differentiated adenocarcinoma.
  • The critical distinction of bronchioloalveolar carcinoma (BAC), well-differentiated adenocarcinoma (WDAC) of lung, adenomatous hyperplasia (AH) and atypical adenomatous hyperplasia (AAH), is based on morphological criteria alone, and is therefore potentially subjective.
  • Neither XIAP nor p63 were detected in normal lung alveolar cells.
  • In contrast, diffuse p63 staining may facilitate the identification of rare cases that may have been misclassified as alveolar in origin based on morphology but may be of BRC origin.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Lung Neoplasms / diagnosis. Membrane Proteins / biosynthesis. Precancerous Conditions / diagnosis. X-Linked Inhibitor of Apoptosis Protein / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Hyperplasia / pathology. Immunohistochemistry. Lung / pathology

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  • (PMID = 18432259.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human
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79. Sonobe M, Manabe T, Wada H, Tanaka F: Lung adenocarcinoma harboring mutations in the ERBB2 kinase domain. J Mol Diagn; 2006 Jul;8(3):351-6
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  • [Title] Lung adenocarcinoma harboring mutations in the ERBB2 kinase domain.
  • Mutations in the ERBB2kinase domain have been reported in non-small cell lung cancer (NSCLC).
  • None of the tumors had a bronchio-alveolar component nor did they have epidermal growth factor receptoror K-rascodon 12 mutations.
  • In conclusion, patients with these tumors tended to be nonsmokers who had clinical features similar to those of lung cancer patients whose tumors expressed epidermal growth factor receptormutations, although their tumors showed slightly different pathological features.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-2. Lung Neoplasms / genetics. Mutation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Non-Small-Cell Lung / genetics. Female. Humans. Male. Middle Aged. Phosphotransferases / genetics. Protein Structure, Tertiary / genetics. Smoking / adverse effects

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  • (PMID = 16825508.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Phosphotransferases
  • [Other-IDs] NLM/ PMC1867605
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80. Ishii A, Suzuki M, Satomi K, Kobayashi H, Sakashita S, Kano J, Pei Y, Minami Y, Ishikawa S, Noguchi M: Increased cytoplasmic S100A6 expression is associated with pulmonary adenocarcinoma progression. Pathol Int; 2009 Sep;59(9):623-30
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  • [Title] Increased cytoplasmic S100A6 expression is associated with pulmonary adenocarcinoma progression.
  • Recently it was reported that S100A6 is one of the genes having higher expression in adenocarcinoma mixed subtype with a bronchioloalveolar carcinoma (BAC) component than in pure BAC.
  • To clarify the association of S100A6 expression with stepwise progression of lung adenocarcinoma, S100A6 protein expression was examined on immunohistochemistry in 92 formalin-fixed and paraffin-embedded lung adenocarcinomas.
  • As a result, although it was not possible to detect any significant correlation between nuclear S100A6 immunoreactivity and tumor progression, advanced adenocarcinoma had significantly higher cytoplasmic S100A6 expression than non-invasive lesions or normal lung tissue (P < 0.05).
  • These findings indicate that S100A6 may be associated with the stepwise progression and/or invasion of lung adenocarcinoma, especially BAC-type adenocarcinoma.
  • The present results suggest the utility of S100A6 immunohistochemistry as a marker for estimation of malignancy in adenocarcinoma with a BAC component.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Biomarkers, Tumor / metabolism. Cell Cycle Proteins / metabolism. Cytoplasm / metabolism. Lung Neoplasms / metabolism. S100 Proteins / metabolism

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  • (PMID = 19712129.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / S100 Proteins; 105504-00-5 / S100A6 protein, human
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81. Kaneda H, Sakaida N, Saito T, Maniwa T, Uemura Y, Saito Y: Appearance of bronchioloalveolar carcinoma and the rapid progression into invasive papillary adenocarcinoma. Gen Thorac Cardiovasc Surg; 2009 Apr;57(4):224-7
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  • [Title] Appearance of bronchioloalveolar carcinoma and the rapid progression into invasive papillary adenocarcinoma.
  • We report the appearance of a pure ground-glass opacity that demonstrates rapid progression into a solid component in the central area, pathologically revealing a minimally invasive papillary adenocarcinoma.
  • Considering the findings of previous reports, as well as our case, we need to pay careful attention to the follow-up of a patient who has even a pure ground-glass opacity when the patient had a history of an invasive lung cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Carcinoma, Papillary / pathology. Lung Neoplasms / pathology. Neoplasms, Second Primary / pathology

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  • (PMID = 19367459.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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82. Borczuk AC, Kim HK, Yegen HA, Friedman RA, Powell CA: Lung adenocarcinoma global profiling identifies type II transforming growth factor-beta receptor as a repressor of invasiveness. Am J Respir Crit Care Med; 2005 Sep 15;172(6):729-37
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  • [Title] Lung adenocarcinoma global profiling identifies type II transforming growth factor-beta receptor as a repressor of invasiveness.
  • RATIONALE: Lung adenocarcinoma histology and clinical outcome are heterogeneous and associated with tumor invasiveness.
  • OBJECTIVES: We hypothesized that invasiveness is associated with a distinct molecular signature and that genes differentially expressed in tumor or adjacent stroma will identify cell surface signal transduction and matrix remodeling pathways associated with the acquisition of invasiveness in lung adenocarcinoma.
  • MAIN RESULTS: Microarray analysis of microdissected noninvasive bronchioloalveolar carcinoma (BAC) and invasive adenocarcinoma and adenocarcinoma-mixed type with BAC features identified transcriptional profiles of lung adenocarcinoma invasiveness.
  • Among the signature set that was lower in adenocarcinoma-mixed compared with BAC was the type II transforming growth factor beta (TGF-beta) receptor, suggesting downregulation of TGFbetaRII is an early event in lung adenocarcinoma metastasis.
  • Repression of TGFbetaRII in lung cancer cells increased tumor cell invasiveness and activated p38 mitogen-activated protein kinases.
  • Microarray analysis of invasive cells identified potential downstream mediators of TGFbetaRII with differential expression in lung adenocarcinomas.
  • CONCLUSIONS: The repression of type II TGF-beta receptor may act as a significant determinant of lung adenocarcinoma invasiveness, an early step in tumor progression toward metastasis.

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  • (PMID = 15976377.001).
  • [ISSN] 1073-449X
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES00354
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
  • [Other-IDs] NLM/ PMC2718552
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83. Kycko A, Reichert M: [Current views on the mechanism of oncogenic cell transformation in ovine pulmonary adenocarcinoma]. Postepy Hig Med Dosw (Online); 2007 Dec 10;61:797-804
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  • [Title] [Current views on the mechanism of oncogenic cell transformation in ovine pulmonary adenocarcinoma].
  • Lung cancer is the most frequently diagnosed of all the human neoplasms leading to death.
  • Because twenty percent of cases are not associated with cigarette smoking, other causes and methods of early diagnosis are being sought.
  • Bronchioloalveolar cancer, which is a subtype of the most common primary lung cancer, adenocarcinoma, is very similar to ovine pulmonary adenocarcinoma (OPA), a naturally occurring lung cancer in sheep.
  • The virus induces neoplastic transformation of secretory epithelial cells of the lung, i.e. alveolar type II pneumocytes and Clara cells.
  • JSRV's tropism for these cells is connected with viral LTR regions interacting with cellular factors that play major roles in the expression of lung-specific genes, e.g. those of surfactant proteins.
  • Morphological and histological similarities with human bronchioloalveolar cancer and the possibility of experimental induction of the tumor in animals makes OPA a good model for the study of oncogenesis and target therapy of lung adenocarcinoma.

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  • (PMID = 18097338.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 55
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84. Fellegara G, D'Adda T, Pilato FP, Froio E, Ampollini L, Rusca M, Rindi G: Genetics of a combined lung small cell carcinoma and large cell neuroendocrine carcinoma with adenocarcinoma. Virchows Arch; 2008 Jul;453(1):107-15
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  • [Title] Genetics of a combined lung small cell carcinoma and large cell neuroendocrine carcinoma with adenocarcinoma.
  • Combined nonneuroendocrine-neuroendocrine lung tumors are relatively infrequent and little is known as for their genetic basis.
  • Here, we report the case of a 69-year-old male with a solitary neoplasm in the upper lobe of the right lung.
  • The main part was an adenocarcinoma of the acinar type.
  • The second part showed morphological and immunohistochemical phenotype of a neuroendocrine carcinoma composed of a small cell lung carcinoma and a large cell neuroendocrine carcinoma.
  • These findings support the true combined nature of this exocrine-neuroendocrine carcinoma of the lung and suggest a common monoclonal origin from a pluripotent epithelial (alveolar or bronchial) precursor cell for the two different tumor components.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Large Cell / diagnosis. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Small Cell / diagnosis. Lung Neoplasms / diagnosis

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  • (PMID = 18551311.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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85. Dacic S: Minimally invasive adenocarcinomas of the lung. Adv Anat Pathol; 2009 May;16(3):166-71
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  • [Title] Minimally invasive adenocarcinomas of the lung.
  • Current World Health Organization (WHO) classification of lung adenocarcinomas includes noninvasive bronchioloalveolar carcinoma (BAC) and several patterns of invasive adenocarcinoma.
  • The most common is a mixed subtype of adenocarcinoma.
  • This group is very heterogenous and includes a wide spectrum of tumors ranging from adenocarcinomas with a dominant BAC growth pattern (lepidic growth) to frankly invasive adenocarcinoma with no BAC component.
  • The change in WHO definition of BAC and introduction of mixed subtype of adenocarcinoma resulted in disconnect between surgical pathologists and clinicians regarding the use of terminology and criteria for diagnosis of BAC and mixed subtype of adenocarcinoma.
  • On the basis of the published data, there is a proposal to define a subcategory of "minimally invasive adenocarcinoma" of the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology. Mixed Tumor, Malignant / pathology

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  • (PMID = 19395880.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 32
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86. Ho C, Murray N, Laskin J, Melosky B, Anderson H, Bebb G: Asian ethnicity and adenocarcinoma histology continues to predict response to gefitinib in patients treated for advanced non-small cell carcinoma of the lung in North America. Lung Cancer; 2005 Aug;49(2):225-31
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  • [Title] Asian ethnicity and adenocarcinoma histology continues to predict response to gefitinib in patients treated for advanced non-small cell carcinoma of the lung in North America.
  • Institutional series suggest specific subgroups of patients with non-small cell lung cancer (NSCLC); female, Asian, non-smokers, respond preferentially to gefitinib.
  • Baseline characteristics at diagnosis; 62% Caucasian, 38% Asian, male 47%, smokers 67%, non-smokers 33%, ECOG 0/1 59%; tumor histology: 57% adenocarcinoma, 13% bronchoalveolar variant, 7% squamous, 23% other.
  • Of the 14 radiological responders, 10 were Asian, 10 ECOG 0/1, 10 female, 8 non-smokers, 8 adenocarcinoma and 4 bronchoalveolar variant.
  • The molecular basis of the improved response rate observed in the subset of female, Asian, non-smokers with adenocarcinoma or bronchoalveolar variant is currently being explored by gene sequencing studies at the British Columbia Cancer Agency Genome Science Centre.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / ethnology. Asian Continental Ancestry Group / ethnology. European Continental Ancestry Group / ethnology. Female. Humans. Male. Middle Aged. North America. Predictive Value of Tests. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Retrospective Studies

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  • (PMID = 15925429.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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87. Takeuchi H, Saoo K, Matsuda Y, Yokohira M, Yamakawa K, Zeng Y, Kuno T, Kamataki T, Imaida K: 8-Methoxypsoralen, a potent human CYP2A6 inhibitor, inhibits lung adenocarcinoma development induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in female A/J mice. Mol Med Rep; 2009 Jul-Aug;2(4):585-8

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  • [Title] 8-Methoxypsoralen, a potent human CYP2A6 inhibitor, inhibits lung adenocarcinoma development induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in female A/J mice.
  • Previously, we demonstrated that 8-methoxypsoralen (methoxsalen), a potent human cytochrome P450 2A6 (CYP2A6) inhibitor, strongly suppresses lung adenoma induction by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in female A/J mice.
  • In the present study, we examined the inhibitory effects of methoxsalen on the development of lung adenocarcinomas, as well as on adenomas and alveolar hyperplasia.
  • The experiments were terminated 52 weeks after the first methoxsalen treatment, and lung adenomas and adenocarcinomas were analyzed histopathologically.
  • These results clearly demonstrate that methoxsalen, a potent human CYP2A6 inhibitor, inhibits not only lung adenoma but also adenocarcinoma development.

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  • (PMID = 21475870.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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88. Kobayashi N, Toyooka S, Ichimura K, Soh J, Yamamoto H, Matsuo K, Otani H, Jida M, Kubo T, Tsukuda K, Kiura K, Sano Y, Date H: Non-BAC component but not epidermal growth factor receptor gene mutation is associated with poor outcomes in small adenocarcinoma of the lung. J Thorac Oncol; 2008 Jul;3(7):704-10
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  • [Title] Non-BAC component but not epidermal growth factor receptor gene mutation is associated with poor outcomes in small adenocarcinoma of the lung.
  • OBJECTIVE: The purpose of this study was to identify risk factors for poor clinical outcome after surgical resection of small lung adenocarcinoma.
  • MATERIALS AND METHODS: Clinical records of 127 patients who had pathologic stage IA lung adenocarcinoma 20 mm or less and who had undergone a lobectomy with mediastinal lymph node dissection were reviewed.
  • CONCLUSION: The high non-BAC component but not EGFR mutation status, is an independent risk factor for both recurrence and poor prognosis in patients with stage IA lung adenocarcinoma <or=20 mm.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Carcinoma, Non-Small-Cell Lung / pathology. Genes, erbB-1 / genetics. Lung Neoplasms / pathology. Mutation

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  • (PMID = 18594314.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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89. Tsujiuchi T, Mori T, Amanuma T, Tanaka N, Tsutsumi M: Establishment and characterization of a rat lung adenocarcinoma cell line with low malignant potential. Cancer Lett; 2005 Jan 10;217(1):97-103
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  • [Title] Establishment and characterization of a rat lung adenocarcinoma cell line with low malignant potential.
  • To investigate characteristic of lung adenocarcinoma growth behavior, we have established a cell line (rat lung cancer in Nara (RLCNR)) from a tumor induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) in a rat.
  • These results indicate that the present newly established cell line originated from an alveolar type II lesion of the lung.
  • It should be useful for further investigation of in vivo growth mechanisms, especially tumor progression, of lung adenocarcinomas, since it has low malignant potential.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / ultrastructure. Cell Line, Tumor / cytology. Lung Neoplasms / ultrastructure. Neoplasm Invasiveness

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  • (PMID = 15596300.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 53609-64-6 / diisopropanolnitrosamine
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90. Summers C, Norval M, De Las Heras M, Gonzalez L, Sharp JM, Woods GM: An influx of macrophages is the predominant local immune response in ovine pulmonary adenocarcinoma. Vet Immunol Immunopathol; 2005 Jul 15;106(3-4):285-94

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An influx of macrophages is the predominant local immune response in ovine pulmonary adenocarcinoma.
  • Infection with a retrovirus, Jaagsiekte sheep retrovirus (JSRV), causes ovine pulmonary adenocarcinoma (OPA).
  • The excess production of surfactant proteins by alveolar tumour cells results in increased production of pulmonary fluid, which is characteristically expelled through the nostrils of affected sheep.
  • When clinical signs of OPA were apparent, the lungs were removed at necropsy and immunohistochemistry (IHC) was performed on lung sections using a panel of mouse anti-sheep mAbs.
  • MHC Class II-positive cells were found intratumourally, peritumourally and in the surrounding alveolar lumina.
  • In the alveolar lumen, the MHC Class II-positive cells were CD14-positive and expressed high levels of IFN-gamma.
  • [MeSH-minor] Animals. Antigens, CD14 / metabolism. Histocompatibility Antigens Class II / metabolism. Immunohistochemistry. Interferon-gamma / biosynthesis. Jaagsiekte sheep retrovirus / pathogenicity. Lung / immunology. Lung / pathology. Sheep

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  • (PMID = 15878202.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Histocompatibility Antigens Class II; 82115-62-6 / Interferon-gamma
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91. Tokiwa H, Sera N, Nakanishi Y: Involvement of alveolar macrophages in the formation of 8-oxodeoxyguanosine associated with exogenous particles in human lungs. Inhal Toxicol; 2005 Oct;17(11):577-85
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  • [Title] Involvement of alveolar macrophages in the formation of 8-oxodeoxyguanosine associated with exogenous particles in human lungs.
  • Lung specimens were collected from 161 non-smoking male patients with carcinoma to determine the deposition of carbon particles and oxidative damage in lung tissues.
  • To determine whether particles in lung tissues were associated with 8-oxo-dG formation, carbon particles deposited in lung tissues were partially purified by cycling of alkali fusion with 1 M KOH; mutagenic chemicals in particles were extracted and excluded by removal with an equal volume of benzene/methanol and dichloromethane.
  • These results were also demonstrated by the occurrence of alveolar macrophages and neutrophils after intratracheal instillation of particles.
  • These observations suggest that small particles from lung cancer patients further promote oxidative damage when used to treat the mouse lung.
  • [MeSH-major] Carbon / administration & dosage. Deoxyguanosine / analogs & derivatives. Lung / metabolism. Macrophages, Alveolar / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Animals. Cell Line. Child. Dose-Response Relationship, Drug. Female. Humans. Lung Neoplasms / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Inbred ICR. Microscopy, Electron, Scanning. Middle Aged. Monocytes / drug effects. Monocytes / metabolism. Particle Size. Pyrenes / chemistry. Pyrenes / metabolism

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  • (PMID = 16033753.001).
  • [ISSN] 0895-8378
  • [Journal-full-title] Inhalation toxicology
  • [ISO-abbreviation] Inhal Toxicol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrenes; 5522-43-0 / 1-nitropyrene; 7440-44-0 / Carbon; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
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92. Sonobe M, Manabe T, Wada H, Tanaka F: Mutations in the epidermal growth factor receptor gene are linked to smoking-independent, lung adenocarcinoma. Br J Cancer; 2005 Aug 8;93(3):355-63
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  • [Title] Mutations in the epidermal growth factor receptor gene are linked to smoking-independent, lung adenocarcinoma.
  • Epidermal growth factor receptor (EGFR) mutations are a potential predictor of the effectiveness of EGFR inhibitors for the treatment of lung cancer.
  • Although EGFR mutations were reported to occur with high frequency in nonsmoking Japanese adenocarcinoma patients, the exact nature has not been fully elucidated.
  • We examined EGFR gene mutations within exons 18-21 and their correlations to clinico-pathological factors and other genetic alterations in tumour specimens from 154 patients who underwent resection for lung cancer at Kyoto University Hospital.
  • Epidermal growth factor receptor mutations were observed in 60 tumours (39.0%), all of which were adenocarcinoma.
  • Among the patients with adenocarcinoma (n=108), EGFR mutations were more frequently observed in nonsmokers than former smokers or current smokers (83.0, 50.0, 15.2%, respectively), in women than men (76.3 vs 34.0%), in tumours with bronchio-alveolar component than those without bronchio-alveolar component (78.9 vs 42.9%), and in well or moderately differentiated tumours than poorly differentiated tumours (72.0, 64.4, 34.2%).
  • Epidermal growth factor receptor mutations may play a key role in the development of smoking-independent adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Genes, erbB-1 / genetics. Lung Neoplasms / genetics. Smoking / adverse effects

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  • (PMID = 16052218.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2361570
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93. Kim CF, Jackson EL, Woolfenden AE, Lawrence S, Babar I, Vogel S, Crowley D, Bronson RT, Jacks T: Identification of bronchioalveolar stem cells in normal lung and lung cancer. Cell; 2005 Jun 17;121(6):823-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of bronchioalveolar stem cells in normal lung and lung cancer.
  • Injury models have suggested that the lung contains anatomically and functionally distinct epithelial stem cell populations.
  • Identified at the bronchioalveolar duct junction, BASCs were resistant to bronchiolar and alveolar damage and proliferated during epithelial cell renewal in vivo.
  • Furthermore, BASCs expanded in response to oncogenic K-ras in culture and in precursors of lung tumors in vivo.
  • These data support the hypothesis that BASCs are a stem cell population that maintains the bronchiolar Clara cells and alveolar cells of the distal lung and that their transformed counterparts give rise to adenocarcinoma.
  • Although bronchiolar cells and alveolar cells are proposed to be the precursor cells of adenocarcinoma, this work points to BASCs as the putative cells of origin for this subtype of lung cancer.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Cell Transformation, Neoplastic / pathology. Lung Neoplasms / pathology. Pulmonary Alveoli / pathology. Stem Cells / pathology


94. Liu S, Cheng H, Yao S, Wang C, Han G, Li X, Liu C: The clinical application value of PET/CT in adenocarcinoma with bronchioloalveolar carcinoma features. Ann Nucl Med; 2010 Aug;24(7):541-7
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  • [Title] The clinical application value of PET/CT in adenocarcinoma with bronchioloalveolar carcinoma features.
  • OBJECTIVE: The goal of our study was to demonstrate the clinical usefulness of positron emission tomography/computed tomography (PET/CT) for adenocarcinoma with bronchioloalveolar carcinoma (BAC) features, through evaluating the relationship between the intrathoracic lymph node metastases and maximum standardized uptake value (SUVmax), tumor size of the primary tumor and the ratio of BAC component and analysing the correlation of SUVmax, tumor size and the ratio of BAC component.
  • Forty-five patients with focal peripheral lung adenocarcinoma with BAC features were included in this study and underwent the PET/CT scan.
  • The diagnosis of the lesion was made by surgical histopathology.
  • CONCLUSIONS: PET/CT would be clinically useful for adenocarcinoma with BAC features, because SUVmax obtained by PET/CT can predict the incidence of intrathoracic lymph node metastases at preoperative stages and even for inoperable patients.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / complications. Positron-Emission Tomography. Tomography, X-Ray Computed

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  • (PMID = 20614257.001).
  • [ISSN] 1864-6433
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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95. Miller VA, Riely GJ, Zakowski MF, Li AR, Patel JD, Heelan RT, Kris MG, Sandler AB, Carbone DP, Tsao A, Herbst RS, Heller G, Ladanyi M, Pao W, Johnson DH: Molecular characteristics of bronchioloalveolar carcinoma and adenocarcinoma, bronchioloalveolar carcinoma subtype, predict response to erlotinib. J Clin Oncol; 2008 Mar 20;26(9):1472-8
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  • [Title] Molecular characteristics of bronchioloalveolar carcinoma and adenocarcinoma, bronchioloalveolar carcinoma subtype, predict response to erlotinib.
  • PURPOSE: We conducted this phase II trial to determine the efficacy of erlotinib in patients with bronchioloalveolar carcinoma (BAC) and adenocarcinoma, BAC subtype, and to determine molecular characteristics associated with response.
  • PATIENTS AND METHODS: Patients (n = 101) with BAC (n = 12) or adenocarcinoma, BAC subtype (n = 89), were enrolled.
  • In patients with pure BAC, the RR and median survival were 20% and 4 months, as compared with 23% and 19 months in those with adenocarcinoma, BAC subtype.
  • CONCLUSION: Erlotinib is active in BAC and adenocarcinoma, mixed subtype, BAC.
  • Testing for EGFR and KRAS mutations can predict RR and PFS after treatment with erlotinib in this histologically enriched subset of patients with non-small-cell lung cancer (NSCLC).
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / genetics. Lung Neoplasms / metabolism. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / metabolism. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Erlotinib Hydrochloride. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. Suppressor of Cytokine Signaling Proteins / genetics. Treatment Outcome. ras Proteins / genetics

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  • (PMID = 18349398.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA08748; United States / NCI NIH HHS / CA / CA68485; United States / NCI NIH HHS / CA / CA90949
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 0 / Suppressor of Cytokine Signaling Proteins; 0 / cytokine inducible SH2-containing protein; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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96. Ishizuka T, Endo S, Tsubochi H, Nakano T, Miwa C, Watanabe K, Koyama S, Nokubi M, Sohara Y: [Mucinous bronchiolo-alveolar cell carcinoma with marked serum elevation of CA19-9: report of a case]. Kyobu Geka; 2009 Jun;62(6):509-12
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  • [Title] [Mucinous bronchiolo-alveolar cell carcinoma with marked serum elevation of CA19-9: report of a case].
  • The pathologic study obtained by a transbronchial tumor biopsy revealed a mucinous adenocarcinoma The patient underwent video-assisted thoracoscopic right middle and lower bi-lobectomies with nodal sampling.
  • Postoperative course was uneventful Pathologic study revealed an adenocarcinoma with mixed subtypes, predominantly composed of mucinous bronchiolo-alveolar cell carcinoma (BAC).
  • Clinico-pathologic features of the lung cancer patients with serum elevation of CA19-9 and CA19-9 positivity in the cancer cells was discussed.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Lung Neoplasms / diagnosis

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  • (PMID = 19522216.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
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97. Sholl LM, Yeap BY, Iafrate AJ, Holmes-Tisch AJ, Chou YP, Wu MT, Goan YG, Su L, Benedettini E, Yu J, Loda M, Jänne PA, Christiani DC, Chirieac LR: Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers. Cancer Res; 2009 Nov 1;69(21):8341-8
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  • [Title] Lung adenocarcinoma with EGFR amplification has distinct clinicopathologic and molecular features in never-smokers.
  • In a subset of lung adenocarcinomas, the epidermal growth factor receptor (EGFR) is activated by kinase domain mutations and/or gene amplification, but the interaction between the two types of abnormalities is complex and unclear.
  • For this study, we selected 99 consecutive never-smoking women of East Asian origin with lung adenocarcinomas that were characterized by histologic subtype.
  • Lung adenocarcinomas with EGFR amplification had significantly more EGFR exon 19 deletion mutations than adenocarcinomas with disomy, and low and high polysomy (100% versus 54%, P = 0.009).
  • EGFR amplification was focally distributed in lung cancer specimens, mostly in regions with solid histology.
  • Lung adenocarcinomas with EGFR amplification have a unique association with exon 19 deletion mutations and show distinct clinicopathologic features associated with a significantly worsened prognosis.

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  • (PMID = 19826035.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / CA092824; United States / NCI NIH HHS / CA / CA074386; United States / NCI NIH HHS / CA / CA090578-01A10003; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R0I CA114465; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / P20 CA090578-01A10003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS143923; NLM/ PMC2783286
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98. Awaya H, Takeshima Y, Amatya VJ, Ishida H, Yamasaki M, Kohno N, Inai K: Loss of expression of E-cadherin and beta-catenin is associated with progression of pulmonary adenocarcinoma. Pathol Int; 2005 Jan;55(1):14-8
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  • [Title] Loss of expression of E-cadherin and beta-catenin is associated with progression of pulmonary adenocarcinoma.
  • The aim of the present study was to determine the association of loss of membranous expression of epithelial (E)-cadherin and beta-catenin with the progression of pulmonary adenocarcinoma.
  • The expression of E-cadherin and beta-catenin was examined in 154 cases of pulmonary adenocarcinoma, including 49 cases of atypical adenomatous hyperplasia (AAH), 40 cases of bronchioloalveolar carcinoma (BAC), 42 cases of BAC-dominant type of adenocarcinoma with mixed subtypes (early MX) and 23 cases of BAC-recessive type of adenocarcinoma with mixed subtypes (overt MX), by immunohistochemistry.
  • Loss of expression of E-cadherin and beta-catenin may play an important role in the progression of pulmonary adenocarcinoma, and these events occur before structural destruction of the alveolar wall by invasion of carcinoma cell.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cadherins / biosynthesis. Cytoskeletal Proteins / biosynthesis. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Trans-Activators / biosynthesis

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  • (PMID = 15660698.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
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99. Schoen K, Block G, Newell SM, Coronado GS: Hypercalcemia of malignancy in a cat with bronchogenic adenocarcinoma. J Am Anim Hosp Assoc; 2010 Jul-Aug;46(4):265-7
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  • [Title] Hypercalcemia of malignancy in a cat with bronchogenic adenocarcinoma.
  • Histopathology diagnosed a bronchogenic adenocarcinoma, and calcium levels returned to normal limits after excision of the mass.
  • While bronchogenic adenocarcinoma has been a suspected cause for hypercalcemia in cats, to the authors' knowledge, this is the first proven account.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / veterinary. Cat Diseases / diagnosis. Hypercalcemia / veterinary. Lung Neoplasms / veterinary

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  • (PMID = 20610700.001).
  • [ISSN] 1547-3317
  • [Journal-full-title] Journal of the American Animal Hospital Association
  • [ISO-abbreviation] J Am Anim Hosp Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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100. Vasin VA, Mnikhovich MV, Vasin IV, Snegur SV: [Clinicomorphological observation of bronchioloalveolar carcinoma of the lung]. Arkh Patol; 2008 Mar-Apr;70(2):43-5
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  • [Title] [Clinicomorphological observation of bronchioloalveolar carcinoma of the lung].
  • The authors analyze rare lung diseases and describe a clinicomorphological case of bronioloalveolar carcinoma of the lung as one of rare bronchopulmonary diseases.
  • According to the WHO histological classification (1999), the tumor is adenocarcinoma that is represented solely by bronchioloalveolar vegetations as a monolayer of the cells lining the walls of pre-existing alveoles without invasion of the stroma, vessels, and pleura.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Bronchi / pathology. Lung Neoplasms / pathology. Pulmonary Alveoli / pathology. Rare Diseases / pathology

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  • (PMID = 18540442.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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