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1. 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.
  • 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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2. Vazquez MF, Koizumi JH, Henschke CI, Yankelevitz DF: Reliability of cytologic diagnosis of early lung cancer. Cancer; 2007 Aug 25;111(4):252-8
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  • [Title] Reliability of cytologic diagnosis of early lung cancer.
  • BACKGROUND: Baseline screening for lung cancer of 2968 high-risk men and women utilizing HRCT enrolled in ELCAP (Early Lung Cancer Action Project) was performed between 1993-2002.
  • Among them, 65 people had surgical resection of their screen-diagnosed lung cancer, 53 of them on the basis of a diagnosis of malignancy or atypical bronchioloalveolar proliferation (ABP) on fine needle aspiration (FNA) biopsy at Weill Medical College of Cornell University (WMC) prior to surgery.
  • The authors compared the diagnosis obtained from the FNA with the subsequent diagnosis from the surgical specimen to assess the reliability of a cytologic diagnosis of lung cancer on FNA of these screen-diagnosed lung cancers.
  • ), with preliminary on-site as well as final diagnosis rendered by a cytologist (M.V., J.K.).
  • These results were correlated with histologic diagnoses obtained as a result of consensus diagnosis by a panel of 5 expert pulmonary pathologists.
  • RESULTS: Of the 53 cases of lung cancer resected following FNA, 4 were diagnosed as atypical bronchioloalveolar proliferation (ABP), 14 as adenocarcinoma with bronchioloalveolar features (ADC-BAC), 28 as adenocarcinoma, not otherwise specified (ADC-NOS), 1 as squamous cell carcinoma (SQCC), 4 as nonsmall-cell carcinoma (NSCC), and 2 as typical carcinoid.
  • In the 49 cases with a malignant cytology and 4 cases of ABP, lung cancer was confirmed histologically.
  • The final expert panel histologic diagnosis was adenocarcinoma in 47 cases; of these, 42 were invasive (mixed subtype or acinar subtype), and 5 were a noninvasive (bronchioloalveolar carcinoma, BAC).
  • Two cases classified as nonkeratinizing SQCC and 2 cases of large cell neuroendocrine carcinoma on histology were misclassified as ADC-NOS by FNA.
  • CONCLUSIONS: Preoperative diagnosis of lung cancer detected by screening with HRCT could be reliably made by FNA.
  • Difficulty in classification occurs in carcinomas of high nuclear grade with prominent nucleoli, including poorly differentiated SQCC and large cell neuroendocrine carcinoma.
  • These are best diagnosed as NSCC on cytomorphology with further subclassification based on immunohistochemistry, which these authors generally perform on cell-block material.
  • A diagnosis of ABP on FNA may be indicative of noninvasive BAC or an invasive adenocarcinoma with prominent BAC features, usually sampled at its periphery.
  • [MeSH-major] Biopsy, Fine-Needle. Cytodiagnosis / methods. Lung Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Carcinoid Tumor / diagnosis. Carcinoma, Non-Small-Cell Lung / diagnosis. Humans. Neoplasms, Squamous Cell / diagnosis. Reproducibility of Results

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  • [CommentIn] Cancer. 2008 May 15;112(10):2329-30 [18407546.001]
  • (PMID = 17614298.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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3. Iczkowski KA, Montironi R: Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu. J Clin Pathol; 2006 Dec;59(12):1327-30
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  • [Title] Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu.
  • Adenoid cystic/basal cell carcinoma (ACBCC) is a rare neoplasm in the prostate.
  • One patient had metastasis to the lung.
  • Ten acinar adenocarcinomas of varying grades were also immunostained as controls.
  • Protein and mRNA expression were 2+ to 3+ (of 3+) in all patients with ACBCC, compared to a breast cancer control with strong reactivity, whereas protein expression was noted in only one acinar carcinoma and mRNA expression was absent in all acinar carcinomas.
  • [MeSH-major] Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Basal Cell / metabolism. Mixed Tumor, Malignant / metabolism. Prostatic Neoplasms / metabolism. Receptor, ErbB-2 / metabolism


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4. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1746-01-6) in female Harlan Sprague-Dawley rats (Gavage Studies). Natl Toxicol Program Tech Rep Ser; 2006 Apr;(521):4-232
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  • HEPATIC CELL PROLIFERATION DATA: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
  • DETERMINATIONS OF TCDD CONCENTRATIONS IN TISSUES: The tissue disposition of TCDD was analyzed in the liver, lung, fat, and blood of all animals in each group at the 14-, 31-, and 53-week interim evaluations and in 10 animals per group at the end of the 2-year study (105 weeks).
  • At 2 years, there was a significant increase in toxic hepatopathy characterized by increased incidences of numerous nonneoplastic liver lesions including hepatocyte hypertrophy, multinucleated hepatocytes, altered hepatocellular foci, inflammation, pigmentation, diffuse fatty change, necrosis, portal fibrosis, oval cell hyperplasia, bile duct hyperplasia, bile duct cysts, cholangiofibrosis, and nodular hyperplasia At 2 years, the incidence of hepatocellular adenoma was significantly increased in the 100 ng/kg core study group.
  • In the lung, the incidence of cystic keratinizing epithelioma of the lung was significantly increased at 2 years in the 100 ng/kg core study group.
  • Nonneoplastic effects in the lung included increased incidences of bronchiolar metaplasia.
  • The incidence of gingival squamous cell carcinoma of the oral mucosa was significantly increased in the 100 ng/kg core study group at 2 years and was accompanied by an increased incidence of gingival squamous hyperplasia.
  • At 2 years, the incidence of squamous cell carcinoma of the uterus in the 46 ng/kg group was significantly increased, and there were two squamous cell carcinomas in the 100 ng/kg stop-exposure group.
  • At 2 years, one acinar adenoma and two acinar cell carcinomas of the pancreas were seen in the 100 ng/kg core study group; one acinar carcinoma was seen in the 100 ng/kg stop-exposure group.
  • The incidences of acinar cell adenoma or carcinoma (combined) exceeded the historical vehicle control range.
  • Nonneoplastic effects in the lung included acinar cytoplasmic vacuolization, chronic active inflammation, acinar atrophy, and arterial chronic active inflammation. (ABSTRACT TRUNCATED)

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  • (PMID = 16835633.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; DO80M48B6O / Tetrachlorodibenzodioxin
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5. Li HC, Schmidt L, Greenson JK, Chang AC, Myers JL: Primary pulmonary adenocarcinoma with intestinal differentiation mimicking metastatic colorectal carcinoma: case report and review of literature. Am J Clin Pathol; 2009 Jan;131(1):129-33
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  • [Title] Primary pulmonary adenocarcinoma with intestinal differentiation mimicking metastatic colorectal carcinoma: case report and review of literature.
  • Pulmonary adenocarcinoma with intestinal differentiation is rare and typically expresses proteins common to lung primaries.
  • Histologic examination revealed tall columnar cells without goblet cell differentiation arranged in a cribriform and acinar pattern with extensive central necrosis.
  • Metastatic carcinoma was present in multiple hilar lymph nodes.
  • [MeSH-major] Adenocarcinoma / pathology. Colorectal Neoplasms / secondary. Lung Neoplasms / pathology

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  • (PMID = 19095576.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Trans-Activators; 156560-97-3 / Cdx-2-3 protein
  • [Number-of-references] 18
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6. Choudhary R, Li H, Winn RA, Sorenson AL, Weiser-Evans MC, Nemenoff RA: Peroxisome proliferator-activated receptor-gamma inhibits transformed growth of non-small cell lung cancer cells through selective suppression of Snail. Neoplasia; 2010 Mar;12(3):224-34
Hazardous Substances Data Bank. ROSIGLITAZONE .

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  • [Title] Peroxisome proliferator-activated receptor-gamma inhibits transformed growth of non-small cell lung cancer cells through selective suppression of Snail.
  • Work from our laboratory and others has demonstrated that activation of the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) inhibits transformed growth of non-small cell lung cancer (NSCLC) cell lines in vitro and in vivo.
  • The Snail family of transcription factors, which includes Snail (Snail1), Slug (Snail2), and ZEB1, is an important regulator of epithelial-mesenchymal transition, as well as cell survival.
  • Our results indicate that, in two independent NSCLC cell lines, rosiglitazone specifically decreased expression of Snail, with no significant effect on either Slug or ZEB1.
  • Suppression of Snail using short hairpin RNA silencing mimicked the effects of PPARgamma activation, in inhibiting anchorage-independent growth, promoting acinar formation in three-dimensional culture, and inhibiting invasiveness.

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  • (PMID = 20234816.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / CA58187; United States / NCI NIH HHS / CA / R01 CA138528; United States / NCI NIH HHS / CA / CA108610; United States / NCI NIH HHS / CA / R01 CA108610; United States / NCI NIH HHS / CA / CA103618; United States / NCI NIH HHS / CA / R01 CA103618
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Thiazolidinediones; 0 / Transcription Factors; 0 / snail family transcription factors; 05V02F2KDG / rosiglitazone; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2838440
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7. Karafin MS, Cummings CT, Fu B, Iacobuzio-Donahue CA: The developmental transcription factor Gata4 is overexpressed in pancreatic ductal adenocarcinoma. Int J Clin Exp Pathol; 2009 Aug 30;3(1):47-55
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  • Silencing of GATA4 mRNA expression by promoter methylation has been implicated in carcinogenesis of the ovary, lung and colorectum.
  • By contrast, GATA4 mRNA expression is upregulated in pancreatic cancer cell lines and tissues.
  • Both the intensity and percent of labeling was recorded for each carcinoma and correlated to the clinic opathologic features available for each patient.
  • Samples of normal adult (n=26) and fetal pancreatic tissue (n=8) were also immunolabeled for comparison to expression patterns in pancreatic carcinoma tissues.
  • Immunolabeling for GATA4 indicated robust nuclear expression in developing acini in fetal pancreatic tissues, consistent with the role of GATA4 in embryologic development, and in mature pancreatic acinar epithelium.
  • Immunolabeling for GATA4 was also noted within normal duct epithelial cells, although it was always lesser in intensity than for acinar cell nuclei in the same section.

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  • (PMID = 19918328.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA106610; United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2776266
  • [Keywords] NOTNLM ; Pancreatic cancer / development / embryology / transcription factor
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8. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (Cas No. 57117-31-4) in female Harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 Sep;(525):1-198
Hazardous Substances Data Bank. 2,3,4,7,8-PENTACHLORODIBENZOFURAN .

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  • Hepatic Cell Proliferation Data: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine (BrdU) was conducted at the 14-, 31-, and 53-week interim evaluations.
  • Determinations of PeCDF Concentrations in Tissues: The tissue disposition of PeCDF was analyzed in the liver, lung, fat, and blood of all animals at the 14-, 31-, and 53-week interim evaluations, and in 10 animals per group at the end of the 2-year study (105 weeks).
  • Measurable concentrations of PeCDF were not detected in fat or lung from vehicle control rats at any of the interim evaluations or at 105 weeks.
  • Mean levels of PeCDF in the liver, fat, lung, and blood in the 200 ng/kg group at the end of the 2-year study were 500 ng/g, 7.75 ng/g, 0.28 ng/g and 0.04 ng/mL, respectively.
  • In the stop-exposure group, PeCDF concentration in lung was comparable to levels observed in the 6 ng/kg group.
  • A significant dose-dependent increase in hepatic toxicity was observed and was characterized by increased incidences of numerous nonneoplastic lesions including hepatocellular hypertrophy, multinucleated hepatocytes, oval cell hyperplasia, diffuse fatty change, pigmentation, nodular hyperplasia, eosinophilic foci, hepatocellular necrosis, bile duct hyperplasia, bile duct fibrosis, cholangiofibrosis, and toxic hepatopathy.
  • At 2 years, three gingival squamous cell carcinomas of the oral mucosa were seen in the 200 ng/kg core and stop-exposure groups, two occurred in the 6 ng/kg group, and one occurred in each of the vehicle control, 20 ng/kg, and 92 ng/kg groups.
  • The incidence of carcinoma of the uterus was marginally increased in the 92 ng/kg group at 2 years.
  • At 14-weeks, lung weights were significantly increased in the 200 ng/kg group compared to the vehicle controls.
  • A single occurrence of a multiple cystic keratinizing epithelioma of the lung was observed in the 200 ng/kg core study group.
  • One pancreatic acinar adenoma and one pancreatic acinar carcinoma were each observed in the 92 ng/kg group and in the 200 ng/kg stop-exposure group at 2 years.
  • Significantly increased incidences of acinar cytoplasmic vacuolization and arterial chronic active inflammation and increased severity of chronic active inflammation were observed in the 200 ng/kg core study group.
  • Numerous nonneoplastic effects were seen in other organs including thyroid follicular cell hypertrophy, thymic atrophy, adrenal cortex cystic degeneration, nephropathy, cardiomyopathy, and squamous hyperplasia of the forestomach.

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  • (PMID = 17160103.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzofurans; 0 / Carcinogens; 0 / Thyroid Hormones; U4C2RV3124 / 2,3,4,7,8-pentachlorodibenzofuran
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9. Morishima K, Hyodo M, Nihei Y, Sata N, Yasuda Y: [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1]. Gan To Kagaku Ryoho; 2010 Jan;37(1):127-9
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  • [Title] [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1].
  • A 65-year-old man underwent a total gastrectomy and distal pancreatectomy for acinar cell carcinoma of the pancreas.
  • Peritoneal dissemination and multiple lung metastases were found 8 months after liver resection.
  • Acinar cell carcinoma of the pancreas is a rare and highly malignant tumor, and there are few reports regarding treatment with chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / therapy. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / therapy. Tegafur / therapeutic use

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  • (PMID = 20087046.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
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10. Spencer ML, Neto AG, Fuller GN, Luna MA: Intracranial extension of acinic cell carcinoma of the parotid gland. Arch Pathol Lab Med; 2005 Jun;129(6):780-2
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  • [Title] Intracranial extension of acinic cell carcinoma of the parotid gland.
  • We report the case of a 47-year-old woman who experienced multiple recurrences of acinic cell carcinoma, lung metastasis, and intracranial extension of the tumor during a 32-year period.
  • In this report, the clinical, microscopic, histochemical, and electron microscopy features of this acinic cell carcinoma are described, and a review of published information about this neoplasm is presented.
  • [MeSH-major] Brain Neoplasms / secondary. Carcinoma, Acinar Cell / secondary. Neoplasm Recurrence, Local / pathology. Parotid Neoplasms / pathology
  • [MeSH-minor] Biopsy, Fine-Needle. Cytoplasm / ultrastructure. Cytoplasmic Granules / chemistry. Cytoplasmic Granules / ultrastructure. Female. Humans. Lung Neoplasms / secondary. Middle Aged. Periodic Acid-Schiff Reaction

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  • (PMID = 15913428.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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11. Gamal G, Nagashima T, Kawashima O, Sugano M, Sakurai S, Sano T, Nakajima T: Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct. Pathol Int; 2006 Apr;56(4):217-21
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  • [Title] Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct.
  • In the lung, acinic cell carcinoma (ACC) is a rare form of tumor.
  • Reported herein is a unique bronchial gland-type tumor diagnosed as well-differentiated ACC that developed in the B9 bronchus of the left lung.
  • Various immunohistochemical and histochemical staining partly satisfied the diagnosis of ACC.
  • Moreover, this tumor contained various sizes of mucous cysts lined by columnar mucous cells, which produced abundant mucin positive for Alcian blue, which is usually present in mucoepidermoid carcinoma.
  • Therefore, the present case is a unique tumor having a broad spectrum of cell differentiation from the terminal duct--acinar unit to the striated duct and excretory duct.
  • This is the first case of unique bronchial gland-type tumor with mixed histological features of ACC and mucoepidermoid carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Bronchogenic / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry. Male. Middle Aged. Thoracoscopy

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  • (PMID = 16634968.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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12. Ide S, Sawai T, Kaku N, Nagayoshi Y, Soda H, Kohno S: [Case of pulmonary adenocarcinoma with co-existing pulmonary actinomycosis in one region of the lung]. Nihon Kokyuki Gakkai Zasshi; 2009 Sep;47(9):823-7
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  • [Title] [Case of pulmonary adenocarcinoma with co-existing pulmonary actinomycosis in one region of the lung].
  • On a diagnosis of pulmonary actinomycosis, 1500 mg of oral amoxicillin was initiated.
  • A histological examination of the resected tumor showed papillary and acinar adenocarcinoma.
  • Pulmonary actinomycosis requires differentiation from lung cancer.
  • Although lung cancer with coexisting pulmonary actinomycosis is rare, clinicians should take into consideration the fact that lung cancer and pulmonary actinomycosis can co-exist in the same patient.
  • [MeSH-major] Actinomycosis / complications. Adenocarcinoma, Papillary / complications. Carcinoma, Acinar Cell / complications. Lung Diseases / complications. Lung Neoplasms / complications
  • [MeSH-minor] Administration, Oral. Amoxicillin / administration & dosage. Antigens, Neoplasm / blood. Biomarkers, Tumor / blood. Humans. Keratin-19 / blood. Male. Middle Aged. Neoplasms, Multiple Primary. Thoracic Surgery, Video-Assisted

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  • (PMID = 19827588.001).
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Keratin-19; 0 / antigen CYFRA21.1; 804826J2HU / Amoxicillin
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13. Uzaslan E, Stuempel T, Ebsen M, Freudenberg N, Nakamura S, Costabel U, Guzman J: Surfactant protein A detection in primary pulmonary adenocarcinoma without bronchioloalveolar pattern. Respiration; 2005 May-Jun;72(3):249-53
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  • [Title] Surfactant protein A detection in primary pulmonary adenocarcinoma without bronchioloalveolar pattern.
  • BACKGROUND: Immunohistochemical studies in human lung carcinoma reported positive staining of tumor cells for surfactant protein A (SP-A), especially in peripheral airway cell carcinoma, which include bronchioloalveolar carcinoma and in some reports also papillary subtypes.
  • OBJECTIVE: The purpose of this study was to determine the SP-A expression in tumor cells of lung adenocarcinoma without a bronchioloalveolar pattern, classified according to the WHO.
  • METHODS: In total, 169 primary adenocarcinomas of the lung (109 acinar, 32 solid with mucin, 24 papillary and 4 mucinous) were examined by immunohistochemistry for SP-A expression.
  • RESULTS: Twenty-five percent of acinar, 38% of papillary and 3% of solid adenocarcinoma with mucin showed a positive intracytoplasmic SP-A reaction of the tumor cells.
  • This study included the largest number of acinar adenocarcinomas and solid adenocarcinomas with mucin studied for SP-A.
  • We clearly demonstrated that also primary lung adenocarcinoma without a bronchioloalveolar pattern can express SP-A.
  • CONCLUSION: These results support the theory that SP-A-producing cells may generate not only bronchioloalveolar and papillary carcinoma, but also other subtypes of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Lung Neoplasms / metabolism. Pulmonary Surfactant-Associated Protein A / metabolism
  • [MeSH-minor] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / metabolism. Adenocarcinoma, Papillary / pathology. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Humans

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  • [Copyright] Copyright 2005 S. Karger AG, Basel
  • (PMID = 15942293.001).
  • [ISSN] 0025-7931
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Pulmonary Surfactant-Associated Protein A
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14. Dobashi Y, Suzuki S, Matsubara H, Kimura M, Endo S, Ooi A: Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas. Cancer; 2009 Jan 1;115(1):107-18
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  • [Title] Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas.
  • BACKGROUND: Aberrant signaling cascades emanating from epidermal growth factor receptor (EGFR) are involved in the complex network of oncogenic signaling in lung carcinomas.
  • METHODS: The authors investigated the involvement of mTOR in the pathobiologic profiles of 150 specimens of lung carcinoma by immunohistochemistry and immunoblotting in correlation with the upstream and downstream proteins Akt and p70S6-kinase (S6K), respectively.
  • In AC, the frequency of p-mTOR staining was higher in the well differentiated subtype, in particular, in the acinar structure.
  • Conversely, in squamous cell carcinomas, mTOR activation was associated with a significantly higher frequency of lymph node metastasis.
  • Second, the activation of mTOR may play a key role in metastasis in squamous cell carcinoma.
  • Overall, the current results demonstrated the potential for the application of rapamycin, an mTOR inhibitor, as an additional novel component of chemotherapy for a defined subset of patients with lung carcinoma.
  • [MeSH-major] Lung Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Humans. Neoplasm Metastasis. Neoplasms, Squamous Cell / metabolism. Neoplasms, Squamous Cell / pathology. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. TOR Serine-Threonine Kinases

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • (PMID = 19090006.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
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15. Liu YL, Matsuzaki T, Nakazawa T, Murata S, Nakamura N, Kondo T, Iwashina M, Mochizuki K, Yamane T, Takata K, Katoh R: Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues. Hum Pathol; 2007 Jan;38(1):171-8
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  • [Title] Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues.
  • To investigate the expression of AQP3 in normal and neoplastic lung tissues, we studied a series of 149 lung carcinoma tissues and 2 cell lines by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction.
  • In normal lung tissues, immunohistochemical expression of AQP3 was demonstrated in bronchial basal cells, alveolar type II cells, bronchiolar epithelial cells, and secretory cells of submucosal glands.
  • In lung carcinomas, AQP3 expression was observed in 59 (70.2%) of 84 adenocarcinomas.
  • Squamous cell carcinoma and large cell carcinoma had rather low positive ratios (35.8% and 13.4%, respectively).
  • No AQP3 expression was demonstrated in small cell carcinoma, pleomorphic carcinoma, or metastatic colon adenocarcinoma.
  • Papillary subtype also showed a higher positive ratio of AQP3 compared with that in acinar and solid with mucin subtypes.
  • Western blotting and reverse transcriptase-polymerase chain reaction analyses confirmed the expression of AQP3 protein and messenger RNA in cell lines and tissues of lung adenocarcinoma.
  • In addition, lung carcinomas, especially adenocarcinomas, can produce AQP3, possibly in connection with their functional and/or biological nature, although the detailed mechanism of AQP3 expression in lung carcinomas remains to be clarified.
  • [MeSH-major] Aquaporin 3 / genetics. Lung / metabolism. Lung Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Cell Line, Tumor. Female. Gene Expression. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17056099.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 158801-98-0 / Aquaporin 3
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16. Leite KR, Mitteldorf CA, Srougi M, Dall'oglio MF, Antunes AA, Pontes J Jr, Camara-Lopes LH: Cdx2, cytokeratin 20, thyroid transcription factor 1, and prostate-specific antigen expression in unusual subtypes of prostate cancer. Ann Diagn Pathol; 2008 Aug;12(4):260-6
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  • There are some unusual histologic variants of prostate carcinoma, including mucinous, signet-ring cells, and ductal carcinomas that can metastasize in a problematic way and simulate lung, colorectal, or bladder primaries.
  • There were 7 mucinous, 5 ductal, 2 signet-ring cells, and 15 usual acinar adenocarcinomas with focal mucinous differentiation.
  • To compare the results with usual acinar adenocarcinomas, we studied 10 primary and their respective lymph node metastases in a tissue microarray, 2 unusual metastatic adenocarcinomas, and 6 usual acinar high-grade carcinomas.
  • For tumors with special histologic finding, Cdx2 was expressed by 9 (31.0%) mucinous, signet-cell, or with focal mucinous differentiation.

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  • (PMID = 18620992.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / KRT20 protein, human; 0 / Keratin-20; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; EC 3.4.21.77 / Prostate-Specific Antigen
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17. Inamura K, Takeuchi K, Togashi Y, Nomura K, Ninomiya H, Okui M, Satoh Y, Okumura S, Nakagawa K, Soda M, Choi YL, Niki T, Mano H, Ishikawa Y: EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers. J Thorac Oncol; 2008 Jan;3(1):13-7
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  • [Title] EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers.
  • INTRODUCTION: Very recently, we have found a novel fusion product between the echinoderm microtubule-associated protein-like4 (EML4) and the anaplastic lymphoma kinase (ALK) in non-small cell lung cancers (NSCLCs).
  • Herein, we present results of a first large scale study of EML4-ALK fusion in lung cancers.
  • METHODS: Using reverse transcription-polymerase chain reaction for EML4-ALK fusion mRNA, we investigated 149 lung adenocarcinomas, 48 squamous cell carcinomas, 3 large-cell neuroendocrine carcinomas, and 21 small-cell carcinomas.
  • Interestingly, all three variant 2 cases were acinar adenocarcinomas, the link being statistically significant (p = 0.00018).
  • CONCLUSIONS: In the present first investigation of EML4-ALK fusion in a large study of lung cancers (5/221), we found an interesting histotype-genotype relationship.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / pathology. Carcinoma, Squamous Cell / pathology. Cell Cycle Proteins / genetics. Chromosome Inversion. Chromosomes, Human, Pair 2. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Survival Analysis

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  • (PMID = 18166835.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / EML4-ALK fusion protein, human; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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18. 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.
  • Clinical characteristics often differ from other types of non-small cell lung cancers.
  • These include frequent female occurrence, especially in East Asians; no or less smoking history; an often indolent course; distinctive chest computed tomographic findings; frequent presentation as an asymptomatic, sometimes small, peripheral nodule(s)/mass; multifocal/synchronous primary tumors; and less frequently as pneumonic-type consolidation or diffuse, inoperable lesions, the latter two often with bronchorrhea, and with chest-only disease.
  • Lobectomy is the treatment of choice for cure, even with pneumonic consolidation, but lesser procedures such as wedge resection or segmentectomy may be considered for what might be multifocal, synchronous primary tumors and for pulmonary relapses.
  • 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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19. 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.
  • To gain insight into their biological significance, we examined 116 surgically resected lung adenocarcinomas.
  • The resected tumors included 13 bronchioloalveolar carcinomas, 20 mixed type adenocarcinomas with bronchioloalveolar carcinoma components, 57 papillary adenocarcinomas, 22 solid adenocarcinomas with mucin, and 4 acinar adenocarcinomas.
  • In mixed adenocarcinomas with bronchioloalveolar carcinoma components, subepithelial myofibroblasts were present in the bronchioloalveolar carcinoma components, but scanty in the invasive areas, where stromal myofibroblasts emerged between the cancer cell nests.
  • 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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20. National Toxicology Program: Toxicology and carcinogenesis studies of 3,3',4,4'-tetrachloroazobenzene (TCAB) (CAS No. 14047-09-7) in Harlan Sprague-Dawley rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(558):1-206
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  • EROD activities in the lung generally increased with increasing dose and were significantly greater in all treated groups of males and females compared to their respective vehicle controls.
  • The highest concentrations of TCAB were observed in fat tissue with lower concentrations in the liver and lung.
  • Absolute and relative lung weights were significantly greater in 100 mg/kg males and 3 mg/kg or greater females.
  • Hematopoietic cell proliferation occurred in most males administered 3 mg/kg or greater and most females administered 10 mg/kg or greater.
  • In the lung, significantly increased incidences of bronchiolar metaplasia of the alveolar epithelium and interstitial mononuclear cell infiltration occurred in 10, 30, and 100 mg/kg males.
  • The incidence of interstitial mononuclear cell infiltration was also significantly increased in 100 mg/kg females.
  • Significantly increased incidences of hematopoietic cell proliferation of the spleen occurred in males administered 10 mg/kg or greater.
  • In the lung, the incidences of multiple cystic keratinizing epithelioma and single or multiple cystic keratinizing epithelioma (combined) in males and females were significantly increased in all dosed groups (except multiple epithelioma in 10 mg/kg females).
  • A significant dose-related increase in hepatic toxicity was observed in dosed rats and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, centrilobular degeneration, hepatocellular necrosis, pigmentation, fatty change, bile duct hyperplasia, oval cell hyperplasia, nodular hyperplasia, hematopoietic cell proliferation, eosinophilic focus, mixed cell focus, multinucleated hepatocytes, bile duct cyst, toxic hepatopathy, and cholangiofibrosis.
  • Significantly increased incidences of gingival squamous cell carcinoma within the oral mucosa occurred in 10 mg/kg males and 100 mg/kg males and females.
  • The incidences of follicular cell adenoma (single or multiple) of the thyroid gland in 30 and 100 mg/kg males were significantly greater than that in the vehicle control group.
  • The incidences of follicular cell hypertrophy, follicular cell hyperplasia, and inflammation were significantly increased in 30 and 100 mg/kg males.
  • Three incidences of single or multiple squamous cell papilloma of the forestomach occurred in 100 mg/kg females, and single incidences of squamous cell carcinoma of the forestomach occurred in 10 and 100 mg/kg females.
  • Numerous nonneoplastic effects were seen in other organs including atrophy, acinar cytoplasmic vacuolization, and inflammation of the pancreas; blood vessel inflammation; lymphoid follicle atrophy and pigmentation of the spleen; pigmentation and atrophy of the mesenteric lymph node; germinal epithelial degeneration of the testes; and inflammation of the nose.

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  • (PMID = 21383777.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Azo Compounds; 0 / Chlorobenzenes; 14047-09-7 / 3,4,3',4'-tetrachloroazobenzene
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21. Haas M, Laubender RP, Stieber P, Holdenrieder S, Bruns CJ, Wilkowski R, Mansmann U, Heinemann V, Boeck S: Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer. Tumour Biol; 2010 Aug;31(4):351-7
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  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Female. Humans. Kinetics. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Peritoneal Neoplasms / blood. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20480409.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 9007-41-4 / C-Reactive Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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22. Taraseviciute A, Vincent BT, Schedin P, Jones PL: Quantitative analysis of three-dimensional human mammary epithelial tissue architecture reveals a role for tenascin-C in regulating c-met function. Am J Pathol; 2010 Feb;176(2):827-38
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  • In the presence of TN-C, however, acini failed to generate a normal BM, and net epithelial cell proliferation increased.
  • To quantify how TN-C alters 3-D tissue architecture and function, we developed a computational image analysis algorithm, which showed that although TN-C disrupted acinar surface structure, it had no effect on their volume.
  • Thus, TN-C promoted epithelial cell proliferation leading to luminal filling, a process that we hypothesized involved c-met, a proto-oncogene amplified in breast tumors that promotes intraluminal filling.
  • Indeed, TN-C increased epithelial c-met expression and promoted luminal filling, whereas blockade of c-met function reversed this phenotype, resulting in normal BM deposition, proper lumen formation, and decreased cell proliferation.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Ductal / genetics. Carcinoma, Ductal / metabolism. Carcinoma, Ductal / pathology. Cell Culture Techniques. Cell Proliferation. Cell Size. Cells, Cultured. Female. Gene Expression Regulation, Neoplastic. Humans. Imaging, Three-Dimensional. Middle Aged. Models, Biological. Young Adult

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  • (PMID = 20042668.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tenascin; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Other-IDs] NLM/ PMC2808088
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23. National Toxicology Program: Toxicology and carcinogenesis studies of a mixture of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Cas No. 1746-01-6), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (Cas No. 57117-31-4), and 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) in female Harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 Sep;(526):1-180
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  • Hepatic Cell Proliferation Data: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the interim evaluations.
  • Liver and lung EROD (CYP1A1) activities and hepatic A4H (CYP1A2) activities were significantly greater in all dosed groups than in the vehicle controls at all interim evaluations (14, 31, and 53 weeks).
  • Determinations of TCDD, PeCDF, and PCB 126 Concentrations in Tissues: Tissue concentrations of TCDD, PeCDF, and PCB 126 were analyzed in the fat, liver, lung, and blood at each interim evaluation and at the end of the 2-year study (105 weeks).
  • In the lung, PeCDF was present at detectable concentrations in the 46 and 100 ng TEQ/kg groups at 14 and 31 weeks.
  • Measurable concentrations of TCDD and PCB 126 were observed at 14 and 31 weeks in the lung of rats in all dosed groups with the highest concentrations observed in the 100 ng TEQ/kg group.
  • At 53 weeks, concentrations of TCDD, PeCDF, and PCB 126 in the lung generally increased with increasing dose.
  • At 105 weeks, detectable concentrations of TCDD, PeCDF, and PCB 126 in the lung were observed in all dosed groups.
  • There was an increase in hepatic toxicity characterized by increases in the incidences of numerous nonneoplastic lesions including hepatocyte hypertrophy, multinucleated hepatocytes, pigmentation, inflammation, diffuse fatty change, bile duct hyperplasia, oval cell hyperplasia, nodular hyperplasia, eosinophilic focus, cholangiofibrosis, bile duct cysts, necrosis, portal fibrosis, mixed cell focus, and toxic hepatopathy.
  • In the lung, there were dose-dependent increases in the incidences of bronchiolar metaplasia of the alveolar epithelium at 53 weeks and at 2 years and squamous metaplasia at 2 years.
  • In the pancreas, there were increases in the incidences of numerous nonneoplastic lesions including arterial chronic active inflammation, acinar cytoplasmic vacuolization, acinar atrophy, chronic active inflammation, and duct dilatation.
  • At 2 years, incidences of acinar adenoma or acinar carcinoma that exceeded the historical control ranges were seen in all dosed groups except the 100 ng TEQ/kg group.
  • Treatment-related increases in the incidences of nonneoplastic lesions were seen in other organs including hyperplasia, cystic degeneration, atrophy, and cytoplasmic vacuolization of the adrenal cortex; gingival squamous hyperplasia of the oral mucosa; squamous metaplasia of the uterus; atrophy of the thymus (incidence and severity); chronic active inflammation of the ovary; nephropathy of the kidney (incidence and severity); cardiomyopathy; bone marrow hyperplasia; transitional epithelium of the urinary bladder; chronic active inflammation of the mesenteric artery; and follicular cell hypertrophy of the thyroid gland. (ABSTRACT TRUNCATED).

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  • (PMID = 17342195.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzofurans; 0 / Carcinogens; DFC2HB4I0K / Polychlorinated Biphenyls; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; U4C2RV3124 / 2,3,4,7,8-pentachlorodibenzofuran
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24. Donati V, Fontanini G, Dell'Omodarme M, Prati MC, Nuti S, Lucchi M, Mussi A, Fabbri M, Basolo F, Croce CM, Aqeilan RI: WWOX expression in different histologic types and subtypes of non-small cell lung cancer. Clin Cancer Res; 2007 Feb 1;13(3):884-91
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  • [Title] WWOX expression in different histologic types and subtypes of non-small cell lung cancer.
  • PURPOSE: Non-small cell lung cancer (NSCLC) has heterogeneous histopathologic classification and clinical behavior and very low survival rate.
  • EXPERIMENTAL DESIGN: WWOX protein expression was evaluated by immunohistochemistry in 170 patients with NSCLC (101 squamous cell carcinomas, 66 adenocarcinomas, 3 large cell carcinomas) and was correlated with histopathologic (histotype, subtype, grade, tumor-node-metastasis, stage, index of cell proliferation Ki67/MIB1) and clinical (age, gender, local recurrences, distant metastases, overall survival, and disease-free survival) characteristics.
  • RESULTS: WWOX expression was absent/reduced in 84.9% of NSCLCs, whereas it was normal in 80.5% of adjacent normal lung tissues.
  • WWOX expression was strongly associated with tumor histology (P=1.1x10(-5)) and histologic grade (P=0.0081): the percentage of cases with absent/strongly reduced WWOX expression was higher in squamous cell carcinomas and in poorly differentiated tumors.
  • Regarding adenocarcinoma, bronchioloalveolar pattern showed normal WWOX expression in 62.5% of the cases, whereas in solid and acinar patterns, a prevalence of cases with absent/very low WWOX expression was observed (79.2% and 50%, respectively).
  • Finally, weak WWOX staining intensity was related to the high index of cell proliferation (P=0.0012).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Gene Expression Regulation, Neoplastic. Lung Neoplasms / metabolism. Oxidoreductases / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Proliferation. Disease Progression. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Time Factors

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  • (PMID = 17289881.001).
  • [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
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 1.- / Oxidoreductases; EC 1.1.1.- / WWOX protein, human
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25. Chilosi M, Murer B: Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy. Arch Pathol Lab Med; 2010 Jan;134(1):55-65
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  • [Title] Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy.
  • CONTEXT: Lung cancer is one of the most frequent and lethal malignant neoplasms, but knowledge regarding the molecular basis of its pathogenesis is far from complete due to the striking diversity of different forms.
  • The current lung cancer classification (World Health Organization 2004) can efficiently distinguish clinically relevant major subtypes (small cell and non-small cell carcinomas), but its results are partly inadequate when facing prognostic and therapeutic decisions for non-small cell carcinomas, especially for the group of tumors classified as adenocarcinoma.
  • Lung adenocarcinoma comprises a heterogeneous group of tumors characterized by diverse morphologic features and molecular pathogenesis.
  • The category of mixed adenocarcinomas includes most adenocarcinomas (approximately 80%) and, according to World Health Organization criteria, is defined by the occurrence of a mixed array of different patterns (acinar, papillary, bronchioloalveolar, solid with mucin).
  • In this evolving scenario, pathologists face new challenging diagnostic roles that include not only the precise morphologic definition of carcinoma subtypes but also their molecular characterization.
  • OBJECTIVE: To use a comprehensive critical analysis reconciling the overwhelming variety of biologic, morphologic, molecular, and clinical data to define new classification schemes for lung adenocarcinoma.
  • CONCLUSIONS: A new classification approach should redefine lung adenocarcinoma heterogeneity reconciling classic morphology, immunophenotypic and molecular features of neoplastic cells, and also relevant information provided by stem cell biology.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / pathology. Lung Neoplasms / classification. Lung Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Cell Differentiation. Drug Therapy. Humans. Stem Cells / pathology. World Health Organization

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  • (PMID = 20073606.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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26. Wang XQ, Li H, Van Putten V, Winn RA, Heasley LE, Nemenoff RA: Oncogenic K-Ras regulates proliferation and cell junctions in lung epithelial cells through induction of cyclooxygenase-2 and activation of metalloproteinase-9. Mol Biol Cell; 2009 Feb;20(3):791-800
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  • [Title] Oncogenic K-Ras regulates proliferation and cell junctions in lung epithelial cells through induction of cyclooxygenase-2 and activation of metalloproteinase-9.
  • Expression of oncogenic K-Ras is frequently observed in non-small-cell lung cancer.
  • However, oncogenic K-Ras is not sufficient to transform lung epithelial cells and requires collaborating signals that have not been defined.
  • To examine the biological effects of K-Ras in nontransformed lung epithelial cells, stable transfectants were generated in RL-65 cells, a spontaneously immortalized lung epithelial cell line.
  • Epithelial cells expressing oncogenic K-Ras showed increased proliferation in two- and three-dimensional tissue culture and delayed formation of hollow acinar structures in three-dimensional matrigel cultures.
  • These data indicate that although expression of oncogenic K-Ras does not transform lung epithelial cells, it alters the phenotype of the cells by increasing proliferation and decreasing cell-cell contacts characteristic of epithelial cells.

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  • (PMID = 19037103.001).
  • [ISSN] 1939-4586
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / CA58187; United States / NCI NIH HHS / CA / R01 CA138528; United States / NCI NIH HHS / CA / CA108610; United States / NCI NIH HHS / CA / R01 CA108610; United States / NCI NIH HHS / CA / R01 CA116527; United States / NCI NIH HHS / CA / CA103618; United States / NCI NIH HHS / CA / R01 CA103618
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Cyclooxygenase Inhibitors; 0 / Kras protein, rat; 0 / beta Catenin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2633382
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27. 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.
  • Immunohistochemical staining showed Ets-1 expression in 82 cases of 156 carcinomas (53%): 36 of 52 (69%) squamous cell carcinomas, 41 of 96 (43%) adenocarcinomas, and 5 of 8 (63%) other carcinomas.
  • In adenocarcinomas, a higher proportion of acinar type expressed Ets-1 compared to papillary or alveolar type (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.
  • Such relationship was not observed among squamous cell carcinoma patients.
  • 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
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / mortality. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Survival Analysis. Survivors

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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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28. 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.
  • 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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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.
  • 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. Furonaka O, Takeshima Y, Awaya H, Kushitani K, Kohno N, Inai K: Aberrant methylation and loss of expression of O-methylguanine-DNA methyltransferase in pulmonary squamous cell carcinoma and adenocarcinoma. Pathol Int; 2005 Jun;55(6):303-9
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  • [Title] Aberrant methylation and loss of expression of O-methylguanine-DNA methyltransferase in pulmonary squamous cell carcinoma and adenocarcinoma.
  • The methylation status of the MGMT gene was investigated by methylation-specific polymerase chain reaction (PCR) and expression status was investigated by immunohistochemistry in 70 cases of pulmonary squamous cell carcinoma (pulmonary SqCC), including 23 cases of the central type and 47 cases of the peripheral type, and in 53 cases of the peripheral type of pulmonary adenocarcinoma (AC).
  • In AC with mixed subtypes showing MGMT methylation, the level of MGMT expression in the bronchioloalveolar carcinoma (BAC) area (non-invasive status) was significantly higher than that in the papillary or acinar AC area (invasive status; P = 0.0002).
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. DNA Methylation. Lung Neoplasms / pathology. O(6)-Methylguanine-DNA Methyltransferase / genetics

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  • (PMID = 15943786.001).
  • [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 / DNA, Neoplasm; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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31. Chantranuwat C, Sriuranpong V, Huapai N, Chalermchai T, Leungtaweeboon K, Voravud N, Mutirangura A: Histopathologic characteristics of pulmonary adenocarcinomas with and without EGFR mutation. J Med Assoc Thai; 2005 Sep;88 Suppl 4:S322-9
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  • EGFR mutation played crucial role for responsiveness of non-small cell lung cancers to EGFR tyrosine kinase inhibitors.
  • RESULTS: Gland-forming pattern, including bronchiloloalveolar carcinoma (BAC), well-formed acinar, and poorly-formed acinar patterns more frequently contains EGFR mutations than solid pattern (72.7% vs. 23.1%, p = 0.002).
  • CONCLUSION: High frequency of the mutation does not present only in BAC pattern, but also in well-formed and poorly-formed acinar patterns, suggesting them as usual spectrum of EGFR mutated adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Genes, erbB-1 / genetics. Lung Neoplasms / pathology

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  • (PMID = 16623049.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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32. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(559):1-174

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  • There were increases in hepatic cell proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
  • Analysis of PCB 118 concentrations in dosed groups showed dose- and duration of dosing-dependent increases in fat, liver, lung, and blood.
  • The highest concentrations were seen in fat at 2 years with lower concentrations observed in the liver, lung, and blood.
  • At 2 years, a significant dose-related increase in hepatic toxicity was observed and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, inflammation, oval cell hyperplasia, pigmentation, multinucleated hepatocyte, eosinophilic and mixed cell foci, diffuse fatty change, toxic hepatopathy, nodular hyperplasia, necrosis, bile duct hyperplasia and cyst, and cholangiofibrosis.
  • In the lung at 2 years, a significantly increased incidence of cystic keratinizing epithelioma occurred in the 4,600 g/kg core study group compared to the vehicle control group incidence.
  • The incidence of carcinoma of the uterus in the 4,600 g/kg stop-exposure group was significantly greater than those in the vehicle control and 4,600 g/kg core study groups at 2 years.
  • A marginal increase in squamous cell carcinoma occurred in the 220 g/kg group.
  • At 2 years, there were marginally increased incidences of exocrine pancreatic adenoma or carcinoma in the 460, 1,000, and 4,600 g/kg core study groups.
  • Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization, pancreatic acinar cell cytoplasmic vacuolization and arterial chronic active inflammation, follicular cell hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
  • CONCLUSIONS: Under the conditions of this 2-year gavage study, there was clear evidence of carcinogenic activity of PCB 118 in female Harlan Sprague-Dawley rats based on increased incidences of neoplasms of the liver (cholangiocarcinoma, hepatocholangioma, and hepatocellular adenoma) and cystic keratinizing epithelioma of the lung.
  • Occurrences of carcinoma in the uterus were considered to be related to the administration of PCB 118.
  • Occurrences of squamous cell carcinoma of the uterus and acinar neoplasms of the pancreas may have been related to administration of PCB 118.
  • Administration of PCB 118 caused increased incidences of nonneoplastic lesions in the liver, lung, adrenal cortex, pancreas, thyroid gland, nose, and kidney.

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  • (PMID = 21383778.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
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33. Kawakami T, Nabeshima K, Hamasaki M, Iwasaki A, Shirakusa T, Iwasaki H: Small cluster invasion: a possible link between micropapillary pattern and lymph node metastasis in pT1 lung adenocarcinomas. Virchows Arch; 2009 Jan;454(1):61-70
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  • [Title] Small cluster invasion: a possible link between micropapillary pattern and lymph node metastasis in pT1 lung adenocarcinomas.
  • Lung adenocarcinomas with micropapillary pattern (MPP) are associated with frequent nodal metastasis.
  • In this study, we investigated how small micropapillary clusters of carcinoma cells present in tumoral alveolar spaces lead to increased lymph node metastasis.
  • We analyzed 146 cases of pT1 lung adenocarcinomas with reference to the presence of MPP, small cluster invasion (SCI), and lymphatic involvement.
  • SCI was defined as markedly resolved acinar-papillary tumor structures with single or small clusters of carcinoma cells invading stroma within fibrotic foci.
  • Carcinoma cells undergoing SCI demonstrated the same characteristic MUC-1 expression on the outer surface of cell clusters as those undergoing MPP.
  • Thus, SCI could link MPP to nodal metastasis; carcinoma cells with MPP tend to undergo SCI in scars and invade lymphatics in pT1 lung adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Lymphatic Metastasis / pathology

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  • (PMID = 19002492.001).
  • [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
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34. Vidyadhara S, Shetty AP, Rajasekaran S: Widespread metastases from acinic cell carcinoma of parotid gland. Singapore Med J; 2007 Jan;48(1):e13-5
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  • [Title] Widespread metastases from acinic cell carcinoma of parotid gland.
  • Acinic cell carcinoma metastasising to the spine is rare and has been described only once before in the literature.
  • We believe this 40-year-old man to be the first reported case of incompletely resected acinic cell carcinoma of the parotid gland metastasising simultaneously to regional lymph nodes, upper lobes of both lungs, sphenoid bone and dorsal spine with neurological deficits.
  • This case report stresses the need for postoperative radiotherapy following incomplete resection of the primary tumour.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Lung Neoplasms / secondary. Parotid Neoplasms / pathology. Skull Neoplasms / secondary. Sphenoid Bone. Spinal Neoplasms / secondary. Thoracic Vertebrae
  • [MeSH-minor] Adult. Diagnosis, Differential. Follow-Up Studies. Humans. Lymphatic Metastasis. Magnetic Resonance Imaging. Male

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  • (PMID = 17245497.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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35. 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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36. 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).
  • Three of the tumors were of the papillary subtype, and one was a mixed subtype that consisted of acinar, papillary, and solid components.
  • 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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37. Guerra C, Schuhmacher AJ, Cañamero M, Grippo PJ, Verdaguer L, Pérez-Gallego L, Dubus P, Sandgren EP, Barbacid M: Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell; 2007 Mar;11(3):291-302
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  • We report that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acinar/centroacinar cells or their precursors into ductal-like cells.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Genes, ras. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / pathology
  • [MeSH-minor] Animals. Cell Lineage. Cell Transformation, Neoplastic. Ceruletide. Doxycycline / pharmacology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Mice. Mice, Mutant Strains. Mutation. Neoplasm Invasiveness. Pancreas / pathology. Signal Transduction


38. Bhatia P, Srinivasan R, Rajwanshi A, Nijhawan R, Khandelwal N, Wig J, Vasishtha RK: 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions. Acta Cytol; 2008 Sep-Oct;52(5):523-9
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  • Seven cases (2.6%) yielded insufficient material for diagnosis; 260 cases were classified as benign (n=118) and malignant (n=142) lesions.
  • Of the 142 malignant aspirates, the cytodiagnosis was adenocarcinoma in 126, neuroendocrine/carcinoid tumor in 7, papillary solid epithelial neoplasm in 2, mucinous cystadenocarcinoma in 2, acinar cell carcinoma in 1 and metastatic small cell carcinoma in lung in 4 cases.

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  • [CommentIn] Acta Cytol. 2008 Sep-Oct;52(5):521-2 [18833811.001]
  • (PMID = 18833812.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Scheble VJ, Braun M, Wilbertz T, Stiedl AC, Petersen K, Schilling D, Reischl M, Seitz G, Fend F, Kristiansen G, Perner S: ERG rearrangement in small cell prostatic and lung cancer. Histopathology; 2010 Jun;56(7):937-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ERG rearrangement in small cell prostatic and lung cancer.
  • AIMS: Small cell prostatic cancer is a rare but aggressive disease.
  • Currently, its histogenetic origin is unclear and its distinction from metastatic small cell lung cancer is challenging.
  • The aim of our study was to determine whether the ERG rearrangement commonly observed in acinar prostatic cancer can distinguish small cell prostatic cancer from small cell lung cancer samples.
  • METHODS AND RESULTS: We assessed 15 small cell prostatic cancers and 22 small cell lung cancers for ERG rearrangement using fluorescence in situ hybridization.
  • ERG rearrangement occurred in 86% of small cell prostatic cancers but in none of the small cell lung cancers and was the best marker to differentiate between both tumours (P < 0.0001).
  • CONCLUSIONS: The ERG rearrangement is commonly observed in small cell prostatic cancer, supporting the hypothesis that ERG rearrangement occurs in aggressive prostatic cancers.
  • Furthermore, the ERG rearrangement is the most significant marker to differentiate between small cell prostatic cancer and small cell lung cancer.
  • Moreover, our data suggest that small cell prostatic cancer is not a tumour entity on its own, but a dedifferentiated variant of common acinar prostatic cancer.
  • [MeSH-major] Carcinoma, Small Cell / genetics. Gene Rearrangement. Lung Neoplasms / genetics. Prostatic Neoplasms / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Chi-Square Distribution. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Tissue Array Analysis

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  • [CommentIn] Histopathology. 2010 Oct;57(4):633; author reply 633-4 [20955388.001]
  • (PMID = 20636794.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / ERG protein, human; 0 / Trans-Activators
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40. Girard N, Deshpande C, Lau C, Finley D, Rusch V, Pao W, Travis WD: Comprehensive histologic assessment helps to differentiate multiple lung primary nonsmall cell carcinomas from metastases. Am J Surg Pathol; 2009 Dec;33(12):1752-64
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  • [Title] Comprehensive histologic assessment helps to differentiate multiple lung primary nonsmall cell carcinomas from metastases.
  • The pathologic classification of nonsmall cell lung cancer (NSCLC) is evolving.
  • Lung adenocarcinoma is morphologically heterogeneous, with mixtures of acinar, papillary, bronchioloalveolar, and solid patterns in more than 80% of cases.
  • In case of synchronous or metachronous multiple NSCLC, the distinction of intrapulmonary metastases from independent primary tumors is of great clinical importance as it influences staging and potentially the therapeutic strategy.
  • Using the Martini-Melamed criteria, paired tumors were characterized as multiple primary NSCLCs in 21 cases and as intrapulmonary metastases in 3 cases.
  • Genomic and mutational data led to a diagnosis of multiple primaries in 14 cases and of metastases in 8 cases; 2 cases could not be assessed.
  • This molecular characterization contradicted the Martini-Melamed diagnosis in 7 (32%) of the 22 assessable comparisons.
  • We found that comparing adenocarcinomas is a complex issue that requires assessment not only of percentages of the histologic subtypes, but also the recording of additional histologic details such as cytologic features, patterns of stroma, necrosis, discrete nodularity versus miliary growth and variants such as clear cell, signet ring, mucinous, and fetal patterns.
  • We also found that paired squamous cell carcinomas could be compared based on histologic subtyping in addition to cytologic and stromal characteristics.
  • In summary, based on a well characterized cohort with detailed clinical, pathologic and molecular data, we found comprehensive histologic assessment is a powerful tool that seems to be a promising way to determine whether multiple lung adenocarcinomas or squamous cell carcinomas are metastatic or multiple primaries.
  • This has great clinical implications for staging and therapeutic management of lung cancer patients with multiple tumors.

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  • (PMID = 19773638.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124504; United States / NCI NIH HHS / CA / CA124504
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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41. Tavora F, Rassaei N, Shilo K, Foss RD, Galvin JR, Travis WD, Franks TJ: Occult primary parotid gland acinic cell adenocarcinoma presenting with extensive lung metastasis. Arch Pathol Lab Med; 2007 Jun;131(6):970-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occult primary parotid gland acinic cell adenocarcinoma presenting with extensive lung metastasis.
  • Acinic cell adenocarcinoma is a malignant salivary gland neoplasm with a relatively low rate of lymphangitic spread to regional lymph nodes.
  • We encountered an unusual example of acinic cell adenocarcinoma that initially presented in the lung, whereas the primary parotid carcinoma, despite extensive clinical evaluation, only became apparent 1 year after initial diagnosis.
  • The histologic, immunohistochemical, and ultrastructural features of the tumor in the parotid gland and lung were similar.
  • This presentation is unique, showing that peripheral lung tumors of salivary gland type are likely to be metastatic, and careful clinical evaluation is warranted in establishing their primary site of origin.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Lung Neoplasms / secondary. Parotid Neoplasms / pathology

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  • (PMID = 17550329.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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42. Wang Y, Liu XG, Liang MZ, Qin PX, Lin YJ, Yi XP: [Correlation of early phase contrast enhancement of multi-detector row computed tomography to tumor stroma of nodular solid lung adenocarcinoma]. Ai Zheng; 2008 Nov;27(11):1190-6
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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 early phase contrast enhancement of multi-detector row computed tomography to tumor stroma of nodular solid lung adenocarcinoma].
  • BACKGROUND & OBJECTIVE: Dynamic enhanced multi-detector row CT (MDCT) has been used in differential diagnosis of pulmonary nodules, but its mechanism was unclear yet.
  • This study was to evaluate the correlations of early phase enhancement of MDCT to proportion and distribution of stroma in solid lung adenocarcinoma.
  • METHODS: A total of 31 patients with lung adenocarcinoma underwent routine contrast-enhanced MDCT.
  • Most acinar adenocarcinomas had net enhancement of > 20 Hu, which was significantly higher than that of solid adenocarcinomas with mucin subtype (P=0.005).
  • CONCLUSIONS: Extent and pattern of CT enhancement of solid lung adenocarcinoma nodules reflect the proliferation and distribution of stroma, respectively.
  • It is helpful to comprehend some false negative on CT enhancement by adequately understanding of the pathologic features of different subtypes of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography. Solitary Pulmonary Nodule / radiography. Tomography, Spiral Computed / methods
  • [MeSH-minor] Adenocarcinoma, Papillary / pathology. Adenocarcinoma, Papillary / radiography. Adult. Aged. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / radiography. Female. Humans. Male. Microvessels / pathology. Microvessels / radiography. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Radiographic Image Enhancement

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  • (PMID = 19000452.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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43. Schwentner I, Obrist P, Thumfart W, Sprinzl G: Distant metastasis of parotid gland tumors. Acta Otolaryngol; 2006 Apr;126(4):340-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The likelihood of developing distant metastasis is associated with high-grade tumors, such as adenoid cystic carcinoma, salivary duct carcinoma, high-grade mucoepidermoid carcinoma and tumors located in the submandibular gland, posterior tongue and pharyngeal tumors.
  • [MeSH-minor] Aged. Bone Neoplasms / secondary. Brain Neoplasms / secondary. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / secondary. Carcinoma, Adenoid Cystic / pathology. Carcinoma, Adenoid Cystic / secondary. Carcinoma, Mucoepidermoid / pathology. Carcinoma, Mucoepidermoid / secondary. Fatal Outcome. Humans. Immunohistochemistry. Incidence. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Male. Parotid Gland / pathology. Parotid Gland / surgery. Salivary Ducts / pathology. Tomography, X-Ray Computed

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  • (PMID = 16608783.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 32
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44. Ribeiro HB, Paiva TF Jr, Mamprin GP, Gorzoni ML, Rocha AJ, Lancellotti CL: Carcinomatous encephalitis as clinical presentation of occult lung adenocarcinoma: case report. Arq Neuropsiquiatr; 2007 Sep;65(3B):841-4
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] Carcinomatous encephalitis as clinical presentation of occult lung adenocarcinoma: case report.
  • A magnetic resonance imaging (MRI) with gadolinium, the method of choice, presumes the diagnosis.
  • Previous reports of this unusual form of metastatic disease have described patients with prior diagnosis of pulmonary adenocarcinoma.
  • We present the case of carcinomatous encephalitis in a 76-year-old woman as the primary manifestation of occult pulmonary adenocarcinoma with its clinical, imaging, and anatomopathological findings.
  • [MeSH-major] Brain Neoplasms / secondary. Carcinoma, Acinar Cell / secondary. Lung Neoplasms / pathology

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  • (PMID = 17952293.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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45. Young RH: From Krukenberg to today: the ever present problems posed by metastatic tumors in the ovary. Part II. Adv Anat Pathol; 2007 May;14(3):149-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The first tumor discussed is gastric carcinoma of intestinal-type whose ovarian manifestations have been the subject of a recent paper which emphasized its differences from the Krukenberg tumor.
  • The section on pancreatic neoplasms reemphasizes the problems caused by metastatic ductal carcinoma, considered primarily in Part I, and discusses less common issues such as spread of neuroendocrine and acinar cell carcinomas.
  • The limited information on spread of tumors of the gallbladder and extrahepatic bile ducts is then reviewed before more detailed consideration of hepatic neoplasms, prompted by recent contributions on hepatocellular carcinoma and intrahepatic cholangiocarcinoma, the latter based on significant experience with this problem in Thailand.
  • The section on appendiceal neoplasms highlights ovarian spread of diverse tumors ranging from typical intestinal-type adenocarcinoma to signet-ring cell carcinomas with various patterns which in the ovary may prompt diagnoses such as a goblet cell (mucinous) carcinoid tumor, but whose ovarian features place them in the category of a Krukenberg tumor.
  • The diverse problems in differential diagnosis of carcinoid tumor (provoked by nested, acinar, and other patterns, including folliclelike spaces) are then reviewed.
  • That patients with breast cancer have an increased risk of primary ovarian cancer and that the latter is more common than secondary spread of breast cancer is noted.
  • The section on lung tumors largely reflects information in a recent paper that small cell carcinoma and adenocarcinoma are the lung cancers that spread to the ovary most commonly.
  • The extremely broad differential diagnosis posed by metastatic malignant melanoma ranging from that of an oxyphilic tumor, to a small cell tumor, to a follicle-forming neoplasm, is then considered.
  • The sections on renal cell carcinoma and other urinary tract neoplasms emphasize the differential diagnosis of metastatic clear cell carcinoma and primary clear cell carcinoma, an issue usually resolvable by an awareness of the various features of the ovarian variant, rarely or never seen in the renal variant.
  • The endometrial stromal tumors are problematic largely because the history of a primary tumor may be remote, in the ovaries the typical growth and vascular pattern of endometrial stromal neoplasms is not always conspicuous, and some endometrial stromal sarcomas in the ovary show sex cordlike patterns of growth.
  • Recent information has indicated that gastrointestinal stromal tumors may rarely have significant ovarian manifestations and if the primary neoplasm is overlooked, the ovarian tumor may be misdiagnosed, usually as an ovarian fibromatous tumor, but potentially as another primary neoplasm.
  • The sections on ovarian spread of uterine carcinomas emphasize the problems owing to cervical adenocarcinomas, which have a greater tendency to involve the ovaries than squamous cell carcinomas and can simulate primary mucinous or endometrioid cancers.
  • The final neoplasms considered are malignant mesothelioma and the desmoplastic small round cell tumor.
  • The microscopic features of malignant mesothelioma are so different from those of primary ovarian carcinoma in most instances that the diagnosis should be readily established on routine microscopic evaluation.
  • The differential diagnosis of the desmoplastic small round cell tumor is more complex because of the greater overlap with the many other small cell malignant tumors that may involve the ovaries primarily or secondarily.
  • However, as pointed out in brief concluding remarks, despite the aid of that modality, as in surgical pathology overall, careful consideration of the clinical background, distribution of disease, gross characteristics and spectrum of routine microscopic findings, will lead to the correct diagnosis in the majority of cases and at the very least lead to formulation of a considered differential diagnosis such that use of special techniques may be judicious and those results placed in context of the time-honored clinical and pathologic features.
  • [MeSH-major] Carcinoma / secondary. Krukenberg Tumor / secondary. Ovarian Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Female. History, 19th Century. History, 20th Century. Humans

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  • (PMID = 17452813.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
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46. National Toxicology Program: Toxicology and carcinogenesis studies of a binary mixture of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) (CAS No. 35065-27-1) in female Harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 Aug;(530):1-258
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatic Cell Proliferation Data: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
  • Determinations of PCB 126 and PCB 153 Concentrations in Tissues: Concentrations of PCB 126 and PCB 153 were determined in fat, liver, lung, and blood at the 14-, 31-, and 53-week interim evaluations and at the end of the 2-year study (105 weeks).
  • PCB 126 was not detectable in vehicle control animals, but increased with increasing dose of PCB 126 and duration of exposure; the highest concentrations were found in liver and fat, and lower levels were seen in lung and blood.
  • Increasing the proportion of PCB 153 in the mixture relative to PCB 126 led to a general decrease in the amount of PCB 126 in liver and lung at the later time points, whereas in fat and blood, there was generally either no effect of PCB 153 on the disposition of PCB 126, or there was an increase in the amount of PCB 126 in the tissue.
  • In vehicle control animals, PCB 153 was detectable in the fat at all time points, in the lung at all time points except 53 weeks, and in the liver and blood at 2 years.
  • At the end of the 2-year study, there were significantly increased incidences and severities of toxic hepatopathy characterized by hepatocyte hypertrophy, multinucleated hepatocytes, pigmentation, diffuse and focal fatty change, eosinophilic focus, nodular hyperplasia, cholangiofibrosis, oval cell hyperplasia, bile duct cysts, bile duct hyperplasia, necrosis, and portal fibrosis.
  • In addition, two animals in the highest dose group had hepatocellular carcinoma.
  • At 2 years, a significantly increased incidence of cystic keratinizing epithelioma of the lung was observed in Group 7.
  • In addition, single occurrences of squamous cell carcinoma were seen in the top two dose groups.
  • Nonneoplastic effects whose incidences were increased in the lung included bronchiolar metaplasia of the alveolar epithelium and squamous metaplasia.
  • Significantly increased incidences of squamous cell carcinoma (gingival) of the oral mucosa were seen at the end of the 2-year study and were accompanied by increased incidences of gingival squamous hyperplasia.
  • In the pancreas at 53 weeks, the incidence of acinar cytoplasmic vacuolization was significantly increased in the highest dose group.
  • At 2 years, increased incidences of acinar atrophy and acinar cytoplasmic vacuolization were seen in addition to pancreatic acinar neoplasms in dosed groups.
  • In the uterus at 2 years, there was a marginal increase in the incidence of squamous cell carcinoma in Group 5.
  • Numerous nonneoplastic effects were seen in other organs at the interim time points including atrophy of the thymus and follicular cell hypertrophy of the thyroid gland.

  • Hazardous Substances Data Bank. 2,2',4,4',5,5'-HEXACHLOROBIPHENYL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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  • (PMID = 17160104.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; DFC2HB4I0K / Polychlorinated Biphenyls; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; ZRU0C9E32O / 2,4,5,2',4',5'-hexachlorobiphenyl
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47. Elizalde-Torrent A, Fernández-Cortijo J, San José A: [Acinar cell carcinoma of the lung]. Arch Bronconeumol; 2010 Jun;46(6):340-2
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] [Acinar cell carcinoma of the lung].
  • [Transliterated title] Carcinoma de células acinares de pulmón.
  • [MeSH-major] Carcinoma, Acinar Cell. Lung Neoplasms

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  • (PMID = 20181420.001).
  • [ISSN] 1579-2129
  • [Journal-full-title] Archivos de bronconeumología
  • [ISO-abbreviation] Arch. Bronconeumol.
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
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48. Chuah KL, Yap WM, Tan HW, Koong HN: Recurrence of pulmonary acinic cell carcinoma. Arch Pathol Lab Med; 2006 Jul;130(7):932-3
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] Recurrence of pulmonary acinic cell carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Lung Neoplasms / pathology. Neoplasm Recurrence, Local / pathology

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  • [CommentOn] Arch Pathol Lab Med. 2003 Apr;127(4):e216-9 [12683906.001]
  • (PMID = 16831044.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] United States
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49. Ando K, Ohkuni Y, Kaneko N, Narita M: Spontaneous rupture of the splenic metastasis in acinar cell carcinoma. Pancreas; 2009 Oct;38(7):836-8
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous rupture of the splenic metastasis in acinar cell carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Neoplasms / pathology. Spleen / pathology. Splenic Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Immunohistochemistry. Lung Neoplasms / diagnosis. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Male. Middle Aged. Rupture, Spontaneous. alpha 1-Antichymotrypsin / metabolism. alpha 1-Antitrypsin / metabolism

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  • (PMID = 19893460.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha 1-Antichymotrypsin; 0 / alpha 1-Antitrypsin
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