[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 23836
1. Nowak M, Madej JA, Dziegiel P: Correlation between MCM-3 protein expression and grade of malignancy in mammary adenocarcinomas and soft tissue fibrosarcomas in dogs. In Vivo; 2009 Jan-Feb;23(1):49-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation between MCM-3 protein expression and grade of malignancy in mammary adenocarcinomas and soft tissue fibrosarcomas in dogs.
  • Localization of MCM-3 and the extent of its expression were evaluated in mammary adenocarcinomas and soft tissue fibrosarcomas in dogs.
  • MATERIALS AND METHODS: The research material was sampled in the course of surgery in 71 dogs of various breeds, aged 4 to 14 years (50 cases of mammary adenocarcinoma and 21 cases of soft tissue fibrosarcoma).
  • RESULTS: Nuclear expression of MCM-3 was detected in 70% adenocarcinomas and in over 71% of fibrosarcomas.
  • Statistical analysis demonstrated strong positive correlation (r=0.71 for fibrosarcomas, r=0.52 for adenocarcinomas; p<0.05) between MCM-3 expression and grade of malignancy in the studied tumours.
  • [MeSH-major] Adenocarcinoma / pathology. Fibrosarcoma / pathology. Mammary Neoplasms, Animal / pathology. Nuclear Proteins / metabolism. Soft Tissue Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19368124.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins
  •  go-up   go-down


2. Fernández Rivera C, Alonso Hernández Á, Mosquera Reboredo J, Rodríguez Gómez I: Association of bladder adenocarcinoma and BK virus infection in a pancreatico-renal transplant recipient. NDT Plus; 2010 Jun;3(3):300-302
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.
  • [Title] Association of bladder adenocarcinoma and BK virus infection in a pancreatico-renal transplant recipient.
  • We report a case of urinary bladder adenocarcinoma in a pancreatico-renal transplant recipient which was diagnosed 2 years after BKV infection.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pediatr Transplant. 2008 Aug;12(5):600-5 [18652620.001]
  • [Cites] Oncogene. 2006 May 4;25(19):2727-35 [16547506.001]
  • [Cites] Transplantation. 2008 Apr 15;85(7 Suppl):S42-8 [18401263.001]
  • [Cites] NDT Plus. 2009 Jun;2(3):246-9 [25984002.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5192-200 [12910256.001]
  • [Cites] Virus Res. 1989 Apr;12(4):315-30 [2543158.001]
  • [Cites] J Am Soc Nephrol. 2004 Jun;15(6):1582-8 [15153569.001]
  • [Cites] J Infect Dis. 2005 Oct 15;192(8):1349-54 [16170751.001]
  • [Cites] Transplantation. 2005 May 27;79(10):1277-86 [15912088.001]
  • [Cites] Transplantation. 2009 Mar 15;87(5):621-30 [19295303.001]
  • [Cites] Transplantation. 2008 Mar 27;85(6):850-4 [18360267.001]
  • [Cites] Transplantation. 2002 Jun 27;73(12):1933-6 [12131691.001]
  • (PMID = 28657060.001).
  • [ISSN] 1753-0784
  • [Journal-full-title] NDT plus
  • [ISO-abbreviation] NDT Plus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; BK virus / kidney transplantation / renal transplantation / urinary bladder neoplasms
  •  go-up   go-down


3. Abnet CC, Freedman ND, Kamangar F, Leitzmann MF, Hollenbeck AR, Schatzkin A: Non-steroidal anti-inflammatory drugs and risk of gastric and oesophageal adenocarcinomas: results from a cohort study and a meta-analysis. Br J Cancer; 2009 Feb 10;100(3):551-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-steroidal anti-inflammatory drugs and risk of gastric and oesophageal adenocarcinomas: results from a cohort study and a meta-analysis.
  • Use of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) may reduce the risk of gastric or oesophageal adenocarcinomas.
  • We examined the association between self-reported use of aspirin or non-aspirin NSAIDs in the earlier 12 months and gastric non-cardia (N=182), gastric cardia (N=178), and oesophageal adenocarcinomas (N=228) in a prospective cohort (N=311 115) followed for 7 years.
  • Use of any aspirin (HR, 95% CI: 0.64, 0.47-0.86) or other NSAIDs (0.68, 0.51-0.92) was associated with a significantly lower risk of gastric non-cardia adenocarcinoma.
  • We found no significant association between using aspirin (1.00, 0.73-1.37) or other NSAIDs (0.90, 69-1.17) and oesophageal adenocarcinoma.
  • We also performed a meta-analysis of the association between the use of NSAIDs and risk of gastric and oesophageal adenocarcinoma.
  • In this analysis, aspirin use was inversely associated with both gastric and oesophageal adenocarcinomas, with summary odds ratios (95% CI) for non-cardia, cardia, and oesophageal adenocarcinomas of 0.64 (0.52-0.80), 0.82 (0.65-1.04), and 0.64 (0.52-0.79), respectively.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2006 May 1;66(9):4975-82 [16651456.001]
  • [Cites] Int J Cancer. 2006 Jul 1;119(1):202-7 [16450404.001]
  • [Cites] Digestion. 2006;74(2):109-15 [17167266.001]
  • [Cites] PLoS Med. 2007 Feb;4(2):e67 [17326708.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):361-4 [17339621.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):365-75 [17339622.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 4;99(7):545-57 [17405999.001]
  • [Cites] Am J Epidemiol. 2007 Jun 15;165(12):1424-33 [17420181.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Oct;5(10):1154-1159.e3 [17644046.001]
  • [Cites] Expert Rev Cardiovasc Ther. 2008 Jan;6(1):95-107 [18095910.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):126-34 [18187391.001]
  • [Cites] Eur J Cancer. 2008 Feb;44(3):465-71 [18221867.001]
  • [Cites] Gut. 2008 May;57(5):561-7 [18194986.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1169-78 [18483339.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2008 Jun;5(6):321-31 [18446147.001]
  • [Cites] Lancet. 2008 Aug 2;372(9636):350-2 [18675670.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Oct;1(5):329-38 [19138977.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jan;9(1):119-23 [10667472.001]
  • [Cites] BMJ. 2000 Jun 17;320(7250):1642-6 [10856067.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
  • [Cites] Eur J Cancer Prev. 2000 Jun;9(3):185-91 [10954258.001]
  • [Cites] Br J Cancer. 2001 Apr 6;84(7):965-8 [11286478.001]
  • [Cites] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517.001]
  • [Cites] Cancer. 2002 Nov 15;95(10):2096-102 [12412162.001]
  • [Cites] Gastroenterology. 2003 Jan;124(1):47-56 [12512029.001]
  • [Cites] Br J Cancer. 2003 Mar 10;88(5):672-4 [12618872.001]
  • [Cites] Br J Cancer. 2003 Jun 2;88(11):1687-92 [12771981.001]
  • [Cites] Prog Exp Tumor Res. 2003;37:1-24 [12795046.001]
  • [Cites] J Natl Cancer Inst. 2003 Dec 3;95(23):1784-91 [14652240.001]
  • [Cites] BMC Cancer. 2003 Oct 31;3:28 [14588079.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):885-7; author reply 887 [15173278.001]
  • [Cites] Aliment Pharmacol Ther. 2004 Sep 15;20(6):645-55 [15352913.001]
  • [Cites] Anticancer Res. 2004 Sep-Oct;24(5B):3177-84 [15510608.001]
  • [Cites] IARC Sci Publ. 1987;(82):1-406 [3329634.001]
  • [Cites] Cancer Res. 1993 Mar 15;53(6):1322-7 [8443812.001]
  • [Cites] Epidemiology. 1994 Mar;5(2):138-46 [8172988.001]
  • [Cites] Cancer. 1995 Oct 1;76(7):1116-9 [8630885.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):295-9 [8903469.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):97-102 [9488582.001]
  • [Cites] Int J Cancer. 1999 Aug 12;82(4):473-6 [10404057.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):444-50 [15734971.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Lancet Oncol. 2005 Dec;6(12):945-52 [16321762.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4766-72 [16899628.001]
  • (PMID = 19156150.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Other-IDs] NLM/ PMC2658549
  •  go-up   go-down


Advertisement
4. Nowak M, Madej JA, Podhorska-Okolow M, Dziegiel P: Expression of extracellular matrix metalloproteinase (MMP-9), E-cadherin and proliferation-associated antigen Ki-67 and their reciprocal correlation in canine mammary adenocarcinomas. In Vivo; 2008 Jul-Aug;22(4):463-9
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.
  • [Title] Expression of extracellular matrix metalloproteinase (MMP-9), E-cadherin and proliferation-associated antigen Ki-67 and their reciprocal correlation in canine mammary adenocarcinomas.
  • BACKGROUND: The purpose of the present study was to determine the expression of the proteins related to tumour metastatic potential, including matrix metalloproteinase (MMP)-9 and E-cadherin, in correlation with the expression of proliferation-associated antigen (Ki-67) in canine mammary adenocarcinomas.
  • CONCLUSION: The positive correlation (r=0.375) between expressions of MMP-9 and Ki-67 and negative correlations between E-cadherin and Ki-67 (r=-0.383) as well as between MMP-9 and E-cadherin (r=-0.45) could suggest that expression and biological significance of the studied markers in mammary adenocarcinomas in dogs resembles the pattern noted in ductal carcinoma, i.e. in the most frequent histological type of malignant tumour in humans.
  • This may point to suitability of the animal model in studies on mechanism of neoplasia and metastases in humans.
  • [MeSH-major] Adenocarcinoma / metabolism. Cadherins / biosynthesis. Gene Expression Regulation, Neoplastic. Ki-67 Antigen / biosynthesis. Mammary Neoplasms, Animal / metabolism. Matrix Metalloproteinase 9 / biosynthesis
  • [MeSH-minor] Animals. Cell Proliferation. Dog Diseases / metabolism. Dogs. Gene Expression Profiling. Neoplasm Metastasis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18712173.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cadherins; 0 / Ki-67 Antigen; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


5. Partheen K, Levan K, Osterberg L, Claesson I, Sundfeldt K, Horvath G: External validation suggests Integrin beta 3 as prognostic biomarker in serous ovarian adenocarcinomas. BMC Cancer; 2009;9:336
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.
  • [Title] External validation suggests Integrin beta 3 as prognostic biomarker in serous ovarian adenocarcinomas.
  • METHODS: We analysed the gene expression of CLU, ITGB3, CAPG, and PRAME in 30 advanced staged serous adenocarcinomas with quantitative real-time polymerase chain reaction (QPCR) and the protein levels were analysed in 98 serous adenocarcinomas with western blot for semiquantitative analysis.
  • [MeSH-major] Cystadenocarcinoma, Serous / diagnosis. Cystadenocarcinoma, Serous / genetics. Integrin beta3 / genetics. Ovarian Neoplasms / diagnosis. Ovarian Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Microfilament Proteins / genetics. Microfilament Proteins / metabolism. Middle Aged. Neoplasm Staging. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Prognosis

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Jan 1;60(1):28-34 [10646846.001]
  • [Cites] Int J Gynecol Cancer. 2008 Nov-Dec;18(6):1215-33 [18217975.001]
  • [Cites] J Cancer Res Clin Oncol. 2001 Feb;127(2):73-9 [11216917.001]
  • [Cites] Cell Tissue Res. 2001 Sep;305(3):285-98 [11572082.001]
  • [Cites] Int J Cancer. 2002 Jan 10;97(2):186-94 [11774263.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] Clin Exp Metastasis. 2002;19(5):427-36 [12198771.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9482-7 [12874388.001]
  • [Cites] Oncogene. 2004 Mar 25;23(13):2298-304 [14755245.001]
  • [Cites] Clin Cancer Res. 2004 Jul 1;10(13):4307-13 [15240516.001]
  • [Cites] J Clin Invest. 1982 Feb;69(2):263-9 [6460044.001]
  • [Cites] J Clin Invest. 1985 Mar;75(3):896-901 [3156882.001]
  • [Cites] Cell. 1986 Jul 18;46(2):271-82 [3487386.001]
  • [Cites] Bioessays. 1987 Oct;7(4):176-9 [2825660.001]
  • [Cites] Mol Biol Cell. 1993 Sep;4(9):953-61 [8257797.001]
  • [Cites] J Cell Biol. 1994 Feb;124(4):619-26 [8106557.001]
  • [Cites] Gynecol Oncol. 1996 Aug;62(2):260-7 [8751559.001]
  • [Cites] Immunity. 1997 Feb;6(2):199-208 [9047241.001]
  • [Cites] Hum Pathol. 1997 Apr;28(4):443-9 [9104944.001]
  • [Cites] Biochem J. 1997 Nov 15;328 ( Pt 1):45-50 [9359832.001]
  • [Cites] Biochim Biophys Acta. 1998 Dec 10;1448(2):290-7 [9920419.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):6875-81 [10066740.001]
  • [Cites] Cell Mol Life Sci. 2004 Oct;61(19-20):2614-23 [15526166.001]
  • [Cites] J Mol Histol. 2005 Feb;36(1-2):119-29 [15704006.001]
  • [Cites] Gynecol Oncol. 2005 Mar;96(3):684-94 [15721412.001]
  • [Cites] Cell. 2005 Sep 23;122(6):835-47 [16179254.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):572-9 [17019794.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(16):2846-54 [16996261.001]
  • [Cites] Int J Gynaecol Obstet. 2006 Nov;95 Suppl 1:S161-92 [17161157.001]
  • [Cites] Gut. 2007 Jan;56(1):95-106 [16847067.001]
  • [Cites] Differentiation. 2007 Nov;75(9):819-30 [17999741.001]
  • [Cites] Int J Cancer. 2008 Nov 1;123(9):2130-7 [18709641.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 May 23;97(11):5907-12 [10823943.001]
  • (PMID = 19775429.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / ITGB3 protein, human; 0 / Integrin beta3; 0 / Microfilament Proteins; 0 / Nuclear Proteins; 0 / PRAME protein, human; 148412-71-9 / CAPG protein, human
  • [Other-IDs] NLM/ PMC2754489
  •  go-up   go-down


6. Ninomiya H, Hiramatsu M, Inamura K, Nomura K, Okui M, Miyoshi T, Okumura S, Satoh Y, Nakagawa K, Nishio M, Horai T, Miyata S, Tsuchiya E, Fukayama M, Ishikawa Y: Correlation between morphology and EGFR mutations in lung adenocarcinomas Significance of the micropapillary pattern and the hobnail cell type. Lung Cancer; 2009 Feb;63(2):235-40
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.
  • [Title] Correlation between morphology and EGFR mutations in lung adenocarcinomas Significance of the micropapillary pattern and the hobnail cell type.
  • The presence of epidermal growth factor receptor (EGFR) tyrosine kinase (TK) mutations significantly correlates with tumor sensitivity to TK inhibitors, particularly in lung adenocarcinomas, the predominant histological subtype in Japan and the United States.
  • To clarify links between EGFR mutations and pathological findings in Japanese lung cancer, detailed pathological features of adenocarcinomas were examined using the WHO criteria as well as our cell type classification (hobnail, columnar and polygonal).
  • We conclude that characteristic histological features, i.e. the hobnail cell morphology and the presence of BAC component and MPP are good predictors of EGFR mutations in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Lung Cancer. 2009 Feb;63(2):161-3 [19027983.001]
  • (PMID = 18571764.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


7. Gladhaug IP, Westgaard A, Schjølberg AR, Burum-Auensen E, Pomianowska E, Clausen OP: Spindle proteins in resected pancreatic head adenocarcinomas: BubR1 is an independent prognostic factor in pancreatobiliary-type tumours. Histopathology; 2010 Feb;56(3):345-55
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spindle proteins in resected pancreatic head adenocarcinomas: BubR1 is an independent prognostic factor in pancreatobiliary-type tumours.
  • The aim was to examine their possible prognostic impact in resected adenocarcinomas in the pancreatic head.
  • METHODS AND RESULTS: Two hundred and eighteen consecutively resected pancreatobiliary-type (n=145) and intestinal-type (n=73) adenocarcinomas involving the pancreatic head were examined for expression of Aurora A, Mad2 and BubR1 by immunohistochemistry on tissue microarrays.
  • CONCLUSION: BubR1 expression is a novel, independent adverse prognostic factor after pancreatoduodenectomy of pancreatobiliary-type adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Pancreatic Neoplasms / metabolism. Protein-Serine-Threonine Kinases / biosynthesis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20459534.001).
  • [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 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / MAD2L1 protein, human; 0 / Mad2 Proteins; 0 / Repressor Proteins; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / BUB1 protein, human; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


8. Schildhaus HU, Kröckel I, Lippert H, Malfertheiner P, Roessner A, Schneider-Stock R: Promoter hypermethylation of p16INK4a, E-cadherin, O6-MGMT, DAPK and FHIT in adenocarcinomas of the esophagus, esophagogastric junction and proximal stomach. Int J Oncol; 2005 Jun;26(6):1493-500
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.
  • [Title] Promoter hypermethylation of p16INK4a, E-cadherin, O6-MGMT, DAPK and FHIT in adenocarcinomas of the esophagus, esophagogastric junction and proximal stomach.
  • Although the incidence of Barrett's carcinomas (BC) and proximal gastric adenocarcinomas (PGC) is increasing, little is known about different epigenetic changes in these etiopathogenetically distinct entities.
  • Therefore, 29 adenocarcinomas [10 BC, 7 PGC and 12 tumors of the esophagogastric junction (JC)] and corresponding non-tumor controls (NT) were examined using methylation-specific PCR.
  • This is the first report on promoter methylation of death-associated protein kinase (DAPK) and fragile histidine triad gene (FHIT) in BC; both DAPK (BC 0.7, JC 0.92 and PGC 0.86) and FHIT (BC 0.88, JC 1.0 and PGC 1.0) were found to be highly methylated, suggesting that epigenetic silencing of these tumor suppressors is a common event in adenocarcinomas of the upper gastrointestinal tract, including BC.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. Adenocarcinoma / genetics. Cadherins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA Methylation. Esophageal Neoplasms / genetics. Esophagogastric Junction. Neoplasm Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic. Stomach Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15870861.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cadherins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.- / Acid Anhydride Hydrolases
  •  go-up   go-down


9. Afify A, Pang L, Howell L: Diagnostic utility of CD44 standard, CD44v6, and CD44v3-10 expression in adenocarcinomas presenting in serous fluids. Appl Immunohistochem Mol Morphol; 2007 Dec;15(4):446-50
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.
  • [Title] Diagnostic utility of CD44 standard, CD44v6, and CD44v3-10 expression in adenocarcinomas presenting in serous fluids.
  • In contrast to the standard form of CD44, which is almost ubiquitously expressed, splice variants are highly restricted in their expression in normal or malignant tissues.
  • The purpose of this study was to evaluate the extent to which metastatic adenocarcinomas in effusions express CD44s, CD44v6, and CD44v3-10 and to assess their diagnostic utility in distinguishing reactive mesothelial cells from adenocarcinomas.
  • Archival paraffin-embedded cell blocks of serous fluids from 23 cases of benign effusions containing reactive mesothelial cells and 45 cases of malignant effusions with metastatic adenocarcinoma (18 ovarian, 11 pulmonary, 9 gastrointestinal, and 7 breast) were retrieved from the surgical pathology files.
  • The cytopathology of all cases was reviewed to confirm the diagnosis.
  • In contrast neoplastic cells in malignant effusions expressed CD44s in 11 cases (24%), CD44v6 in 21 cases (47%), and CD44v3-10 in 39 cases (87%).
  • CD44s immunostaining can be used as a reliable marker to identify reactive mesothelial cells, meanwhile CD44v3-10 immunostaining can detect majority of adenocarcinomas in malignant effusions.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18091389.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / CD44 protein, human; 0 / CD44v6 antigen; 0 / Glycoproteins
  •  go-up   go-down


10. Krusche CA, Vloet AJ, Classen-Linke I, von Rango U, Beier HM, Alfer J: Class I histone deacetylase expression in the human cyclic endometrium and endometrial adenocarcinomas. Hum Reprod; 2007 Nov;22(11):2956-66
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Class I histone deacetylase expression in the human cyclic endometrium and endometrial adenocarcinomas.
  • Recently, HDAC inhibitors were shown to enhance differentiation of endometrial fibroblasts and endometrial adenocarcinomas.
  • In endometrial adenocarcinomas (n = 17), HDAC-1 expression was studied by immunohistochemistry.
  • Compared to normal endometrium, a high proportion of endometrial adenocarcinomas showed impaired HDAC-1 protein expression in the epithelial and stromal compartment.
  • [MeSH-major] Adenocarcinoma / enzymology. Endometrial Neoplasms / enzymology. Endometrium / enzymology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17728353.001).
  • [ISSN] 0268-1161
  • [Journal-full-title] Human reproduction (Oxford, England)
  • [ISO-abbreviation] Hum. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Repressor Proteins; EC 2.3.1.48 / p300-CBP Transcription Factors; EC 2.3.1.48 / p300-CBP-associated factor; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylase 2; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
  •  go-up   go-down


11. Godoy MC, Naidich DP: Subsolid pulmonary nodules and the spectrum of peripheral adenocarcinomas of the lung: recommended interim guidelines for assessment and management. Radiology; 2009 Dec;253(3):606-22
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subsolid pulmonary nodules and the spectrum of peripheral adenocarcinomas of the lung: recommended interim guidelines for assessment and management.
  • These are now known to frequently, although not invariably, fall into the spectrum of peripheral adenocarcinomas of the lung.
  • As a consequence, recognition of the potential association between subsolid nodules and peripheral adenocarcinomas requires a review of current guidelines for the management of these lesions, further necessitated by a differential diagnosis that includes benign lesions such as focal inflammation, focal fibrosis, and organizing pneumonia.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography. Practice Guidelines as Topic. Solitary Pulmonary Nodule / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans. Imaging, Three-Dimensional. Incidence. Prognosis. Radiographic Image Interpretation, Computer-Assisted. Tomography, Emission-Computed

  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19952025.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 87
  •  go-up   go-down


12. John T, Li M, Panchal D, Hui F, Meng F, Bandarchi-Chamkhaleh B, Kohler D, Zhu C, Shepherd FA, Tsao M: Correlation of primary tumor engraftment in immune deficient mice and relapse rate in patients with early-stage non-small cell lung carcinoma (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):11082

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Squamous cell carcinomas engrafted significantly more than adenocarcinomas (57% versus 26%, p=0.03).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963173.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


13. Ogawa T, Yoshida T, Tsuruta T, Tokuyama W, Adachi S, Kikuchi M, Mikami T, Saigenji K, Okayasu I: Tumor budding is predictive of lymphatic involvement and lymph node metastases in submucosal invasive colorectal adenocarcinomas and in non-polypoid compared with polypoid growths. Scand J Gastroenterol; 2009;44(5):605-14
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor budding is predictive of lymphatic involvement and lymph node metastases in submucosal invasive colorectal adenocarcinomas and in non-polypoid compared with polypoid growths.
  • OBJECTIVE: Early colorectal carcinomas (submucosal invasive adenocarcinomas) can be classified into polypoid and non-polypoid growth types, the latter progressing more rapidly to advanced malignancy.
  • Tumor budding was examined using anti-cytokeratin antibodies in 98 colorectal submucosal invasive adenocarcinomas and compared with the clinicopathological findings.
  • [MeSH-major] Adenocarcinoma / secondary. Colonic Polyps / pathology. Colorectal Neoplasms / pathology. Lymph Nodes / pathology. Neoplasm Invasiveness / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Confidence Intervals. Disease Progression. Female. Follow-Up Studies. Humans. Immunohistochemistry. Intestinal Mucosa / pathology. Logistic Models. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Odds Ratio. Predictive Value of Tests. Probability. Registries. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Tumor Burden

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19221929.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  •  go-up   go-down


14. Resnick MB, Gavilanez M, Newton E, Konkin T, Bhattacharya B, Britt DE, Sabo E, Moss SF: Claudin expression in gastric adenocarcinomas: a tissue microarray study with prognostic correlation. Hum Pathol; 2005 Aug;36(8):886-92
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Claudin expression in gastric adenocarcinomas: a tissue microarray study with prognostic correlation.
  • Tissue microarrays were created from paraffinized samples from 146 patients with distal gastric adenocarcinomas (61 intestinal and 85 diffuse or mixed subtypes).
  • Moderate to strong staining of claudins 1, 3, 4, and ZO-1 was detected in 74%, 48%, 62%, and 74% of the intestinal but in only 46%, 24%, 45%, and 36% of the diffuse subtype of adenocarcinomas (P < .05).
  • Cox multivariate analysis revealed that tumor stage, diffuse subtype, and moderate to strong claudin 4 staining were associated with decreased survival (P < .02).
  • In conclusion, claudins 1, 3, and 4 and ZO-1 are strongly expressed in most gastric intestinal-type adenocarcinomas but less frequently in diffuse gastric cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Membrane Proteins / biosynthesis. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16112005.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 P20 RR017596-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Phosphoproteins; 0 / TJP1 protein, human; 0 / Zonula Occludens-1 Protein
  •  go-up   go-down


15. Jung JH, Jung CK, Choi HJ, Jun KH, Yoo J, Kang SJ, Lee KY: Diagnostic utility of expression of claudins in non-small cell lung cancer: different expression profiles in squamous cell carcinomas and adenocarcinomas. Pathol Res Pract; 2009;205(6):409-16
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] Diagnostic utility of expression of claudins in non-small cell lung cancer: different expression profiles in squamous cell carcinomas and adenocarcinomas.
  • Claudin-1 expression was stronger in squamous cell carcinomas than in adenocarcinomas, whereas claudin-4 and claudin-5 expression was stronger in adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Membrane Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Biomarkers, Tumor / analysis. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / mortality. Carcinoma, Non-Small-Cell Lung / pathology. Claudin-1. Claudin-3. Claudin-4. Claudin-5. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Korea. Male. Middle Aged. Neoplasm Staging. Tissue Array Analysis. Young Adult

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19231096.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN1 protein, human; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN5 protein, human; 0 / Claudin-1; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudin-5; 0 / Membrane Proteins
  •  go-up   go-down


16. Yamada N, Kusumoto M, Maeshima A, Suzuki K, Matsuno Y: Correlation of the solid part on high-resolution computed tomography with pathological scar in small lung adenocarcinomas. Jpn J Clin Oncol; 2007 Dec;37(12):913-7
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] Correlation of the solid part on high-resolution computed tomography with pathological scar in small lung adenocarcinomas.
  • OBJECTIVE: To predict the grade of invasion in small (</=3 cm in diameter) lung adenocarcinomas from preoperative high-resolution computed tomography (HRCT), we measured CT numbers of the solid part and compared these with pathological features.
  • METHODS: We reviewed 131 cases of lung adenocarcinoma (</=3 cm in diameter) surgically resected between January 1999 and December 2000, which had >10% ground glass opacity (GGO) area on HRCT.
  • CONCLUSIONS: Small lung adenocarcinomas with a solid part CT number under -40 in on HRCT usually show no invasion or micro-invasion.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Predictive Value of Tests. Prognosis. Retrospective Studies

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18211981.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


17. Wang KL, Wu TT, Resetkova E, Wang H, Correa AM, Hofstetter WL, Swisher SG, Ajani JA, Rashid A, Hamilton SR, Albarracin CT: Expression of annexin A1 in esophageal and esophagogastric junction adenocarcinomas: association with poor outcome. Clin Cancer Res; 2006 Aug 1;12(15):4598-604
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.
  • [Title] Expression of annexin A1 in esophageal and esophagogastric junction adenocarcinomas: association with poor outcome.
  • However, the role of ANXA1 in esophageal adenocarcinoma is unclear.
  • Our goal was to evaluate ANXA1 expression and determine its prognostic significance in adenocarcinoma of the esophagus and esophagogastric junction.
  • EXPERIMENTAL DESIGN: This study included 104 consecutive patients with primary resected esophageal and esophagogastric junction adenocarcinomas (11 stage I, 24 stage II, 53 stage III, and 16 stage IV).
  • CONCLUSION: Our results indicate that high ANXA1 expression is frequent in esophageal and esophagogastric junction adenocarcinomas, correlates with more advanced pathologic T stage and the presence of distant metastasis, and is an independent prognostic factor for patient survival.
  • [MeSH-major] Adenocarcinoma / metabolism. Annexin A1 / biosynthesis. Esophageal Neoplasms / metabolism. Esophagogastric Junction / metabolism. Esophagogastric Junction / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Prognosis. Survival Analysis. Tissue Array Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16899607.001).
  • [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 / Annexin A1
  •  go-up   go-down


18. Ebert MP, Model F, Mooney S, Hale K, Lograsso J, Tonnes-Priddy L, Hoffmann J, Csepregi A, Röcken C, Molnar B, Schulz HU, Malfertheiner P, Lofton-Day C: Aristaless-like homeobox-4 gene methylation is a potential marker for colorectal adenocarcinomas. Gastroenterology; 2006 Nov;131(5):1418-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aristaless-like homeobox-4 gene methylation is a potential marker for colorectal adenocarcinomas.
  • METHODS: Using methylation-specific arbitrarily primed polymerase chain reaction, a fragment of the Aristaless-like homeobox-4 (ALX4) gene that was highly methylated in colon adenomas and cancer was identified.
  • Methylation of ALX4 was analyzed in colorectal adenomas and cancers, in the liver metastases of patients with colorectal cancer, and in 61 other neoplasias, including gastric, esophageal, and hepatocellular cancer and cholangiocarcinoma.
  • RESULTS: ALX4 gene methylation was confirmed in colon adenomas (11/13) and more frequently present in primary colorectal cancers (30/47) compared with the normal colon mucosa (0/21) (P < .0001).
  • In addition, ALX4 methylation was frequently observed in adenocarcinomas of the esophagus (12/14), stomach (11/15), and bile ducts (4/5) compared with all other cancers (P < .001).
  • CONCLUSIONS: Apart from colon adenomas and primary and metastatic colorectal cancers, ALX4 is frequently methylated in adenocarcinomas of the gastrointestinal tract.
  • [MeSH-major] Adenocarcinoma / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Colonic Polyps / genetics. DNA Methylation. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Neoplasm Metastasis. Precancerous Conditions / genetics

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17101318.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ALX4 protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  •  go-up   go-down


19. van Dekken H, Tilanus HW, Hop WC, Dinjens WN, Wink JC, Vissers KJ, van Marion R: Array comparative genomic hybridization, expression array, and protein analysis of critical regions on chromosome arms 1q, 7q, and 8p in adenocarcinomas of the gastroesophageal junction. Cancer Genet Cytogenet; 2009 Feb;189(1):37-42
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array comparative genomic hybridization, expression array, and protein analysis of critical regions on chromosome arms 1q, 7q, and 8p in adenocarcinomas of the gastroesophageal junction.
  • Survival rates of adenocarcinomas of the gastroesophageal junction (GEJ) are low, because these tumors are generally in an advanced stage by the time they are detected.
  • To delineate overexpressed genes, we performed array comparative genomic hybridization (aCGH) and mRNA expression analysis of 15 GEJ adenocarcinoma samples using a fine-tiling cDNA array covering chromosome segments 1q31.3~q41 (193.9-215.8 Mb: 21.9 Mb), 7q11.23~q22.1 (72.3-103.0 Mb: 30.7 Mb), and 8p23.1~p21.3 (11.1-20.7 Mb: 9.6 Mb).
  • In conclusion, using a straightforward approach we constructed a targeted gene profile for GEJ adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 8 / genetics. Esophageal Neoplasms / genetics. Esophagogastric Junction / metabolism. Stomach Neoplasms / genetics
  • [MeSH-minor] Comparative Genomic Hybridization. Female. Gene Expression Profiling. Genome, Human. Humans. Male. Middle Aged. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. RNA, Messenger / metabolism


20. Pineda-Daboin K, Neto A, Ochoa-Perez V, Luna MA: Nasopharyngeal adenocarcinomas: a clinicopathologic study of 44 cases including immunohistochemical features of 18 papillary phenotypes. Ann Diagn Pathol; 2006 Aug;10(4):215-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nasopharyngeal adenocarcinomas: a clinicopathologic study of 44 cases including immunohistochemical features of 18 papillary phenotypes.
  • Nasopharyngeal adenocarcinomas (NPACs) are uncommon neoplasms with a diverse histomorphology and clinical behavior.
  • There were 28 salivary gland type, 13 conventional low-grade papillary NPACs of surface origin, and 3 metastatic adenocarcinomas, 2 thyroid and 1 lung.
  • In contrast, 18 (64.2%) of the 28 patients with salivary gland-type NPACs had died of the disease or were living with disease at follow-up.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Immunoenzyme Techniques / methods. Nasopharyngeal Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Child. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Phenotype. Retrospective Studies. Salivary Glands / chemistry. Salivary Glands / pathology. Survival Rate. Thyroid Neoplasms / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16844563.001).
  • [ISSN] 1092-9134
  • [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 / Biomarkers, Tumor
  •  go-up   go-down


21. Yamamori M, Taniguchi M, Maeda S, Nakamura T, Okamura N, Kuwahara A, Iwaki K, Tamura T, Aoyama N, Markova S, Kasuga M, Okumura K, Sakaeda T: VEGF T-1498C polymorphism, a predictive marker of differentiation of colorectal adenocarcinomas in Japanese. Int J Med Sci; 2008;5(2):80-6
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF T-1498C polymorphism, a predictive marker of differentiation of colorectal adenocarcinomas in Japanese.
  • BACKGROUND: Previously, MDR1 T-129C polymorphism, encoding multidrug resistant transporter MDR1/P-glycoprotein, was reported to be predictive of poorly-differentiated colorectal adenocarcinomas.
  • Treatment of a colorectal adenocarcinoma cell line, HCT-15, with sodium butyrate, a typical differentiating agent, resulted in an increase of alkaline phosphatase activity and MDR1 mRNA expression, but in a decrease of VEGF mRNA expression.
  • CONCLUSIONS: VEGF T-1498C polymorphism is also a candidate marker predictive of poorly-differentiated colorectal adenocarcinomas, but further investigations with a large number of patients should be addressed to draw a conclusion.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / genetics. Vascular Endothelial Growth Factor A / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Histopathology. 2000 Feb;36(2):121-6 [10672056.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2401-7 [10873092.001]
  • [Cites] Biol Pharm Bull. 2006 Jul;29(7):1449-53 [16819187.001]
  • [Cites] Breast Cancer Res Treat. 2000 May;61(1):13-20 [10930086.001]
  • [Cites] Cytokine. 2000 Aug;12(8):1232-5 [10930302.001]
  • [Cites] J Vasc Res. 2000 Nov-Dec;37(6):443-8 [11146397.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Jun;280(6):C1358-66 [11350730.001]
  • [Cites] Nature. 2001 May 24;411(6836):494-8 [11373684.001]
  • [Cites] Int J Clin Oncol. 2001 Oct;6(5):221-8 [11723743.001]
  • [Cites] J Am Soc Nephrol. 2002 Jan;13(1):260-4 [11752046.001]
  • [Cites] J Cell Sci. 2001 Dec;114(Pt 24):4557-65 [11792820.001]
  • [Cites] Am J Hematol. 2002 Apr;69(4):247-54 [11921018.001]
  • [Cites] Diabetes. 2002 May;51(5):1635-9 [11978667.001]
  • [Cites] Lab Invest. 2002 May;82(5):555-62 [12003996.001]
  • [Cites] J Med Genet. 2002 May;39(5):340-6 [12011154.001]
  • [Cites] Anticancer Res. 2002 Jan-Feb;22(1A):121-8 [12017273.001]
  • [Cites] Genes Immun. 2002 Jun;3(4):229-32 [12058259.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3369-72 [12067976.001]
  • [Cites] Pharm Res. 2002 Sep;19(9):1323-9 [12403069.001]
  • [Cites] Biol Pharm Bull. 2002 Nov;25(11):1391-400 [12419946.001]
  • [Cites] Vascul Pharmacol. 2002 Nov;39(4-5):225-37 [12747962.001]
  • [Cites] World J Gastroenterol. 2003 Jun;9(6):1227-30 [12800229.001]
  • [Cites] FEBS Lett. 2003 Jun 19;545(2-3):144-50 [12804765.001]
  • [Cites] Biochem Pharmacol. 2003 Jul 1;66(1):163-70 [12818377.001]
  • [Cites] Pharmacogenomics. 2003 Jul;4(4):397-410 [12831320.001]
  • [Cites] Int J Cancer. 2003 Sep 10;106(4):468-71 [12845639.001]
  • [Cites] J Exp Clin Cancer Res. 2003 Jun;22(2):229-37 [12866573.001]
  • [Cites] Oncologist. 2004;9 Suppl 1:2-10 [15178810.001]
  • [Cites] Curr Top Med Chem. 2004;4(13):1385-98 [15379652.001]
  • [Cites] J Surg Oncol. 1982 Nov;21(3):143-8 [7132366.001]
  • [Cites] Science. 1983 Feb 25;219(4587):983-5 [6823562.001]
  • [Cites] J Neurosurg. 1988 Aug;69(2):254-62 [3134521.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Jun 15;161(2):851-8 [2735925.001]
  • [Cites] J Clin Invest. 1989 Nov;84(5):1470-8 [2478587.001]
  • [Cites] Science. 1989 Dec 8;246(4935):1306-9 [2479986.001]
  • [Cites] Science. 1989 Dec 8;246(4935):1309-12 [2479987.001]
  • [Cites] Cell. 1991 Jul 12;66(1):85-94 [1712673.001]
  • [Cites] World J Surg. 1995 Mar-Apr;19(2):178-83 [7754620.001]
  • [Cites] Histopathology. 1997 Aug;31(2):123-33 [9279562.001]
  • [Cites] Histol Histopathol. 1998 Oct;13(4):1233-42 [9810514.001]
  • [Cites] Br J Cancer. 1998 Nov;78(10):1379-84 [9823983.001]
  • [Cites] Int J Cancer. 1999 Jun 11;81(6):845-50 [10362127.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Dec 3;325(1):144-50 [15522212.001]
  • [Cites] Hepatogastroenterology. 2004 Nov-Dec;51(60):1698-702 [15532808.001]
  • [Cites] Drug Metab Pharmacokinet. 2005 Dec;20(6):391-414 [16415525.001]
  • [Cites] Curr Pharm Des. 2006;12(3):273-86 [16454744.001]
  • [Cites] Drug Metab Pharmacokinet. 2006 Apr;21(2):126-32 [16702732.001]
  • (PMID = 18414651.001).
  • [ISSN] 1449-1907
  • [Journal-full-title] International journal of medical sciences
  • [ISO-abbreviation] Int J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Butyrates; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Vascular Endothelial Growth Factor A; EC 3.1.3.1 / Alkaline Phosphatase
  • [Other-IDs] NLM/ PMC2293643
  • [Keywords] NOTNLM ; colorectal adenocarcinoma / differentiation / genetic polymorphism / predictive marker / vascular endothelial growth factor
  •  go-up   go-down


22. Crist KA, Zhang Z, You M, Gunning WT, Conran PB, Steele VE, Lubet RA: Characterization of rat ovarian adenocarcinomas developed in response to direct instillation of 7,12-dimethylbenz[a]anthracene (DMBA) coated suture. Carcinogenesis; 2005 May;26(5):951-7
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of rat ovarian adenocarcinomas developed in response to direct instillation of 7,12-dimethylbenz[a]anthracene (DMBA) coated suture.
  • Human ovarian cancer is predominantly of epithelial cell origin (>90% of malignant tumors) and most often presents at an advanced stage with poor prognosis.
  • Most animal models of ovarian carcinoma yield thecal/granulosa cell tumors, rather than adenocarcinomas.
  • Induction of adenocarcinoma in 10-45% of rats following an ovarian implantation of 7,12-dimethylbenz[a]anthracene (DMBA) coated silk suture has been reported.
  • Tumor histology was distributed as well differentiated adenocarcinoma (1/23), poorly differentiated adenocarcinoma (8/23), thecal/granulosa cell tumor (8/23), undifferentiated sarcoma (5/23) and one undifferentiated carcinoma with no adeno character.
  • Adenocarcinomas appeared to originate from the ovarian surface epithelium, with focal papillary extension into cystic space.
  • Vimentin positive epithelial cells when present in adenocarcinomas (4/7), showed perinuclear staining, quite distinct from the uniformly stained stromal cells in thecal/granulosa cell tumors (8/8).
  • [MeSH-major] 9,10-Dimethyl-1,2-benzanthracene / pharmacology. Adenocarcinoma / chemically induced. Carcinogens / pharmacology. Ovarian Neoplasms / chemically induced

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15695234.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-05103
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
  •  go-up   go-down


23. Deka J, Wiedemann N, Anderle P, Murphy-Seiler F, Bultinck J, Eyckerman S, Stehle JC, André S, Vilain N, Zilian O, Robine S, Delorenzi M, Basler K, Aguet M: Bcl9/Bcl9l are critical for Wnt-mediated regulation of stem cell traits in colon epithelium and adenocarcinomas. Cancer Res; 2010 Aug 15;70(16):6619-28
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bcl9/Bcl9l are critical for Wnt-mediated regulation of stem cell traits in colon epithelium and adenocarcinomas.
  • Adenocarcinomas with aberrant Wnt signaling arose with similar incidence in wild-type and mutant mice.
  • [MeSH-major] Adenocarcinoma / pathology. Colonic Neoplasms / pathology. Intracellular Signaling Peptides and Proteins / metabolism. Neoplastic Stem Cells / pathology. Wnt Proteins / metabolism


24. Shimizu K, Itsuzaki Y, Fujii H, Honoki K, Tsujiuchi T: Reduced expression of the Rassf1a gene and its aberrant DNA methylation in pancreatic duct adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine in hamsters. Mol Carcinog; 2008 Feb;47(2):80-7
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] Reduced expression of the Rassf1a gene and its aberrant DNA methylation in pancreatic duct adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine in hamsters.
  • Alterations of the Rassf1a gene were investigated in pancreatic duct adenocarcinomas (PDAs) induced by N-nitrosobis(2-oxopropyl)amine (BOP) in hamsters.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinogens / toxicity. DNA Methylation. Nitrosamines / toxicity. Pancreatic Neoplasms / genetics. Tumor Suppressor Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17849420.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA Primers; 0 / Nitrosamines; 0 / Tumor Suppressor Proteins; 60599-38-4 / nitrosobis(2-oxopropyl)amine
  •  go-up   go-down


25. Alberty J, Möllers A, Stoll W: [Expert assessment of adenocarcinomas of the nasal cavity and the paranasal sinuses caused by wood dust]. Laryngorhinootologie; 2009 Feb;88(2):106-11
MedlinePlus Health Information. consumer health - Occupational Health.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expert assessment of adenocarcinomas of the nasal cavity and the paranasal sinuses caused by wood dust].
  • BACKGROUND: Adenocarcinomas of the nasal cavity and the paranasal sinuses after occupational exposure to sawdust from oak and beech have been listed as occupational diseases in Germany since 1988.
  • MATERIALS AND METHODS: A retrospective analysis of 43 cases which had been evaluated between March 1994 and February 2007 for an occupational disease #4203, in the Ear-Nose-Throat clinic of the Münster University Hospital, Germany.
  • CONCLUSIONS: The use of the revised guidelines is recommended for expert assessment of adenocarcinomas of the nasal cavity and the paranasal sinuses caused by wood dust.
  • [MeSH-major] Adenocarcinoma / etiology. Dust. Expert Testimony / legislation & jurisprudence. Nasal Cavity. Nose Neoplasms / etiology. Occupational Diseases / etiology. Occupational Exposure / adverse effects. Paranasal Sinus Neoplasms / etiology. Wood / adverse effects
  • [MeSH-minor] Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / etiology. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Postoperative Complications / diagnosis. Postoperative Complications / etiology. Practice Guidelines as Topic. Radiation Injuries / diagnosis. Radiation Injuries / etiology. Radiotherapy, Adjuvant. Retrospective Studies. Workers' Compensation / legislation & jurisprudence

  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18651374.001).
  • [ISSN] 0935-8943
  • [Journal-full-title] Laryngo- rhino- otologie
  • [ISO-abbreviation] Laryngorhinootologie
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dust
  •  go-up   go-down


26. Cook MB, Kamangar F, Whiteman DC, Freedman ND, Gammon MD, Bernstein L, Brown LM, Risch HA, Ye W, Sharp L, Pandeya N, Webb PM, Wu AH, Ward MH, Giffen C, Casson AG, Abnet CC, Murray LJ, Corley DA, Nyrén O, Vaughan TL, Chow WH: Cigarette smoking and adenocarcinomas of the esophagus and esophagogastric junction: a pooled analysis from the international BEACON consortium. J Natl Cancer Inst; 2010 Sep 8;102(17):1344-53
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cigarette smoking and adenocarcinomas of the esophagus and esophagogastric junction: a pooled analysis from the international BEACON consortium.
  • BACKGROUND: Previous studies that showed an association between smoking and adenocarcinomas of the esophagus and esophagogastric junction were limited in their ability to assess differences by tumor site, sex, dose-response, and duration of cigarette smoking cessation.
  • METHODS: We used primary data from 10 population-based case-control studies and two cohort studies from the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium.
  • Patients were classified as having esophageal adenocarcinoma (n = 1540), esophagogastric junctional adenocarcinoma (n = 1450), or a combination of both (all adenocarcinoma; n = 2990).
  • Associations between pack-years of cigarette smoking and risks of adenocarcinomas were assessed, as well as their potential modification by sex and duration of smoking cessation.
  • RESULTS: The summary odds ratios demonstrated strong associations between cigarette smoking and esophageal adenocarcinoma (OR = 1.96, 95% confidence interval [CI] = 1.64 to 2.34), esophagogastric junctional adenocarcinoma (OR = 2.18, 95% CI = 1.84 to 2.58), and all adenocarcinoma (OR = 2.08, 95% CI = 1.83 to 2.37).
  • Compared with current smokers, longer smoking cessation was associated with a decreased risk of all adenocarcinoma after adjusting for pack-years (<10 years of smoking cessation: OR = 0.82, 95% CI = 0.60 to 1.13; and > or =10 years of smoking cessation: OR = 0.71, 95% CI = 0.56 to 0.89).
  • CONCLUSIONS: Cigarette smoking is associated with increased risks of adenocarcinomas of the esophagus and esophagogastric junction in white men and women; compared with current smoking, smoking cessation was associated with reduced risks.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Quitting Smoking.
  • MedlinePlus Health Information. consumer health - Smoking.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):340-6 [10652424.001]
  • [Cites] Br J Cancer. 2009 Sep 1;101(5):855-9 [19672254.001]
  • [Cites] Int J Epidemiol. 2000 Aug;29(4):645-54 [10922340.001]
  • [Cites] Ann Otol Rhinol Laryngol. 2001 Feb;110(2):190-3 [11219528.001]
  • [Cites] Cancer Causes Control. 2001 Oct;12(8):721-32 [11562112.001]
  • [Cites] Gastroenterology. 2001 Dec;121(6):1286-93 [11729107.001]
  • [Cites] Am J Clin Nutr. 2002 Jan;75(1):137-44 [11756071.001]
  • [Cites] Int J Cancer. 2002 Jun 20;99(6):860-8 [12115489.001]
  • [Cites] Am J Epidemiol. 2002 Nov 1;156(9):813-23 [12396999.001]
  • [Cites] Surg Oncol Clin N Am. 2002 Apr;11(2):235-56 [12424848.001]
  • [Cites] BMJ. 2003 Sep 6;327(7414):557-60 [12958120.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):733-44 [14570033.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):826-34 [15173266.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438 [15285078.001]
  • [Cites] J Natl Cancer Inst. 2004 Sep 15;96(18):1383-7 [15367571.001]
  • [Cites] J Natl Cancer Inst. 1994 Sep 7;86(17):1340-5 [8064893.001]
  • [Cites] Cancer Causes Control. 1994 Jul;5(4):333-40 [8080945.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Mar;4(2):85-92 [7742727.001]
  • [Cites] Am J Gastroenterol. 1995 Oct;90(10):1785-90 [7572895.001]
  • [Cites] Int J Cancer. 1997 Aug 7;72(4):565-73 [9259392.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1277-84 [9293918.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):150-5 [9450576.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] N Engl J Med. 1999 Mar 18;340(11):825-31 [10080844.001]
  • [Cites] Ann Intern Med. 1999 Jun 1;130(11):883-90 [10375336.001]
  • [Cites] Am J Epidemiol. 1999 Sep 1;150(5):469-75 [10472946.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):620-5 [15767340.001]
  • [Cites] Cancer Causes Control. 2005 Nov;16(9):1065-74 [16184472.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):517-23 [16537710.001]
  • [Cites] Am J Epidemiol. 2006 Jun 1;163(11):1053-64 [16624970.001]
  • [Cites] Dis Esophagus. 2006;19(5):321-8 [16984526.001]
  • [Cites] World J Gastroenterol. 2007 Mar 14;13(10):1585-94 [17461453.001]
  • [Cites] Am J Epidemiol. 2007 Jun 15;165(12):1424-33 [17420181.001]
  • [Cites] Am J Epidemiol. 2007 Aug 15;166(4):479-89 [17548786.001]
  • [Cites] Epidemiology. 2007 Sep;18(5):639-48 [17700253.001]
  • [Cites] Epidemiology. 2007 Sep;18(5):649-51 [17700254.001]
  • [Cites] MMWR Morb Mortal Wkly Rep. 2007 Nov 9;56(44):1157-61 [17989644.001]
  • [Cites] Int J Cancer. 2008 Mar 1;122(5):1118-29 [17990321.001]
  • [Cites] Gut. 2008 Feb;57(2):173-80 [17932103.001]
  • [Cites] Nicotine Tob Res. 2008 Feb;10(2):287-99 [18236293.001]
  • [Cites] Eur J Cancer. 2008 Feb;44(3):465-71 [18221867.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):352-8 [18268119.001]
  • [Cites] Gut. 2008 Mar;57(3):298-305 [17965056.001]
  • [Cites] Am J Epidemiol. 2008 Apr 15;167(8):970-5 [18250081.001]
  • [Cites] Lancet Oncol. 2008 Jul;9(7):649-56 [18556244.001]
  • [Cites] J Natl Cancer Inst. 2008 Aug 20;100(16):1184-7 [18695138.001]
  • [Cites] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1174-82 [19293308.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):127-32 [10883680.001]
  • (PMID = 20716718.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA057949-03; United States / PHS HHS / / R21DKO77742; United States / NCI NIH HHS / CA / U01-CA57923; United States / NCI NIH HHS / CA / U01-CA57983; United States / NIDDK NIH HHS / DK / R01 DK063616; United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NCI NIH HHS / CA / K05 CA124911; United States / NCI NIH HHS / CA / U01-CA57949; United States / NCI NIH HHS / CA / CA59636; United States / NCI NIH HHS / CA / R01-CA30022; United States / NCI NIH HHS / CA / U01 CA057949; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / R01 CA57947-03; United States / Intramural NIH HHS / / ZIA CP010136-15; United States / NCI NIH HHS / CA / R37-CA41530; United Kingdom / Chief Scientist Office / /
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2935475
  •  go-up   go-down


27. Marxfeld H, Staedtler F, Harleman JH: Gene expression in fibroadenomas of the rat mammary gland in contrast to spontaneous adenocarcinomas and normal mammary gland. Exp Toxicol Pathol; 2006 Nov;58(2-3):145-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression in fibroadenomas of the rat mammary gland in contrast to spontaneous adenocarcinomas and normal mammary gland.
  • However, the entity adenocarcinoma arising in fibroadenoma does exist and in humans there is evidence of certain forms of fibroadenomas to confer greater risk of subsequent breast cancer.
  • In this study, we aim to elucidate the molecular features of both spontaneous fibroadenomas and adenocarcinomas.
  • We conclude that in the tumours examined here, no progression to adenocarcinoma is likely.
  • Further studies are needed, examining a greater number of tumours and including cases of adenocarcinoma arising in fibroadenoma.
  • [MeSH-major] Adenocarcinoma / genetics. Fibroadenoma / genetics. Gene Expression Profiling. Mammary Glands, Animal / metabolism. Mammary Neoplasms, Animal / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16905299.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Thy-1; 9007-34-5 / Collagen; EC 4.2.1.11 / Phosphopyruvate Hydratase
  •  go-up   go-down


28. Chandrasoma P, Wickramasinghe K, Ma Y, DeMeester T: Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia? Dis Esophagus; 2007;20(1):36-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia?
  • Adenocarcinoma of the distal esophagus and gastroesophageal junction are believed to arise in Barrett's esophagus with intestinal metaplasia.
  • Whether adenocarcinoma can arise in columnar lined esophagus without intestinal metaplasia is in doubt.
  • Whether adenocarcinoma of the gastric cardia arises in intestinal metaplasia of the gastric cardia is also in doubt.
  • We aim to evaluate the relationship of size and stage of adenocarcinoma of the distal esophagus, gastroesophageal junction and gastric cardia to intestinal metaplasia and other types of columnar epithelium.
  • Seventy-four patients who had esophagogastrectomy for adenocarcinomas in this region were examined histologically to assess the frequency of residual intestinal metaplasia in the surrounding epithelium.
  • These data strongly support the contention that adenocarcinomas of this region, including those in the gastric cardia, arise in intestinal metaplastic epithelium.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17227308.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


29. von Rahden BH, Stein HJ, Feith M, Becker K, Siewert JR: Lymphatic vessel invasion as a prognostic factor in patients with primary resected adenocarcinomas of the esophagogastric junction. J Clin Oncol; 2005 Feb 1;23(4):874-9
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphatic vessel invasion as a prognostic factor in patients with primary resected adenocarcinomas of the esophagogastric junction.
  • PURPOSE: To evaluate the value of lymphatic vessel invasion (LVI) as a predictor of survival in patients with primary resected adenocarcinomas of the esophagogastric junction (AEG).
  • PATIENTS AND METHODS: We prospectively evaluated 459 patients undergoing primary surgical resection for tumors of the esophagogastric junction at our institution between 1992 and 2000 (180 adenocarcinomas of the distal esophagus, AEG I; 140 carcinomas of the cardia, AEG II; and 139 subcardial gastric cancers, AEG III).
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction. Lymphatic Vessels / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness. Prognosis. Prospective Studies

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15681533.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


30. Lai TC, Chow KC, Lin TY, Chiang IP, Fang HY, Chen CY, Ho SP: Expression of 53BP1 as a cisplatin-resistant marker in patients with lung adenocarcinomas. Oncol Rep; 2010 Aug;24(2):321-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of 53BP1 as a cisplatin-resistant marker in patients with lung adenocarcinomas.
  • DNA repair is one of the major causes of spontaneous drug and radiation resistance in patients with lung adenocarcinomas (LADC).
  • [MeSH-major] Adenocarcinoma / genetics. Cisplatin / therapeutic use. Drug Resistance, Neoplasm / genetics. Intracellular Signaling Peptides and Proteins / genetics. Lung Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20596616.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Pharmacological; 0 / Biomarkers, Tumor; 0 / Intracellular Signaling Peptides and Proteins; 0 / TP53BP1 protein, human; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


31. Terry MB, Gammon MD, Zhang FF, Vaughan TL, Chow WH, Risch HA, Schoenberg JB, Mayne ST, Stanford JL, West AB, Rotterdam H, Blot WJ, Fraumeni JF Jr, Santella RM: Alcohol dehydrogenase 3 and risk of esophageal and gastric adenocarcinomas. Cancer Causes Control; 2007 Nov;18(9):1039-46
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol dehydrogenase 3 and risk of esophageal and gastric adenocarcinomas.
  • OBJECTIVES: Alcohol increases esophageal squamous carcinoma risk but has been less consistently associated with esophageal adenocarcinoma.
  • METHODS: We undertook a study to examine whether a common polymorphism in the alcohol dehydrogenase 3 gene was associated with a higher risk of esophageal adenocarcinoma using data and biological samples collected for the Esophageal and Gastric Cancer Study (n = 114 esophageal and gastric cardia adenocarcinoma, n = 60 non-cardia gastric carcinoma, n = 23 cases of esophageal squamous cell carcinoma and 160 controls).
  • RESULTS: Individuals homozygous for ADH ( 3 ) (1-1) had a higher risk of each tumor type compared to individuals who had ADH ( 3 ) (2-2) or ADH ( 3 ) (1-2) genotype (OR = 1.7, 95% CI = 1.0-2.9 for esophageal and gastric cardia adenocarcinomas; OR = 1.7, 95% CI = 0.7-4.3 for esophageal squamous cell carcinoma; and OR = 2.8, 95% CI = 1.5-5.1 for non-cardia gastric cancer).
  • CONCLUSION: These data suggest ADH3 genotype may be associated with risk of esophageal and gastric cardia adenocarcinomas.

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17665311.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01-CA57923; United States / NCI NIH HHS / CA / U01-CA57983; United States / NCI NIH HHS / CN / N01-CN05230; United States / NCI NIH HHS / CA / U01-CA57949; United States / NCI NIH HHS / CP / N02-CP40501; United States / NIEHS NIH HHS / ES / P30-ES09089; United States / NIEHS NIH HHS / ES / P30-ES10126; United States / NIEHS NIH HHS / ES / P30 ES009089
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
  •  go-up   go-down


32. Bondi J, Pretorius M, Bukholm I, Danielsen H: Large-scale genomic instability in colon adenocarcinomas and correlation with patient outcome. APMIS; 2009 Oct;117(10):730-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large-scale genomic instability in colon adenocarcinomas and correlation with patient outcome.
  • The purpose of this study was to evaluate the association between DNA content in colon adenocarcinomas using high-resolution image cytometry and patient outcome.
  • Tumours from 219 patients operated for colon adenocarcinoma were analysed using high-resolution image cytometry.
  • The results were related to disease-free survival and to cancer-specific death.
  • DNA content in colon adenocarcinomas measured by image cytometry is an independent predictor of prognosis in our patients operated for colon adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Colonic Neoplasms / genetics. Genomic Instability
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Aneuploidy. Female. Humans. Male. Middle Aged. Neoplasm Staging. Ploidies

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19775341.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  •  go-up   go-down


33. Veras E, Srodon M, Neijstrom ES, Ronnett BM: Metastatic HPV-related cervical adenocarcinomas presenting with thromboembolic events (Trousseau Syndrome): clinicopathologic characteristics of 2 cases. Int J Gynecol Pathol; 2009 Mar;28(2):134-9
MedlinePlus Health Information. consumer health - Cervical Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic HPV-related cervical adenocarcinomas presenting with thromboembolic events (Trousseau Syndrome): clinicopathologic characteristics of 2 cases.
  • Two cases of systemic thromboembolism (Trousseau syndrome) associated with metastatic human papillomavirus (HPV)-related endocervical adenocarcinomas are reported.
  • Lymph node biopsy revealed metastatic mucinous adenocarcinoma with focal signet ring cell differentiation.
  • Imaging studies demonstrated metastatic disease without a defined primary site.
  • Autopsy examination revealed widespread metastatic adenocarcinoma with a 2 cm cervical adenocarcinoma.
  • Diagnostic laparoscopy with biopsies and left oophorectomy revealed metastatic mucinous adenocarcinoma with signet ring cell differentiation involving peritoneum, ovary, cervix, and bladder without a defined primary site.
  • Progressive thromboembolic disease with acute renal failure and multiple cerebral infarcts developed and the patient expired shortly after initiation of chemotherapy, 2 months after presentation.
  • High-risk HPV-related endocervical adenocarcinomas occasionally exhibit signet ring cell differentiation and can present with Trousseau syndrome.
  • These features more commonly suggest metastatic adenocarcinoma of upper gastrointestinal tract origin but the presence of HPV DNA within the tumors establishes them as cervical in origin.
  • [MeSH-major] Adenocarcinoma / complications. Papillomavirus Infections / complications. Thromboembolism / etiology. Uterine Cervical Neoplasms / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19188822.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


34. Maddocks OD, Short AJ, Donnenberg MS, Bader S, Harrison DJ: Attaching and effacing Escherichia coli downregulate DNA mismatch repair protein in vitro and are associated with colorectal adenocarcinomas in humans. PLoS One; 2009;4(5):e5517
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Attaching and effacing Escherichia coli downregulate DNA mismatch repair protein in vitro and are associated with colorectal adenocarcinomas in humans.
  • BACKGROUND: Mucosa-associated Escherichia coli are frequently found in the colonic mucosa of patients with colorectal adenocarcinoma, but rarely in healthy controls.
  • Adenocarcinoma and normal colonic mucosa from colorectal cancer patients (n = 20) was probed by immunofluorescence and PCR for AEEC.
  • Mucosa-associated E. coli were found on 10/20 (50%) adenocarcinomas and 3/20 (15%) normal mucosa samples (P<0.05).
  • AEEC were detected on 5/20 (25%) adenocarcinomas, but not normal mucosa samples (P<0.05).

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Infect Immun. 2001 May;69(5):3315-22 [11292754.001]
  • [Cites] J Clin Invest. 2001 Mar;107(5):621-9 [11238563.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15107-12 [11742074.001]
  • [Cites] Cell Microbiol. 2002 Apr;4(4):235-43 [11952640.001]
  • [Cites] Mutat Res. 2002 Jun;511(2):145-78 [12052432.001]
  • [Cites] J Immunol Methods. 2002 Jul 1;265(1-2):39-47 [12072177.001]
  • [Cites] Gastroenterology. 2002 Aug;123(2):542-53 [12145807.001]
  • [Cites] Cell. 2002 Oct 18;111(2):241-50 [12408868.001]
  • [Cites] Environ Mol Mutagen. 2002;40(4):243-50 [12489114.001]
  • [Cites] Carcinogenesis. 2003 Feb;24(2):217-24 [12584170.001]
  • [Cites] DNA Repair (Amst). 2003 May 13;2(5):571-80 [12713814.001]
  • [Cites] J Clin Microbiol. 2003 Jun;41(6):2289-93 [12791838.001]
  • [Cites] Infect Immun. 2003 Jul;71(7):3995-4002 [12819087.001]
  • [Cites] Clin Microbiol Rev. 2003 Jul;16(3):365-78 [12857773.001]
  • [Cites] Microbes Infect. 2004 Jan;6(1):38-50 [14738892.001]
  • [Cites] Microbiology. 2004 Mar;150(Pt 3):527-38 [14993302.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):40-4 [15043999.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):20127-36 [14988394.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):80-93 [15236175.001]
  • [Cites] Nucleic Acids Res. 2004;32(12):e100 [15249596.001]
  • [Cites] Cell Microbiol. 2004 Nov;6(11):1097-111 [15469437.001]
  • [Cites] Annu Rev Cell Dev Biol. 2004;20:695-723 [15473857.001]
  • [Cites] J Med Microbiol. 2004 Nov;53(Pt 11):1137-44 [15496393.001]
  • [Cites] Emerg Infect Dis. 2004 Oct;10(10):1797-805 [15504266.001]
  • [Cites] Nat Rev Cancer. 2004 Oct;4(10):769-80 [15510158.001]
  • [Cites] J Clin Invest. 1969 Aug;48(8):1423-32 [5796354.001]
  • [Cites] J Biol Chem. 1973 Apr 10;248(7):2542-8 [4698231.001]
  • [Cites] J Cell Biol. 1974 Aug;62(2):329-43 [4609988.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1259-64 [8577751.001]
  • [Cites] Infect Immun. 1996 Mar;64(3):966-73 [8641808.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):808-11 [9041175.001]
  • [Cites] Infect Immun. 1997 Jul;65(7):2528-36 [9199415.001]
  • [Cites] Infect Immun. 1997 Aug;65(8):3277-85 [9234787.001]
  • [Cites] Clin Microbiol Rev. 1998 Jan;11(1):142-201 [9457432.001]
  • [Cites] Infect Immun. 1998 Apr;66(4):1570-8 [9529083.001]
  • [Cites] Mutat Res. 1998 Feb 26;398(1-2):93-9 [9626969.001]
  • [Cites] Gastroenterology. 1998 Aug;115(2):281-6 [9679033.001]
  • [Cites] J Biol Chem. 1998 Sep 25;273(39):25436-42 [9738012.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3911-5 [10097137.001]
  • [Cites] Mutat Res. 1999 Jun 30;427(2):67-78 [10393261.001]
  • [Cites] Nat Cell Biol. 2005 Feb;7(2):137-47 [15619620.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1317-9 [16174847.001]
  • [Cites] Infect Immun. 2006 Sep;74(9):5419-21 [16926439.001]
  • [Cites] Cancer Res. 2006 Sep 15;66(18):9036-44 [16982745.001]
  • [Cites] Curr Opin Microbiol. 2007 Feb;10(1):76-81 [17208515.001]
  • [Cites] Mol Cancer Res. 2007 Feb;5(2):165-70 [17293392.001]
  • [Cites] Cell Microbiol. 2007 May;9(5):1352-64 [17474908.001]
  • [Cites] Cancer Res. 1977 Dec;37(12):4352-60 [922726.001]
  • [Cites] Infect Immun. 1983 Sep;41(3):1340-51 [6350186.001]
  • [Cites] Epidemiol Rev. 1984;6:31-51 [6386503.001]
  • [Cites] Cancer Res. 1985 Jun;45(6):2405-14 [3886132.001]
  • [Cites] Infect Immun. 1987 Jan;55(1):69-77 [3539808.001]
  • [Cites] Cancer Res. 1988 Apr 1;48(7):1936-42 [3349466.001]
  • [Cites] Infect Immun. 1993 Jan;61(1):350-5 [8418061.001]
  • [Cites] J Bacteriol. 1993 Aug;175(15):4670-80 [8393004.001]
  • [Cites] Nat Genet. 1995 Jan;9(1):48-55 [7704024.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2111-5 [7743510.001]
  • [Cites] J Clin Microbiol. 1995 Aug;33(8):2064-8 [7559949.001]
  • [Cites] Science. 2000 Feb 25;287(5457):1497-500 [10688800.001]
  • [Cites] J Infect Dis. 2000 Apr;181(4):1496-500 [10762584.001]
  • [Cites] J Biol Chem. 1971 Sep 10;246(17):5466-76 [10970180.001]
  • [Cites] J Infect Dis. 2001 Jul 15;184(2):227-30 [11424022.001]
  • (PMID = 19436735.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA141038; United Kingdom / Cancer Research UK / / 617SUR R40245; United Kingdom / Cancer Research UK / / C505/A7328; United Kingdom / Medical Research Council / / MRCDTGG122/5
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins
  • [Other-IDs] NLM/ PMC2677459
  •  go-up   go-down


35. Georgel T, Jankowski R, Henrot P, Baumann C, Kacha S, Grignon B, Toussaint B, Graff P, Kaminsky MC, Geoffrois L, Vignaud JM: CT assessment of woodworkers' nasal adenocarcinomas confirms the origin in the olfactory cleft. AJNR Am J Neuroradiol; 2009 Aug;30(7):1440-4
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CT assessment of woodworkers' nasal adenocarcinomas confirms the origin in the olfactory cleft.
  • BACKGROUND AND PURPOSE: Endoscopic endonasal surgery let us observe that woodworkers' nasal adenocarcinomas originate in the olfactory cleft.
  • Our aim was the identification of CT imaging features that corroborate the olfactory cleft as the site of origin for woodworkers' adenocarcinoma.
  • MATERIALS AND METHODS: We designed a retrospective study to compare CT scans of 27 unilateral olfactory cleft adenocarcinomas with 30 cases of nasosinusal polyposis (NSP) and 33 healthy sinus controls.
  • RESULTS: The nasal septum was significantly bulging across the midline in adenocarcinoma (4.6 +/- 3 mm; range, -0.1-13.7 mm) compared with NSP (0.7 +/- 1 mm; range, -2.1-2.3 mm) or healthy sinus controls (0.5 +/- 1 mm; range, -1.2-2 mm) (P < .001).
  • The olfactory cleft was significantly wider in adenocarcinoma (15.1 +/- 4.5 mm; range, 8.6-25.7 mm) than in NSP (3.6 +/- 0.4 mm; range, 2.8-4.6 mm) or healthy sinus controls (3.3 +/- 0.7 mm; range, 1.4-4.6 mm).
  • The ethmoidal labyrinth width was significantly smaller on the pathologic side in adenocarcinoma (7.2 +/- 2.7 mm; range, 3.2-14.2 mm) than in the control groups (P < .001).
  • Whereas the angle between the conchal lamina and vertical midline was close to zero degrees in NSP (0.03 +/- 2.25 degrees ; range, -5 degrees -3 degrees ) and healthy sinus controls (0.45 +/- 2.13 degrees , range, -5 degrees -5 degrees ), it reached 39.76 +/- 13.83 degrees (P < .001) in adenocarcinoma.
  • CONCLUSIONS: Radiologists should suspect nasal adenocarcinoma on sinus CT scans showing a unilateral expanding opacity of the olfactory cavity.
  • [MeSH-major] Adenocarcinoma / radiography. Nasal Cavity / radiography. Nose Neoplasms / radiography. Occupational Diseases / radiography. Tomography, X-Ray Computed / methods

  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • MedlinePlus Health Information. consumer health - Occupational Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19541776.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


36. Inamura K, Togashi Y, Okui M, Ninomiya H, Hiramatsu M, Satoh Y, Okumura S, Nakagawa K, Shimoji T, Noda T, Ishikawa Y: HOXB2 as a novel prognostic indicator for stage I lung adenocarcinomas. J Thorac Oncol; 2007 Sep;2(9):802-7
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] HOXB2 as a novel prognostic indicator for stage I lung adenocarcinomas.
  • BACKGROUND: Outcomes of patients with lung adenocarcinomas can be predicted to some extent from the pathologic stage (p-stage).
  • Although all attempts are made to fully remove cancer lesions, still a number of p-stage I patients without metastatic disease at the time of surgery develop recurrences and die of cancer.
  • Using real-time reverse-transcriptase polymerase chain reaction analysis, we investigated the transcriptional levels of the top metastasis-related genes using 96 independent test lung adenocarcinoma samples and investigated their correlations with the prognosis.
  • [MeSH-major] Adenocarcinoma. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Lung Neoplasms. RNA, Neoplasm / genetics. Transcription Factors / genetics
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Female. Humans. Male. Neoplasm Staging. Nuclear Proteins. Prognosis. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Thorac Oncol. 2008 Jan;3(1):100. Ishikawa, Yuichi [added]
  • (PMID = 17805056.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HOXB2 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / RNA, Neoplasm; 0 / Transcription Factors
  •  go-up   go-down


37. Langer R, Mutze K, Becker K, Feith M, Ott K, Höfler H, Keller G: Expression of class I histone deacetylases (HDAC1 and HDAC2) in oesophageal adenocarcinomas: an immunohistochemical study. J Clin Pathol; 2010 Nov;63(11):994-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of class I histone deacetylases (HDAC1 and HDAC2) in oesophageal adenocarcinomas: an immunohistochemical study.
  • AIMS: To investigate the expression of class I histone deacetylase (HDAC) isoforms 1 and 2 in oesophageal adenocarcinomas.
  • CONCLUSIONS: High HDAC2 expression is associated with aggressive tumour behaviour in oesophageal adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism. Histone Deacetylase 1 / metabolism. Histone Deacetylase 2 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Esophagectomy. Female. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Prognosis. Survival Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20924032.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / HDAC2 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylase 2
  •  go-up   go-down


38. Ridgway PF, Ziprin P, Alkhamesi N, Paraskeva PA, Peck DH, Darzi AW: Hypoxia augments gelatinase activity in a variety of adenocarcinomas in vitro. J Surg Res; 2005 Apr;124(2):180-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia augments gelatinase activity in a variety of adenocarcinomas in vitro.
  • BACKGROUND: Hypoxia within solid adenocarcinomas and protease up-regulation has been independently implicated as poor prognostic indicators in a variety of tumor types.
  • This suggests a mechanism explaining the poorer prognosis seen in patients with protease-secreting solid adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Anoxia / metabolism. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Breast Neoplasms. Cell Line, Tumor. Cell Survival. Colonic Neoplasms. Enzyme Inhibitors / pharmacology. Humans. In Vitro Techniques. Matrix Metalloproteinase Inhibitors. Neoplasm Invasiveness. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Up-Regulation

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15820246.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


39. Park SY, Lee HS, Choe G, Chung JH, Kim WH: Clinicopathological characteristics, microsatellite instability, and expression of mucin core proteins and p53 in colorectal mucinous adenocarcinomas in relation to location. Virchows Arch; 2006 Jul;449(1):40-7
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.
  • [Title] Clinicopathological characteristics, microsatellite instability, and expression of mucin core proteins and p53 in colorectal mucinous adenocarcinomas in relation to location.
  • However, there have been few studies of mucinous adenocarcinoma (MA) in relation to location.
  • Ninety-six consecutive colorectal MAs and ninety-eight nonmucinous adenocarcinomas (nMAs) were investigated.
  • Right-sided MAs, by comparison with those on the left side, were characterized by older age, larger tumor size, lower stage at presentation, peritumoral lymphocytic response, background of serrated adenoma, MSI-H phenotype, higher MUC2 and MUC5AC expression, and lower p53 protein overexpression.
  • In univariate analysis, right-sided location had a favorable effect on disease specific survival of the patients with MA, although it is not an independent predictor of survival.
  • [MeSH-major] Adenocarcinoma, Mucinous / genetics. Chromosomal Instability / genetics. Colorectal Neoplasms / genetics. Mucins / biosynthesis. Tumor Suppressor Protein p53 / metabolism

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16645863.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


40. Johnson SK, Haun RS: The gamma-aminobutyric acid A receptor pi subunit is overexpressed in pancreatic adenocarcinomas. JOP; 2005 Mar;6(2):136-42
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.
  • [Title] The gamma-aminobutyric acid A receptor pi subunit is overexpressed in pancreatic adenocarcinomas.
  • SETTING: Five pancreatic ductal adenocarcinomas and 5 bulk pancreatic ducts isolated from independent pancreatic specimens without malignancies were analyzed by differential display.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Gene Expression Regulation, Neoplastic. Protein Subunits / genetics. Receptors, GABA-A / genetics
  • [MeSH-minor] Biomarkers, Tumor / analysis. Cell Proliferation. DNA, Complementary. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Gene Expression Profiling. Humans. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology. RNA, Messenger / analysis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • Guide to Pharmacology. gene/protein/disease-specific - GABAA receptor pi subunit - data and references .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15767729.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Protein Subunits; 0 / RNA, Messenger; 0 / Receptors, GABA-A
  •  go-up   go-down


41. Bastide K, Ugolin N, Levalois C, Bernaudin JF, Chevillard S: Are adenosquamous lung carcinomas a simple mix of adenocarcinomas and squamous cell carcinomas, or more complex at the molecular level? Lung Cancer; 2010 Apr;68(1):1-9
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.
  • [Title] Are adenosquamous lung carcinomas a simple mix of adenocarcinomas and squamous cell carcinomas, or more complex at the molecular level?
  • Adenocarcinomas (AC), squamous cell carcinomas (SCC) and adenosquamous carcinomas (ASC) are three histological subtypes of non-small-cell lung carcinomas (NSCLC).
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Adenosquamous / genetics. Carcinoma, Squamous Cell / genetics. Lung / metabolism. Lung Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. RADON, RADIOACTIVE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20004040.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GATA6 Transcription Factor; 0 / Gata6 protein, rat; 0 / Mucin-1; 0 / Receptor, Notch2; Q74S4N8N1G / Radon
  • [Number-of-references] 61
  •  go-up   go-down


42. Tang M, Asamoto M, Ogawa K, Naiki-Ito A, Sato S, Takahashi S, Shirai T: Induction of apoptosis in the LNCaP human prostate carcinoma cell line and prostate adenocarcinomas of SV40T antigen transgenic rats by the Bowman-Birk inhibitor. Pathol Int; 2009 Nov;59(11):790-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of apoptosis in the LNCaP human prostate carcinoma cell line and prostate adenocarcinomas of SV40T antigen transgenic rats by the Bowman-Birk inhibitor.
  • The present study was undertaken to evaluate the effects of BBI on androgen-sensitive/dependent prostate cancers using a human prostate cancer cell (LNCaP) and the transgenic rats developing adenocarcinoma of the prostate (TRAP) model.
  • Feeding of 3% roughly prepared BBI (BBIC) to TRAP from the age 3 weeks to 13 weeks resulted in significant reduction of the relative epithelial areas within the acinus and multiplicity of the adenocarcinomas in the lateral prostate lobes.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Prostatic Neoplasms / drug therapy. Trypsin Inhibitor, Bowman-Birk Soybean / pharmacology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19883429.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Connexin 43; 0 / Trypsin Inhibitor, Bowman-Birk Soybean
  •  go-up   go-down


43. Lee JH, Kim JH, Choi JW, Kim YS: The presence of a micropapillary component predicts aggressive behaviour in early and advanced gastric adenocarcinomas. Pathology; 2010;42(6):560-3
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The presence of a micropapillary component predicts aggressive behaviour in early and advanced gastric adenocarcinomas.
  • However, little is known about the clinicopathological significance of the MC in gastric adenocarcinoma.
  • METHODS: We investigated the clinicopathological characteristics of gastric adenocarcinoma with a MC and compared them with those of conventional gastric adenocarcinoma.
  • The presence of a MC in gastric adenocarcinoma was significantly associated with the depth of invasion, lymph node metastasis, lymphovascular invasion, perineural invasion, higher clinical stages, and poor overall survival rates, but not with age, gender, tumour size, location, and Lauren histological types.
  • CONCLUSIONS: Recognition of a MC in early and advanced gastric adenocarcinomas is very important as it can predict cancer invasion and metastasis leading to a poor clinical outcome.
  • [MeSH-major] Adenocarcinoma / pathology. Neoplasm Invasiveness / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Prognosis. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20854075.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


44. Sales KJ, List T, Boddy SC, Williams AR, Anderson RA, Naor Z, Jabbour HN: A novel angiogenic role for prostaglandin F2alpha-FP receptor interaction in human endometrial adenocarcinomas. Cancer Res; 2005 Sep 1;65(17):7707-16
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel angiogenic role for prostaglandin F2alpha-FP receptor interaction in human endometrial adenocarcinomas.
  • In the present study, we found elevated FP receptor and vascular endothelial growth factor (VEGF) expression colocalized in glandular epithelial and vascular cells lining the blood vessels in endometrial adenocarcinomas.
  • We investigated the signaling pathways activated by the FP receptor and their role in modulating VEGF expression in endometrial adenocarcinoma (Ishikawa) cells.
  • Finally, we confirmed that PGF2alpha could potentiate angiogenesis in endometrial adenocarcinoma explants by transactivation of the EGFR and induction of VEGF mRNA expression.
  • [MeSH-major] Adenocarcinoma / blood supply. Adenocarcinoma / metabolism. Dinoprost / metabolism. Endometrial Neoplasms / blood supply. Endometrial Neoplasms / metabolism. MAP Kinase Signaling System / physiology. Receptors, Prostaglandin / metabolism

  • Hazardous Substances Data Bank. PROSTAGLANDIN F2ALPHA .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Obstet Gynaecol. 1988 Feb;95(2):162-5 [2894838.001]
  • [Cites] J Pharmacol Exp Ther. 1999 Sep;290(3):1278-84 [10454504.001]
  • [Cites] Prostaglandins. 1993 May;45(5):413-26 [8321911.001]
  • [Cites] Int J Cancer. 1994 Jan 2;56(1):26-30 [8262674.001]
  • [Cites] J Biol Chem. 1994 Jan 28;269(4):2632-6 [8300593.001]
  • [Cites] Mol Pharmacol. 1994 Sep;46(3):477-84 [7935328.001]
  • [Cites] Hum Pathol. 1995 Aug;26(8):892-6 [7635451.001]
  • [Cites] Nature. 1996 Feb 8;379(6565):557-60 [8596637.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):454-60 [8697391.001]
  • [Cites] EXS. 1997;79:1-8 [9002217.001]
  • [Cites] J Biol Chem. 1998 Mar 20;273(12):6689-97 [9506966.001]
  • [Cites] Adv Cancer Res. 1998;74:49-139 [9561267.001]
  • [Cites] Mol Endocrinol. 1998 Jun;12(6):815-24 [9626657.001]
  • [Cites] Cell. 1998 May 29;93(5):705-16 [9630216.001]
  • [Cites] FASEB J. 1998 Sep;12(12):1063-73 [9737710.001]
  • [Cites] Am J Orthop (Belle Mead NJ). 1999 Mar;28(3 Suppl):8-12 [10193997.001]
  • [Cites] Curr Opin Cell Biol. 1999 Apr;11(2):177-83 [10209148.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Jun;31(6):637-43 [10404636.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9572-80 [10734107.001]
  • [Cites] Nat Med. 2000 Sep;6(9):1024-8 [10973323.001]
  • [Cites] Trends Endocrinol Metab. 2000 Apr;11(3):91-9 [10707049.001]
  • [Cites] Oncogene. 2001 Mar 26;20(13):1540-6 [11313900.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2243-9 [11344234.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4143-54 [11358838.001]
  • [Cites] J Biol Chem. 2001 Feb 16;276(7):4554-63 [11083862.001]
  • [Cites] J Clin Invest. 2001 Jul;108(1):25-30 [11435452.001]
  • [Cites] Nat Med. 2001 Sep;7(9):1048-51 [11533709.001]
  • [Cites] Br J Cancer. 2001 Sep 28;85(7):1023-31 [11592775.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):424-32 [11809691.001]
  • [Cites] Cancer Res. 2002 Jan 15;62(2):506-11 [11809702.001]
  • [Cites] Endocrinology. 2002 Mar;143(3):1018-25 [11861527.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13926-31 [12242329.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3592-600 [12429651.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5669-73 [14522881.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1134-6 [14561696.001]
  • [Cites] Reproduction. 2003 Nov;126(5):559-67 [14611628.001]
  • [Cites] Exp Cell Res. 2004 Jan 1;292(1):201-8 [14720519.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):986-93 [14764825.001]
  • [Cites] Endocrinology. 2004 May;145(5):2228-44 [14736735.001]
  • [Cites] Mol Endocrinol. 2004 Jun;18(6):1533-45 [15044590.001]
  • [Cites] Am J Obstet Gynecol. 1978 Mar 15;130(6):640-6 [637076.001]
  • [Cites] Br J Obstet Gynaecol. 1981 Apr;88(4):434-42 [7225303.001]
  • [Cites] J Clin Endocrinol Metab. 1983 Aug;57(2):360-6 [6134747.001]
  • [Cites] Br J Obstet Gynaecol. 1983 Dec;90(12):1135-40 [6580910.001]
  • [Cites] Br J Obstet Gynaecol. 1984 Jul;91(7):673-80 [6589016.001]
  • [Cites] Science. 1989 Dec 8;246(4935):1306-9 [2479986.001]
  • (PMID = 16140938.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U127684438; United Kingdom / Medical Research Council / / U.1276.00.004.00002.01/2(61014)
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin; 0 / Vascular Endothelial Growth Factor A; 0 / prostaglandin F2alpha receptor; B7IN85G1HY / Dinoprost; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2694301; NLM/ UKMS2436
  •  go-up   go-down


45. Gümüs-Akay G, Unal AE, Elhan AH, Bayar S, Karadayt K, Sunguroglu A, Kadikiran A, Tükün A: DNA copy number changes in gastric adenocarcinomas: high resolution-comparative genomic hybridization study in Turkey. Arch Med Res; 2009 Oct;40(7):551-60
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA copy number changes in gastric adenocarcinomas: high resolution-comparative genomic hybridization study in Turkey.
  • The aim of this study was to identify the genomic imbalances of gains and/or losses in gastric adenocarcinomas from Turkish patients and to investigate their association with development and progression of this type of cancer.
  • METHODS: Forty three patients with gastric adenocarcinoma were enrolled in this study and genomic imbalances were analyzed by high-resolution-comparative genomic hybridization (HR-CGH).
  • RESULTS: In 36/43 cases (84%) of gastric adenocarcinomas, genomic imbalances have involved all chromosomes in various combinations.
  • CONCLUSIONS: A series of gains, losses and amplifications concerned with gastric adenocarcinoma identified in this study are presented in detail.
  • [MeSH-major] Adenocarcinoma / genetics. Comparative Genomic Hybridization / methods. DNA Copy Number Variations. Stomach Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Male. Middle Aged. Turkey / epidemiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2009 IMSS. Published by Elsevier Inc.
  • (PMID = 20082868.001).
  • [ISSN] 1873-5487
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


46. Nakayama H, Yamada K, Saito H, Oshita F, Ito H, Kameda Y, Noda K: Sublobar resection for patients with peripheral small adenocarcinomas of the lung: surgical outcome is associated with features on computed tomographic imaging. Ann Thorac Surg; 2007 Nov;84(5):1675-9
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] Sublobar resection for patients with peripheral small adenocarcinomas of the lung: surgical outcome is associated with features on computed tomographic imaging.
  • BACKGROUND: Sublobar resection for peripheral small adenocarcinomas of the lung remains controversial.
  • METHODS: A total of 123 patients with adenocarcinoma of the lung underwent sublobar resection of clinical T1N0M0 tumors measuring 2 cm or less in diameter on high-resolution computed tomography.
  • CONCLUSIONS: Sublobar resection might be an acceptable procedure for the treatment of small air-containing type adenocarcinomas of the lung on preoperative high-resolution computed tomography.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery. Pneumonectomy / methods. Radiography, Thoracic / methods. Tomography, X-Ray Computed / methods

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Ann Thorac Surg. 2008 Nov;86(5):1723-4; author reply 1724-5 [19049798.001]
  • (PMID = 17954084.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  •  go-up   go-down


47. Solis LM, Raso MG, Kalhor N, Behrens C, Wistuba II, Moran CA: Primary oncocytic adenocarcinomas of the lung: a clinicopathologic, immunohistochemical, and molecular biologic analysis of 16 cases. Am J Clin Pathol; 2010 Jan;133(1):133-40
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.
  • [Title] Primary oncocytic adenocarcinomas of the lung: a clinicopathologic, immunohistochemical, and molecular biologic analysis of 16 cases.
  • Sixteen cases of primary oncocytic adenocarcinomas of the lung are reported.
  • Surgical staging disclosed 14 patients (88%) with stage I disease, 1 (6%) with stage II, and 1 (6%) with stage III.
  • These cases represent an unusual variant of pulmonary adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Oxyphil Cells / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. DNA Mutational Analysis. DNA, Neoplasm / analysis. Fatal Outcome. Female. Humans. Lung / pathology. Lung / surgery. Male. Middle Aged. Mutation. Neoplasm Recurrence, Local. Neoplasm Staging. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics. ras Proteins / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20023269.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


48. Sakao Y, Miyamoto H, Oh S, Takahashi N, Inagaki T, Miyasaka Y, Akaboshi T, Sakuraba M: The impact of cigarette smoking on prognosis in small adenocarcinomas of the lung: the association between histologic subtype and smoking status. J Thorac Oncol; 2008 Sep;3(9):958-62
MedlinePlus Health Information. consumer health - Smoking.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The impact of cigarette smoking on prognosis in small adenocarcinomas of the lung: the association between histologic subtype and smoking status.
  • OBJECTIVE: In this retrospective study, we clarified the impact of smoking on prognosis and the association of clinicopathological factors, particularly histologic subtype, in patients with small adenocarcinoma of the lung.
  • METHODS: Between 1996 and December 2006, 121 patients presenting with adenocarcinomas that had a diameter </=2 cm were analyzed.
  • The clinicopathological records of the patients were examined for age, gender, nodal status (c-N and p-N), tumor size, serum carcinoembryonic antigen level, histologic subtype, and smoking history.
  • A histologic subtype was defined using a modified World Health Organization classification.
  • These subtypes are bronchioloalveolar carcinoma (BAC), adenocarcinoma with little or no BAC component (Non or min BAC), and mixed bronchioloalveolar carcinoma with other adenocarcinoma components.
  • Gender, serum carcinoembryonic antigen level, and histologic subtype were significantly associated with smoking status.
  • Histologic subtype (Non or min BAC) was the only significant prognostic factor in multivariate analyses.
  • The prevalence of smoking by histologic subtype was 27.3% for BAC, 43.2% for mixed bronchioloalveolar carcinoma, and 74.6% for Non or min BAC.
  • CONCLUSIONS: When adenocarcinomas were small (diameter </=2 cm) cigarette smoking and male gender were associated with Non or min BAC histologic subtypes, which are thought to have more aggressive biologic features resulting in poorer outcome compared with other subtypes.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Lung Neoplasms / pathology. Smoking / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Risk Factors. Survival Rate

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18758296.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


49. Langer R, Feith M, Siewert JR, Wester HJ, Hoefler H: Expression and clinical significance of glucose regulated proteins GRP78 (BiP) and GRP94 (GP96) in human adenocarcinomas of the esophagus. BMC Cancer; 2008;8:70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and clinical significance of glucose regulated proteins GRP78 (BiP) and GRP94 (GP96) in human adenocarcinomas of the esophagus.
  • In this study we investigated the glucose regulated proteins GRP78 (BiP) and GRP94 (GP96) in a series of human esophageal adenocarcinomas to determine their implications in cancer progression and prognosis.
  • METHODS: Formalin-fixed, paraffin-embedded tissues of primary resected esophageal (Barrett) adenocarcinomas (n = 137) and corresponding normal tissue were investigated. mRNA-gene expression levels of GRP78 and GRP94 were determined by quantitative real-time RT-PCR after mRNA extraction.
  • CONCLUSION: We could demonstrate an association of GRP78 and GRP94 mRNA and protein expression with tumor stage and behaviour in esophageal adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. HSP70 Heat-Shock Proteins / metabolism. Heat-Shock Proteins / metabolism. Membrane Proteins / metabolism. Molecular Chaperones / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / complications. Disease Progression. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / analysis. Survival Analysis. Up-Regulation

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Oncol Rep. 2003 May;5(3):203-9 [12667417.001]
  • [Cites] Int J Epidemiol. 2000 Aug;29(4):645-54 [10922340.001]
  • [Cites] J Natl Cancer Inst. 2004 Sep 1;96(17):1300-10 [15339968.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 1994;4(1):1-18 [7987045.001]
  • [Cites] Br J Surg. 1998 Nov;85(11):1457-9 [9823902.001]
  • [Cites] Breast Cancer Res Treat. 1999 Mar;54(2):135-46 [10424404.001]
  • [Cites] World J Gastroenterol. 2005 Jan 21;11(3):429-32 [15637761.001]
  • [Cites] World J Gastroenterol. 2005 Feb 21;11(7):1056-9 [15742415.001]
  • [Cites] World J Gastroenterol. 2005 Apr 14;11(14):2072-9 [15810071.001]
  • [Cites] Cell Stress Chaperones. 2005 Spring;10(1):46-58 [15832947.001]
  • [Cites] Lung Cancer. 2005 Jul;49(1):55-62 [15949590.001]
  • [Cites] Cell Stress Chaperones. 2005 Summer;10(2):86-103 [16038406.001]
  • [Cites] Am J Pathol. 2001 Feb;158(2):419-29 [11159180.001]
  • [Cites] Trends Biochem Sci. 2001 Aug;26(8):504-10 [11504627.001]
  • [Cites] Surg Oncol. 2000 Jul;9(1):35-41 [11525305.001]
  • [Cites] Scand J Gastroenterol Suppl. 2001;(234):51-60 [11768562.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):123-30 [11756233.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] FEBS Lett. 2007 Jul 31;581(19):3641-51 [17481612.001]
  • [Cites] Cancer Detect Prev. 2005;29(6):544-51 [16297569.001]
  • [Cites] N Engl J Med. 2005 Dec 29;353(26):2821-2; author reply 2821-2 [16382552.001]
  • [Cites] Clin Chim Acta. 2006 Feb;364(1-2):308-15 [16182273.001]
  • [Cites] Curr Mol Med. 2006 Feb;6(1):45-54 [16472112.001]
  • [Cites] Arch Biochem Biophys. 2006 Mar 15;447(2):155-66 [16497268.001]
  • [Cites] Electrophoresis. 2006 May;27(9):1840-52 [16645950.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7849-53 [16912156.001]
  • [Cites] Cancer Biol Ther. 2006 Jul;5(7):741-4 [16861902.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):5987-93 [17062670.001]
  • [Cites] Toxicology. 2007 Jan 18;229(3):253-61 [17161515.001]
  • [Cites] Cell Stress Chaperones. 2006 Winter;11(4):334-42 [17278882.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3496-9 [17440054.001]
  • [Cites] Recent Results Cancer Res. 2000;155:1-14 [10693234.001]
  • [Cites] Toxicol Appl Pharmacol. 2000 Mar 15;163(3):260-6 [10702365.001]
  • [Cites] Breast Cancer Res Treat. 2000 Jan;59(1):15-26 [10752676.001]
  • [Cites] J Cell Biochem. 2000 Apr;77(3):396-408 [10760948.001]
  • [Cites] Cell Stress Chaperones. 2004 Mar;9(1):76-87 [15270080.001]
  • (PMID = 18331622.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Membrane Proteins; 0 / Molecular Chaperones; 0 / RNA, Messenger; 0 / glucose-regulated proteins; 0 / molecular chaperone GRP78
  • [Other-IDs] NLM/ PMC2270853
  •  go-up   go-down


50. Roedl JB, Colen RR, Holalkere NS, Fischman AJ, Choi NC, Blake MA: Adenocarcinomas of the esophagus: response to chemoradiotherapy is associated with decrease of metabolic tumor volume as measured on PET-CT. Comparison to histopathologic and clinical response evaluation. Radiother Oncol; 2008 Dec;89(3):278-86
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenocarcinomas of the esophagus: response to chemoradiotherapy is associated with decrease of metabolic tumor volume as measured on PET-CT. Comparison to histopathologic and clinical response evaluation.
  • PATIENTS AND METHODS: A total of 51 study subjects with adenocarcinomas (Type I due to Siewert classification) of the esophagus underwent PET-CT scans before and after neoadjuvant chemoradiotherapy.
  • CONCLUSIONS: Tumor volume and TLG can be used to assess treatment response and survival in patients with esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Radiother Oncol. 2009 Aug;92(2):291 [19264369.001]
  • (PMID = 18701180.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


51. Vazquez M, Carter D, Brambilla E, Gazdar A, Noguchi M, Travis WD, Huang Y, Zhang L, Yip R, Yankelevitz DF, Henschke CI, International Early Lung Cancer Action Program Investigators: Solitary and multiple resected adenocarcinomas after CT screening for lung cancer: histopathologic features and their prognostic implications. Lung Cancer; 2009 May;64(2):148-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solitary and multiple resected adenocarcinomas after CT screening for lung cancer: histopathologic features and their prognostic implications.
  • PURPOSE: To study the histopathologic features of CT screen-detected Stage IA adenocarcinomas to determine whether survival differed by the proportion of bronchioloalveolar component (BAC) or by the presence of multiple lesions in node-negative patients.
  • METHODS: Five pathologists with expertise in pulmonary pathology examined 279 resected cases of adenocarcinomas, 30 mm or less in length diagnosed by CT screening for lung cancer.
  • The panel determined the consensus diagnosis for each case, identified additional cancers, and classified each case as solitary or non-solitary.
  • RESULTS: Of the cases of adenocarcinoma, 20 (7%) were BAC subtype, 246 (88%) mixed subtype and 13 (5%) adenocarcinoma-OTHER.
  • Kaplan-Meier 10-year survival rates were 100% for BAC and adeno-MIXED with 90-99% BAC cases, 95% for mixed with 1-90% BAC, 90% for those without a BAC component, and 75% for other cases.
  • Contrary to staging predictions, cases of non-solitary node-negative adenocarcinoma had the same excellent prognosis as solitary node-negative cases, suggesting that most of the small, node-negative multiple carcinomas probably represent multiple primaries rather than intrapulmonary metastasis.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Histopathology. 2005 Jun;46(6):677-84 [15910599.001]
  • [Cites] Chest. 2005 Mar;127(3):768-77 [15764756.001]
  • [Cites] Am J Surg Pathol. 2006 May;30(5):606-13 [16699315.001]
  • [Cites] Ann Thorac Surg. 2006 Nov;82(5):1808-13; discussion 1813-4 [17062253.001]
  • [Cites] N Engl J Med. 2006 Oct 26;355(17):1763-71 [17065637.001]
  • [Cites] Ann Thorac Surg. 2007 Jan;83(1):209-14 [17184664.001]
  • [Cites] Radiology. 2007 Feb;242(2):555-62 [17255425.001]
  • [Cites] Ann Thorac Surg. 2007 Feb;83(2):397-400 [17257959.001]
  • [Cites] Mod Pathol. 2007 Feb;20(2):233-41 [17192789.001]
  • [Cites] J Thorac Oncol. 2006 Nov;1(9 Suppl):S13-9 [17409995.001]
  • [Cites] Lung Cancer. 2007 May;56(2):193-9 [17239983.001]
  • [Cites] J Cardiovasc Surg (Torino). 2007 Jun;48(3):369-74 [17505443.001]
  • [Cites] Ann Thorac Surg. 2007 Sep;84(3):934-8; discussion 939 [17720402.001]
  • [Cites] AJR Am J Roentgenol. 2000 Mar;174(3):763-8 [10701622.001]
  • [Cites] Lung Cancer. 2000 Sep;29(3):179-88 [10996420.001]
  • [Cites] Cancer. 2001 Jul 1;92(1):153-9 [11443621.001]
  • [Cites] Ann Diagn Pathol. 2001 Dec;5(6):321-9 [11745069.001]
  • [Cites] Lung Cancer. 2002 Apr;36(1):9-14 [11891027.001]
  • [Cites] AJR Am J Roentgenol. 2002 May;178(5):1053-7 [11959700.001]
  • [Cites] Ann Thorac Surg. 2002 Oct;74(4):988-93; discussion 993-4 [12400733.001]
  • [Cites] Am J Surg Pathol. 2003 Jan;27(1):101-9 [12502932.001]
  • [Cites] Lung Cancer. 2003 Feb;39(2):231-2 [12581579.001]
  • [Cites] Eur J Cardiothorac Surg. 2003 Mar;23(3):409-14 [12614815.001]
  • [Cites] Ann Thorac Surg. 2003 Jun;75(6):1745-51; discussion 1751 [12822610.001]
  • [Cites] Anticancer Res. 2003 Nov-Dec;23(6D):4959-65 [14981952.001]
  • [Cites] J Thorac Cardiovasc Surg. 2004 Mar;127(3):857-61 [15001917.001]
  • [Cites] Lung Cancer. 2004 Apr;44(1):43-51 [15013582.001]
  • [Cites] J Thorac Cardiovasc Surg. 2004 Jun;127(6):1574-8 [15173709.001]
  • [Cites] Ann Thorac Surg. 2004 Oct;78(4):1194-9 [15464469.001]
  • [Cites] J Thorac Cardiovasc Surg. 1970 Aug;60(2):275-90 [5451072.001]
  • [Cites] Cancer. 1976 Mar;37(3):1389-96 [1260659.001]
  • [Cites] Cancer. 1977 Apr;39(4):1647-55 [192433.001]
  • [Cites] Cancer. 1981 Mar 1;47(5 Suppl):1182-7 [6263446.001]
  • [Cites] Am Rev Respir Dis. 1984 Oct;130(4):549-54 [6091505.001]
  • [Cites] Am Rev Respir Dis. 1984 Oct;130(4):555-60 [6091506.001]
  • [Cites] Am Rev Respir Dis. 1984 Oct;130(4):561-5 [6091507.001]
  • [Cites] J Natl Cancer Inst. 1988 Nov 2;80(17):1404-7 [3172266.001]
  • [Cites] Cancer Res. 1995 Jan 1;55(1):135-40 [7805023.001]
  • [Cites] Cancer. 1995 Jun 15;75(12):2844-52 [7773933.001]
  • [Cites] Cancer. 1997 Mar 1;79(5):906-14 [9041152.001]
  • [Cites] Cancer. 1997 Apr 15;79(8):1521-6 [9118033.001]
  • [Cites] Chest. 1997 Jun;111(6):1710-7 [9187198.001]
  • [Cites] Lancet. 1999 Jul 10;354(9173):99-105 [10408484.001]
  • [Cites] Histol Histopathol. 2006 Jun;21(6):627-32 [16528673.001]
  • (PMID = 18951650.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA070907-109001; United States / NCI NIH HHS / CA / R01 CA078905; United States / NCI NIH HHS / CA / R01-CA-78905; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / P50 CA070907-109001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Other-IDs] NLM/ NIHMS146973; NLM/ PMC2849638
  •  go-up   go-down


52. Pérez Escuredo J, Llorente JL, Melón S, de Oña M, García Martínez J, Alvarez Marcos C, Hermsen M: [Viral infection of herpes simplex, Epstein-Barr, varicela zoster, human papilloma, cytomegalovirus, or adenovirus are not related to sinonasal adenocarcinomas]. Acta Otorrinolaringol Esp; 2007 Aug-Sep;58(7):311-5
MedlinePlus Health Information. consumer health - Shingles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Viral infection of herpes simplex, Epstein-Barr, varicela zoster, human papilloma, cytomegalovirus, or adenovirus are not related to sinonasal adenocarcinomas].
  • [Transliterated title] Las infecciones por virus herpes simplex, Epstein-Barr, varicela zoster, papiloma humano, citomegalovirus o adenovirus no tienen relación con los adenocarcinomas nasosinusales.
  • However, until now sinonasal adenocarcinomas (ACN) have not been studied.
  • [MeSH-major] Adenocarcinoma / virology. Adenoviridae Infections / genetics. Epstein-Barr Virus Infections / genetics. Herpes Simplex / genetics. Herpes Zoster / genetics. Papillomavirus Infections / genetics. Paranasal Sinus Neoplasms / virology

  • MedlinePlus Health Information. consumer health - Herpes Simplex.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17683698.001).
  • [ISSN] 0001-6519
  • [Journal-full-title] Acta otorrinolaringológica española
  • [ISO-abbreviation] Acta Otorrinolaringol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / DNA, Viral
  •  go-up   go-down


53. Deng H, Makizumi R, Ravikumar TS, Dong H, Yang W, Yang WL: Bone morphogenetic protein-4 is overexpressed in colonic adenocarcinomas and promotes migration and invasion of HCT116 cells. Exp Cell Res; 2007 Mar 10;313(5):1033-44
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone morphogenetic protein-4 is overexpressed in colonic adenocarcinomas and promotes migration and invasion of HCT116 cells.
  • In an analysis of human colon normal mucosa and tumors at different stages by immunohistochemistry, we observed that the intensity of BMP-4 staining in late-adenocarcinomas was stronger than that in normal mucosa and adenomas, while there was no difference in the staining of its receptors (BMPR-IA and BMPR-II) at all stages.
  • [MeSH-major] Adenocarcinoma / metabolism. Bone Morphogenetic Proteins / metabolism. Cell Movement. Colonic Neoplasms / metabolism. Intestinal Mucosa / metabolism. Liver Neoplasms / secondary

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17275810.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
  •  go-up   go-down


54. Li AR, Chitale D, Riely GJ, Pao W, Miller VA, Zakowski MF, Rusch V, Kris MG, Ladanyi M: EGFR mutations in lung adenocarcinomas: clinical testing experience and relationship to EGFR gene copy number and immunohistochemical expression. J Mol Diagn; 2008 May;10(3):242-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR mutations in lung adenocarcinomas: clinical testing experience and relationship to EGFR gene copy number and immunohistochemical expression.
  • Lung adenocarcinomas responsive to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors possess EGFR mutations and often increased EGFR copy number.
  • [MeSH-major] Adenocarcinoma / genetics. Genes, erbB-1. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2003 Oct 15;21(20):3798-807 [12953099.001]
  • [Cites] Mod Pathol. 2008 May;21 Suppl 2:S16-22 [18437168.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2858-65 [9256129.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 [15741570.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] PLoS Med. 2005 Jan;2(1):e17 [15696205.001]
  • [Cites] Mod Pathol. 2005 Aug;18(8):1027-33 [15920544.001]
  • [Cites] J Mol Diagn. 2005 Aug;7(3):396-403 [16049312.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):6838-45 [15998906.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):6829-37 [15998907.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):8081-92 [16204011.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):751-8 [16467085.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):839-44 [16467097.001]
  • [Cites] Am J Clin Pathol. 2006 Jun;125(6):860-5 [16690485.001]
  • [Cites] Nat Med. 2006 Jul;12(7):852-5 [16799556.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 2):4403s-4408s [16857818.001]
  • [Cites] Cancer Sci. 2006 Aug;97(8):753-9 [16863509.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):587-95 [17290067.001]
  • [Cites] Clin Cancer Res. 2007 May 15;13(10):2890-6 [17504988.001]
  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):4954-5 [17785543.001]
  • [Cites] Mod Pathol. 2007 Oct;20(10):1028-35 [17673923.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1472-8 [18349398.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • (PMID = 18403609.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA129243
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2329789
  •  go-up   go-down


55. Haroon M, Kwong WY, Cantwell B, Walker F: A case of cetuximab-related tumour lysis syndrome in metastatic rectal carcinoma. NDT Plus; 2010 Jun;3(3):271-272

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 60-year-old man was diagnosed with a moderately differentiated adenocarcinoma in November 2006.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2008 May 10;26(14):2406-8 [18467734.001]
  • [Cites] Ann Oncol. 2005 May;16 Suppl 4:iv50-55 [15923430.001]
  • [Cites] J Natl Cancer Inst. 1998 May 6;90(9):675-84 [9586664.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2643-8 [17363584.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):299-304 [11208819.001]
  • [Cites] Eur J Cancer. 2001 Sep;37 Suppl 4:S16-22 [11597400.001]
  • (PMID = 28657052.001).
  • [ISSN] 1753-0784
  • [Journal-full-title] NDT plus
  • [ISO-abbreviation] NDT Plus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


56. Goldstein NS: Small colonic microsatellite unstable adenocarcinomas and high-grade epithelial dysplasias in sessile serrated adenoma polypectomy specimens: a study of eight cases. Am J Clin Pathol; 2006 Jan;125(1):132-45
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.
  • [Title] Small colonic microsatellite unstable adenocarcinomas and high-grade epithelial dysplasias in sessile serrated adenoma polypectomy specimens: a study of eight cases.
  • Eight sessile serrated adenoma (SSA), right colon polypectomies with focal invasive adenocarcinoma or high-grade dysplasia were studied to identify features indicating a high risk of transformation and characterize the morphologic features of serrated dysplasia; 6 cases had invasive adenocarcinoma; 2 were high-grade dysplasia.
  • In the 6 invasive adenocarcinomas, the neoplasm extended directly down into the submucosa without lateral intramucosal spread.
  • The mean maximum dimension of the invasive adenocarcinoma was 2.9 mm (range, 2-4 mm).
  • Small proximal SSAs can transform into adenocarcinoma without a component of adenomatous dysplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Chromosomal Instability. Colonic Neoplasms / pathology. Microsatellite Repeats

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16483002.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins
  •  go-up   go-down


57. Balasenthil S, Broaddus RR, Kumar R: Expression of metastasis-associated protein 1 (MTA1) in benign endometrium and endometrial adenocarcinomas. Hum Pathol; 2006 Jun;37(6):656-61
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.
  • [Title] Expression of metastasis-associated protein 1 (MTA1) in benign endometrium and endometrial adenocarcinomas.
  • We investigated the expression profile of MTA1 in different stages of benign endometrium as well as in endometrial endometrioid adenocarcinoma using immunohistochemistry and Western blotting.
  • Immunohistochemical staining performed on tumor microarray containing 70 endometrial endometrioid adenocarcinomas of various grades showed increased expression of MTA1 in 53 (75.7%) tumors.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Neoplasm Staging

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16733204.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 098823
  • [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 / Repressor Proteins; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


58. McChesney PA, Aiyar SE, Lee OJ, Zaika A, Moskaluk C, Li R, El-Rifai W: Cofactor of BRCA1: a novel transcription factor regulator in upper gastrointestinal adenocarcinomas. Cancer Res; 2006 Feb 1;66(3):1346-53
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.
  • [Title] Cofactor of BRCA1: a novel transcription factor regulator in upper gastrointestinal adenocarcinomas.
  • In this work, we show that COBRA1 is overexpressed in the majority of primary upper gastrointestinal adenocarcinomas (UGC), and its overexpression correlates with down-regulation of TFF1.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Nuclear Proteins / genetics. Stomach Neoplasms / genetics. Transcription Factor AP-1 / metabolism
  • [MeSH-minor] Binding Sites. Cell Line, Tumor. DNA, Neoplasm / metabolism. Gene Expression Regulation, Neoplastic. Humans. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transcription Factors. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16452188.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 106176; United States / NCI NIH HHS / CA / CA 93999; United States / NIDDK NIH HHS / DK / DK 064604
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / TFF1 protein, human; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / negative elongation factor
  •  go-up   go-down


59. Fong D, Hermann M, Untergasser G, Pirkebner D, Draxl A, Heitz M, Moser P, Margreiter R, Hengster P, Amberger A: Dkk-3 expression in the tumor endothelium: a novel prognostic marker of pancreatic adenocarcinomas. Cancer Sci; 2009 Aug;100(8):1414-20
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] Dkk-3 expression in the tumor endothelium: a novel prognostic marker of pancreatic adenocarcinomas.
  • Here we analyzed the clinical relevance of Dkk-3 expression in pancreas adenocarcinomas and determined its role on endothelial cell growth in vitro.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Endothelium / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Pancreatic Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19493271.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DKK3 protein, human; 0 / Intercellular Signaling Peptides and Proteins
  •  go-up   go-down


60. Balko JM, Black EP: Ovarian carcinoma as a surrogate tumor for lung adenocarcinomas in evaluating the chemo-stability of a gene expression signature. Cancer Biol Ther; 2009 Jan;8(2):167-73
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ovarian carcinoma as a surrogate tumor for lung adenocarcinomas in evaluating the chemo-stability of a gene expression signature.
  • Expression patterns in multiple epithelial tumors were compared to lung adenocarcinomas (LAC).
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Cell Line, Tumor. Erlotinib Hydrochloride. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Oligonucleotide Array Sequence Analysis. Quinazolines. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Regression Analysis. Reproducibility of Results. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19029813.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


61. Aamodt R, Jonsdottir K, Andersen SN, Bondi J, Bukholm G, Bukholm IR: Differences in protein expression and gene amplification of cyclins between colon and rectal adenocarcinomas. Gastroenterol Res Pract; 2009;2009:285830
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.
  • [Title] Differences in protein expression and gene amplification of cyclins between colon and rectal adenocarcinomas.
  • Adenocarcinomas of rectum and colon may be different with regard to the cellular biological basis for cancer development.

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 1994 Nov 18;79(4):551-5 [7954821.001]
  • [Cites] Cell. 1994 Nov 18;79(4):563-71 [7954823.001]
  • [Cites] Oncogene. 1993 Aug;8(8):2127-33 [8336939.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3685-9 [8386381.001]
  • [Cites] Curr Opin Cell Biol. 1997 Feb;9(1):93-8 [9013668.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Br J Cancer. 1997;75(12):1774-8 [9192980.001]
  • [Cites] Int J Biochem Cell Biol. 1997 Apr;29(4):559-73 [9363633.001]
  • [Cites] Cancer Res. 1998 Mar 1;58(5):985-90 [9500460.001]
  • [Cites] Int J Oncol. 1998 May;12(5):1007-11 [9538120.001]
  • [Cites] Am J Pathol. 1998 Sep;153(3):963-72 [9736045.001]
  • [Cites] Clin Cancer Res. 1997 Aug;3(8):1399-404 [9815824.001]
  • [Cites] Clin Cancer Res. 1996 Oct;2(10):1781-5 [9816130.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):1-11 [9858526.001]
  • [Cites] Oncogene. 1999 May 13;18(19):3004-16 [10378696.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2885-90 [10383150.001]
  • [Cites] Leuk Lymphoma. 1999 Sep;35(1-2):147-57 [10512172.001]
  • [Cites] Eur J Cancer. 1999 Jun;35(6):942-5 [10533476.001]
  • [Cites] Curr Biol. 1999 Nov 4;9(21):1255-8 [10556095.001]
  • [Cites] Am J Pathol. 2000 Jun;156(6):2135-47 [10854234.001]
  • [Cites] EMBO J. 1992 Mar;11(3):961-71 [1312467.001]
  • [Cites] Nature. 1991 Nov 28;354(6351):314-7 [1659666.001]
  • [Cites] Cell. 1991 Dec 20;67(6):1169-79 [1836977.001]
  • [Cites] Semin Surg Oncol. 1987;3(3):152-8 [2821605.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):3046-50 [7708772.001]
  • [Cites] Mol Cell Biol. 1995 May;15(5):2612-24 [7739542.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Jul 1;128(1):43-5 [11454429.001]
  • [Cites] J Pathol. 2001 Sep;195(2):171-8 [11592095.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1134-8 [11861394.001]
  • [Cites] Br J Cancer. 2002 Feb 1;86(3):402-8 [11875707.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Apr;87(4):1810-3 [11932322.001]
  • [Cites] Lung Cancer. 2002 Jun;36(3):277-82 [12009238.001]
  • [Cites] Arch Pathol Lab Med. 2002 Sep;126(9):1079-86 [12204057.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2003 Mar;11(1):9-14 [12610350.001]
  • [Cites] Oral Oncol. 2003 Jul;39(5):476-82 [12747972.001]
  • [Cites] Anal Cell Pathol. 2003;25(3):103-14 [12775914.001]
  • [Cites] Hum Pathol. 2003 May;34(5):471-8 [12792921.001]
  • [Cites] World J Gastroenterol. 2003 Nov;9(11):2450-4 [14606074.001]
  • [Cites] Expert Rev Anticancer Ther. 2004 Apr;4(2):289-302 [15056059.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):4015-21 [15217933.001]
  • [Cites] J Clin Pathol. 2005 May;58(5):509-14 [15858123.001]
  • [Cites] Virchows Arch. 2005 Jun;446(6):626-33 [15891905.001]
  • [Cites] Eur J Haematol. 2005 Aug;75(2):106-15 [16004607.001]
  • [Cites] Hum Pathol. 2005 Jul;36(7):828-37 [16084954.001]
  • [Cites] Br J Cancer. 2005 Sep 5;93(5):515-9 [16091759.001]
  • [Cites] Hum Pathol. 2005 Sep;36(9):994-1002 [16153463.001]
  • [Cites] Oncol Rep. 2006 Sep;16(3):443-9 [16865241.001]
  • [Cites] Anticancer Res. 2006 Nov-Dec;26(6B):4415-21 [17201163.001]
  • (PMID = 20029639.001).
  • [ISSN] 1687-630X
  • [Journal-full-title] Gastroenterology research and practice
  • [ISO-abbreviation] Gastroenterol Res Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2796221
  •  go-up   go-down


62. Pérez LO, Abba MC, Dulout FN, Golijow CD: Evaluation of p53 codon 72 polymorphism in adenocarcinomas of the colon and rectum in La Plata, Argentina. World J Gastroenterol; 2006 Mar 7;12(9):1426-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of p53 codon 72 polymorphism in adenocarcinomas of the colon and rectum in La Plata, Argentina.
  • AIM: To evaluate the potential association between p53 codon 72 polymorphism and sporadic colorectal adenocarcinoma development,and human papillomavirus (HPV) infection.
  • Lack of association was found between p53 polymorphism and HPV infection in the set of adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Codon / genetics. Colorectal Neoplasms / genetics. Genes, p53. Polymorphism, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Argentina. Case-Control Studies. Causality. Genetic Predisposition to Disease. Humans. Middle Aged. Papillomaviridae. Papillomavirus Infections / genetics. Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Radiology. 2000 May;215(2):327-35 [10796903.001]
  • [Cites] Mol Cell Biol. 1999 Feb;19(2):1092-100 [9891044.001]
  • [Cites] J Microbiol Immunol Infect. 2001 Jun;34(2):87-91 [11456365.001]
  • [Cites] Res Commun Mol Pathol Pharmacol. 2001 Jul;109(1-2):25-34 [11458982.001]
  • [Cites] Cancer Invest. 2001;19(7):678-83 [11577808.001]
  • [Cites] Ann Intern Med. 2002 Oct 1;137(7):603-12 [12353948.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1684-8 [12496062.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2003 Jul 1;109(1):63-6 [12818446.001]
  • [Cites] Oncogene. 2003 Aug 14;22(34):5252-60 [12917626.001]
  • [Cites] Biol Res. 2003;36(2):279-83 [14513722.001]
  • [Cites] Cancer Sci. 2004 Jan;95(1):7-11 [14720320.001]
  • [Cites] Oncogene. 2004 Mar 11;23(10):1954-6 [14647431.001]
  • [Cites] World J Gastroenterol. 2004 Oct 1;10(19):2775-8 [15334668.001]
  • [Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]
  • [Cites] J Clin Microbiol. 1992 Apr;30(4):987-92 [1315341.001]
  • [Cites] Am J Surg. 1993 Dec;166(6):738-40; discussion 741-2 [8273860.001]
  • [Cites] Hum Hered. 1994 Sep-Oct;44(5):266-70 [7927355.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):594-8 [10203277.001]
  • [Cites] Gynecol Oncol. 1999 Oct;75(1):108-12 [10502435.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 Dec;130(12):728-32 [15365822.001]
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):529-35 [15548361.001]
  • [Cites] World J Gastroenterol. 2005 Jan 14;11(2):289-92 [15633234.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):2862-7 [15837733.001]
  • [Cites] Colorectal Dis. 2005 Sep;7(5):492-5 [16108887.001]
  • [Cites] Gut. 1995 Jul;37(1):87-90 [7672688.001]
  • [Cites] Carcinogenesis. 1996 Feb;17(2):261-4 [8625447.001]
  • [Cites] Nature. 1998 May 21;393(6682):229-34 [9607760.001]
  • [Cites] Nat Genet. 2000 May;25(1):47-54 [10802655.001]
  • (PMID = 16552814.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Codon
  • [Other-IDs] NLM/ PMC4124323
  •  go-up   go-down


63. Couvelard A, O'Toole D, Leek R, Turley H, Sauvanet A, Degott C, Ruszniewski P, Belghiti J, Harris AL, Gatter K, Pezzella F: Expression of hypoxia-inducible factors is correlated with the presence of a fibrotic focus and angiogenesis in pancreatic ductal adenocarcinomas. Histopathology; 2005 Jun;46(6):668-76
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] Expression of hypoxia-inducible factors is correlated with the presence of a fibrotic focus and angiogenesis in pancreatic ductal adenocarcinomas.
  • AIMS: To study the expression of hypoxia-regulated markers in pancreatic ductal adenocarcinomas (PA) in relationship to the presence of a fibrotic focus, angiogenesis quantification and clinical outcome.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / analysis. Basic Helix-Loop-Helix Transcription Factors. Carbonic Anhydrases / analysis. Female. Fibrosis. Follow-Up Studies. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Immunohistochemistry. Lymphatic Metastasis. Male. Middle Aged. Necrosis. Neoplasm Staging. Pancreas / blood supply. Pancreas / chemistry. Pancreas / pathology. Survival Analysis. Transcription Factors / analysis. Vascular Endothelial Growth Factor A / analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15910598.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  •  go-up   go-down


64. Zhou Y, Rideout WM 3rd, Zi T, Bressel A, Reddypalli S, Rancourt R, Woo JK, Horner JW, Chin L, Chiu MI, Bosenberg M, Jacks T, Clark SC, Depinho RA, Robinson MO, Heyer J: Chimeric mouse tumor models reveal differences in pathway activation between ERBB family- and KRAS-dependent lung adenocarcinomas. Nat Biotechnol; 2010 Jan;28(1):71-8
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chimeric mouse tumor models reveal differences in pathway activation between ERBB family- and KRAS-dependent lung adenocarcinomas.
  • Adenocarcinomas arising in an allelic series of lung cancer models containing HER2 (also known as ERBB2), KRAS or EGFR oncogenes exhibit features of advanced malignancies.
  • [MeSH-major] Adenocarcinoma / metabolism. Chimera / metabolism. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Proto-Oncogene Proteins p21(ras) / metabolism. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Disease Models, Animal. Embryonic Stem Cells / drug effects. Embryonic Stem Cells / metabolism. Mice. Mice, Transgenic. Mutation / genetics. Phenotype. Piperazines / pharmacology. Quinazolines / pharmacology. Respiratory Insufficiency / metabolism. Respiratory Insufficiency / pathology


65. Shibata T, Noguchi T, Takeno S, Gabbert HE, Ramp U, Kawahara K: Disturbed XIAP and XAF1 expression balance is an independent prognostic factor in gastric adenocarcinomas. Ann Surg Oncol; 2008 Dec;15(12):3579-87
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.
  • [Title] Disturbed XIAP and XAF1 expression balance is an independent prognostic factor in gastric adenocarcinomas.
  • METHODS: XIAP, Smac/DIABLO, and XAF1 expression was analyzed by immunohistochemistry (IHC) in 187 gastric adenocarcinomas.
  • Disease-specific survival after surgery was examined.
  • Individually, XIAP, Smac, and XAF1 were not significantly associated with disease-specific survival.
  • CONCLUSION: The expression balance of XIAP and XAF1 is an independent prognostic factor in gastric adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Mitochondrial Proteins / metabolism. Neoplasm Proteins / metabolism. Stomach Neoplasms / metabolism. X-Linked Inhibitor of Apoptosis Protein / metabolism

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18807090.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DIABLO protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitochondrial Proteins; 0 / Neoplasm Proteins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XAF1 protein, human; 0 / XIAP protein, human
  •  go-up   go-down


66. Schneider AR, Seifert H, Trojan J, Stein J, Hoepffner NM: Frequency of colorectal polyps in patients with sporadic adenomas or adenocarcinomas of the papilla of vater--an age-matched, controlled study. Z Gastroenterol; 2005 Oct;43(10):1123-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of colorectal polyps in patients with sporadic adenomas or adenocarcinomas of the papilla of vater--an age-matched, controlled study.
  • Patients with familial adenomatous polyposis bear a particularly increased risk for periampullary tumors.
  • METHODS: 26 consecutive patients (16 women, 10 men; median age 59 years) with sporadic adenomas (n = 19) or adenocarcinomas (n = 7) of the ampulla of Vater were retrospectively evaluated.
  • However, the finding of 2 rectal carcinomas among patients with ampullary neoplasms supports the place of screening colonoscopy for the diagnostic work-up of ampullary tumors.
  • [MeSH-major] Adenocarcinoma / complications. Adenoma / complications. Ampulla of Vater. Common Bile Duct Neoplasms / complications. Intestinal Polyps / epidemiology
  • [MeSH-minor] Adenoma, Villous / complications. Adenoma, Villous / surgery. Adenomatous Polyposis Coli / epidemiology. Adult. Aged. Aged, 80 and over. Colonic Polyps / diagnosis. Colonic Polyps / epidemiology. Colonoscopy. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / epidemiology. Data Interpretation, Statistical. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prevalence. Retrospective Studies. Risk Factors. Time Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16220451.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


67. Zhu W, Michael CW: WT1, monoclonal CEA, TTF1, and CA125 antibodies in the differential diagnosis of lung, breast, and ovarian adenocarcinomas in serous effusions. Diagn Cytopathol; 2007 Jun;35(6):370-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] WT1, monoclonal CEA, TTF1, and CA125 antibodies in the differential diagnosis of lung, breast, and ovarian adenocarcinomas in serous effusions.
  • The distinction between metastatic adenocarcinomas of lung (LAC), breast (BAC), and ovary (OAC) in serous effusions can be very difficult since they all can present as tight cell clusters.
  • This is particularly challenging when the malignant effusion is the patient's initial presentation or when the patient has a history of more than one primary.
  • The aim of this study is to evaluate the usefulness of WT1, monoclonal CEA (mCEA), TTF1, and CA125 antibodies in the differential diagnosis of metastatic adenocarcinoma from the lung, breast and ovary in serous effusions.
  • A positive TTF1 staining supports the diagnosis of metastatic carcinoma originating from lung rather than breast, while a negative TTF1 favors the diagnosis of a breast primary.
  • Immunohistochemical studies with WT1, TTF1, and mCEA antibodies are useful in the differential diagnosis of metastatic adenocarcinomas of lung, breast, and ovary.
  • [MeSH-major] Adenocarcinoma / diagnosis. Antibodies, Monoclonal. CA-125 Antigen / immunology. Carcinoembryonic Antigen / immunology. Nuclear Proteins / immunology. Pleural Effusion, Malignant / diagnosis. Transcription Factors / immunology. WT1 Proteins / immunology
  • [MeSH-minor] Breast Neoplasms / diagnosis. Diagnosis, Differential. Female. Humans. Lung Neoplasms / diagnosis. Ovarian Neoplasms / diagnosis

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17497661.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / CA-125 Antigen; 0 / Carcinoembryonic Antigen; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / WT1 Proteins; 0 / thyroid nuclear factor 1
  •  go-up   go-down


68. Alves MK, Lima VP, Ferrasi AC, Rodrigues MA, De Moura Campos Pardini MI, Rabenhorst SH: CDKN2A promoter methylation is related to the tumor location and histological subtype and associated with Helicobacter pylori flaA(+) strains in gastric adenocarcinomas. APMIS; 2010 Apr;118(4):297-307
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CDKN2A promoter methylation is related to the tumor location and histological subtype and associated with Helicobacter pylori flaA(+) strains in gastric adenocarcinomas.
  • Therefore, we examined a series of gastric adenocarcinomas to assess the association between p16INK4A inactivation and H. pylori genotype (vacA, cagA, cagE, virB11 and flaA) according to the location and histological subtype of the tumors. p16INK4A expression and CDKN2A promoter methylation were found in 77 gastric adenocarcinoma samples by immunohistochemistry and methylation-specific PCR, respectively.
  • In diffuse subtype tumors, the inactivation of p16INK4A by promoter methylation was unique in noncardia tumors (p=0.022).
  • [MeSH-major] Adenocarcinoma / genetics. Genes, p16. Helicobacter Infections / genetics. Stomach Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20402675.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
  •  go-up   go-down


69. Li LG, Xu HM: Inducible nitric oxide synthase, nitrotyrosine and apoptosis in gastric adenocarcinomas and their correlation with a poor survival. World J Gastroenterol; 2005 May 7;11(17):2539-44
Hazardous Substances Data Bank. L-TYROSINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inducible nitric oxide synthase, nitrotyrosine and apoptosis in gastric adenocarcinomas and their correlation with a poor survival.
  • AIM: To detect the presence of inducible nitric oxide synthase (iNOS), nitrotyrosine (NT) and apoptosis in gastric adenocarcinomas and their possible correlations with the clinicopathological characteristics and prognosis of gastric adenocarcinoma.
  • METHODS: Sixty-six specimens of gastric adenocarcinoma and corresponding adjacent normal gastric tissues were studied.
  • RESULTS: Results showed that iNOS expression was detected at an intermediate or high level in 41 of 66 (62%) specimens of gastric adenocarcinoma.
  • Many clinicopathologic characteristics of gastric adenocarcinoma, such as tumor size, depth of invasion, lymph node metastasis and TNM staging, were related to iNOS and NT expressions (P<0.05).
  • CONCLUSION: NO produced by iNOS may play a stronger role in promoting gastric adenocarcinoma growth than in suppressing its growth. iNOS and NT expressions by gastric adenocarcinoma may correlate with a poor survival.
  • [MeSH-major] Adenocarcinoma / metabolism. Apoptosis. Nitric Oxide Synthase / metabolism. Stomach Neoplasms / metabolism. Tyrosine / analogs & derivatives. Tyrosine / metabolism

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15849807.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  • [Other-IDs] NLM/ PMC4305739
  •  go-up   go-down


70. Wang X, Fu Y, Chen X, Ye J, Lü B, Ye F, Lü W, Xie X: The expressions of bHLH gene HES1 and HES5 in advanced ovarian serous adenocarcinomas and their prognostic significance: a retrospective clinical study. J Cancer Res Clin Oncol; 2010 Jul;136(7):989-96
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expressions of bHLH gene HES1 and HES5 in advanced ovarian serous adenocarcinomas and their prognostic significance: a retrospective clinical study.
  • METHODS: Formalin-fixed, paraffin embedded tissues and clinic-pathological parameters from 61 patients with FIGO stage IIIc-IV ovarian serous adenocarcinoma were collected, the expression of HES1 and HES5 protein were immunohistochemically detected, and the association of HES1 and HES5 expression with survival of the patients were analyzed.
  • RESULTS: The expressions of both HES1 and HES5 in adenocarcinoma were significantly higher than those in adenoma and normal control (chi(2) = 32.915, P = 0.000 and chi(2) = 46.863, P = 0.000 respectively).
  • Overall survival and disease-free period were longer in HES1 low-expression patients (median 43.0 and 22.0 months) than those in high-expression patients (median 24.0 and 14.5 months).
  • Univariate analysis and multivariate Cox regression model did not show that HES1 or HES5 expression was a factor associated with survival of advanced ovarian serous adenocarcinoma patients.
  • CONCLUSIONS: The expressions of bHLH gene HES1 and HES5 are increased in advanced ovarian serous adenocarcinomas, and HES1 high-expression probably is a potential poor prognostic factor for the patients.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Cystadenocarcinoma, Serous / diagnosis. Cystadenocarcinoma, Serous / metabolism. Disease Progression. Homeodomain Proteins / biosynthesis. Ovarian Neoplasms / diagnosis. Ovarian Neoplasms / metabolism. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cutan Pathol. 2003 Jan;30(1):23-8 [12534800.001]
  • [Cites] Oncogene. 2000 Nov 30;19(51):5951-3 [11127827.001]
  • [Cites] Blood. 2004 May 1;103(9):3503-10 [14670925.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):341-7 [15288259.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):207-14 [7459811.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):501-8 [10080591.001]
  • [Cites] Development. 1999 Sep;126(17):3925-35 [10433920.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):298-305 [15671559.001]
  • [Cites] Br J Cancer. 2005 Jan 31;92(2):334-41 [15655552.001]
  • [Cites] J Immunol. 2005 Mar 1;174(5):2507-16 [15728456.001]
  • [Cites] Gynecol Oncol. 2005 Apr;97(1):26-34 [15790433.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 May;55(5):461-5 [15690203.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1354-68 [15887117.001]
  • [Cites] Br J Cancer. 2005 Sep 19;93(6):709-18 [16136053.001]
  • [Cites] Surgery. 2005 Dec;138(6):1137-42; discussion 1142 [16360401.001]
  • [Cites] Mol Endocrinol. 2006 Mar;20(3):698-705 [16282371.001]
  • [Cites] Genes Chromosomes Cancer. 2006 May;45(5):470-81 [16444749.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4715-24 [16651424.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Cancer Sci. 2007 Feb;98(2):155-62 [17297654.001]
  • [Cites] Gynecol Oncol. 2007 Apr;105(1):66-73 [17234259.001]
  • [Cites] Int J Gynecol Cancer. 2007 Nov-Dec;17(6):1293-9 [17388915.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Jan;65(1):43-53 [17644000.001]
  • [Cites] Nature. 2008 Jan 3;451(7174):76-80 [18172499.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2220-9 [18039953.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):36-44 [10615124.001]
  • [Cites] Development. 2000 Sep;127(18):3913-21 [10952889.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):171-8 [15013216.001]
  • (PMID = 20091184.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / Repressor Proteins; 148591-48-4 / HES5 protein, human; 149348-15-2 / HES1 protein, human
  • [Other-IDs] NLM/ PMC2874490
  •  go-up   go-down


71. López-Malpartida AV, Ludeña MD, Varela G, García Pichel J: Differential ErbB receptor expression and intracellular signaling activity in lung adenocarcinomas and squamous cell carcinomas. Lung Cancer; 2009 Jul;65(1):25-33
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.
  • [Title] Differential ErbB receptor expression and intracellular signaling activity in lung adenocarcinomas and squamous cell carcinomas.
  • Adenocarcinomas (AC) and squamous cell carcinomas (SCC) are NSCLC subtypes with distinct clinico-pathological features, and responses to ErbB-targeted inhibitors treatment.
  • [MeSH-major] Adenocarcinoma / enzymology. Carcinoma, Squamous Cell / enzymology. Lung Neoplasms / enzymology. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, ErbB-2 / biosynthesis


72. Lo SS, Khorana AA, Javle M, Simon S, Kiefer G, Rajasenan K, Wang H, Hantel A, Shayne M, Hwang J, Schmotzer A, Ramanathan RK: A phase II study of weekly docetaxel in combination with capecitabine in advanced gastric and gastroesophageal adenocarcinomas. Oncology; 2010;78(2):125-9
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of weekly docetaxel in combination with capecitabine in advanced gastric and gastroesophageal adenocarcinomas.
  • This multi-institutional phase II trial evaluates the combination of docetaxel and capecitabine as first- or second-line treatment in patients with advanced gastric and GE adenocarcinomas.
  • CONCLUSIONS: The regimen of docetaxel and capecitabine is a well-tolerated, easily administered and active outpatient regimen for advanced gastric and GE adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Deoxycytidine / analogs & derivatives. Esophageal Neoplasms / drug therapy. Fluorouracil / analogs & derivatives. Stomach Neoplasms / drug therapy. Taxoids / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / toxicity. Capecitabine. Female. Humans. Male. Middle Aged. Neoplasm Staging. Outpatients. Patient Selection. Survival Analysis. Young Adult

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CAPECITABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20389134.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 15H5577CQD / docetaxel; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
  •  go-up   go-down


73. Postawski K, Gałecka-Josse M, Baranowski W: Is global DNA methylation in sporadic uterine adenocarcinomas in women a result of histological and clinical tumor advancement? Ginekol Pol; 2009 Nov;80(11):824-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is global DNA methylation in sporadic uterine adenocarcinomas in women a result of histological and clinical tumor advancement?
  • AIM: To find out the relationship, if any between the extent of the overall genomic DNA methylation, and clinical and pathological features of the sporadic endometrial adenocarcinomas in women.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation / genetics. Endometrial Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. DNA / genetics. Female. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Middle Aged. Neoplasm Staging. Poland. Uterine Neoplasms / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20088395.001).
  • [ISSN] 0017-0011
  • [Journal-full-title] Ginekologia polska
  • [ISO-abbreviation] Ginekol. Pol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9007-49-2 / DNA
  •  go-up   go-down


74. Mees ST, Mardin WA, Wendel C, Baeumer N, Willscher E, Senninger N, Schleicher C, Colombo-Benkmann M, Haier J: EP300--a miRNA-regulated metastasis suppressor gene in ductal adenocarcinomas of the pancreas. Int J Cancer; 2010 Jan 1;126(1):114-24
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] EP300--a miRNA-regulated metastasis suppressor gene in ductal adenocarcinomas of the pancreas.
  • Genetic and epigenetic alterations during development of pancreatic ductal adenocarcinomas (PDACs) are well known.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. E1A-Associated p300 Protein / genetics. MicroRNAs / genetics. Neoplasm Metastasis / genetics. Pancreatic Neoplasms / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19569050.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 2.3.1.48 / EP300 protein, human
  •  go-up   go-down


75. Wilting SM, Snijders PJ, Meijer GA, Ylstra B, van den Ijssel PR, Snijders AM, Albertson DG, Coffa J, Schouten JP, van de Wiel MA, Meijer CJ, Steenbergen RD: Increased gene copy numbers at chromosome 20q are frequent in both squamous cell carcinomas and adenocarcinomas of the cervix. J Pathol; 2006 Jun;209(2):220-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased gene copy numbers at chromosome 20q are frequent in both squamous cell carcinomas and adenocarcinomas of the cervix.
  • The genomic profiles of nine squamous cell carcinomas (SCCs) and seven adenocarcinomas (AdCAs), as well as four human papillomavirus (HPV)-immortalized keratinocyte cell lines, were assessed.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Squamous Cell / genetics. Chromosomes, Human, Pair 20 / genetics. Uterine Cervical Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Chromosome Aberrations. Chromosome Mapping / methods. Chromosomes, Human / genetics. DNA (Cytosine-5-)-Methyltransferase / genetics. Female. Genome, Human / genetics. Humans. In Situ Hybridization, Fluorescence / methods. Middle Aged. Oligonucleotide Array Sequence Analysis / methods. Papillomaviridae. RNA, Messenger / analysis. RNA, Neoplasm / analysis

  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2006 Pathological Society of Great Britain and Ireland.
  • [CommentIn] J Pathol. 2006 Oct;210(2):258-9; author reply 260 [16841301.001]
  • (PMID = 16538612.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90421
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3B
  •  go-up   go-down


76. Herzog CR, Desai D, Amin S: Array CGH analysis reveals chromosomal aberrations in mouse lung adenocarcinomas induced by the human lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Biochem Biophys Res Commun; 2006 Mar 17;341(3):856-63
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array CGH analysis reveals chromosomal aberrations in mouse lung adenocarcinomas induced by the human lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.
  • Each of these chromosomes contains sites of orthology with those altered in human lung adenocarcinomas, suggesting similar roles in human lung cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinogens / pharmacology. Chromosome Aberrations. Lung Neoplasms / chemically induced. Lung Neoplasms / genetics. Nitrosamines / pharmacology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16455056.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 9007-49-2 / DNA
  •  go-up   go-down


77. Schmid K, Oehl N, Wrba F, Pirker R, Pirker C, Filipits M: EGFR/KRAS/BRAF mutations in primary lung adenocarcinomas and corresponding locoregional lymph node metastases. Clin Cancer Res; 2009 Jul 15;15(14):4554-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR/KRAS/BRAF mutations in primary lung adenocarcinomas and corresponding locoregional lymph node metastases.
  • EXPERIMENTAL DESIGN: Direct bidirectional sequencing of EGFR gene exons 18 to 21, KRAS gene codons 12/13 and 61 to 68, and BRAF exon 15 was done on 96 paired samples of primary lung adenocarcinomas and corresponding locoregional lymph node metastases.
  • [MeSH-major] Adenocarcinoma / pathology. Genes, ras / genetics. Mutation. Proto-Oncogene Proteins B-raf / genetics. Receptor, Epidermal Growth Factor / genetics


78. Erman M, Grunenwald D, Penault-Llorca F, Grenier J, Besse B, Validire P, Morat L, Girard P, Le Chevalier T, Sabatier L, Soria JC: Epidermal growth factor receptor, HER-2/neu and related pathways in lung adenocarcinomas with bronchioloalveolar features. Lung Cancer; 2005 Mar;47(3):315-23
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.
  • [Title] Epidermal growth factor receptor, HER-2/neu and related pathways in lung adenocarcinomas with bronchioloalveolar features.
  • Lung adenocarcinomas with bronchioalveolar features (ABAF), formerly called bronchioloalveolar cancers (BAC), constitute a distinct clinical, radiological and pathological entity among lung malignancies.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / physiopathology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / physiopathology. Gene Expression Profiling. Lung Neoplasms / genetics. Lung Neoplasms / physiopathology. Protein-Serine-Threonine Kinases / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, ErbB-3 / biosynthesis


79. Kimchi-Sarfaty C, Vieira WD, Dodds D, Sherman A, Kreitman RJ, Shinar S, Gottesman MM: SV40 Pseudovirion gene delivery of a toxin to treat human adenocarcinomas in mice. Cancer Gene Ther; 2006 Jul;13(7):648-57
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SV40 Pseudovirion gene delivery of a toxin to treat human adenocarcinomas in mice.
  • Human KB adenocarcinomas growing in mice were treated with intratumoral injection of PE38 packaged in vitro, and tumor size decreased significantly.

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Appl Microbiol Biotechnol. 1999 Oct;52(4):524-33 [10570800.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):6889-93 [8041715.001]
  • [Cites] Appl Microbiol Biotechnol. 2000 May;53(5):558-67 [10855716.001]
  • [Cites] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661.001]
  • [Cites] Expert Opin Biol Ther. 2001 Mar;1(2):291-300 [11727536.001]
  • [Cites] Hum Gene Ther. 2002 Jan 20;13(2):299-310 [11812285.001]
  • [Cites] World J Surg. 2002 Jul;26(7):783-9 [11948367.001]
  • [Cites] Drug Discov Today. 2002 Apr 15;7(8):479-85 [11965397.001]
  • [Cites] Hum Gene Ther. 2003 Jan 20;14(2):167-77 [12614568.001]
  • [Cites] Cancer Immunol Immunother. 2003 May;52(5):338-41 [12700949.001]
  • [Cites] Cancer Gene Ther. 2003 Jul;10(7):501-8 [12833130.001]
  • [Cites] J Neurooncol. 2003 Oct;65(1):15-25 [14649882.001]
  • [Cites] Hum Gene Ther. 2003 Dec 10;14(18):1787-98 [14670129.001]
  • [Cites] Expert Opin Biol Ther. 2004 Apr;4(4):519-30 [15102601.001]
  • [Cites] Int J Med Microbiol. 2004 Apr;293(7-8):577-82 [15149034.001]
  • [Cites] J Immunol. 2004 Jul 1;173(1):61-7 [15210759.001]
  • [Cites] Ann Thorac Surg. 2004 Aug;78(2):436-43; discussion 436-43 [15276492.001]
  • [Cites] Biotechniques. 2004 Aug;37(2):270-5 [15335219.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6231-8 [15448012.001]
  • [Cites] J Med Chem. 2004 Nov 4;47(23):5690-9 [15509168.001]
  • [Cites] Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953.001]
  • [Cites] J Biol Chem. 1990 Sep 25;265(27):16306-10 [2118903.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8291-5 [2236041.001]
  • [Cites] J Urol. 1993 Jun;149(6):1626-32 [8501821.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7538-42 [8356052.001]
  • [Cites] Ann N Y Acad Sci. 1993 Jun 23;685:740-5 [8363279.001]
  • [Cites] Blood. 1994 Jan 15;83(2):426-34 [8286741.001]
  • [Cites] Ann N Y Acad Sci. 1994 May 31;716:126-38; discussion 138-43 [7912913.001]
  • [Cites] Hum Gene Ther. 1997 May 1;8(7):843-9 [9143910.001]
  • [Cites] Virology. 1997 Oct 27;237(2):414-21 [9356352.001]
  • [Cites] J Mol Biol. 1998 Aug 21;281(3):475-83 [9698563.001]
  • [Cites] Hum Gene Ther. 1999 Apr 10;10(6):923-34 [10223726.001]
  • [Cites] Immunol Res. 2004;30(3):339-49 [15531774.001]
  • [Cites] Curr Pharm Biotechnol. 2004 Oct;5(5):451-8 [15544493.001]
  • [Cites] Blood. 2005 May 1;105(9):3707-13 [15626735.001]
  • [Cites] Cancer Gene Ther. 2000 Jan;7(1):91-6 [10678361.001]
  • (PMID = 16498428.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / BC / Z01 BC005598-16; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Virulence Factors; 80168379AG / Doxorubicin; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
  • [Other-IDs] NLM/ NIHMS7889; NLM/ PMC1482740
  •  go-up   go-down


80. Broët P, Tan P, Alifano M, Camilleri-Broët S, Richardson S: Finding exclusively deleted or amplified genomic areas in lung adenocarcinomas using a novel chromosomal pattern analysis. BMC Med Genomics; 2009;2:43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Finding exclusively deleted or amplified genomic areas in lung adenocarcinomas using a novel chromosomal pattern analysis.
  • BACKGROUND: Genomic copy number alteration (CNA) that are recurrent across multiple samples often harbor critical genes that can drive either the initiation or the progression of cancer disease.
  • We applied this model to a homogeneous series of 65 lung adenocarcinomas.
  • Most of the known oncogenes or tumor suppressor genes associated with lung adenocarcinoma were located within these areas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genome Res. 2006 Sep;16(9):1149-58 [16899652.001]
  • [Cites] Bioinformatics. 2006 Apr 15;22(8):911-8 [16455750.001]
  • [Cites] Int J Cancer. 2006 Mar 15;118(6):1556-64 [16187286.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9625-30 [15983384.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):338-41 [15549096.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Jul;25(3):195-204 [10379865.001]
  • [Cites] Genomics. 2007 May;89(5):647-53 [17276656.001]
  • [Cites] Nat Med. 2004 Aug;10(8):789-99 [15286780.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • (PMID = 19594952.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2718000
  •  go-up   go-down


81. Salcedo R, Worschech A, Cardone M, Jones Y, Gyulai Z, Dai RM, Wang E, Ma W, Haines D, O'hUigin C, Marincola FM, Trinchieri G: MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18. J Exp Med; 2010 Aug 2;207(8):1625-36
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.
  • [Title] MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18.
  • The inability of Myd88(-/-) mice to heal ulcers generated upon injury creates an altered inflammatory environment that induces early alterations in expression of genes encoding proinflammatory factors, as well as pathways regulating cell proliferation, apoptosis, and DNA repair, resulting in a dramatic increase in adenoma formation and progression to infiltrating adenocarcinomas with frequent clonal mutations in the beta-catenin gene.

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2000 Mar;24(3):227-35 [10700174.001]
  • [Cites] PLoS One. 2009;4(6):e6026 [19551144.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3581-6 [12097256.001]
  • [Cites] Clin Genet. 2009 Jul;76(1):1-18 [19659756.001]
  • [Cites] Cancer Cell. 2009 Sep 8;16(3):208-19 [19732721.001]
  • [Cites] Nat Rev Cancer. 2009 Nov;9(11):798-809 [19851315.001]
  • [Cites] Immunity. 2010 Mar 26;32(3):379-91 [20303296.001]
  • [Cites] Immunity. 2010 Mar 26;32(3):367-78 [20226691.001]
  • [Cites] Carcinogenesis. 2003 Jan;24(1):91-7 [12538353.001]
  • [Cites] Scand J Gastroenterol. 2003 Aug;38(8):837-44 [12940437.001]
  • [Cites] Cell. 2004 Jul 23;118(2):229-41 [15260992.001]
  • [Cites] Cell. 2004 Aug 6;118(3):285-96 [15294155.001]
  • [Cites] Eur J Immunol. 2004 Sep;34(9):2347-55 [15307167.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1790-2 [9065403.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):99-104 [15615857.001]
  • [Cites] J Gastroenterol. 2005 Jan;40(1):16-23 [15692785.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):695-702 [15765149.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 May;288(5):G1055-65 [15826931.001]
  • [Cites] Nat Med. 2005 Aug;11(8):845-52 [16041381.001]
  • [Cites] Gastroenterology. 2005 Sep;129(3):913-27 [16143131.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):2953-61 [16540643.001]
  • [Cites] J Exp Med. 2006 Jun 12;203(6):1391-7 [16717119.001]
  • [Cites] Nat Rev Immunol. 2006 Nov;6(11):836-48 [17063185.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):258-69 [17200722.001]
  • [Cites] Semin Nephrol. 2007 Jan;27(1):98-114 [17336692.001]
  • [Cites] Nature. 2007 Mar 29;446(7135):557-61 [17361131.001]
  • [Cites] Immunity. 2007 Apr;26(4):461-75 [17398123.001]
  • [Cites] Science. 2007 Jul 6;317(5834):121-4 [17615358.001]
  • [Cites] Science. 2007 Jul 6;317(5834):124-7 [17615359.001]
  • [Cites] Cell Cycle. 2007 Oct 1;6(19):2344-7 [17700066.001]
  • [Cites] World J Gastroenterol. 2007 Nov 14;13(42):5560-70 [17948929.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):1869-81 [18054559.001]
  • [Cites] J Clin Invest. 2007 Dec;117(12):3909-21 [18008007.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jan 15;105(2):652-6 [18178624.001]
  • [Cites] J Clin Invest. 2008 May;118(5):1727-38 [18431520.001]
  • [Cites] Am J Hum Genet. 2008 May;82(5):1202-10 [18439550.001]
  • [Cites] Curr Drug Targets. 2008 May;9(5):369-74 [18473764.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20858-63 [19075245.001]
  • [Cites] Cancer Cell. 2009 Feb 3;15(2):103-13 [19185845.001]
  • [Cites] Mol Med. 2000 Dec;6(12):1016-27 [11474118.001]
  • (PMID = 20624890.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / PHS HHS / / HHSN261200800001E; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Il18r1 protein, mouse; 0 / Interleukin-18; 0 / Interleukin-18 Receptor alpha Subunit; 0 / Myd88 protein, mouse; 0 / Myeloid Differentiation Factor 88; 0 / Receptors, Interleukin-1 Type I; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 6.5.1.- / DNA Repair Enzymes; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ PMC2916129
  •  go-up   go-down


82. Salaria SN, Illei P, Sharma R, Walter KM, Klein AP, Eshleman JR, Maitra A, Schulick R, Winter J, Ouellette MM, Goggins M, Hruban R: Palladin is overexpressed in the non-neoplastic stroma of infiltrating ductal adenocarcinomas of the pancreas, but is only rarely overexpressed in neoplastic cells. Cancer Biol Ther; 2007 Mar;6(3):324-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Palladin is overexpressed in the non-neoplastic stroma of infiltrating ductal adenocarcinomas of the pancreas, but is only rarely overexpressed in neoplastic cells.
  • DESIGN: Immunohistochemical labeling of tissue microarrays was used to define the patterns of palladin protein expression in 177 ductal adenocarcinomas of the pancreas.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Pathol. 2002 Jan;160(1):91-9 [11786403.001]
  • [Cites] J Gastrointest Surg. 2006 Nov;10(9):1199-210; discussion 1210-1 [17114007.001]
  • [Cites] PLoS Med. 2006 Dec;3(12):e516 [17194196.001]
  • [Cites] J Cell Sci. 2006 Mar 15;119(Pt 6):995-1004 [16492705.001]
  • [Cites] Am J Pathol. 2004 Mar;164(3):903-14 [14982844.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Mar;13(3):487-91 [15006928.001]
  • [Cites] FEBS Lett. 2004 May 21;566(1-3):30-4 [15147863.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):263-9 [9665487.001]
  • [Cites] Mod Pathol. 2005 Jun;18(6):779-87 [15791284.001]
  • [Cites] Int Rev Cytol. 2005;246:31-58 [16164966.001]
  • [Cites] Nat Genet. 2005 Oct;37(10):1099-103 [16142235.001]
  • [Cites] Lab Invest. 2005 Aug;85(8):1003-12 [15924149.001]
  • [Cites] FEBS J. 2006 Jan;273(1):26-33 [16367745.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):319-25 [17235047.001]
  • [Cites] J Cell Biochem. 2007 Apr 1;100(5):1288-300 [17115415.001]
  • [Cites] J Cell Biol. 2000 Aug 7;150(3):643-56 [10931874.001]
  • [Cites] Mol Biol Cell. 2001 Oct;12(10):3060-73 [11598191.001]
  • [Cites] Am J Hum Genet. 2002 Apr;70(4):1044-8 [11870593.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Feb 21;301(4):1038-44 [12589817.001]
  • [Cites] Am J Pathol. 2003 Jul;163(1):217-29 [12819026.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3735-42 [12839967.001]
  • [Cites] Oncogene. 2003 Aug 7;22(32):5021-30 [12902985.001]
  • [Cites] J Cell Sci. 2006 Aug 15;119(Pt 16):3316-24 [16868024.001]
  • (PMID = 17404500.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924-110011; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA062924-110011; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA062924-100011; United States / NCI NIH HHS / CA / CA90709; United States / NCI NIH HHS / CA / P50 CA062924-100011; United States / NCI NIH HHS / CA / R01 CA090709
  • [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 / Cytoskeletal Proteins; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / palladin protein, human
  • [Other-IDs] NLM/ NIHMS184318; NLM/ PMC3144721
  •  go-up   go-down


83. Han CP, Kok LF, Wang PH, Wu TS, Tyan YS, Cheng YW, Lee MY, Yang SF: Scoring of p16(INK4a) immunohistochemistry based on independent nuclear staining alone can sufficiently distinguish between endocervical and endometrial adenocarcinomas in a tissue microarray study. Mod Pathol; 2009 Jun;22(6):797-806
International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scoring of p16(INK4a) immunohistochemistry based on independent nuclear staining alone can sufficiently distinguish between endocervical and endometrial adenocarcinomas in a tissue microarray study.
  • Endocervical adenocarcinomas and endometrial adenocarcinomas are malignancies that affect uterus; however, their biological behaviors are quite different.
  • The purpose of this study is to evaluate four different scoring methods of p16(INK4a) immunohistochemical staining in distinguishing between primary endocervical adenocarcinomas and endometrial adenocarcinomas from limited sizes of tissue specimens.
  • A tissue microarray was constructed using formalin-fixed, paraffin-embedded tissue from hysterectomy specimens, including 14 endocervical adenocarcinomas and 21 endometrial adenocarcinomas.
  • Of the four scoring methods for p16(INK4a) expression, Method Nucleus, Method Dominant Cytoplasm or Nucleus, and Method Mean of Cytoplasm plus Nucleus showed significant (P values <0.05), but Method Cytoplasm did not show significant (P=0.432), frequency distinction between endocervical adenocarcinomas and endometrial adenocarcinomas.
  • According to the data in this tissue microarray study, Method Nucleus is the most convenient and efficient method to distinguish between endocervical adenocarcinomas and endometrial adenocarcinomas.
  • Method Cytoplasm is of no use in the diagnostic distinction between endocervical adenocarcinomas and endometrial adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / diagnosis. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Endometrial Neoplasms / diagnosis. Tissue Array Analysis. Uterine Cervical Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19347018.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
  •  go-up   go-down


84. Mazzer M, Zanon E, Foltran L, De Pauli F, Cardellino G, Iaiza E, Ermacora P, Aprile G, Fasola G: Second-line pemetrexed-oxaliplatin combination for advanced pancreatic adenocarcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e15597

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second-line pemetrexed-oxaliplatin combination for advanced pancreatic adenocarcinoma.
  • However, there is growing evidence suggesting that second-line treatment may provide further disease control in selected pts.
  • METHODS: Pancreatic cancer pts with advanced disease, PS>60, age>18 years, who progressed after a gemcitabine-based therapy were enrolled in a phase II trial, and treated with pemetrexed 500 mg/mq followed by oxaliplatin 120 mg/mq, day 1 every 3 weeks, together with adequate oral folinic acid and intramuscular vitamin B12 supplementation.
  • Three among the treated patients died within 30 days from last delivered cycle due to progressive disease.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962879.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


85. Zhang H, Zhao Q, Chen Y, Wang Y, Gao S, Mao Y, Li M, Peng A, He D, Xiao X: Selective expression of S100A7 in lung squamous cell carcinomas and large cell carcinomas but not in adenocarcinomas and small cell carcinomas. Thorax; 2008 Apr;63(4):352-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective expression of S100A7 in lung squamous cell carcinomas and large cell carcinomas but not in adenocarcinomas and small cell carcinomas.
  • The specific expression of this protein and its cellular distribution were investigated in 145 paraffin embedded lung cancer samples, six benign lung disease and 21 normal lung tissues by immunohistochemistry.
  • RESULTS: Specific expression of both S100A7 mRNA and protein was found in squamous cell carcinomas, adenosquamous carcinomas and large cell lung carcinomas, whereas neither was detected in adenocarcinomas or paired non-cancerous lung tissues.
  • Our most important finding is that elevated S100A7 protein could be detected in the sera of patients with squamous cell carcinomas.
  • CONCLUSION: S100A7 was only expressed in squamous cell carcinomas and large cell lung carcinomas and an increase in the level of S100A7 protein in serum may serve as a potential marker for lung cancer diagnosis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Calcium-Binding Proteins / metabolism. Carcinoma, Large Cell / diagnosis. Carcinoma, Squamous Cell / diagnosis. Lung Neoplasms / diagnosis. Neoplasm Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18364444.001).
  • [ISSN] 1468-3296
  • [Journal-full-title] Thorax
  • [ISO-abbreviation] Thorax
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Neoplasm Proteins; 0 / S100 Proteins; 0 / S100A7 protein, human
  •  go-up   go-down


86. von Rahden BH, Kircher S, Kafka M, Stuermer L, Reiber C, Gattenlöhner S, Germer CT, Grimm M: Glucocorticoid-induced TNFR family-related receptor (GITR)-expression in tumor infiltrating leucocytes (TILs) is associated with the pathogenesis of esophageal adenocarcinomas with and without Barrett's mucosa. Cancer Biomark; 2010;7(6):285-94
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucocorticoid-induced TNFR family-related receptor (GITR)-expression in tumor infiltrating leucocytes (TILs) is associated with the pathogenesis of esophageal adenocarcinomas with and without Barrett's mucosa.
  • BACKGROUND: Esophageal adenocarcinomas (EACs) arise due to gastroesophageal reflux, with Barrett's esophagus (BE) regarded as precancerous lesion.
  • METHODS: Immunohistochemical analysis of GITR expression was analyzed in esophageal cancer (n=70: 41 EAC with BE, 19 EAC without BE, and n=10 esophageal squamous-cell carcinomas, ESCC), the adenocarcinoma cell line OE-33, and peripheral blood leucocytes (PBLs) of EAC patients, furthermore in biopsies of BE without intraepithelial neoplasia (IN) (n=18).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Glucocorticoid-Induced TNFR-Related Protein / biosynthesis. Leukocytes / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21694467.001).
  • [ISSN] 1875-8592
  • [Journal-full-title] Cancer biomarkers : section A of Disease markers
  • [ISO-abbreviation] Cancer Biomark
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glucocorticoid-Induced TNFR-Related Protein
  •  go-up   go-down


87. Han CP, Lee MY, Tyan YS, Kok LF, Yao CC, Wang PH, Hsu JD, Tseng SW: p16 INK4 and CEA can be mutually exchanged with confidence between both relevant three-marker panels (ER/Vim/CEA and ER/Vim/p16 INK4) in distinguishing primary endometrial adenocarcinomas from endocervical adenocarcinomas in a tissue microarray study. Virchows Arch; 2009 Oct;455(4):353-61
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.
  • [Title] p16 INK4 and CEA can be mutually exchanged with confidence between both relevant three-marker panels (ER/Vim/CEA and ER/Vim/p16 INK4) in distinguishing primary endometrial adenocarcinomas from endocervical adenocarcinomas in a tissue microarray study.
  • The accurate distinction between primary endocervical adenocarcinomas (ECA) and endometrial adenocarcinomas (EMA) may require the use of multiple ancillary monoclonal antibodies in panels of immunohistochemistry stains.
  • CEA and p16(INK4) can be interchanged with confidence without significantly influencing the panel presentations and efficiencies in distinguishing between adenocarcinomas of endocervical and endometrial origin.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Carcinoembryonic Antigen / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Endometrial Neoplasms / diagnosis. Uterine Cervical Neoplasms / diagnosis


88. Sumikawa H, Johkoh T, Nagareda T, Sekiguchi J, Matsuo K, Fujita Y, Natsag J, Inoue A, Mihara N, Honda O, Tomiyama N, Minami M, Okumura M, Nakamura H: Pulmonary adenocarcinomas with ground-glass attenuation on thin-section CT: quantification by three-dimensional image analyzing method. Eur J Radiol; 2008 Jan;65(1):104-11
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] Pulmonary adenocarcinomas with ground-glass attenuation on thin-section CT: quantification by three-dimensional image analyzing method.
  • METHODS: The study included 49 patients with histologically diagnosed adenocarcinomas smaller than 2 cm in diameter.
  • [MeSH-major] Adenocarcinoma / radiography. Imaging, Three-Dimensional. Lung Neoplasms / radiography. Tomography, X-Ray Computed / methods

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17466475.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  •  go-up   go-down


89. Bonnetain F, Maillard E, Seitz J, Mitry E, Ychou M, Gasmi M, Raoul J, Mariette C, Bedenne L, Dahan L: Longitudinal analysis of quality of life (QoL) within a randomized phase III trial in patients (pts) with metastatic pancreatic adenocarcinoma (MPA). J Clin Oncol; 2009 May 20;27(15_suppl):e17544

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Longitudinal analysis of quality of life (QoL) within a randomized phase III trial in patients (pts) with metastatic pancreatic adenocarcinoma (MPA).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963761.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


90. Kelsen D, Jhawer M, Ilson D, Tse A, Randazzo J, Robinson E, Capanu M, Shah MA: Analysis of survival with modified docetaxel, cisplatin, fluorouracil (mDCF), and bevacizumab (BEV) in patients with metastatic gastroesophageal (GE) adenocarcinoma: Results of a phase II clinical trial. J Clin Oncol; 2009 May 20;27(15_suppl):4512

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of survival with modified docetaxel, cisplatin, fluorouracil (mDCF), and bevacizumab (BEV) in patients with metastatic gastroesophageal (GE) adenocarcinoma: Results of a phase II clinical trial.
  • : 4512 Background: Metastatic GE cancer is an aggressive disease with poor patient (pt) outcomes.
  • In 39 patients with measurable disease we observed 26 confirmed partial responses (67%, 95% CI 50%- 81%), and 12 (31%) stable disease.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962705.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


91. Dahan L, Methy N, Seitz J, Mitry E, Ychou M, Gasmi M, Raoul J, Mariette C, Bedenne L, Bonnetain F: Impact of first-line and second-line PFS definitions within a randomized phase III trial in patients (pts) with metastatic pancreatic adenocarcinoma (MPA). J Clin Oncol; 2009 May 20;27(15_suppl):e15583

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of first-line and second-line PFS definitions within a randomized phase III trial in patients (pts) with metastatic pancreatic adenocarcinoma (MPA).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962358.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


92. Hsu JD, Yao CC, Lee MY, Kok LF, Wang PH, Tyan YS, Han CP: True cytokeratin 8/18 immunohistochemistry is of no use in distinguishing between primary endocervical and endometrial adenocarcinomas in a tissue microarray study. Int J Gynecol Pathol; 2010 May;29(3):282-9
International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] True cytokeratin 8/18 immunohistochemistry is of no use in distinguishing between primary endocervical and endometrial adenocarcinomas in a tissue microarray study.
  • The choice of appropriate therapeutic plans for primary endocervical adenocarcinomas and endometrial adenocarcinomas depends on the site of origin of the tumor.
  • The purpose of this study was to make clear whether the immunohistochemistry of the true cytokeratin 8/18 monoclonal antibody (Leica Microsystems, Newcastle, United Kingdom), instead of CAM 5.2 (Becton Dickinson Biosciences, San Jose, CA), has potential use in distinguishing between endocervical adenocarcinomas and endometrial adenocarcinomas.
  • A tissue microarray was constructed using paraffin-embedded, formalin-fixed tissues from 34 hysterectomy specimens, including 14 endocervical adenocarcinomas and 20 endometrial adenocarcinomas.
  • The immunohistochemical expressions of all 3 markers, cytokeratin 8, 18, and 8/18 showed nonsignificant (P>0.05) frequency differences between the immunostaining results (positive vs. negative) in tumors of both gynecologic adenocarcinomas.
  • Although CAM 5.2 has been reported to be helpful in distinguishing between primary endocervical adenocarcinomas and endometrial adenocarcinomas, we could not verify this point of view using the true cytokeratin 8/18 monoclonal antibody (Leica Microsystems).
  • In conclusion, the true cytokeratin 8/18 monoclonal antibody is of no use in distinguishing between primary endocervical adenocarcinomas and endometrial adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Endometrial Neoplasms / metabolism. Keratin-18 / metabolism. Keratin-8 / metabolism. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Retrospective Studies. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • International Agency for Research on Cancer - Screening Group. diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20407331.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Keratin-18; 0 / Keratin-8
  •  go-up   go-down


93. Anagnostou V, Lowery F, Syrigos K, Frangia K, Zolota V, Panagopoulos N, Dougenis D, Tanoue L, Detterbeck F, Homer R, Rimm D: Association of expression of bcl-2 with outcome in non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e22039

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Tumors expressed BCL-2 in 57% and 53% of the cases in training and validation cohorts respectively and squamous cell carcinomas expressed higher levels of BCL-2 expression compared to adenocarcinomas (mean AQUA score 42 and 26 respectively, p=0.007); BCL-2 was not associated with other standard clinical or pathological characteristics.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963158.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


94. Zhong W, Yang X, Guo A, Su J, Zhang X, Chen H, Qiao G, Liao R, Yang J, Wu Y: Genetic evolution of EGFR and the clonal origin of adenocarcinomas exhibiting various degrees of bronchioloalveolar carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e22050

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic evolution of EGFR and the clonal origin of adenocarcinomas exhibiting various degrees of bronchioloalveolar carcinoma.
  • This study was performed to determine whether sequential adenocarcinoma with BAC features emerges in the lung field arises from a single clone or multiple clones in the same individual.
  • METHODS: Samples of adenocarcinomas exhibiting various degrees of BAC were obtained by thoracotomy.
  • RESULTS: Based on an analysis of EGFR in tumor specimens from 428 lung cancer patients, fifteen cases of sequential BAC-related adenocarcinoma obtained by thoracotomy were identified.
  • Together with alterations in BAC/adenocarcinoma components, the EGFR-TKI untreated series with at least one episode of EGFR-activating mutations represented three typical models: no significant EGFR evolution for a single clone, genetic alterations from mutant to wild-type EGFR for multifocal lesions, and a switch from wild-type to mutant EGFR, which might exhibit uncertain circumstances of cancer progression.
  • The single clone model indicates subsequent disease progression, whereas genetic alterations from mutations to wild-type EGFR are suggestive of secondary primary carcinoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963232.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


95. Yap JC, Yang GY, Fakih M, Mashtare T, Bullard Dunn K, Kuvshinoff BW, Smith J, Khushalani NI, Gibbs JF: Primary adenocarcinoma of the anus: a 22-year SEER population database analysis. J Clin Oncol; 2009 May 20;27(15_suppl):e15072

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary adenocarcinoma of the anus: a 22-year SEER population database analysis.
  • Adenocarcinoma (AdenoCa) is rare and accounts for approximately 10% of anal cancers.
  • All pts had single diagnosis of anal cancer with localized disease without nodal involvement.
  • This database lacks information on use of chemotherapy and local disease control.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964572.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


96. Bellizzi AM, Bloomston M, Bellizzi SM, Marsh WL, Frankel WL: Assessment of prognostic factors in pancreatic ductal adenocarcinoma: Focus on the retroperitoneal margin. J Clin Oncol; 2009 May 20;27(15_suppl):e15670

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of prognostic factors in pancreatic ductal adenocarcinoma: Focus on the retroperitoneal margin.
  • : e15670 Background: Pancreatic ductal adenocarcinoma (PDA) is a leading cause of cancer death in the West, with a nearly superimposable incidence and mortality.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962842.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


97. Seki M, Akasaka Y: Multiple lung adenocarcinomas and AAH treated by surgical resection. Lung Cancer; 2007 Feb;55(2):237-40
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] Multiple lung adenocarcinomas and AAH treated by surgical resection.
  • Atypical adenomatous hyperplasia (AAH) is often found in the lungs of patients with multiple primary lung adenocarcinoma; however, treatment for such patients has not been clearly defined.
  • This report presents a case of multiple primary lung adenocarcinoma with multiple AAH treated by surgery.
  • Thirteen tumorous lesions were resected; 10 lesions were diagnosed as primary lung adenocarcinoma and the others as AAH.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17118487.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  •  go-up   go-down


98. Siewert JR, Ott K: Are squamous and adenocarcinomas of the esophagus the same disease? Semin Radiat Oncol; 2007 Jan;17(1):38-44
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.
  • [Title] Are squamous and adenocarcinomas of the esophagus the same disease?
  • Esophageal cancer can be divided in squamous-cell cancer (SCC) and adenocarcinoma (Barrett cancer: AEG I) by histopathology.
  • [MeSH-major] Adenocarcinoma / therapy. Carcinoma, Squamous Cell / therapy. Esophageal Neoplasms / therapy

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17185196.001).
  • [ISSN] 1053-4296
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
  •  go-up   go-down


99. van Dieren JM, Wink JC, Vissers KJ, van Marion R, Hoogmans MM, Dinjens WN, Schouten WR, Tanke HJ, Szuhai K, Kuipers EJ, van der Woude CJ, van Dekken H: Chromosomal and microsatellite instability of adenocarcinomas and dysplastic lesions (DALM) in ulcerative colitis. Diagn Mol Pathol; 2006 Dec;15(4):216-22
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal and microsatellite instability of adenocarcinomas and dysplastic lesions (DALM) in ulcerative colitis.
  • Longstanding ulcerative colitis (UC) is associated with a high risk of developing UC-related colonic adenocarcinoma (UCC).
  • Immunohistochemical analysis of mismatch repair genes MLH1, PMS2, MSH2, and MSH6 showed negative immunostaining in 1 neoplasm (5%).
  • MSI of BAT25 and BAT26 was seen in 3 tumors (14%) including the neoplasm with aberrant immunostaining.
  • [MeSH-major] Adenocarcinoma / pathology. Chromosomal Instability. Colitis, Ulcerative / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Microsatellite Instability


100. Zhao ZR, Zhang ZY, Cui DS, Jiang L, Zhang HJ, Wang MW, Sun XF: Particularly interesting new cysteine-histidine rich protein expression in colorectal adenocarcinomas. World J Gastroenterol; 2006 Jan 14;12(2):298-301
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Particularly interesting new cysteine-histidine rich protein expression in colorectal adenocarcinomas.
  • METHODS: The expression of PINCH was examined by immumohistochemistry in 141 samples of primary colorectal adenocarcinoma and 92 normal samples of colorectal mucosa.
  • [MeSH-major] Adenocarcinoma / chemistry. Colorectal Neoplasms / chemistry. DNA-Binding Proteins / analysis

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2000 Jul 28;275(30):22607-10 [10801899.001]
  • [Cites] Neoplasia. 2004 Nov-Dec;6(6):796-801 [15720806.001]
  • [Cites] Cancer. 2002 Sep 15;95(6):1387-95 [12216108.001]
  • [Cites] Glia. 2003 Feb;41(3):213-23 [12528177.001]
  • [Cites] Cancer. 1976 Apr;37(4):1891-1900 [177180.001]
  • [Cites] Adv Cancer Res. 1988;50:159-96 [3287842.001]
  • [Cites] Cancer Res. 1991 Aug 15;51(16):4436-42 [1868464.001]
  • [Cites] Int J Cancer. 1991 Sep 9;49(2):220-3 [1652568.001]
  • [Cites] J Surg Oncol. 1992 Sep;51(1):60-4 [1325577.001]
  • [Cites] Am J Gastroenterol. 1994 May;89(5):665-9 [8172135.001]
  • [Cites] Am J Clin Pathol. 1996 May;105(5):604-12 [8623770.001]
  • [Cites] Cancer Lett. 1996 Jun 5;103(2):163-70 [8635153.001]
  • [Cites] Annu Rev Cell Dev Biol. 1995;11:379-416 [8689563.001]
  • [Cites] Annu Rev Cell Dev Biol. 1995;11:549-99 [8689569.001]
  • [Cites] J Pathol. 1996 May;179(1):15-9 [8691338.001]
  • [Cites] Am J Gastroenterol. 1996 Oct;91(10):2195-9 [8855747.001]
  • [Cites] Annu Rev Cell Dev Biol. 1996;12:463-518 [8970735.001]
  • [Cites] J Pathol. 1997 Aug;182(4):380-4 [9306957.001]
  • [Cites] Mol Biol Cell. 1998 Dec;9(12):3367-82 [9843575.001]
  • [Cites] J Cell Biol. 1999 Jan 11;144(1):45-57 [9885243.001]
  • [Cites] Mol Cell Biol. 1999 Mar;19(3):2425-34 [10022929.001]
  • [Cites] Int J Oncol. 1999 Jun;14(6):1057-61 [10339657.001]
  • [Cites] J Biol Chem. 2001 Feb 16;276(7):4932-9 [11078733.001]
  • (PMID = 16482633.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LIMS1 protein, human; 0 / Membrane Proteins
  • [Other-IDs] NLM/ PMC4066042
  •  go-up   go-down






Advertisement