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1. 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
Hazardous Substances Data Bank. 3,4,3',4'-Tetrachloroazobenzene .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 3,3',4,4'-Tetrachloroazobenzene (TCAB) is not commercially manufactured but is formed as an unwanted by-product in the manufacture of 3,4-dichloroaniline and its herbicidal derivatives Propanil, Linuron, and Diuron.
  • It occurs from the degradation of chloroanilide herbicides (acylanilides, phenylcarbamates, and phenylureas) in soil by peroxide-producing microorganisms; and is formed by the photolysis and biolysis of 3,4-dichloroaniline.
  • TCAB was nominated by the United States Environmental Protection Agency for toxicity and carcinogenicity testing based on its structural and biological similarity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the potential for human exposure from the consumption of crops contaminated with 3,4-dichloroaniline-derived herbicides.
  • 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.
  • TCAB concentrations were significantly increased in a dose-dependent manner in all tissues from dosed groups relative to vehicle controls.
  • 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.
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Humans. Male. Mice. Mice, Inbred Strains. Organ Size / drug effects. Rats. Rats, Sprague-Dawley

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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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2. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Structurally related compounds that bind to the AhR and exhibit biological actions similar to TCDD are commonly referred to as "dioxin-like compounds"(DLCs).
  • Manufacture and use of these chemicals were stopped because of increased PCB residues in the environment, but they continue to be released into the environment through the use and disposal of products containing PCBs, as by-products during the manufacture of certain organic chemicals, during combustion of some waste materials, and during atmospheric recycling.
  • In general, exposure to PCB 118 lead to dose-dependent decreases in the concentrations of serum total thyroxine (T4) and free T4 in all dosed groups.
  • There were increases in hepatic cell proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
  • Administration of PCB 118 led to dose-dependent increases in CYP1A1-associated 7-ethoxyresorufin-O-deethylase, CYP1A2-associated acetanilide4-hydroxylase, and CYP2B-associated pentoxyresorufin-O-deethylase activities at the 14-, 31-, and 53-week interim evaluations.
  • 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.
  • [MeSH-minor] Animals. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Humans. Male. Rats. Rats, Sprague-Dawley. Tetrachlorodibenzodioxin / toxicity

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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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Structurally related compounds that bind to the AhR and exhibit biological actions similar to TCDD are commonly referred to as "dioxin-like compounds" (DLCs).
  • The main sources of TCDD releases into the environment are from combustion and incineration; metal smelting, refining, and processing; chemical manufacturing and processing; biological and photochemical processes; and existing reservoir sources that reflect past releases.
  • 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).
  • Exposure led to a treatment-related increase in hepatic toxicity with a broad spectrum of lesions.
  • 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.
  • The highest incidence of cholangiocarcinoma was seen in the 100 ng/kg core study group and included a significant number of animals with multiple cholangiocarcinomas.
  • 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)
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Female. Mice. Neoplasms, Experimental / chemically induced. Organ Size / drug effects. Rats. Rats, Sprague-Dawley

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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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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • Diagnostic problems are mainly related to the poor reproducibility of histologic criteria, especially when applied in small biopsies and cytology, and to the difficulty in assigning each form to a precisely defined entity, as needed by updated therapeutic approaches.
  • 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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5. 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
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] Aberrant methylation and loss of expression of O-methylguanine-DNA methyltransferase in pulmonary squamous cell carcinoma and adenocarcinoma.
  • O(6)-Methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein that protects cells against the carcinogenic effects of alkylating agents.
  • 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 SqCC, the frequency of MGMT methylation was 26% in the central type and 40% in the peripheral type; a significant correlation was not found (P = 0.29).
  • 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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6. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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 affects were mediated through COX-2-dependent activation of beta-catenin signaling and inhibition of apoptosis.
  • 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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8. 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
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] [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
  • [MeSH-minor] Aged. Drug Combinations. Gastrectomy. Hepatectomy. Humans. Male. Pancreatectomy

  • MedlinePlus Health Information. consumer health - Liver Cancer.
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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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