[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 7399
1. Kanzaki H, Ouchida M, Hanafusa H, Yamamoto H, Suzuki H, Yano M, Aoe M, Imai K, Date H, Nakachi K, Shimizu K: The association between RAD18 Arg302Gln polymorphism and the risk of human non-small-cell lung cancer. J Cancer Res Clin Oncol; 2008 Feb;134(2):211-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association between RAD18 Arg302Gln polymorphism and the risk of human non-small-cell lung cancer.
  • Single nucleotide polymorphism (SNP) of arginine (Arg, CGA) or glutamine (Gln, CAA) at codon 302 is known on RAD18; however, the association between the SNP and the risk of any human cancers including non-small-cell lung cancer (NSCLC) has not been reported.
  • As to the relationship of the SNP with clinicopathological parameters of NSCLC, significantly higher risks were detected in lung squamous cell carcinoma (LSC) (OR = 4.40, 95% CI = 1.60-12.1).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. DNA-Binding Proteins / metabolism. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Aged. Alleles. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Case-Control Studies. Cohort Studies. Female. Genotype. Humans. Male. Polymerase Chain Reaction. Risk Factors. Ubiquitin-Protein Ligases



2. Al-Wadei HA, Takahashi T, Schuller HM: Growth stimulation of human pulmonary adenocarcinoma cells and small airway epithelial cells by beta-carotene via activation of cAMP, PKA, CREB and ERK1/2. Int J Cancer; 2006 Mar 15;118(6):1370-80
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth stimulation of human pulmonary adenocarcinoma cells and small airway epithelial cells by beta-carotene via activation of cAMP, PKA, CREB and ERK1/2.
  • An alpha-tocopherol, beta-carotene supplementation trial (ATBC) and a chemoprevention trial with beta-carotene and retinoids (CARET trial) were conducted in the 1990s in populations at risk for the development of lung cancer.
  • Both trials had to be discontinued due to significant increases in lung cancer and cardiovascular mortality.
  • Clinical trials to test the cancer preventive effects of beta-carotene are still ongoing, and high concentrations of this provitamin are contained in numerous dietary supplements.
  • Using a cell line derived from a human pulmonary adenocarcinoma (PAC) of Clara cell lineage and immortalized human small airway epithelial cells, our data show that low concentrations of beta-carotene that can be realistically expected in human tissues after oral administration caused a significant increase in intracellular cAMP and activated PKA, as well as in phosphorylation of ERK1/2 and CREB.
  • Control experiments with retinol also showed stimulation of cell proliferation and activation of PKA in both cell lines.
  • In light of the fact that PAC is the leading type of lung cancer, these findings suggest that the growth promoting effects of beta-carotene on this cancer type observed in our experiments may have contributed to the unfortunate outcome of the ATBC and CARET trials.
  • Our data challenge the widely accepted view that beta-carotene may be useful as a cancer preventive agent.
  • [MeSH-major] Cell Proliferation / drug effects. Cyclic AMP / metabolism. Cyclic AMP Response Element-Binding Protein / metabolism. Epithelial Cells / drug effects. Protein-Serine-Threonine Kinases / metabolism. beta Carotene / pharmacology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Analysis of Variance. Blotting, Western. Cell Line. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / metabolism. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Humans. Lung / cytology. Lung / drug effects. Lung / metabolism. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation / drug effects. Time Factors. Vitamins / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BETA-CAROTENE .
  • 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 = 16206275.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088809; United States / NCI NIH HHS / CA / R01 CA096128
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Vitamins; 01YAE03M7J / beta Carotene; E0399OZS9N / Cyclic AMP; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  •  go-up   go-down



3. Fujimoto N, Kiura K, Takigawa N, Fujiwara Y, Toyooka S, Umemura S, Tabata M, Ueoka H, Tanimoto M: Triplet chemotherapy with cisplatin, docetaxel, and irinotecan for patients with recurrent or refractory non-small cell lung cancer. Acta Med Okayama; 2010 Feb;64(1):33-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Triplet chemotherapy with cisplatin, docetaxel, and irinotecan for patients with recurrent or refractory non-small cell lung cancer.
  • We examined the feasibility of triplet chemotherapy using cisplatin, docetaxel, and irinotecan for patients with recurrent or refractory non-small cell lung cancer (NSCLC), retrospectively.
  • Most patients had performance status 1 (16/25), stage IV disease (18/25) and adenocarcinoma-histology (16/25).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / mortality. Adult. Aged. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / mortality. Carcinoma, Signet Ring Cell / drug therapy. Carcinoma, Signet Ring Cell / mortality. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / mortality. Cisplatin / administration & dosage. Cisplatin / adverse effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Quinazolines / administration & dosage. Quinazolines / adverse effects. Retrospective Studies. Survival Analysis. Taxoids / administration & dosage. Taxoids / adverse effects

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20200582.001).
  • [ISSN] 0386-300X
  • [Journal-full-title] Acta medica Okayama
  • [ISO-abbreviation] Acta Med. Okayama
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Quinazolines; 0 / Taxoids; 0H43101T0J / irinotecan; 15H5577CQD / docetaxel; Q20Q21Q62J / Cisplatin; S65743JHBS / gefitinib; XT3Z54Z28A / Camptothecin
  •  go-up   go-down



Advertisement
4. Wakelee HA, Chang ET, Gomez SL, Keegan TH, Feskanich D, Clarke CA, Holmberg L, Yong LC, Kolonel LN, Gould MK, West DW: Lung cancer incidence in never smokers. J Clin Oncol; 2007 Feb 10;25(5):472-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer incidence in never smokers.
  • PURPOSE: Lung cancer is a leading cause of cancer death worldwide.
  • Although smoking remains the predominant cause of lung cancer, lung cancer in never smokers is an increasingly prominent public health issue.
  • However, data on this topic, particularly lung cancer incidence rates in never smokers, are limited.
  • METHODS: We reviewed the existing literature on lung cancer incidence and mortality rates among never smokers and present new data regarding rates in never smokers from the following large, prospective cohorts: Nurses' Health Study; Health Professionals Follow-Up Study; California Teachers Study; Multiethnic Cohort Study; Swedish Lung Cancer Register in the Uppsala/Orebro region; and First National Health and Nutrition Examination Survey Epidemiologic Follow-Up Study.
  • RESULTS: Truncated age-adjusted incidence rates of lung cancer among never smokers age 40 to 79 years in these six cohorts ranged from 14.4 to 20.8 per 100,000 person-years in women and 4.8 to 13.7 per 100,000 person-years in men, supporting earlier observations that women are more likely than men to have non-smoking-associated lung cancer.
  • The distinct biology of lung cancer in never smokers is apparent in differential responses to epidermal growth factor receptor inhibitors and an increased prevalence of adenocarcinoma histology in never smokers.
  • CONCLUSION: Lung cancer in never smokers is an important public health issue, and further exploration of its incidence patterns, etiology, and biology is needed.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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).
  • 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] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):582-5 [15767333.001]
  • [Cites] J Clin Oncol. 2005 May 10;23(14):3175-85 [15886304.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5076-83 [15958551.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):123-32 [16014882.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):133-44 [16014883.001]
  • [Cites] J Epidemiol. 2005 Jun;15 Suppl 2:S134-9 [16127225.001]
  • [Cites] Cancer Causes Control. 2005 Nov;16(9):1009-19 [16184466.001]
  • [Cites] Lancet. 2005 Oct 29-Nov 4;366(9496):1527-37 [16257339.001]
  • [Cites] Carcinogenesis. 2005 Dec;26(12):2207-12 [16051642.001]
  • [Cites] J Clin Oncol. 2005 Nov 20;23(33):8396-405 [16293870.001]
  • [Cites] Ann Oncol. 2005 Dec;16(12):1906-14 [16219624.001]
  • [Cites] Mutat Res. 2005 Dec 30;592(1-2):45-57 [16009381.001]
  • [Cites] N Engl J Med. 2006 Jan 26;354(4):333-42 [16436765.001]
  • [Cites] Int J Cancer. 2006 Apr 1;118(7):1798-804 [16217766.001]
  • [Cites] Br J Cancer. 2006 Feb 13;94(3):450-4 [16434986.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1647-53 [16533793.001]
  • [Cites] J Clin Oncol. 2006 Apr 10;24(11):1700-4 [16505411.001]
  • [Cites] J Toxicol Environ Health A. 2006 Apr;69(7):533-97 [16608828.001]
  • [Cites] J Toxicol Environ Health A. 2006 Apr;69(7):633-54 [16608830.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):762-8 [16614121.001]
  • [Cites] J Natl Cancer Inst. 2006 May 17;98(10):691-9 [16705123.001]
  • [Cites] Oncol Rep. 2006 Jul;16(1):183-9 [16786144.001]
  • [Cites] Clin Lung Cancer. 2006 Jul;8(1):22-9 [16870042.001]
  • [Cites] Int J Cancer. 2006 Sep 15;119(6):1462-7 [16642467.001]
  • [Cites] Lung Cancer. 2005 Mar;47(3):351-9 [15713518.001]
  • [Cites] Am J Epidemiol. 2000 Feb 15;151(4):346-57 [10695593.001]
  • [Cites] BMJ. 2000 Aug 5;321(7257):323-9 [10926586.001]
  • [Cites] Epidemiology. 2000 Nov;11(6):673-9 [11055628.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 15;92(22):1812-23 [11078758.001]
  • [Cites] Br J Radiol. 2000 Dec;73(876):1252-9 [11205667.001]
  • [Cites] J Natl Cancer Inst. 2001 Feb 21;93(4):277-83 [11181774.001]
  • [Cites] Am J Epidemiol. 2001 Apr 15;153(8):807-14 [11296155.001]
  • [Cites] Int J Cancer. 2001 Nov15;94(4):591-3 [11745449.001]
  • [Cites] J Thorac Imaging. 2002 Jul;17(3):189-97 [12082370.001]
  • [Cites] Cancer Causes Control. 2002 Sep;13(7):625-35 [12296510.001]
  • [Cites] Curr Top Microbiol Immunol. 2003;275:225-48 [12596901.001]
  • [Cites] Int J Epidemiol. 2003 Feb;32(1):60-3 [12690010.001]
  • [Cites] J Epidemiol Community Health. 2004 Feb;58(2):156; author reply 156-7 [14729900.001]
  • [Cites] Int J Cancer. 2004 Mar10;109(1):125-31 [14735478.001]
  • [Cites] Br Med Bull. 2003;68:71-94 [14757710.001]
  • [Cites] Rev Environ Health. 2003 Oct-Dec;18(4):251-67 [15025189.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):826-34 [15173266.001]
  • [Cites] Chest. 2004 Aug;126(2):347-51 [15302716.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] Cancer. 2004 Sep 15;101(6):1428-36 [15368331.001]
  • [Cites] Br J Cancer. 2004 Oct 4;91(7):1280-6 [15292933.001]
  • [Cites] Cancer Causes Control. 2004 Oct;15(8):819-27 [15456995.001]
  • [Cites] Am J Epidemiol. 1990 Jun;131(6):1068-71 [2343859.001]
  • [Cites] Chest. 1992 Jan;101(1):19-25 [1729068.001]
  • [Cites] Comput Biol Med. 1992 Sep;22(5):351-61 [1424580.001]
  • [Cites] MMWR CDC Surveill Summ. 1994 Nov 18;43(3):1-43 [7969014.001]
  • [Cites] Cancer. 1995 Jan 1;75(1):29-33 [7804973.001]
  • [Cites] Cancer Lett. 1995 Jan 6;88(1):1-5 [7850764.001]
  • [Cites] Am J Epidemiol. 1995 Jun 1;141(11):1023-32 [7771438.001]
  • [Cites] Annu Rev Public Health. 1995;16:61-81 [7639884.001]
  • [Cites] Am J Epidemiol. 1996 Mar 15;143(6):535-42 [8610670.001]
  • [Cites] J Womens Health. 1997 Feb;6(1):49-62 [9065374.001]
  • [Cites] Int J Epidemiol. 1997 Apr;26(2):256-63 [9169159.001]
  • [Cites] Am J Epidemiol. 1997 Aug 1;146(3):231-43 [9247007.001]
  • [Cites] Cancer Causes Control. 1998 Mar;9(2):173-82 [9578294.001]
  • [Cites] Am J Epidemiol. 1998 Aug 1;148(3):259-62 [9690362.001]
  • [Cites] Am J Public Health. 1998 Oct;88(10):1503-9 [9772852.001]
  • [Cites] Am J Epidemiol. 1999 Jan 1;149(1):13-20 [9883789.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 21;91(8):675-90 [10218505.001]
  • [Cites] JAMA. 2004 Dec 22;292(24):2984-90 [15613666.001]
  • [Cites] Carcinogenesis. 2005 Feb;26(2):395-401 [15528218.001]
  • [Cites] BMJ. 2005 Jan 29;330(7485):223 [15613366.001]
  • [Cites] BMJ. 2005 Feb 5;330(7486):277 [15681570.001]
  • [CommentIn] J Clin Oncol. 2007 Feb 10;25(5):469-71 [17290053.001]
  • (PMID = 17290054.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA087969; United States / NCI NIH HHS / CA / P01 CA055075; United States / NCI NIH HHS / CA / R01 CA077398-09; United States / NCI NIH HHS / CA / CA087969-01; United States / NCI NIH HHS / CA / R01 CA077398; United States / NCI NIH HHS / CA / R01 CA77398; United States / NCI NIH HHS / CA / P01 CA087969-01; United States / NCI NIH HHS / PC / N01 PC035136-21-0-0; None / None / / N01 PC035136-21-0-0; United States / NCI NIH HHS / CA / CA055075-09S10001; United States / NCI NIH HHS / CA / P01 CA055075-09S10001
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS150119; NLM/ PMC2764546
  •  go-up   go-down



5. Singh A, Misra V, Thimmulappa RK, Lee H, Ames S, Hoque MO, Herman JG, Baylin SB, Sidransky D, Gabrielson E, Brock MV, Biswal S: Dysfunctional KEAP1-NRF2 interaction in non-small-cell lung cancer. PLoS Med; 2006 Oct;3(10):e420
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dysfunctional KEAP1-NRF2 interaction in non-small-cell lung cancer.
  • METHODS AND FINDINGS: Here we report a systematic analysis of the KEAP1 genomic locus in lung cancer patients and cell lines that revealed deletion, insertion, and missense mutations in functionally important domains of KEAP1 and a very high percentage of loss of heterozygosity at 19p13.2, suggesting that biallelic inactivation of KEAP1 in lung cancer is a common event.
  • Sequencing of KEAP1 in 12 cell lines and 54 non-small-cell lung cancer (NSCLC) samples revealed somatic mutations in KEAP1 in a total of six cell lines and ten tumors at a frequency of 50% and 19%, respectively.
  • Evaluation of loss of heterozygosity at 19p13.2 revealed allelic losses in 61% of the NSCLC cell lines and 41% of the tumor samples.
  • Decreased KEAP1 activity in cancer cells induced greater nuclear accumulation of NRF2, causing enhanced transcriptional induction of antioxidants, xenobiotic metabolism enzymes, and drug efflux pumps.
  • Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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] Cancer Res. 2000 Sep 1;60(17):4894-906 [10987304.001]
  • [Cites] Cell Death Differ. 2006 Oct;13(10):1763-75 [16485034.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1798-804 [11410522.001]
  • [Cites] Toxicol Appl Pharmacol. 2001 Jun 15;173(3):154-60 [11437637.001]
  • [Cites] Surg Today. 2001;31(10):936-8 [11759895.001]
  • [Cites] Cancer. 2001 Dec 1;92(11):2911-9 [11753966.001]
  • [Cites] Annu Rev Med. 2002;53:615-27 [11818492.001]
  • [Cites] Anal Biochem. 1969 Mar;27(3):502-22 [4388022.001]
  • [Cites] Cancer Res. 1985 Apr;45(4):1437-43 [2983882.001]
  • [Cites] Biochim Biophys Acta. 1989 Dec 17;989(2):163-77 [2557085.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5196-203 [12234984.001]
  • [Cites] Annu Rev Med. 2003;54:73-87 [12471176.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2003;43:233-60 [12359864.001]
  • [Cites] Cancer Res. 2003 Jan 15;63(2):312-8 [12543781.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Oct 24;310(3):824-9 [14550278.001]
  • [Cites] Nat Genet. 2003 Nov;35(3):238-45 [14517554.001]
  • [Cites] Oncogene. 2003 Dec 18;22(58):9275-81 [14681686.001]
  • [Cites] Curr Oncol Rep. 2004 Mar;6(2):116-22 [14751089.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2040-5 [14764894.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7130-9 [15282312.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Nov;41(3):250-6 [15334548.001]
  • [Cites] Trends Cell Biol. 2000 Jan;10(1):17-24 [10603472.001]
  • [Cites] J Natl Cancer Inst. 1993 Jun 2;85(11):897-901 [8098377.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4313-20 [8044778.001]
  • [Cites] Genes Chromosomes Cancer. 1998 Apr;21(4):308-19 [9559342.001]
  • [Cites] Prostate. 1999 Jan 1;38(1):46-54 [9973109.001]
  • [Cites] J Clin Invest. 2004 Nov;114(9):1248-59 [15520857.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(24):10941-53 [15572695.001]
  • [Cites] Int J Oncol. 2005 Jan;26(1):201-10 [15586241.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(3):1089-99 [15657435.001]
  • [Cites] Curr Opin Pulm Med. 2005 Jul;11(4):287-91 [15928493.001]
  • [Cites] J Exp Med. 2005 Jul 4;202(1):47-59 [15998787.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Oct;2(10):518-25 [16205771.001]
  • [Cites] Mol Cell. 2006 Mar 3;21(5):689-700 [16507366.001]
  • [Cites] J Clin Invest. 2006 Apr;116(4):984-95 [16585964.001]
  • [Cites] Biochem J. 2006 May 1;395(3):599-609 [16426233.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3410-5 [11248092.001]
  • (PMID = 17020408.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES 038819; United States / NHLBI NIH HHS / HL / R01 HL081205-03; United States / NHLBI NIH HHS / HL / R01 HL081205; United States / NCI NIH HHS / CA / P50 CA058184; United States / NHLBI NIH HHS / HL / HL081205; United States / NHLBI NIH HHS / HL / HL081205-03
  • [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 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human
  • [Other-IDs] NLM/ PMC1584412
  •  go-up   go-down



6. Ohtsubo K, Watanabe H, Yamada T, Tsuchiyama T, Mouri H, Yamashita K, Yasumoto K, Ikeda H, Nakanuma Y, Yano S: Cancer of unknown primary site in which tumor marker-oriented chemotherapy was effective and pancreatic cancer was finally confirmed at autopsy. Intern Med; 2009;48(18):1651-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer of unknown primary site in which tumor marker-oriented chemotherapy was effective and pancreatic cancer was finally confirmed at autopsy.
  • We report a 47-year-old man with cancer of unknown primary site in whom pancreatic cancer was confirmed at autopsy.
  • Although a primary lesion was not confirmed, we planned to perform tumor marker-oriented chemotherapy because pancreatic cancer was suspected as the primary lesion based on tumor markers and pathological findings from metastatic lymph node.
  • Microscopic examination at autopsy revealed poorly differentiated adenocarcinoma in the pancreatic head, although a pancreatic mass was not clear macroscopically.
  • [MeSH-major] Neoplasms, Unknown Primary / diagnosis. Neoplasms, Unknown Primary / drug therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Antigens, Neoplasm / metabolism. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Autopsy. Biomarkers, Tumor / metabolism. Cisplatin / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Lung Neoplasms / diagnosis. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19755768.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DU-PAN-2 antigen, human; 0 / pancreatic associated antigen, SPan-1; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin
  •  go-up   go-down



7. Cassoni P, Daniele L, Maldi E, Righi L, Tavaglione V, Novello S, Volante M, Scagliotti GV, Papotti M: Caveolin-1 expression in lung carcinoma varies according to tumour histotype and is acquired de novo in brain metastases. Histopathology; 2009 Jul;55(1):20-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Caveolin-1 expression in lung carcinoma varies according to tumour histotype and is acquired de novo in brain metastases.
  • AIMS: To study caveolin-1 (Cav-1) expression in metastatic lung carcinomas.
  • METHODS AND RESULTS: Cav-1 expression was investigated in a series of 121 lung carcinomas and it was shown that 18/121 tumours (14.9%) were Cav-1+.
  • None of the pure bronchioloalveolar carcinomas proved to be positive, vs. 42.8% of the large cell carcinomas (neuroendocrine subtype excluded).
  • Adenocarcinomas (8.5%), large cell neuroendocrine carcinomas (20%) and squamous cell carcinomas (29.6%) displayed an intermediate percentage of positive cases, suggesting a gradient of Cav-1 expression according to tumour histotype-related aggressiveness.
  • Moreover, the percentage of Cav-1+ tumours with distant metastases was almost double that of non-metastatic tumours (17.8% vs. 8.1%), irrespective of the histotype.
  • In 34 tumours metastatic to the brain, primary and secondary lesions were compared and 53% of brain metastases were Cav-1+ vs. 20.6% of primaries, indicating a de novo acquisition of Cav-1 expression.
  • CONCLUSIONS: Cav-1 immunoreactivity in lung carcinoma is histotype-dependent and acquired de novo in brain metastases, suggesting a site-specific phenotypic shift in secondary lesions.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Carcinoma, Large Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Caveolin 1 / metabolism. Lung Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • (PMID = 19614763.001).
  • [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 / Caveolin 1; 0 / DNA, Neoplasm; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down



8. Peng Z, Shan C, Wang H: [Value of promoter methylation of RASSF1A, p16, and DAPK genes in induced sputum in diagnosing lung cancers]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2010 Mar;35(3):247-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Value of promoter methylation of RASSF1A, p16, and DAPK genes in induced sputum in diagnosing lung cancers].
  • OBJECTIVE: To determine the aberrant methylation status of RASSF1A,p16 and DAPK gene promoter region in induced sputum from lung cancer patients and the value of their combined detection in diagnosing lung cancers.
  • METHODS: Methylation-specific PCR (MSP) was used to detect the promoter methylation status of RASSF1A, p16, and DAPK genes in induced sputum and pathological tissues from 82 patients with lung cancers and 25 patients with pulmonary benign lesion.
  • RESULTS: The positive rates of promoter methylation of RASSF1A, p16, and DAPK genes in pathological tissues from patients with lung cancers were 63.4%, 59.8%, and 58.5%, respectively,and those in induced sputum were 54.9%, 48.8%, and 51.2%, respectively.
  • The promoter methylation of RASSF1A,p16, and DAPK genes were not detected in patients with pulmonary benign lesion.
  • There was a significant difference between the lung cancer group and pulmonary benign lesion group (P<0.05).
  • The methylation rate of RASSF1A gene was significantly lower in the middle and high differentiation and non-metastastic lymph node of lung cancer tissues than that in the poor differentiation and the metastatic lymph node of lung cancer tissues(P<0.05), and was not correlated with age, sex, smoking index, clinical stage, and pathological types.The methylation rate of p16, and DAPK genes was not significantly correlated with all the above mentioned factors (P>0.05).
  • CONCLUSION: Joint detection for promoter hypermethylation of RASSF1A, p16, and DAPK genes in induced sputum may be used as a simple and effective index of the diagnosis and prognose of lung cancers, and can improve the positive rate.
  • [MeSH-major] Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Lung Neoplasms / diagnosis. Sputum / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Aged. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / genetics. DNA Methylation. Death-Associated Protein Kinases. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Promoter Regions, Genetic / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20360646.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  •  go-up   go-down



9. Sithanandam G, Smith GT, Fields JR, Fornwald LW, Anderson LM: Alternate paths from epidermal growth factor receptor to Akt in malignant versus nontransformed lung epithelial cells: ErbB3 versus Gab1. Am J Respir Cell Mol Biol; 2005 Nov;33(5):490-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alternate paths from epidermal growth factor receptor to Akt in malignant versus nontransformed lung epithelial cells: ErbB3 versus Gab1.
  • In many human lung adenocarcinoma cell lines, a pathway involving epidermal growth factor receptor (EGFR), ErbB2 and ErbB3 receptors, phosphatidyl inositol 3-kinase (PI3K), Akt, glycogen synthase kinase 3-beta (GSK3-beta), and cyclin D1 controls cell growth, survival, and invasiveness.
  • We have investigated this pathway in paired transformed/nontransformed cell lines from murine peripheral lung epithelium, E9/E10 and A5/C10.
  • The E9 and A5 carcinoma lines expressed ErbB3 and transforming growth factor-alpha (TGF-alpha) and responded to TGF-alpha stimulation with protein complex formation including the p85 regulatory subunit of PI3K, activation of Akt, phosphorylation of GSK3-beta, and increased cyclin D1 protein and the cell cycle.
  • ErbB3 and TGF-alpha were not detected in the nontransformed E10 and C10 cell lines.
  • Nevertheless, exposure of E10 or C10 cells to TGF-alpha activated PI3K and Akt and increased cyclin D1 and cell growth.
  • Thus, alternate pathways downstream of EGFR regulate mitosis in these paired malignant versus nontransformed lung cell lines.



10. Lee EB, Jeon HS, Yoo SS, Choi YY, Kang HG, Cho S, Cha SI, Choi JE, Park TI, Lee BH, Park RW, Kim IS, Kang YM, Kim CH, Jheon S, Jung TH, Park JY: Polymorphisms in apoptosis-related genes and survival of patients with early-stage non-small-cell lung cancer. Ann Surg Oncol; 2010 Oct;17(10):2608-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphisms in apoptosis-related genes and survival of patients with early-stage non-small-cell lung cancer.
  • PURPOSE: This study was conducted to determine the association between single-nucleotide polymorphisms (SNPs) in apoptosis-related genes and survival outcomes of patients with early-stage non-small-cell lung cancer (NSCLC).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Intracellular Signaling Peptides and Proteins / genetics. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. Receptors, Tumor Necrosis Factor, Type I / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / mortality. Carcinoma, Squamous Cell / pathology. DNA, Neoplasm / genetics. Female. Genotype. Humans. Male. Middle Aged. Neoplasm Staging. Polymerase Chain Reaction. Prognosis. Survival Rate

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20422457.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Repressor Proteins; 0 / TNFRSF10B protein, human; 0 / TNFRSF1A protein, human
  •  go-up   go-down



11. Matsuoka K, Sumitomo S, Nakashima N, Nakajima D, Misaki N: Prognostic value of carcinoembryonic antigen and CYFRA21-1 in patients with pathological stage I non-small cell lung cancer. Eur J Cardiothorac Surg; 2007 Sep;32(3):435-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of carcinoembryonic antigen and CYFRA21-1 in patients with pathological stage I non-small cell lung cancer.
  • BACKGROUND: The aim of this retrospective study was to assess the prognostic value of serum tumor markers (carcinoembryonic antigen (CEA) and CYFRA21-1) in patients with pathologic (p-) stage I non-small cell lung cancer (NSCLC) undergoing complete resection.
  • Patients who had received preoperative chemotherapy or radiotherapy were excluded, as were patients who had multiple malignancies including multiple lung cancer.
  • RESULTS: The histological classification was adenocarcinoma in 193 patients, squamous cell carcinoma in 71, large cell carcinoma in 5, and other histological type in 6.
  • The positive ratio of CEA and CYFRA21-1 was 25.7% and 13.7%, respectively, and in relation to histological type was 27.8% and 7.8% in adenocarcinoma, and 20.6% and 28.4% in squamous cell carcinoma.
  • In patients with adenocarcinoma, a CEA level above 5.0 ng/ml was associated with shorter survival and early recurrence, whereas CYFRA21-1 showed no such association.
  • In patients with squamous cell carcinoma, elevated preoperative CEA was not related to survival and recurrence.
  • In these patients, preoperative CYFRA21-1 level exceeding 2.8 ng/ml was associated with a poorer outcome, whereas preoperative CYFRA21-1 level was not associated with cancer recurrence.
  • CONCLUSION: The patients with p-stage I adenocarcinoma whose preoperative CEA level was high might be considered as good candidates for adjuvant chemotherapy.
  • [MeSH-major] Antigens, Neoplasm / blood. Biomarkers, Tumor / blood. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Keratins / blood. Lung Neoplasms / blood
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Keratin-19. Male. Middle Aged. Prognosis. Pulmonary Surgical Procedures. Regression Analysis. Retrospective Studies. Survival Analysis

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17611117.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / antigen CYFRA21.1; 68238-35-7 / Keratins
  •  go-up   go-down



12. Balendiran GK: Fibrates in the chemical action of daunorubicin. Curr Cancer Drug Targets; 2009 May;9(3):366-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Natural product, daunorubicin a toxic analogue of anthracycline is reduced to less toxic daunorubicinol by the AKR1B10, enzyme, which is overexpressed in most cases of smoking associate squamous cell carcinoma (SCC) and adenocarcinoma.
  • In addition, AKR1B10 was discovered as an enzyme overexpressed in human liver, cervical and endometrial cancer cases in samples from uterine cancer patients.
  • Also, the expression of AKR1B10 was associated with tumor recurrence after surgery and keratinization of squamous cell carcinoma in cervical cancer and estimated to have the potential as a tumor intervention target colorectal cancer cells (HCT-8) and diagnostic marker for non-small-cell lung cancer.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • 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 = 19442055.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R15 DK085496
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 53PF01Q249 / Clofibric Acid; EC 1.1.1.- / AKR1B10 protein, human; EC 1.1.1.21 / Aldehyde Reductase; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 39
  •  go-up   go-down



13. Takeda S, Funakoshi Y, Kadota Y, Koma M, Maeda H, Kawamura S, Matsubara Y: Fall in diffusing capacity associated with induction therapy for lung cancer: a predictor of postoperative complication? Ann Thorac Surg; 2006 Jul;82(1):232-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fall in diffusing capacity associated with induction therapy for lung cancer: a predictor of postoperative complication?
  • BACKGROUND: Pulmonary resection after induction therapy is associated with high rates of pulmonary morbidity and mortality.
  • However, the impact of induction therapy on the pulmonary toxicity and associated pulmonary complications has not been fully investigated in the setting of lung cancer surgery.
  • METHODS: We assessed the 66 consecutive patients who underwent a pulmonary resection after induction therapy, 48 of whom received chemoradiotherapy and 18, chemotherapy alone.
  • Results of pulmonary function before and after induction therapy were compared, and logistic regression analyses utilized to explore the risk factors of pulmonary morbidity.
  • The diffusing capacity of lung for carbon monoxide (D(LCO)) was decreased significantly by 21% (from 90.3% +/- 18.3% to 71.1% +/- 12.5%; p < 0.0005).
  • Univariate and multivariate analyses revealed that predicted postoperative %D(LCO) alone was an independent factor to predict postoperative pulmonary morbidity.
  • CONCLUSIONS: For patients who undergo a pulmonary resection after induction therapy, predicted postoperative %D(LCO) is more important to predict pulmonary morbidity rather than static pulmonary function (predicted postoperative %VC or %FEV1).
  • We believe that the impact of diffusion limitation after induction therapy should to be emphasized to decrease the pulmonary morbidity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / physiopathology. Lung Neoplasms / physiopathology. Pneumonectomy. Postoperative Complications / epidemiology. Pulmonary Diffusing Capacity
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / physiopathology. Adenocarcinoma / radiotherapy. Adenocarcinoma / surgery. Aged. Anoxia / etiology. Carbon Monoxide / analysis. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / physiopathology. Carcinoma, Large Cell / radiotherapy. Carcinoma, Large Cell / surgery. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / physiopathology. Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / surgery. Cisplatin / administration & dosage. Combined Modality Therapy. Empyema, Pleural / etiology. Female. Forced Expiratory Volume. Forecasting. Humans. Male. Middle Aged. Mitomycin / administration & dosage. Pneumonia / etiology. Predictive Value of Tests. Pulmonary Atelectasis / etiology. Pulmonary Embolism / etiology. Pulmonary Embolism / mortality. Pulmonary Gas Exchange. Radiotherapy / adverse effects. Remission Induction. Respiratory Distress Syndrome, Adult / etiology. Respiratory Distress Syndrome, Adult / mortality. Respiratory Insufficiency / etiology. Retrospective Studies. Risk Factors. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives. Vindesine / administration & dosage. Vital Capacity

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • Hazardous Substances Data Bank. VINDESINE .
  • Hazardous Substances Data Bank. Carbon monoxide .
  • Hazardous Substances Data Bank. VINORELBINE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16798220.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 5V9KLZ54CY / Vinblastine; 7U1EE4V452 / Carbon Monoxide; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine; RSA8KO39WH / Vindesine
  •  go-up   go-down



14. Sullivan JP, Spinola M, Dodge M, Raso MG, Behrens C, Gao B, Schuster K, Shao C, Larsen JE, Sullivan LA, Honorio S, Xie Y, Scaglioni PP, DiMaio JM, Gazdar AF, Shay JW, Wistuba II, Minna JD: Aldehyde dehydrogenase activity selects for lung adenocarcinoma stem cells dependent on notch signaling. Cancer Res; 2010 Dec 1;70(23):9937-48
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aldehyde dehydrogenase activity selects for lung adenocarcinoma stem cells dependent on notch signaling.
  • Aldehyde dehydrogenase (ALDH) is a candidate marker for lung cancer cells with stem cell-like properties.
  • Immunohistochemical staining of a large panel of primary non-small cell lung cancer (NSCLC) samples for ALDH1A1, ALDH3A1, and CD133 revealed a significant correlation between ALDH1A1 (but not ALDH3A1 or CD133) expression and poor prognosis in patients including those with stage I and N0 disease.
  • Flow cytometric analysis of a panel of lung cancer cell lines and patient tumors revealed that most NSCLCs contain a subpopulation of cells with elevated ALDH activity, and that this activity is associated with ALDH1A1 expression.
  • Isolated ALDH(+) lung cancer cells were observed to be highly tumorigenic and clonogenic as well as capable of self-renewal compared with their ALDH(-) counterparts.
  • Suppression of the Notch pathway by treatment with either a γ-secretase inhibitor or stable expression of shRNA against NOTCH3 resulted in a significant decrease in ALDH(+) lung cancer cells, commensurate with a reduction in tumor cell proliferation and clonogenicity.
  • Therapeutic targeting of the Notch pathway reduces this ALDH(+) component, implicating Notch signaling in lung cancer stem cell maintenance.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Metastasis Rev. 2010 Mar;29(1):61-72 [20094757.001]
  • [Cites] Cancer Res. 2010 Feb 15;70(4):1469-78 [20145124.001]
  • [Cites] Cancer Res. 2010 Aug 15;70(16):6477-85 [20663904.001]
  • [Cites] J Natl Cancer Inst. 2010 Sep 8;102(17):1310-21 [20679594.001]
  • [Cites] Am J Respir Crit Care Med. 2007 Mar 15;175(6):547-53 [17158280.001]
  • [Cites] J Thorac Oncol. 2006 Mar;1(3):231-9 [17409862.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4827-33 [17510412.001]
  • [Cites] Cytometry B Clin Cytom. 2007 Jul;72(4):281-9 [17111384.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1423-30 [17476279.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7954-9 [17804701.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8051-7 [17804716.001]
  • [Cites] Int J Cancer. 2008 Feb 15;122(4):761-8 [17955491.001]
  • [Cites] Cell Death Differ. 2008 Mar;15(3):504-14 [18049477.001]
  • [Cites] Lung Cancer. 2008 Mar;59(3):340-9 [17920722.001]
  • [Cites] Cancer Res. 2008 Mar 15;68(6):1820-5 [18339862.001]
  • [Cites] J Clin Invest. 2008 Jun;118(6):2111-20 [18497886.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):755-68 [18784658.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393.001]
  • [Cites] Mol Cancer. 2008;7:87 [19025616.001]
  • [Cites] Cancer Res. 2009 Feb 1;69(3):845-54 [19176379.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3249-62 [11751631.001]
  • [Cites] Dev Biol. 2002 May 1;245(1):42-56 [11969254.001]
  • [Cites] Oncogene. 2003 Apr 3;22(13):1988-97 [12673204.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):357-64 [15288261.001]
  • [Cites] Cancer Gene Ther. 1996 Jan-Feb;3(1):24-30 [8785707.001]
  • [Cites] J Cell Biochem Suppl. 1996;24:32-91 [8806092.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3555-61 [15867348.001]
  • [Cites] Stem Cells. 2005 Jun-Jul;23(6):752-60 [15917471.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):1883-90; discussion 1895-6 [16488983.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1111-5 [16564000.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11707-12 [16857736.001]
  • [Cites] Mol Imaging. 2004 Apr;3(2):117-24 [15296676.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7445-52 [16885340.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):823-6 [16799564.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):181-6 [17185413.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Stem Cells. 2007 Mar;25(3):807-15 [17158237.001]
  • [Cites] Mol Cancer Res. 2009 Mar;7(3):330-8 [19276181.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3382-9 [19336570.001]
  • [Cites] Br J Cancer. 2009 Jun 16;100(12):1879-88 [19513078.001]
  • [Cites] Int J Cancer. 2010 Feb 15;126(4):950-8 [19676044.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):709-18 [20068161.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):632-8 [20068176.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Dec 29;106(52):22293-8 [20007775.001]
  • [Cites] Cell Stem Cell. 2010 Jul 2;7(1):127-33 [20621056.001]
  • (PMID = 21118965.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA070907-13; United States / NCI NIH HHS / CA / P50 CA070907-14; United States / NCI NIH HHS / CA / P50 CA070907-12; United States / NCI NIH HHS / CA / CA070907-12; United States / NCI NIH HHS / CA / P50CA70907; United States / NCI NIH HHS / CA / P50 CA070907-13; None / None / / P50 CA070907-11; United States / NCI NIH HHS / CA / U24 CA126608-05; United States / NCI NIH HHS / CA / P50 CA070907-11; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / U24 CA126608
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH3 protein, human; 0 / Receptors, Notch; EC 1.2.1.3 / ALDH1A1 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Other-IDs] NLM/ NIHMS244831; NLM/ PMC3058307
  •  go-up   go-down



15. Wagner M, Besse B, Balleyguier C, Soria JC: Leptomeningeal and medullary response to second-line erlotinib in lung adenocarcinoma. J Thorac Oncol; 2008 Jun;3(6):677-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leptomeningeal and medullary response to second-line erlotinib in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / pathology. Meningeal Neoplasms / secondary. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
  • [MeSH-minor] Cerebrospinal Fluid / cytology. Diagnosis, Differential. Dose-Response Relationship, Drug. Erlotinib Hydrochloride. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18520813.001).
  • [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] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down



16. Zhou XF, Coburn RA, Morris ME: Effects of new 4-aryl-1,4-dihydropyridines and 4-arylpyridines on drug efflux mediated by multidrug resistance-associated protein 1. J Pharm Sci; 2005 Oct;94(10):2256-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A [3H]vinblastine accumulation study was conducted in human small cell lung cancer H69AR (overexpressing MRP1) and wild type H69 cells.
  • Daunomycin accumulation studies, determined using a flow cytometric assay, were also performed in H69AR and human pancreatic adenocarcinoma Panc-1 cells and the results were highly correlated with those obtained from the [3H]vinblastine accumulation studies.
  • [MeSH-minor] Cell Line, Tumor / drug effects. Cell Survival / drug effects. Daunorubicin / toxicity. Drug Interactions. Drug Resistance, Multiple / drug effects. Glutathione / metabolism. Humans. Inhibitory Concentration 50. Time Factors. Vinblastine / metabolism

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • 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) 2005 Wiley-Liss, Inc. and the American Pharmacists Association
  • (PMID = 16136554.001).
  • [ISSN] 0022-3549
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dihydropyridines; 0 / Multidrug Resistance-Associated Proteins; 0 / Pyridines; 0 / multidrug resistance-associated protein 1; 5V9KLZ54CY / Vinblastine; GAN16C9B8O / Glutathione; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down



17. McKenna RJ Jr: New approaches to the minimally invasive treatment of lung cancer. Cancer J; 2005 Jan-Feb;11(1):73-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New approaches to the minimally invasive treatment of lung cancer.
  • Diagnoses were as follows: benign disease (53), pulmonary met (27), Lymphoma (5) and lung cancer (1015).
  • 641 (63.1%) of the primary lung cancers were adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Carcinoma, Non-Small-Cell Lung / surgery. Laparoscopy / methods. Lung Neoplasms / surgery. Pneumonectomy / methods. Postoperative Complications



18. Stojsic J, Radojicic J, Markovic J, Milenkovic B, Maric D, Adzic T, Milovanovic I: Gender and age trends of histological types of lung cancer in a 20-year period: pathological perspective. J BUON; 2010 Jan-Mar;15(1):136-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gender and age trends of histological types of lung cancer in a 20-year period: pathological perspective.
  • PURPOSE: To find out the trends of distribution in different histological types of lung cancer in both genders in a period of 20 years.
  • METHODS: The most frequent histological types of lung cancer in tissue specimens obtained by bronchoscopy or percutaneous needle biopsy were analysed in terms of age and gender.
  • RESULTS: Squamous cell carcinoma (SCC) prevailed in the total number of patients in all investigated years (58.0%), and separately in male (60.4%) and female (45.7%) patients.
  • Continuous campaign against smoking and helping its cessation, improving working and socioeconomic conditions is a strategy for decreasing all histological types of lung cancer patients.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / pathology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / epidemiology. Lung Neoplasms / pathology. Small Cell Lung Carcinoma / epidemiology. Small Cell Lung Carcinoma / pathology

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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 = 20414941.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down



19. Movsas B, Scott C, Watkins-Bruner D: Pretreatment factors significantly influence quality of life in cancer patients: a Radiation Therapy Oncology Group (RTOG) analysis. Int J Radiat Oncol Biol Phys; 2006 Jul 1;65(3):830-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pretreatment factors significantly influence quality of life in cancer patients: a Radiation Therapy Oncology Group (RTOG) analysis.
  • PURPOSE: The purpose of this analysis was to assess the impact of pretreatment factors on quality of life (QOL) in cancer patients.
  • METHODS AND MATERIALS: Pretreatment QOL (via Functional Assessment of Cancer Therapy [FACT], version 2) was obtained in 1,428 patients in several prospective Radiation Therapy Oncology Group (RTOG) trials including nonmetastatic head-and-neck (n = 1139), esophageal (n = 174), lung (n = 51), rectal (n = 47), and prostate (n = 17) cancer patients.
  • The potentially devastating impact of a cancer diagnosis, particularly in young and minority patients, must be addressed.
  • [MeSH-minor] Adenocarcinoma / radiotherapy. Adult. Aged. Carcinoma, Squamous Cell / radiotherapy. Esophageal Neoplasms / radiotherapy. Female. Head and Neck Neoplasms / radiotherapy. Humans. Karnofsky Performance Status. Lung Neoplasms / radiotherapy. Male. Middle Aged. Multivariate Analysis. Prospective Studies. Prostatic Neoplasms / radiotherapy. Randomized Controlled Trials as Topic. Rectal Neoplasms / radiotherapy. Socioeconomic Factors. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16564646.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down



20. Tian Q, Chen LA, Wang HS, Zhu BH, Tian L, Yang Z, An Y: Endobronchial ultrasound-guided transbronchial needle aspiration of undiagnosed mediastinal lymphadenopathy. Chin Med J (Engl); 2010 Aug;123(16):2211-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: EBUS-TBNA was diagnostic in 33 (63%) patients, with diagnosis of lung cancer in 23 patients (14 patients of small cell lung cancer, eight patients with adenocarcinoma, and one patient of squamous carcinoma).
  • One patient with negative EBUS-TBNA results died of cancer cachexia.
  • The sensitivity, specificity, and positive and negative predictive value of EBUS-TBNA for the diagnosis of neoplastic disease were 85%, 100%, 100%, and 50% respectively.
  • The sensitivity, specificity, and positive and negative predictive value of EBUS-TBNA for the diagnosis of sarcoidosis were 56%, 100%, 100%, and 13%, respectively.
  • Five patients with no definite diagnosis from EBUS-TNBA examination are under close follow-up.
  • It also adds pathological information needed to make the diagnosis of sarcoidosis.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Endosonography / methods. Lung Neoplasms / diagnosis. Lymphatic Diseases / diagnosis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lymphatic Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20819667.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  •  go-up   go-down



21. De Petris L, Migliorino MR, Ceribelli A, Martelli O, Di Molfetta M, Mancuso A, De Santis S, Di Salvia R, De Marinis F: Docetaxel administered every two weeks as second-line chemotherapy for advanced non-small cell lung cancer: a phase II study. Anticancer Res; 2005 Nov-Dec;25(6C):4713-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel administered every two weeks as second-line chemotherapy for advanced non-small cell lung cancer: a phase II study.
  • BACKGROUND: The aim of this phase II study was to evaluate efficacy and toxicity of single-agent docetaxel, administered every two weeks as second-line treatment for patients with recurrent non-small cell lung cancer (NSCLC).
  • PATIENTS AND METHODS: Forty-eight patients with confirmed NSCLC were enrolled in this trial The median age was 56.5 years (range 43-76), median PS was 1, and the main histology type was adenocarcinoma (54%).
  • Though non-hematological toxicity is significantly reduced, myelosuppression is still a matter of concern.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Taxoids / administration & dosage

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16334165.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel
  •  go-up   go-down



22. Findeis-Hosey JJ, Yang Q, Spaulding BO, Wang HL, Xu H: IMP3 expression is correlated with histologic grade of lung adenocarcinoma. Hum Pathol; 2010 Apr;41(4):477-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IMP3 expression is correlated with histologic grade of lung adenocarcinoma.
  • This study aimed to determine the correlation of insulin-like growth factor II mRNA binding protein 3 expression with histologic grade of lung adenocarcinoma.
  • Eighty-nine cases, including 11 atypical adenomatous hyperplasias, 10 pure bronchioloalveolar carcinomas, 36 well-differentiated adenocarcinomas and 41 moderately or poorly differentiated adenocarcinomas, were immunohistochemically studied using a monoclonal antibody against insulin-like growth factor II mRNA binding protein 3.
  • Twenty-nine (70.7%) of 41 moderately to poorly differentiated adenocarcinomas were positive for insulin-like growth factor II mRNA binding protein 3, with 26 (89.7%) tumors demonstrating either a strong staining or staining in greater than 30% of tumor cells.
  • Four (40.0%) of 10 bronchioloalveolar carcinomas and 13 (36.1%) of 36 well-differentiated adenocarcinomas exhibited insulin-like growth factor II mRNA binding protein 3 positivity with a variable degree and percentage of tumor cells staining.
  • When bronchioloalveolar carcinomas were present in a pure form or as a component of adenocarcinomas, positive insulin-like growth factor II mRNA binding protein 3 staining was always patchy, with less than 20% of tumor cells stained.
  • Overall, the frequency of positive insulin-like growth factor II mRNA binding protein 3 staining was lower in bronchioloalveolar carcinomas and well-differentiated adenocarcinomas compared to moderately/poorly differentiated adenocarcinomas (P < .01).
  • These findings show that insulin-like growth factor II mRNA binding protein 3 is strongly and diffusely expressed in a large proportion of moderately/poorly differentiated lung adenocarcinomas, in particular in the solid component of mixed subtype adenocarcinomas, less frequently expressed in well-differentiated adenocarcinomas and bronchioloalveolar carcinomas, and negative in atypical adenomatous hyperplasias.
  • The higher frequency of expression in moderately/poorly differentiated adenocarcinomas suggests that insulin-like growth factor II mRNA binding protein 3 expression may be associated with an aggressive biological behavior.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasm Proteins / biosynthesis. RNA-Binding Proteins / biosynthesis
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Humans. Hyperplasia. Immunohistochemistry. Lung / metabolism. Lung / pathology. Neoplasm Invasiveness. Neoplasm Staging. Precancerous Conditions / metabolism

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc.
  • (PMID = 20004948.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IMP3 protein, human; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins
  •  go-up   go-down



23. Lockwood WW, Chari R, Coe BP, Thu KL, Garnis C, Malloff CA, Campbell J, Williams AC, Hwang D, Zhu CQ, Buys TP, Yee J, English JC, Macaulay C, Tsao MS, Gazdar AF, Minna JD, Lam S, Lam WL: Integrative genomic analyses identify BRF2 as a novel lineage-specific oncogene in lung squamous cell carcinoma. PLoS Med; 2010 Jul 27;7(7):e1000315
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrative genomic analyses identify BRF2 as a novel lineage-specific oncogene in lung squamous cell carcinoma.
  • BACKGROUND: Traditionally, non-small cell lung cancer is treated as a single disease entity in terms of systemic therapy.
  • Emerging evidence suggests the major subtypes--adenocarcinoma (AC) and squamous cell carcinoma (SqCC)--respond differently to therapy.
  • METHODS AND FINDINGS: We used an integrative genomics approach, combing high-resolution comparative genomic hybridization and gene expression microarray profiles, to compare AC and SqCC tumors in order to uncover alterations at the DNA level, with corresponding gene transcription changes, which are selected for during development of lung cancer subtypes.
  • Through the analysis of multiple independent cohorts of clinical tumor samples (>330), normal lung tissues and bronchial epithelial cells obtained by bronchial brushing in smokers without lung cancer, we identified the overexpression of BRF2, a gene on Chromosome 8p12, which is specific for development of SqCC of lung.
  • Genetic activation of BRF2, which encodes a RNA polymerase III (Pol III) transcription initiation factor, was found to be associated with increased expression of small nuclear RNAs (snRNAs) that are involved in processes essential for cell growth, such as RNA splicing.
  • Frequent activation of BRF2 in >35% preinvasive bronchial carcinoma in situ, as well as in dysplastic lesions, provides evidence that BRF2 expression is an early event in cancer development of this cell lineage.
  • CONCLUSIONS: This is the first study, to our knowledge, to show that the focal amplification of a gene in Chromosome 8p12, plays a key role in squamous cell lineage specificity of the disease.
  • Our data suggest that genetic activation of BRF2 represents a unique mechanism of SqCC lung tumorigenesis through the increase of Pol III-mediated transcription.
  • It can serve as a marker for lung SqCC and may provide a novel target for therapy.

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2008 Jan 31;358(5):502-11 [18234754.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Cell. 2008 Apr 4;133(1):78-89 [18394991.001]
  • [Cites] BMC Bioinformatics. 2008;9:243 [18492270.001]
  • [Cites] Mol Cell Biol. 2008 Jun;28(12):4204-14 [18391023.001]
  • [Cites] Oncogene. 2008 Jun 5;27(25):3635-40 [18212743.001]
  • [Cites] J Biol Chem. 2008 Jul 11;283(28):19184-91 [18456653.001]
  • [Cites] Oncogene. 2008 Jul 31;27(33):4615-24 [18391978.001]
  • [Cites] BMC Mol Biol. 2008;9:74 [18700021.001]
  • [Cites] Cell Cycle. 2007 Oct 1;6(19):2323-6 [17938580.001]
  • [Cites] N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398.001]
  • [Cites] J Pathol. 2009 Jan;217(1):65-72 [18932182.001]
  • [Cites] Oncology. 2009;76(4):239-46 [19246948.001]
  • [Cites] Oncologist. 2009 Mar;14(3):253-63 [19221167.001]
  • [Cites] Nat Genet. 2009 Nov;41(11):1238-42 [19801978.001]
  • [Cites] Genes Dev. 2000 Oct 15;14(20):2650-63 [11040218.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Nature. 2001 Apr 26;410(6832):1111-6 [11323676.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Mar;125(2):87-99 [11369051.001]
  • [Cites] Oncogene. 2001 Oct 4;20(45):6551-8 [11641780.001]
  • [Cites] J Biol Chem. 2001 Nov 16;276(46):43056-64 [11564744.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3249-62 [11751631.001]
  • [Cites] Clin Chest Med. 2002 Mar;23(1):65-81, viii [11901921.001]
  • [Cites] Genes Dev. 2002 Oct 15;16(20):2593-620 [12381659.001]
  • [Cites] Genes Dev. 2003 Feb 15;17(4):419-37 [12600935.001]
  • [Cites] Cell Cycle. 2003 May-Jun;2(3):181-4 [12734418.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]
  • [Cites] Eur J Surg Oncol. 2003 Nov;29(9):764-5 [14602497.001]
  • [Cites] Nat Genet. 2004 Mar;36(3):299-303 [14981516.001]
  • [Cites] Eur J Cancer. 2004 May;40(7):1082-94 [15093586.001]
  • [Cites] Oncogene. 2004 Apr 19;23(18):3208-16 [15094770.001]
  • [Cites] BMC Bioinformatics. 2004 Feb 9;5:13 [15040819.001]
  • [Cites] Lancet. 1997 May 24;349(9064):1498-504 [9167458.001]
  • [Cites] Genes Dev. 1998 Sep 1;12(17):2664-72 [9732265.001]
  • [Cites] Bioinformatics. 2004 Dec 12;20(18):3636-7 [15201182.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9027-34 [15604268.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jan;6(1):69-78 [15688068.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Biochem Soc Trans. 2005 Jun;33(Pt 3):447-9 [15916538.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5561-70 [15994928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9625-30 [15983384.001]
  • [Cites] Oncogene. 2005 Jul 14;24(30):4806-12 [15870700.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7561-7 [16140918.001]
  • [Cites] Mol Cell Biol. 2005 Nov;25(21):9406-18 [16227591.001]
  • [Cites] BMC Bioinformatics. 2005;6:274 [16297240.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):353-7 [16273092.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2116-28 [16489012.001]
  • [Cites] Biochem Soc Symp. 2006;(73):141-54 [16626295.001]
  • [Cites] Br J Cancer. 2006 Jun 19;94(12):1927-35 [16705311.001]
  • [Cites] Nat Rev Cancer. 2006 Aug;6(8):593-602 [16862190.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:25-34 [16869735.001]
  • [Cites] Trends Genet. 2006 Aug;22(8):447-55 [16787682.001]
  • [Cites] Int J Cancer. 2007 Jan 15;120(2):436-43 [17096350.001]
  • [Cites] Hum Genet. 2007 Feb;120(6):795-805 [17051368.001]
  • [Cites] Am J Respir Crit Care Med. 2007 Mar 15;175(6):547-53 [17158280.001]
  • [Cites] J Thorac Oncol. 2007 Apr;2(4):327-43 [17409807.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6007-11 [17616654.001]
  • [Cites] BMC Genomics. 2007;8:297 [17727719.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16663-8 [17925434.001]
  • [Cites] Annu Rev Pathol. 2006;1:331-48 [18039118.001]
  • [Cites] Trends Genet. 2007 Dec;23(12):614-22 [17977614.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • (PMID = 20668658.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA070907; Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BRF2 protein, human; 0 / Biomarkers, Tumor; 0 / Transcription Factor TFIIIB
  • [Other-IDs] NLM/ PMC2910599
  •  go-up   go-down



24. Su JL, Yang CY, Shih JY, Wei LH, Hsieh CY, Jeng YM, Wang MY, Yang PC, Kuo ML: Knockdown of contactin-1 expression suppresses invasion and metastasis of lung adenocarcinoma. Cancer Res; 2006 Mar 1;66(5):2553-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Knockdown of contactin-1 expression suppresses invasion and metastasis of lung adenocarcinoma.
  • Numerous genetic changes are associated with cancer cell metastasis and invasion.
  • In search for key regulators of invasion and metastasis, a panel of lung cancer cell lines with different invasive ability was screened.
  • Suppression of contactin-1 expression abolished the ability of lung adenocarcinoma cells to invade Matrigel in vitro as well as the polymerization of filamentous-actin and the formation of focal adhesion structures.
  • Contactin-1 is proposed to function importantly in the invasion and metastasis of lung adenocarcinoma cells via RhoA-mediated mechanisms.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Adhesion Molecules, Neuronal / biosynthesis. Cell Adhesion Molecules, Neuronal / deficiency. Lung Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16510572.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / CNTN1 protein, human; 0 / Cell Adhesion Molecules, Neuronal; 0 / Cntn1 protein, mouse; 0 / Contactin 1; 0 / Contactins; 124671-05-2 / RHOA protein, human; EC 3.6.5.2 / rhoA GTP-Binding Protein
  •  go-up   go-down



25. Yoshiya K, Motono N, Yamato Y, Koike T: [Bronchoplastic procedures for lung cancer]. Kyobu Geka; 2008 Oct;61(11):927-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Bronchoplastic procedures for lung cancer].
  • Bronchoplastic procedures for patients with lung cancer are designed to achieve radical cure with preservation of functioning lung parenchyma.
  • The operative results of 139 cases of lung cancer who underwent bronchoplasty between 1963 through 2007 were reviewed.
  • Squamous cell carcinoma was the most frequently encountered histological type of disease (78%), followed by adenocarcinoma (12%) and other histological types (10%).
  • The 5-year survival rate in the patients with squamous cell carcinoma was 63.2%, and in patients with adenocarcinoma was 26.3%.
  • SS for patients with early-stage squamous cell carcinoma of the segmental bronchus is a curative operation with preservation of the pulmonary function.
  • Bronchoplasty without lung resection (SR, WR) is a reliable method for patients with low-grade malignant polypoid tumors arising from the bronchus.
  • Patients with adenocarcinoma, N2 disease or major bronchial anastomotic complication show a worse prognosis.
  • [MeSH-major] Adenocarcinoma / surgery. Bronchi / surgery. Carcinoma, Squamous Cell / surgery. Lung Neoplasms / surgery. Reconstructive Surgical Procedures / methods. Thoracic Surgical Procedures / methods



26. Sato T, Soejima K, Nakayama S, Satomi R, Sayama K, Asano K: [A case of fat embolism syndrome associated with pathological femoral fracture caused by metastatic adenocarcinoma of the lung]. Nihon Kokyuki Gakkai Zasshi; 2010 Oct;48(10):765-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of fat embolism syndrome associated with pathological femoral fracture caused by metastatic adenocarcinoma of the lung].
  • A 76-year-old woman with multiple bone metastases from lung adenocarcinoma was admitted due to a pathological femoral fracture.
  • Computed tomography of the chest revealed diffuse ground glass opacities in both lungs, and magnetic resonance imaging of the brain showed multiple acute infarctions.
  • Fat embolism syndrome should be considered as a differential diagnosis if consciousness disturbance and respiratory failure occur in patients with metastatic bone carcinoma and pathological long bone fractures.
  • [MeSH-major] Adenocarcinoma / complications. Embolism, Fat / etiology. Femoral Fractures / etiology. Fractures, Spontaneous / etiology. Lung Neoplasms / complications

  • Genetic Alliance. consumer health - Embolism.
  • MedlinePlus Health Information. consumer health - Leg Injuries and Disorders.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21066866.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down



27. Schuchert MJ, Luketich JD: Management of Barrett's esophagus. Oncology (Williston Park); 2007 Oct;21(11):1382-9, 1392; discussion 1392, 1394, 1396
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Typically arising in the setting of chronic gastroesophageal reflux disease, the presence of Barrett's esophagus carries a 50- to 100-fold increased risk of developing esophageal cancer.
  • Aggressive medical or surgical antireflux therapy may ameliorate symptoms, but have not yet been proven to affect the risk of developing esophageal adenocarcinoma in randomized trials.
  • There have been no studies to establish that endoscopic screening/surveillance programs decrease the rates of death from cancer.
  • Fit patients with Barrett's esophagus and high-grade dysplasia should undergo esophagectomy to prevent the risk of developing esophageal adenocarcinoma.
  • For non-operative candidates, endoscopic ablative approaches may represent a reasonable therapeutic alternative.

  • Genetic Alliance. consumer health - Barrett's Esophagus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18080619.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 62
  •  go-up   go-down



28. Carpizo DR, D'Angelica M: Liver resection for metastatic colorectal cancer in the presence of extrahepatic disease. Lancet Oncol; 2009 Aug;10(8):801-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liver resection for metastatic colorectal cancer in the presence of extrahepatic disease.
  • Early studies of liver resection for colorectal cancer metastases identified patients with concomitant extrahepatic disease as a group with poor outcomes.
  • In this paper, we review the published work on metastatic colorectal cancer, pertaining to the role of surgery in patients with liver metastases and concomitant extrahepatic disease.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / surgery. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Liver Neoplasms / secondary. Liver Neoplasms / surgery
  • [MeSH-minor] Hepatectomy. Humans. Lung Neoplasms / mortality. Lung Neoplasms / secondary. Lymphatic Metastasis / pathology. Neoplasm Metastasis / pathology. Peritoneal Neoplasms / mortality. Peritoneal Neoplasms / secondary



29. Taylor MD, Smith PW, Brix WK, Wick MR, Theodosakis N, Swenson BR, Kozower BD, Lau CL, Jones DR: Fluorodeoxyglucose positron emission tomography and tumor marker expression in non-small cell lung cancer. J Thorac Cardiovasc Surg; 2009 Jan;137(1):43-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fluorodeoxyglucose positron emission tomography and tumor marker expression in non-small cell lung cancer.
  • Both FDG-PET maximal standardized uptake values and selected tumor markers have been shown to correlate with stage, nodal disease, and survival in non-small cell lung cancer (NSCLC).
  • In addition, increasing maximal standardized uptake values correlated with increased expression of glucose transporter 1 (P < .0001) and p53 (P = .04) in adenocarcinoma.
  • CONCLUSION: FDG-PET maximal standardized uptake values correlate with an increased expression of glucose transporter 1 and p53 in lung adenocarcinoma, but not squamous cell cancer.



30. Park K, Goto K: A review of the benefit-risk profile of gefitinib in Asian patients with advanced non-small-cell lung cancer. Curr Med Res Opin; 2006 Mar;22(3):561-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A review of the benefit-risk profile of gefitinib in Asian patients with advanced non-small-cell lung cancer.
  • BACKGROUND: Improvements in first-line therapy of advanced non-small-cell lung cancer (NSCLC) have increased the need for effective second-line treatment options.
  • In a Phase II trial of the anticancer drug gefitinib (IRESSA), greater efficacy was observed in Japanese compared with non-Japanese patients.
  • Furthermore, results from a placebo-controlled Phase III trial (IRESSA Survival Evaluation in Lung cancer [ISEL]) showed that treatment with gefitinib was not associated with a statistically significant improvement in survival in either the overall or adenocarcinoma co-primary populations, although there was marked heterogeneity in survival outcomes between patient groups, with patients of Asian origin achieving a significant survival benefit with gefitinib compared with placebo.
  • Female gender, adenocarcinoma histology, non-smoking history, good PS and the presence of multiple lung metastases are associated with improved responsiveness to gefitinib.
  • The incidence of interstitial lung disease appears to be higher in Japanese than non-Japanese patients, although the reasons for this are not clear.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16574039.001).
  • [ISSN] 0300-7995
  • [Journal-full-title] Current medical research and opinion
  • [ISO-abbreviation] Curr Med Res Opin
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
  • [Number-of-references] 79
  •  go-up   go-down



31. Howell NR, Zheng W, Cheng L, Tornos C, Kane P, Pearl M, Chalas E, Liang SX: Carcinomas of ovary and lung with clear cell features: can immunohistochemistry help in differential diagnosis? Int J Gynecol Pathol; 2007 Apr;26(2):134-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinomas of ovary and lung with clear cell features: can immunohistochemistry help in differential diagnosis?
  • Metastatic lung carcinomas with clear cell morphology can be confused with primary ovarian clear cell carcinomas.
  • We performed immunohistochemical stains in 14 cases of non-small cell lung carcinomas with clear cell features and 14 cases of ovarian clear cell carcinomas using a panel of markers, including thyroid transcription factor 1 (TTF-1), carcinoembryonic antigen (CEA), Wilms tumor gene 1, octamer-binding transcription factor 4 (OCT-4), cancer antigen 125 (CA-125), estrogen receptor, and progesterone receptor.
  • Among non-small cell lung carcinomas with clear cell features, 87.5% of adenocarcinomas (or 50% overall frequency in lung carcinomas) were positive for TTF-1, whereas none of the ovarian clear cell carcinomas were positive (P = 0.002).
  • All 14 ovarian clear cell carcinomas stained for CA-125 as compared with 1 non-small cell lung carcinoma (P < 0.001).
  • On the other hand, 85% of non-small cell lung carcinomas stained for CEA, whereas none of the ovarian clear cell carcinomas did (P < 0.001).
  • Interestingly, 4 ovarian clear cell carcinomas (28%) showed positive staining for the germ cell marker OCT-4.
  • Either lung or ovarian carcinomas stained for Wilms tumor gene 1, estrogen receptor, or progesterone receptor very infrequently; and the difference between the 2 groups was not statistically significant.
  • Our results suggest that an immunohistochemical panel consisting of TTF-1, CEA, CA-125, and OCT-4 is helpful in distinguishing most pulmonary and ovarian carcinomas with clear cell features.
  • [MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Carcinoma, Non-Small-Cell Lung / diagnosis. Lung Neoplasms / diagnosis. Ovarian Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. CA-125 Antigen / genetics. CA-125 Antigen / metabolism. Carcinoembryonic Antigen / genetics. Carcinoembryonic Antigen / metabolism. Diagnosis, Differential. Female. Gene Expression Regulation, Neoplastic. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Octamer Transcription Factor-3 / genetics. Octamer Transcription Factor-3 / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

  • 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 = 17413979.001).
  • [ISSN] 0277-1691
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Carcinoembryonic Antigen; 0 / Nuclear Proteins; 0 / Octamer Transcription Factor-3; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
  •  go-up   go-down



32. Gormus U, Ergen A, Yaylim-Eraltan I, Yilmaz H, Turna A, Bozkurt N, Isbir T: Fas-1377 A/G polymorphism in lung cancer. In Vivo; 2007 Jul-Aug;21(4):663-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fas-1377 A/G polymorphism in lung cancer.
  • BACKGROUND: Reduced expression of Fas and/or increased expression of FasL is known to exist in some cancer types including lung cancer, so the Fas/FasL system may play a role in the course of cancer.
  • Lack of cell surface Fas expression is one of the main routes of apoptotic resistance in tumor formation and progression.
  • Functional mutations in the Fas gene that impair apoptotic signal transduction are associated with susceptibility to various types of cancer.
  • In this study, we focused on lung cancer.
  • RESULTS: We did not find any relationship between Fas-1377 G-->A polymorphism and lung cancer.
  • CONCLUSION: There was no relationship between Fas-1377 G-->A polymorphism and lung cancer, but it was statistically significant that smoking might increase the possibility of creating lung cancer in AG genotypes more than in other genotypes.
  • [MeSH-major] Antigens, CD95 / genetics. Carcinoma, Squamous Cell / genetics. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Apoptosis / physiology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Small Cell / genetics. Carcinoma, Small Cell / pathology. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Point Mutation. Promoter Regions, Genetic / genetics. Signal Transduction

  • Genetic Alliance. consumer health - Lung Cancer.
  • 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
  • (PMID = 17708363.001).
  • [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 / Antigens, CD95
  •  go-up   go-down



33. Mireskandari M, Shafaii AF, Kayser G, Kayser K: Lack of CD117 and rare bcl-2 expression in stomach cancer by immunohistochemistry. An immunohistochemical study with review of the literature. Diagn Pathol; 2006;1:7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of CD117 and rare bcl-2 expression in stomach cancer by immunohistochemistry. An immunohistochemical study with review of the literature.
  • BACKGROUND: Gastric adenocarcinoma is one of the most frequent malignancies worldwide including Iran.
  • This study was designed to immunohistochemically evaluate the CD117 and bcl-2 expression in gastric carcinomas and their potential use as therapeutic targets in the treatment of patients with advanced stage gastric cancer.
  • MATERIALS AND METHODS: Representative paraffin blocks obtained from 38 operated gastric adenocarcinoma patients were retrieved from Afzalipour Hospital pathology department archive, Kerman, Iran.
  • In addition, the cases were evaluated immunohistochemically for apoptosis-related protein (bcl-2), to evaluating a potential association of CD117 expression with the cell proliferation regulatory pathways.
  • RESULTS: No positive reaction for CD117 was seen in gastric carcinoma tumor cells irrespective to the cell type, grade, and stage, proliferation and apoptosis rate.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2004 May 15;103(10):3644-54 [14726395.001]
  • [Cites] Fertil Steril. 1999 Jan;71(1):85-9 [9935121.001]
  • [Cites] Exp Hematol. 2004 Apr;32(4):390-6 [15050750.001]
  • [Cites] Anticancer Drugs. 2004 Apr;15(4):405-9 [15057146.001]
  • [Cites] Mol Cancer Ther. 2004 May;3(5):527-35 [15141010.001]
  • [Cites] Br J Cancer. 2004 May 4;90(9):1825-9 [15150607.001]
  • [Cites] Gynecol Oncol. 2004 Jun;93(3):718 [15196872.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):264-76 [15665303.001]
  • [Cites] World J Gastroenterol. 2005 Feb 28;11(8):1228-31 [15754411.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2162-71 [15800309.001]
  • [Cites] Pathol Res Pract. 2005;201(2):71-81 [15901127.001]
  • [Cites] World J Gastroenterol. 2005 Jun 28;11(24):3655-9 [15968715.001]
  • [Cites] Gan To Kagaku Ryoho. 2005 Oct;32(11):1540-5 [16315863.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2575-82 [2249198.001]
  • [Cites] Am J Clin Pathol. 1990 Jan;93(1):8-13 [2403744.001]
  • [Cites] Cell Growth Differ. 1995 Jun;6(6):769-79 [7545433.001]
  • [Cites] Cell Growth Differ. 1995 Sep;6(9):1111-8 [8519688.001]
  • [Cites] Anticancer Res. 1996 Nov-Dec;16(6B):3397-402 [9042197.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3192-203 [10880433.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1267-73 [10942367.001]
  • [Cites] Am J Gastroenterol. 2001 Jan;96(1):16-26 [11197247.001]
  • [Cites] J Biol Regul Homeost Agents. 2001 Jan-Mar;15(1):90-4 [11388751.001]
  • [Cites] Dig Dis Sci. 2002 Jan;47(1):107-13 [11837709.001]
  • [Cites] Am J Clin Pathol. 2002 Feb;117(2):183-5 [11863213.001]
  • [Cites] Am J Clin Pathol. 2002 Feb;117(2):188-93 [11865845.001]
  • [Cites] Cancer Genet Cytogenet. 2002 May;135(1):1-22 [12072198.001]
  • [Cites] Exp Hematol. 2002 Jul;30(7):767-73 [12135675.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4879-83 [12208734.001]
  • [Cites] Int J Cancer. 2003 Mar 10;104(1):60-5 [12532420.001]
  • [Cites] Exp Hematol. 2003 Feb;31(2):109-17 [12591275.001]
  • [Cites] Gene Expr Patterns. 2003 Mar;3(1):53-8 [12609603.001]
  • [Cites] Lung Cancer. 2003 May;40(2):173-80 [12711118.001]
  • [Cites] Anticancer Res. 2003 May-Jun;23(3B):2329-33 [12894511.001]
  • [Cites] Acta Pathol Microbiol Scand. 1965;64:31-49 [14320675.001]
  • [Cites] Anticancer Res. 2003 Sep-Oct;23(5b):4305-8 [14666642.001]
  • [Cites] Expert Rev Anticancer Ther. 2003 Dec;3(6):757-66 [14686698.001]
  • [Cites] Am J Pathol. 2004 Jan;164(1):305-13 [14695343.001]
  • [Cites] J Natl Cancer Inst. 2004 Jan 7;96(1):46-55 [14709738.001]
  • [Cites] World J Gastroenterol. 2005 Oct 7;11(37):5899-901 [16270406.001]
  • [Cites] J Cell Physiol. 1997 Jul;172(1):1-11 [9207920.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):327-33 [9440029.001]
  • [Cites] Clin Cancer Res. 2004 Jan 15;10(2):751-61 [14760098.001]
  • (PMID = 16759362.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1475889
  •  go-up   go-down



34. Jonsson H, Bergdahl IA, Akerblom G, Eriksson K, Andersson K, Kågström L, Järvholm B, Damber L: Lung cancer risk and radon exposure in a cohort of iron ore miners in Malmberget, Sweden. Occup Environ Med; 2010 Aug;67(8):519-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer risk and radon exposure in a cohort of iron ore miners in Malmberget, Sweden.
  • OBJECTIVES: Lung cancer caused by radon in miners is a well-known risk.
  • As this mine has relatively low radon levels, the results are highly relevant for risk estimation in non-uranium underground mines.
  • 122 lung cancer cases occurred during the follow-up period of 1958-2000.
  • The results for squamous cell and small cell lung cancer were 0.049 and 0.072, respectively.
  • However, no increased risk was observed for adenocarcinoma (0.000 ERR per kBq year/m(3), 95% CI -0.017 to 0.017).
  • Radon did not increase the risk for adenocarcinoma in the lung.
  • [MeSH-major] Iron / toxicity. Lung Neoplasms / epidemiology. Neoplasms, Radiation-Induced / epidemiology. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects. Radon / toxicity



35. Mountzios G, Planchard D, Besse B, Validire P, Girard P, Devisme C, Dimopoulos MA, Soria JC, Fouret P: Mitogen-activated protein kinase activation in lung adenocarcinoma: a comparative study between ever smokers and never smokers. Clin Cancer Res; 2008 Jul 1;14(13):4096-102
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitogen-activated protein kinase activation in lung adenocarcinoma: a comparative study between ever smokers and never smokers.
  • PURPOSE: There are major differences affecting genes in adenocarcinomas in ever and never smokers.
  • EXPERIMENTAL DESIGN: Expression of activated extracellular signal-regulated kinases, c-Jun NH(2)-terminal kinases, and P38 enzymes (pP38) were evaluated by means of immunohistochemistry in 188 chemonaïve patients with surgically resected lung adenocarcinoma.
  • Cell viability of the lung adenocarcinoma cell line HCC827 was studied after treatment with cisplatin or the P38 MAPK inhibitor SB 203580.
  • Cell viability of HCC827 was significantly reduced after exposure to SB203580 alone or when combined with cisplatin.
  • CONCLUSIONS: Life-long nonsmoking is associated with high activated P38 levels in patients with lung adenocarcinoma.
  • Activated P38 can contribute to the viability of adenocarcinoma cells in never smokers, but is not predictive for overall survival.
  • [MeSH-major] Adenocarcinoma / enzymology. Gene Expression Regulation, Neoplastic. Lung Neoplasms / enzymology. Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Enzyme Activation. Female. Humans. MAP Kinase Signaling System. Male. Middle Aged. Smoking

  • MedlinePlus Health Information. consumer health - Lung 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18593986.001).
  • [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] EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  •  go-up   go-down



36. Xia T, Li H, Sun Q, Wang Y, Fan N, Yu Y, Li P, Chang JY: Promising clinical outcome of stereotactic body radiation therapy for patients with inoperable Stage I/II non-small-cell lung cancer. Int J Radiat Oncol Biol Phys; 2006 Sep 1;66(1):117-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promising clinical outcome of stereotactic body radiation therapy for patients with inoperable Stage I/II non-small-cell lung cancer.
  • PURPOSE: To evaluate the efficacy and toxicity of hypofractionated stereotactic body radiotherapy in patients with Stage I/II non-small-cell lung cancer.
  • METHODS AND MATERIALS: Forty-three patients with inoperable Stage I/II non-small-cell lung cancer underwent treatment prospectively using the stereotactic gamma-ray whole-body therapeutic system (body gamma-knife radiosurgery) with 30 rotary conical-surface Co(60) sources focused on the target volume.
  • [MeSH-major] Adenocarcinoma / surgery. Carcinoma, Non-Small-Cell Lung / surgery. Carcinoma, Squamous Cell / surgery. Lung Neoplasms / surgery. Radiosurgery / methods



37. Peng Q, Liu M, Song SM, Li XH, Du YH, Zhi Y, Wang MY: The recruitment of exogenous endothelial progenitor cells in lung tumor model of nude mice. Chin J Cancer; 2010 Nov;29(11):952-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The recruitment of exogenous endothelial progenitor cells in lung tumor model of nude mice.
  • In this study, we investigated the recruitment of exogenous EPCs in human lung adenocarcinoma model of nude mice.
  • METHODS: EPCs labeled with green fluorescence protein (GFP) were transplanted into nude mice bearing human lung adenocarcinoma.
  • The tumor tissues were stained for CD133, hypoxia-inducible factor-1alpha (HIF-1α), stromal cell-derived factor-1α (SDF-1α), and vascular endothelial growth factor receptor (KDR).
  • [MeSH-major] Adenocarcinoma / pathology. Bone Marrow / pathology. Endothelial Cells / transplantation. Lung Neoplasms / pathology. Stem Cell Transplantation. Stem Cells / pathology
  • [MeSH-minor] Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Cell Line, Tumor. Chemokine CXCL12 / genetics. Chemokine CXCL12 / metabolism. Female. Glycoproteins / genetics. Glycoproteins / metabolism. Green Fluorescent Proteins / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic. Peptides / genetics. Peptides / metabolism. RNA, Messenger / metabolism. Transfection. Tumor Burden. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20979695.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Chemokine CXCL12; 0 / Glycoproteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Peptides; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 147336-22-9 / Green Fluorescent Proteins; Adenocarcinoma of lung
  •  go-up   go-down



38. Agarwala A, Fisher W, Bruetman D, McClean J, Taber D, Titzer M, Juliar B, Yu M, Breen T, Einhorn LH, Hanna N: Gefitinib plus celecoxib in chemotherapy-naïve patients with stage IIIB/IV non-small cell lung cancer: a phase II study from the Hoosier Oncology Group. J Thorac Oncol; 2008 Apr;3(4):374-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib plus celecoxib in chemotherapy-naïve patients with stage IIIB/IV non-small cell lung cancer: a phase II study from the Hoosier Oncology Group.
  • BACKGROUND: Gefitinib, an inhibitor of the epidermal growth factor receptor (EGFR) pathway, has single agent activity in non-small cell lung cancer (NSCLC).
  • RESULTS: From January 2004 to November 2004, 31 patients were enrolled: male/female 13/18; median age 70 years (range, 19-93); 68% had adenocarcinoma; Eastern Cooperative Oncology Group PS 0/1 13/18; stage IIIb/IV 2/29.
  • Two patients died of interstitial lung disease due to treatment.
  • All responders were females with adenocarcinoma, two were remote or never smokers and three were former smokers.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Celecoxib. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Pyrazoles / administration & dosage. Quinazolines / administration & dosage. Sulfonamides / administration & dosage. Survival Rate

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CELECOXIB .
  • 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 = 18379355.001).
  • [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] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrazoles; 0 / Quinazolines; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib; S65743JHBS / gefitinib
  •  go-up   go-down



39. Tse LA, Yu IT, Au JS, Yu KS, Kwok KP, Qiu H, Wong TW: Environmental tobacco smoke and lung cancer among Chinese nonsmoking males: might adenocarcinoma be the culprit? Am J Epidemiol; 2009 Mar 1;169(5):533-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Environmental tobacco smoke and lung cancer among Chinese nonsmoking males: might adenocarcinoma be the culprit?
  • No studies have specifically reported the association of lung adenocarcinoma with environmental tobacco smoke (ETS) exposure among nonsmoking males.
  • The objective of this study was to examine the exposure-response relation between ETS exposure and lung cancer among nonsmoking males.
  • In particular, the association with adenocarcinoma of the lung was studied.
  • A total of 132 Chinese male nonsmokers with newly diagnosed primary lung cancer and 536 nonsmoking community referents were interviewed about ETS exposures from the household and/or workplace, including ever ETS exposure, sources of exposure, number of smoking cohabitants/coworkers, and smoker-years.
  • Univariate logistic regression analyses showed a weak association between all lung cancers and ever ETS exposure from the household and/or workplace (odds ratio (OR) = 1.11, 95% confidence interval (CI): 0.74, 1.67), but an increased risk was restricted to adenocarcinoma (OR = 1.68, 95% CI: 1.00, 2.38).
  • After adjustment for family cancer history and other confounders, excess risk (OR = 1.62, 95% CI: 0.91, 2.88) still persisted for adenocarcinoma, although it was no longer statistically significant.
  • Exposure-response relations for adenocarcinoma were found with increasing levels of all ETS indices when exposures from the household and workplaces were combined.
  • The consistent exposure-response relations between ETS exposures and adenocarcinoma suggested a probable causal link, which would have to be confirmed by future larger studies.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Lung Neoplasms / epidemiology. Lung Neoplasms / etiology. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adult. Age Distribution. Aged. Carcinoma, Large Cell / epidemiology. Carcinoma, Large Cell / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Case-Control Studies. Hong Kong / epidemiology. Humans. Interviews as Topic. Logistic Models. Male. Middle Aged. Occupational Exposure / adverse effects. Risk Factors. Smoking Cessation

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Secondhand Smoke.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19126588.001).
  • [ISSN] 1476-6256
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tobacco Smoke Pollution
  •  go-up   go-down



40. Carretta A, Ciriaco P, Melloni G, Bandiera A, Libretti L, Puglisi A, Giovanardi M, Zannini P: Surgical treatment of multiple primary adenocarcinomas of the lung. Thorac Cardiovasc Surg; 2009 Feb;57(1):30-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical treatment of multiple primary adenocarcinomas of the lung.
  • INTRODUCTION: The incidence of lung adenocarcinomas has steadily increased over the last decades.
  • The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (MPAL) analyzing the radiological and histological features.
  • Histology revealed 26 adenocarcinomas, five adenocarcinomas with a bronchioloalveolar (BAC) pattern and 21 BAC.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery. Neoplasms, Multiple Primary. Pneumonectomy. Thoracic Surgery, Video-Assisted. Thoracotomy

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19169994.001).
  • [ISSN] 0171-6425
  • [Journal-full-title] The Thoracic and cardiovascular surgeon
  • [ISO-abbreviation] Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down



41. Yoshimura M, Imamura F, Ueno K, Uchida J: Gemcitabine/carboplatin in a modified 21-day administration schedule for advanced-stage non-small-cell lung cancer. Clin Lung Cancer; 2006 Nov;8(3):208-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemcitabine/carboplatin in a modified 21-day administration schedule for advanced-stage non-small-cell lung cancer.
  • PURPOSE: Gemcitabine/carboplatin is active for advanced-stage non-small-cell lung cancer.
  • PATIENTS AND METHODS: Thirty-one patients with stage IIIB or stage IV non-small cell lung cancer received gemcitabine 1000 mg/m(2) on days 1 and 8 and carboplatin at an area under the curve of 5 mg capital ZE, Cyrillic minute/mL on day 8, every 21 days.
  • Grade 3/4 thrombocytopenia, according to the National Cancer Institute Common Toxicity Criteria, version 3.0, was observed in 2 patients (6.5%) in the first 2 cycles.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carboplatin / administration & dosage. Carcinoma, Squamous Cell / drug therapy. Deoxycytidine / analogs & derivatives. Lung Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17239297.001).
  • [ISSN] 1525-7304
  • [Journal-full-title] Clinical lung cancer
  • [ISO-abbreviation] Clin Lung Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
  •  go-up   go-down



42. Shih YW, Chien ST, Chen PS, Lee JH, Wu SH, Yin LT: Alpha-mangostin suppresses phorbol 12-myristate 13-acetate-induced MMP-2/MMP-9 expressions via alphavbeta3 integrin/FAK/ERK and NF-kappaB signaling pathway in human lung adenocarcinoma A549 cells. Cell Biochem Biophys; 2010 Sep;58(1):31-44
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-mangostin suppresses phorbol 12-myristate 13-acetate-induced MMP-2/MMP-9 expressions via alphavbeta3 integrin/FAK/ERK and NF-kappaB signaling pathway in human lung adenocarcinoma A549 cells.
  • The purpose of this study is to investigate the anti-metastatic effect of alpha-mangostin on phorbol 12-myristate 13-acetate (PMA)-induced matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) expressions in A549 human lung adenocarcinoma cells.
  • Finally, the transient transfection of ERK siRNA significantly down-regulated the expressions of MMP-2 and MMP-9 concomitantly with a marked inhibition on cell invasion and migration.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Integrin alphaVbeta3 / metabolism. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 9 / biosynthesis. NF-kappa B / metabolism. Neoplasm Metastasis / prevention & control. Xanthones / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Movement / drug effects. Focal Adhesion Kinase 1 / metabolism. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. RNA, Small Interfering. Signal Transduction. Tetradecanoylphorbol Acetate / antagonists & inhibitors. Tetradecanoylphorbol Acetate / pharmacology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • Hazardous Substances Data Bank. Mangostin .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20652762.001).
  • [ISSN] 1559-0283
  • [Journal-full-title] Cell biochemistry and biophysics
  • [ISO-abbreviation] Cell Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Xanthones; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.11.24 / MAPK1 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate; U6RIV93RU1 / mangostin
  •  go-up   go-down



43. Pan TC, Zheng Z, Li J, Chen T, Liu LG, Wei X: [Appropriate extent of lymph node dissection for clinical I a stage non-small cell lung cancer]. Ai Zheng; 2007 Mar;26(3):303-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Appropriate extent of lymph node dissection for clinical I a stage non-small cell lung cancer].
  • BACKGROUND & OBJECTIVE: There is no agreement on the appropriate extent of lymph node dissection for lung cancer, especially for early non-small cell lung cancer (NSCLC).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / surgery. Lung Neoplasms / surgery. Lymph Node Excision / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Adult. Aged. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Female. Follow-Up Studies. Humans. Lung / pathology. Lymph Nodes / surgery. Lymphatic Metastasis. Male. Mediastinum / pathology. Mediastinum / surgery. Middle Aged. Neoplasm Staging. Pneumonectomy / methods. Survival Rate



44. Koh WP, Yuan JM, Wang R, Seow A, Lee HP, Yu MC: Chronic rhinosinusitis and risk of lung cancer in the Singapore Chinese Health Study. Int J Cancer; 2008 Sep 15;123(6):1398-402
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic rhinosinusitis and risk of lung cancer in the Singapore Chinese Health Study.
  • Epidemiologic evidence suggests that chronic inflammatory conditions of the lung may increase lung cancer risk.
  • These chronic conditions, such as chronic obstructive pulmonary disease and asthma, commonly coexist with chronic rhinosinusitis.
  • We prospectively examined if chronic rhinitis or sinusitis was associated with lung cancer risk in the Singapore Chinese Health Study, a population-based cohort of 63,257 Singapore Chinese, who were aged 45-74 years when recruited between 1993 and 1998.
  • Each subject completed a comprehensive interview on medical conditions, dietary and lifestyle factors at recruitment, and cancer occurrence and survival status were determined via linkage to population-based registries.
  • As of 31 December, 2005, 954 cohort participants had developed lung cancer.
  • Compared with subjects without such history, subjects who reported a history of physician-diagnosed rhinitis or sinusitis at baseline, whether allergic or nonallergic, had a statistically significant 59% increase in risk of lung cancer (hazard ratio [HR] = 1.59; confidence interval [CI] = 1.06-2.37).
  • This association was significant and stronger in women (HR = 2.32; 95% CI = 1.23-4.39) compared to men, and for the adenocarcinoma cell type (HR = 1.91; 95% CI = 1.07-3.42) compared to other histologies.
  • Overall, a history of asthma, hay fever, allergic dermatitis, food allergy or any other allergic conditions asked in a single question was not related to lung cancer risk (HR = 1.11; 95% CI = 0.90-1.36).
  • Chronic rhinosinusitis may be a marker of pan-airway inflammation and its association with lung cancer risk provides evidence linking inflammation to lung carcinogenesis, especially among women.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Sinusitis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • [Cites] Thorax. 2004 Apr;59(4):303-7 [15047949.001]
  • [Cites] Cancer Causes Control. 2003 May;14(4):327-34 [12846363.001]
  • [Cites] Cancer. 1979 Feb;43(2):636-42 [217523.001]
  • [Cites] Am J Epidemiol. 1985 Jul;122(1):66-74 [4014202.001]
  • [Cites] Am J Pathol. 1985 Dec;121(3):531-51 [3907369.001]
  • [Cites] Am J Surg Pathol. 1985 Jun;9(6):391-400 [3004243.001]
  • [Cites] Ann Intern Med. 1987 Apr;106(4):512-8 [3826952.001]
  • [Cites] Br J Cancer. 1990 Dec;62(6):982-7 [2257230.001]
  • [Cites] Am J Epidemiol. 1992 Sep 15;136(6):623-32 [1442729.001]
  • [Cites] Am J Epidemiol. 1995 Jun 1;141(11):1023-32 [7771438.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):135-40 [9488588.001]
  • [Cites] Am J Respir Crit Care Med. 1998 Jun;157(6 Pt 1):1907-12 [9620926.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Sep;7(9):775-81 [9752985.001]
  • [Cites] Respiration. 1998;65(6):450-7 [9817959.001]
  • [Cites] Am J Epidemiol. 1999 Jan 1;149(1):13-20 [9883789.001]
  • [Cites] J Laryngol Otol. 1998 Nov;112(11):1019-30 [10197137.001]
  • [Cites] Allergy. 1999 Mar;54(3):242-8 [10321560.001]
  • [Cites] Eur Respir J. 2004 Nov;24(5):758-64 [15516669.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8919-23 [15604253.001]
  • [Cites] Arch Intern Med. 2003 Jun 23;163(12):1475-80 [12824098.001]
  • [Cites] J Allergy Clin Immunol. 2003 Jun;111(6):1171-83; quiz 1184 [12789212.001]
  • [Cites] Respir Med. 2003 Aug;97(8):909-14 [12924517.001]
  • [Cites] J Allergy Clin Immunol. 2001 Mar;107(3):469-76 [11240947.001]
  • [Cites] Eur Respir J. 2001 Apr;17(4):596-603 [11401051.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Sep 1;164(5):726-7 [11549521.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Nov 15;164(10 Pt 2):S76-80 [11734472.001]
  • [Cites] Nutr Cancer. 2001;39(2):187-95 [11759279.001]
  • [Cites] Allergy. 2002 Feb;57(2):150-4 [11929419.001]
  • [Cites] Allergy. 2002 Sep;57(9):841-55 [12169183.001]
  • [Cites] Curr Allergy Asthma Rep. 2003 Nov;3(6):513-8 [14531973.001]
  • [Cites] Nihon Jibiinkoka Gakkai Kaiho. 2003 Oct;106(10):1030-7 [14631770.001]
  • [Cites] Am J Rhinol. 2004 Jan-Feb;18(1):15-21 [15035566.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 [15741570.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):773-8 [15824142.001]
  • [Cites] Steroids. 2005 May-Jun;70(5-7):372-81 [15862820.001]
  • [Cites] Am J Epidemiol. 2005 Sep 15;162(6):542-7 [16093291.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):257-62 [16231326.001]
  • [Cites] Int J Cancer. 2006 Apr 1;118(7):1798-804 [16217766.001]
  • [Cites] Carcinogenesis. 2006 Jun;27(6):1240-4 [16344268.001]
  • [Cites] Chest. 2006 Aug;130(2):429-35 [16899841.001]
  • [Cites] Proc Am Thorac Soc. 2006 Aug;3(6):535-7 [16921139.001]
  • [Cites] Steroids. 2007 Feb;72(2):135-43 [17276470.001]
  • [Cites] COPD. 2007 Jun;4(2):163-6 [17530509.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6520-7 [17596594.001]
  • [Cites] Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2007 May;42(5):378-84 [17629011.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Sep;12(9):890-8 [14504200.001]
  • [Cites] J Allergy Clin Immunol. 2000 Nov;106(5 Suppl):S201-5 [11080732.001]
  • [Cites] Lancet. 2000 Aug 26;356(9231):724-9 [11085692.001]
  • [Cites] J Allergy Clin Immunol. 2003 Feb;111(2 Suppl):S520-9 [12592298.001]
  • [Cites] Am J Epidemiol. 2003 Apr 1;157(7):606-12 [12672680.001]
  • [Cites] J Manag Care Pharm. 2004 Jul-Aug;10(4):310-7 [15298529.001]
  • (PMID = 18548585.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA80205; United States / NCI NIH HHS / CA / R01 CA55069; United States / NCI NIH HHS / CA / R01 CA080205-09; United States / NCI NIH HHS / CA / R35 CA053890; United States / NCI NIH HHS / CA / R01 CA055069; United States / NCI NIH HHS / CA / R01 CA080205; United States / NCI NIH HHS / CA / R35 CA53890
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS122744; NLM/ PMC2728457
  •  go-up   go-down



45. Wang XH, Wang Z, Duan BC, Song JT, He JB, Ou LW, Zhang P: [Inhibitory effect of fumagillol combined with cyclophosphamide on metastasis of lung adenocarcinoma cell line LA795 xenograft in mice]. Ai Zheng; 2005 Dec;24(12):1448-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Inhibitory effect of fumagillol combined with cyclophosphamide on metastasis of lung adenocarcinoma cell line LA795 xenograft in mice].
  • This study was designed to observe the synergetic inhibitory effect of fumagillol (TNP-470) in combination with cyclophosphamide (CTX) on metastasis of lung adenocarcinoma cell line LA795 xenograft in mouse, and to explore the related mechanism of suppressing tumor metastasis by TNP-470.
  • The metastatic tumor foci on lung surface in mice were counted to calculate occurrence rate and inhibitory rate of metastases on lung surface.
  • TNP-470 plus CTX showed synergetic effect on inhibiting metastasis on lung surface with a Q value of 1.21.
  • The metastatic foci on lung surface were significantly fewer in combination group, TNP-470 group, and CTX group than in control group (1.75+/-1.71, 4.75+/-3.34, and 8.50+/-2.67 vs. 12.13+/-4.02, P<0.05).
  • CONCLUSIONS: TNP-470 and CTX have synergetic inhibitory effect on lung metastasis of LA795 xenograft tumor.
  • TNP-470 may inhibit lung metastasis of LA795 xenograft tumor by suppressing the expression of P-selectin.
  • [MeSH-major] Adenocarcinoma / pathology. Cyclohexanes / pharmacology. Cyclophosphamide / pharmacology. Lung Neoplasms / pathology. P-Selectin / metabolism. Sesquiterpenes / pharmacology
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Antineoplastic Agents, Alkylating / pharmacology. Cell Line, Tumor. Drug Synergism. Lung / pathology. Male. Mice. Mice, Nude. Microcirculation / drug effects. Neoplasm Metastasis. Random Allocation

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16351790.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Alkylating; 0 / Cyclohexanes; 0 / P-Selectin; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down



46. Qian XP, Liu BR, Wan L, Hu J, Zhu LJ, Yu LX: [Anti-angiogenic effect of vinorelbine in combination with cetuximab in vitro and in vivo]. Zhonghua Zhong Liu Za Zhi; 2010 Apr;32(4):253-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Human lung adenocarcinoma A549 cells were used as control group.
  • Furthermore, we used Transwell chambers, capillary tube formation and flow cytometry to observe the effects of vinorelbine combined with cetuximab on HUVEC migration, tube formation and cell apoptosis, respectively.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antibodies, Monoclonal / pharmacology. Lung Neoplasms / pathology. Neovascularization, Pathologic / prevention & control. Vinblastine / analogs & derivatives
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / pathology. Animals. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Cetuximab. Chick Embryo. Drug Synergism. Endothelial Cells / cytology. Humans. Umbilical Veins / cytology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CETUXIMAB .
  • Hazardous Substances Data Bank. VINORELBINE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20510073.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 5V9KLZ54CY / Vinblastine; PQX0D8J21J / Cetuximab; Q6C979R91Y / vinorelbine
  •  go-up   go-down



47. Wani Y, Notohara K, Tsukayama C: Mesonephric adenocarcinoma of the uterine corpus: a case report and review of the literature. Int J Gynecol Pathol; 2008 Jul;27(3):346-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesonephric adenocarcinoma of the uterine corpus: a case report and review of the literature.
  • Mesonephric adenocarcinoma (MA) is a rare tumor of the female genital tract, mainly in the cervix and vagina, which is usually associated with mesonephric remnants or mesonephric hyperplasia.
  • A 73-year-old woman presented with multiple nodules in the bilateral lung.
  • In addition, the ductal pattern simulating endometrioid adenocarcinoma was also noted.
  • Other elements consisted of a retiform pattern, serous adenocarcinoma-like papillary budding, and glomeruloid morphology.
  • We review the previously published cases of MA and discuss the principal differential diagnosis of MA in the uterine corpus.
  • [MeSH-major] Adenocarcinoma / pathology. Uterine Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Uterine Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18580312.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 15
  •  go-up   go-down



48. Tsuta K, Ishii G, Nitadori J, Murata Y, Kodama T, Nagai K, Ochiai A: Comparison of the immunophenotypes of signet-ring cell carcinoma, solid adenocarcinoma with mucin production, and mucinous bronchioloalveolar carcinoma of the lung characterized by the presence of cytoplasmic mucin. J Pathol; 2006 May;209(1):78-87
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of the immunophenotypes of signet-ring cell carcinoma, solid adenocarcinoma with mucin production, and mucinous bronchioloalveolar carcinoma of the lung characterized by the presence of cytoplasmic mucin.
  • The latest World Health Organization (WHO) classification divides adenocarcinoma mainly into adenocarcinoma mixed subtypes, acinar adenocarcinoma, papillary adenocarcinoma, bronchioloalveolar carcinoma, and solid adenocarcinoma with mucin production, and it mentions several variants, including fetal adenocarcinoma, mucinous ("colloid") adenocarcinoma, mucinous cystadenocarcinoma, signet-ring adenocarcinoma, and clear cell adenocarcinoma.
  • In general, the mucin-producing adenocarcinoma of the lung comprises signet-ring cell carcinoma (SRCC), solid adenocarcinoma with mucin production (SA), and mucinous bronchioloalveolar carcinoma (m-BAC), mucinous ("colloid") adenocarcinomas and/or mucinous cystadenocarcinoma, and mucoepidermoid carcinoma.
  • In this study we analysed SRCC, SA, m-BAC, normal lung, and foregut-related secretory tissue for immunohistochemical differences using tissue microarrays.
  • These immunohistochemical findings support the results of our previous clinicopathological analysis of SRCC of the lung showing that SRCC occurs anatomically in the peripheral portion of the lung rather than in the bronchial gland-bearing portion.
  • [MeSH-major] Adenocarcinoma / immunology. Lung Neoplasms / immunology. Mucins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / immunology. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Mucinous / immunology. Adenocarcinoma, Mucinous / metabolism. Carcinoma, Signet Ring Cell / immunology. Carcinoma, Signet Ring Cell / metabolism. Humans. Immunoenzyme Techniques. Immunophenotyping. Protein Array Analysis / methods



49. Hashibe M, Morgenstern H, Cui Y, Tashkin DP, Zhang ZF, Cozen W, Mack TM, Greenland S: Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study. Cancer Epidemiol Biomarkers Prev; 2006 Oct;15(10):1829-34
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study.
  • We conducted a population-based case-control study of the association between marijuana use and the risk of lung and upper aerodigestive tract cancers in Los Angeles.
  • METHODS: Our study included 1,212 incident cancer cases and 1,040 cancer-free controls matched to cases on age, gender, and neighborhood.
  • RESULTS: Although using marijuana for > or =30 joint-years was positively associated in the crude analyses with each cancer type (except pharyngeal cancer), no positive associations were observed when adjusting for several confounders including cigarette smoking.
  • The adjusted odds ratio estimate (and 95% confidence limits) for > or =60 versus 0 joint-years was 1.1 (0.56, 2.1) for oral cancer, 0.84 (0.28, 2.5) for laryngeal cancer, and 0.62 (0.32, 1.2) for lung cancer; the adjusted odds ratio estimate for > or =30 versus 0 joint-years was 0.57 (0.20, 1.6) for pharyngeal cancer, and 0.53 (0.22, 1.3) for esophageal cancer.
  • CONCLUSIONS: Our results may have been affected by selection bias or error in measuring lifetime exposure and confounder histories; but they suggest that the association of these cancers with marijuana, even long-term or heavy use, is not strong and may be below practically detectable limits.
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Adolescent. Adult. Aged. Alcohol Drinking / adverse effects. Carcinoma, Large Cell / epidemiology. Carcinoma, Large Cell / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Case-Control Studies. Confounding Factors (Epidemiology). Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / etiology. Female. Humans. Incidence. Laryngeal Neoplasms / epidemiology. Laryngeal Neoplasms / etiology. Los Angeles / epidemiology. Male. Middle Aged. Mouth Neoplasms / epidemiology. Mouth Neoplasms / etiology. Pharyngeal Neoplasms / epidemiology. Pharyngeal Neoplasms / etiology. Population Surveillance. Risk Factors. Time Factors

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17035389.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA11386; United States / NCI NIH HHS / CA / CA96134; United States / NCI NIH HHS / CA / T32 CA009142; United States / NCI NIH HHS / CA / CA77954; United States / NIEHS NIH HHS / ES / ES011667; United States / NCI NIH HHS / CA / CA90833; United States / NCI NIH HHS / CA / CA09142
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



50. Cen WJ, Pan Y, Li WX, Yang SQ: [Comparison of DNA-dependent protein kinase catalytic subunit expression in two lung adenocarcinoma cell lines with different radiosensitivity]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Nov;29(11):2241-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Comparison of DNA-dependent protein kinase catalytic subunit expression in two lung adenocarcinoma cell lines with different radiosensitivity].
  • OBJECTIVE: To investigate DNA-dependent protein kinase catalytic subunit (DNA-PKcs) content and activity in lung adenocarcinoma cell lines and its correlation with radiosensitivity.
  • METHODS: The content and activity of DNA-PKcs were analyzed in two lung adenocarcinoma cell lines A549 and H1299 by Western blotting and the Signa TECT DNA-PK assay kit.
  • The dose-survival relationship for two cell lines was analyzed using clonogenic formation assay.
  • The survival fractions at 2 Gy (SF2) were 0.7412 in A549 cell line and 0.2473 in H1299 cell line.
  • CONCLUSION: DNA-PKcs is an important factor to affect the radiosensitivity of lung adenocarcinoma cell lines.
  • [MeSH-major] Adenocarcinoma / enzymology. Calcium-Binding Proteins / metabolism. Lung Neoplasms / enzymology. Radiation Tolerance
  • [MeSH-minor] Cell Line, Tumor. Humans

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19923078.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CIB1 protein, human; 0 / Calcium-Binding Proteins
  •  go-up   go-down



51. Park SK, Cho LY, Yang JJ, Park B, Chang SH, Lee KS, Kim H, Yoo KY, Lee CT, Scientific Committee, Korean Academy of Tuberculosis and Respiratory Diseases: Lung cancer risk and cigarette smoking, lung tuberculosis according to histologic type and gender in a population based case-control study. Lung Cancer; 2010 Apr;68(1):20-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer risk and cigarette smoking, lung tuberculosis according to histologic type and gender in a population based case-control study.
  • We recruited cases from the Korean Academy of Tuberculosis and Respiratory Diseases and controls from Chungju, a local site of the Korean Multi-Center Cancer Cohort.
  • We used unconditional logistic regression to calculate the odds ratio (OR) and 95% confidence interval (CI) to estimate lung cancer risk by histologic type for males and females separately.
  • The OR (95% CI) of 40 or more pack-years smoked relative to never smokers was 6.78 (4.17-11.00), 3.49 (1.83-6.33), and 2.72 (1.57-4.72) for males, and 13.72 (3.23-58.18), 12.18 (3.12-47.57), and 7.11 (1.78-28.43) for females for squamous cell, adenocarcinoma, and small cell carcinoma, respectively.
  • Among males, the respective OR (95% CI) for past and current history of lung tuberculosis was 3.21 (2.12-4.90), 2.69 (1.63-4.45), and 1.52 (0.83-2.78), and for females was 2.40 (1.30-4.42), 4.20 (2.75-6.39), and 1.37 (0.61-3.06).
  • Our findings provide additional evidence that women are more susceptible to the carcinogenic effects of tobacco, smoking has a higher risk for squamous cell and small cell carcinoma than adenocarcinoma, and tuberculosis is a potential risk factor for certain lung cancer histologic types.
  • [MeSH-major] Carcinoma / epidemiology. Lung Neoplasms / epidemiology. Tuberculosis, Pulmonary / epidemiology

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Tuberculosis.
  • 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
  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19545930.001).
  • [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
  • [Publication-country] Ireland
  •  go-up   go-down



52. Kulke MH, Muzikansky A, Clark J, Enzinger PC, Fidias P, Kinsella K, Michelini A, Fuchs CS: A Phase II trial of vinorelbine in patients with advanced gastroesophageal adenocarcinoma. Cancer Invest; 2006 Jun-Jul;24(4):346-50
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Phase II trial of vinorelbine in patients with advanced gastroesophageal adenocarcinoma.
  • Platinum-based combination chemotherapy regimens increasingly are accepted as a first-line treatment option for patients with advanced gastroesophageal adenocarcinoma.
  • Vinorelbine is both well tolerated and active in patients with advanced breast, lung cancer, and squamous cell carcinoma of the esophagus, but has not previously been evaluated as a single agent in gastroesophageal adenocarcinoma.
  • Twenty-nine patients with previously treated or untreated metastatic gastroesophageal adenocarcinoma were treated with weekly vinorelbine, administered at a dose of 25 mg/m2, and were followed for evidence of radiologic response, toxicity, and survival.
  • We conclude that vinorelbine has minimal toxicity but only minor antitumor activity in patients with advanced gastroesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Phytogenic / adverse effects. Esophageal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy. Vinblastine / analogs & derivatives

  • 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 .
  • Hazardous Substances Data Bank. VINORELBINE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16777685.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA 093401; United States / NHLBI NIH HHS / HL / K30 HL04095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5V9KLZ54CY / Vinblastine; Q6C979R91Y / vinorelbine
  •  go-up   go-down



53. Okita R, Yamashita M, Nakata M, Teramoto N, Bessho A, Mogami H: Multiple ground-glass opacity in metastasis of malignant melanoma diagnosed by lung biopsy. Ann Thorac Surg; 2005 Jan;79(1):e1-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple ground-glass opacity in metastasis of malignant melanoma diagnosed by lung biopsy.
  • Focal ground-glass opacity (GGO) on computed tomography has been reported in several disorders including inflammatory disease and primary neoplastic lesion of the lung.
  • We report a case of malignant melanoma of the nasal cavity metastatic to the lungs in which multiple pulmonary nodules showed GGO.
  • Lung biopsy specimen demonstrated melanoma cells proliferating in a lepidic fashion along the thickened alveolar wall simulating bronchioloalveolar carcinoma.
  • Metastatic lung tumor showing GGO is uncommon.
  • [MeSH-major] Lung Neoplasms / radiography. Lung Neoplasms / secondary. Melanoma / radiography. Melanoma / secondary. Nasal Cavity / pathology. Nose Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / radiography. Adenocarcinoma, Bronchiolo-Alveolar / radiography. Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Chemotherapy, Adjuvant. Dacarbazine / therapeutic use. Diagnosis, Differential. Female. Humans. Melanocytes / pathology. Middle Aged. Picibanil / administration & dosage. Tegafur / administration & dosage. Tomography, X-Ray Computed. Uracil / administration & dosage

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15620900.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 1548R74NSZ / Tegafur; 39325-01-4 / Picibanil; 56HH86ZVCT / Uracil; 7GR28W0FJI / Dacarbazine
  •  go-up   go-down



54. Kishi K, Homma S, Kurosaki A, Motoi N, Yoshimura K: High-resolution computed tomography findings of lung cancer associated with idiopathic pulmonary fibrosis. J Comput Assist Tomogr; 2006 Jan-Feb;30(1):95-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution computed tomography findings of lung cancer associated with idiopathic pulmonary fibrosis.
  • OBJECTIVE: The purpose of this study was to evaluate high-resolution computed tomography (HRCT) findings of lung cancer associated with idiopathic pulmonary fibrosis (IPF).
  • METHODS: Thirty patients with lung cancer who had preceding IPF and were receiving regular follow-up between 1993 and 2002 were examined.
  • RESULTS: In 28 of the 30 patients, the most common HRCT pattern of lung cancer was a nodular lesion with soft tissue attenuation.
  • Squamous cell carcinoma and adenocarcinoma were the most frequent histologic types.
  • CONCLUSIONS: The typical HRCT findings of lung cancer were well-defined nodular lesions with lobulation in peripheral areas of the lung.
  • [MeSH-major] Lung Neoplasms / complications. Lung Neoplasms / radiography. Pulmonary Fibrosis / complications. Pulmonary Fibrosis / radiography. Tomography, X-Ray Computed / methods



55. Miller VA, Hirsch FR, Johnson DH: Systemic therapy of advanced bronchioloalveolar cell carcinoma: challenges and opportunities. J Clin Oncol; 2005 May 10;23(14):3288-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic therapy of advanced bronchioloalveolar cell carcinoma: challenges and opportunities.
  • Bronchioloalveolar cell carcinoma (BAC) has fascinated physicians with its unique epidemiology, pathology, clinical manifestations, and natural history when compared with other non-small-cell lung cancer (NSCLC) subtypes.
  • The recognition that pure BAC and adenocarcinoma with BAC features behave similarly and as such represent a relatively common entity will facilitate accrual to BAC specific studies.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lung Neoplasms / drug therapy



56. Maruyama M, Shiono S, Kato H, Sato T, Yanagawa N: [Surgical resection of metachronous multiple lung cancer after complete response of small cell lung cancer; report of a case]. Kyobu Geka; 2006 Feb;59(2):164-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical resection of metachronous multiple lung cancer after complete response of small cell lung cancer; report of a case].
  • A 76-year-old man underwent combination chemotherapy with cisplatin and etoposide and 50 Gy radiotherapy for left-sided small cell lung cancer in 1999.
  • In December 2004, chest computed tomography (CT) revealed a 1 cm nodule in the right lung.
  • Although no diagnosis could be made by bronchoscope, we suspected metachronous multiple lung cancer because of high 18fluorodeoxyglucose uptake with positron emission tomography (PET).
  • The patient underwent video-assisted thoracoscopic surgery in May 2005; the frozen section diagnosis was adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Lung Neoplasms / surgery. Neoplasms, Second Primary / surgery
  • [MeSH-minor] Aged. Carcinoma, Small Cell / drug therapy. Carcinoma, Small Cell / radiotherapy. Combined Modality Therapy. Humans. Male. Positron-Emission Tomography. Remission Induction. Thoracic Surgery, Video-Assisted. Thoracic Surgical Procedures. Tomography, X-Ray Computed

  • 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
  • (PMID = 16482915.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down



57. Paleiron N, André M, Pottier E, Natali F: [Slow progression of a ground glass lesion - need for long term vigilance]. Rev Mal Respir; 2009 Mar;26(3):315-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Slow progression of a ground glass lesion - need for long term vigilance].
  • The final diagnosis was stage I adenocarcinoma.
  • CONCLUSIONS: The management of a ground glass opacity differs from solid nodules of the lung.
  • Long term follow up is necessary because of the long doubling time in these neoplasms.
  • [MeSH-major] Adenocarcinoma / radiography. Lung Neoplasms / radiography

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19367205.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down



58. Foeglé J, Hédelin G, Lebitasy MP, Purohit A, Velten M, Quoix E: Specific features of non-small cell lung cancer in women: a retrospective study of 1738 cases diagnosed in Bas-Rhin between 1982 and 1997. J Thorac Oncol; 2007 Jun;2(6):466-74
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific features of non-small cell lung cancer in women: a retrospective study of 1738 cases diagnosed in Bas-Rhin between 1982 and 1997.
  • INTRODUCTION: The literature suggests that lung cancer may represent a different disease in women compared with men and that gender specificities have been reported mostly in clinical trials patients.
  • METHODS: We conducted a retrospective, population-based study of a sample of 1738 patients diagnosed with a non-small cell lung cancer (NSCLC) in the department of Bas-Rhin (northeastern France) between 1982 and 1997.
  • More NSCLC were metastatic at diagnosis in women than in men (41.1% versus 29.9%).
  • Adenocarcinoma predominated in women (54.4%), whereas squamous cell carcinoma predominated in men (65.9%).
  • Invasive procedures, such as transthoracic needle biopsy, contributed more frequently to histological diagnosis in women.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / pathology

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17545840.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down



59. Delgado J, Martinez LM, Sánchez TT, Ramirez A, Iturria C, González-Avila G: Lung cancer pathogenesis associated with wood smoke exposure. Chest; 2005 Jul;128(1):124-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer pathogenesis associated with wood smoke exposure.
  • BACKGROUND: Tobacco is considered the most important cause of lung cancer, but other factors could also be involved in its pathogenesis.
  • The aim of the present work was to establish an association between wood smoke exposure and lung cancer pathogenesis, and to analyze the effects of wood smoke on p53 and murine double minute 2 (MDM2) protein expression.
  • DESIGN: Blood samples were obtained from 62 lung cancer patients, 9 COPD patients, and 9 control subjects.
  • Of the 62 lung cancer patients, 23 were tobacco smokers (lung cancer associated with tobacco [LCT] group), 24 were exposed to wood smoke (lung cancer associated with wood smoke [LCW] group), and 15 could not be included in these groups.
  • RESULTS: Approximately 38.7% of the lung cancer patients examined had an association with wood smoke exposure, most of them women living in rural areas.
  • Adenocarcinoma was present in 46.7% of these patients.
  • The p53 and phospho-p53 proteins were significantly increased in LCW samples (56,536.8 +/- 4,629 densitometry units [DU] and 58,244.8 +/- 7,492 DU, respectively [+/- SD]), in comparison with the other groups.
  • The 57-kD MDM2 isoform plasma concentration was very high in LCW and LCT samples (75,696.4 +/- 11,979 DU and 78,551.7 +/- 11,548 DU, respectively).
  • This correlates with the low concentration of p53 observed in the COPD group (13,657 +/- 2,012 DU), and could explain the different clinic evolution of this smoker population in comparison with the LCT subjects.
  • CONCLUSION: This study suggests that there is a possible association of lung cancer with wood smoke exposure.
  • [MeSH-major] Adenocarcinoma / etiology. Environmental Exposure. Lung Neoplasms / etiology. Smoke / adverse effects. Wood

  • Genetic Alliance. consumer health - Lung Cancer.
  • 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] Chest. 2005 Jul;128(1):6-8 [16002905.001]
  • (PMID = 16002925.001).
  • [ISSN] 0012-3692
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Smoke; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down



60. Bai XY, Shen H: [Quantitative study of thyroid transcription factor-1 protein expression in lung carcinoma cell nucleus by tissue microarray]. Nan Fang Yi Ke Da Xue Xue Bao; 2006 Oct;26(10):1423-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Quantitative study of thyroid transcription factor-1 protein expression in lung carcinoma cell nucleus by tissue microarray].
  • OBJECTIVE: To investigate thyroid transcription factor-1 (TTF-1) expression in normal human adult type II alveolar epithelial cells, embryonic pneumocytes, lung carcinoma cells and lymph node metastases of lung cancer.
  • METHODS: Lung carcinoma tissue microarray was constructed containing 765 cores of 20 normal adult lung tissues, 15 embryonic lung tissues, 100 lung carcinomas and 55 corresponding lymph node metastases.
  • The nuclei of lung carcinoma cells had smaller TTF-1 PU than normal adult type II alveolar epithelial cells and embryonic pneumocyte nuclei (P<0.001).
  • The lung adenocarcinoma and small cell lung carcinoma cell nuclei had greater TTF-1 PU than squamous cell carcinoma and large cell lung carcinoma cell nuclei (P<0.001).
  • TTF-1 PU was greater in squamous cell carcinoma cell nuclei than in large cell lung carcinoma cell nuclei (P<0.001).
  • In lung adenocarcinoma, squamous cell lung carcinoma and large cell lung carcinoma, TTF-1 PU was greater in the cancerous cell nuclei of lymph node metastases than in the corresponding primary carcinoma cell nuclei (P<0.001, P<0.001, and P<0.05, respectively).
  • In small cell lung carcinoma, TTF-1 PU of the cancerous cell nuclei of lymph node metastases was similar to that of primary carcinomas (P>0.05).
  • TTF-1 PU was greater in lung carcinoma with lymph node metastases than in those without metastalsis (P<0.001).
  • TTF-1 PU of the cell nuclei was not associated with the tumor growth pattern, differentiation and patients' gender (P>0.05), but was greater in TNM stage II-IV than in stage I (P<0.001).
  • CONCLUSIONS: The amount of TTF-1 in the cell nuclei decreases in the order of normal adult type II alveolar epithelial cells, embryonic pneumocytes and lung carcinoma cells.
  • TTF-1 expression is higher in adenocarcinoma and small cell carcinoma and lower in squamous carcinoma and large cell carcinoma.
  • Stronger TTF-1 expression is associated with greater likeliness of lung carcinoma metastatie, and can be an important hallmark for metastasis potential of lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma.
  • [MeSH-major] Cell Nucleus / metabolism. Lung Neoplasms / metabolism. Nuclear Proteins / biosynthesis. Tissue Array Analysis / methods. Transcription Factors / biosynthesis
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Small Cell / metabolism. Carcinoma, Small Cell / pathology. Humans. Immunohistochemistry. Lymphatic Metastasis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17062341.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
  •  go-up   go-down



61. Miyaishi A, Osawa K, Osawa Y, Inoue N, Yoshida K, Kasahara M, Tsutou A, Tabuchi Y, Sakamoto K, Tsubota N, Takahashi J: MUTYH Gln324His gene polymorphism and genetic susceptibility for lung cancer in a Japanese population. J Exp Clin Cancer Res; 2009;28:10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MUTYH Gln324His gene polymorphism and genetic susceptibility for lung cancer in a Japanese population.
  • BACKGROUND: Genetic polymorphisms of DNA repair enzymes in the base excision repair (BER) pathway, may lead to genetic instability and lung cancer carcinogenesis.
  • We investigated the interactions among the gene polymorphisms in DNA repair genes and lung cancer.
  • METHODS: We analyzed associations among OGG1 Ser326Cys and MUTYH Gln324His gene polymorphisms in relation to lung cancer risk using PCR-RFLP.
  • The study involved 108 lung cancer patients and 121 non-cancer controls divided into non-smokers, smokers according to pack-years smoked in Japanese.
  • RESULTS: The results showed that the MUTYH His/His genotype compared with Gln/Gln genotype showed an increased risk for lung cancer (adjusted odds ratio [OR] 3.03, confidence interval [95%CI], 1.31-7.00, p = 0.010), whereas there was no significant increase for the Gln/His genotype (adjusted OR 1.35, 95%CI 0.70-2.61, p = 0.376).
  • The MUTYH His/His genotype was at a borderline increased risk for both adenocarcinoma and squamous cell carcinoma (adjusted OR 2.50, 95%CI 0.95-6.62, p = 0.065 for adenocarcinoma; adjusted OR 3.20, 95%CI 0.89-11.49, p = 0.075 for squamous cell carcinoma, respectively).
  • However, the OGG1 Ser/Cys or Cys/Cys genotypes compared with the Ser/Ser genotype did not have significantly increased risk for lung cancer, containing either adenocarcinoma or squamous cell carcinoma.
  • The joint effect of tobacco exposure and the MUTYH His/His genotype compared with the Gln/Gln genotype showed a significant association with lung cancer risk in smokers, and there was not significantly increased in non-smokers (adjusted OR 3.82, 95%CI 1.22-12.00, p = 0.022 for smokers; adjusted OR 2.60, 95%CI 0.60-11.25, p = 0.200 for non-smokers, respectively).
  • The effect of tobacco exposure and the OGG1 Ser326Cys showed also no significant risk for lung cancer.
  • CONCLUSION: Our findings suggest that the MUTYH Gln324His polymorphism appear to play an important role in modifying the risk for lung cancer in the Japanese population.
  • [MeSH-major] DNA Glycosylases / genetics. Lung Neoplasms / enzymology. Lung Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Aged. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / genetics. Case-Control Studies. Female. Genetic Predisposition to Disease. Humans. Japan / epidemiology. Male. Middle Aged. Polymorphism, Genetic. Risk Factors. Smoking / genetics. Smoking / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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] Nucleic Acids Res. 2000 Mar 15;28(6):1355-64 [10684930.001]
  • [Cites] J Exp Clin Cancer Res. 2008;27:49 [18823566.001]
  • [Cites] Science. 2001 Feb 16;291(5507):1284-9 [11181991.001]
  • [Cites] Nat Genet. 2002 Feb;30(2):227-32 [11818965.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Apr;11(4):409-12 [11927502.001]
  • [Cites] Hum Genet. 2004 Jan;114(2):207-10 [14579148.001]
  • [Cites] Nature. 1991 Jan 31;349(6308):431-4 [1992344.001]
  • [Cites] Int J Cancer. 1994 Apr 1;57(1):123-8 [8150530.001]
  • [Cites] Chest. 1997 Dec;112(6):1474-9 [9404741.001]
  • [Cites] Hum Genet. 2004 Nov;115(6):498-503 [15449173.001]
  • [Cites] Mutat Res. 2005 Oct 15;578(1-2):430-3 [15890374.001]
  • [Cites] Am J Epidemiol. 2005 Nov 15;162(10):925-42 [16221808.001]
  • [Cites] Cancer Sci. 2006 Aug;97(8):724-8 [16800823.001]
  • [Cites] Lung Cancer. 2006 Dec;54(3):267-83 [16982113.001]
  • [Cites] Asian Pac J Cancer Prev. 2007 Jan-Mar;8(1):103-8 [17477782.001]
  • [Cites] Cancer Sci. 2008 Feb;99(2):355-60 [18271935.001]
  • [Cites] Clin Genet. 2008 Jun;73(6):545-53 [18422726.001]
  • [Cites] Cancer Lett. 2008 Jul 18;266(1):60-72 [18374480.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jul;17(7):1739-45 [18628426.001]
  • [Cites] Gastroenterology. 2008 Aug;135(2):499-507 [18534194.001]
  • [Cites] Arch Biochem Biophys. 2000 May 1;377(1):1-8 [10775435.001]
  • (PMID = 19161591.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  • [Other-IDs] NLM/ PMC2656466
  •  go-up   go-down



62. Huang YD, Hung YC, Yeh LS, Chiang IP, Zeng GC, Chang WC: Synchronous ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma. Taiwan J Obstet Gynecol; 2006 Sep;45(3):264-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synchronous ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma.
  • OBJECTIVE: We report a rare case of synchronous cancer consisting of ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma.
  • Histology showed moderately to poorly differentiated endometrioid adenocarcinoma of the right ovary with extensive lymphovascular permeation, as well as paraaortic and bilateral pelvic lymph node metastases.
  • Endocervical adenocarcinoma, < 3 mm in depth, was also identified on the cervix.
  • The final surgical-pathologic stage of ovarian endometrioid adenocarcinoma was stage IIIc and of endocervical mucinous adenocarcinoma was stage IA1.
  • Adjuvant chemotherapy with carboplatin and paclitaxel was prescribed postoperatively, but the malignancy was not controlled due to lung, brain and vulva metastases.
  • Diagnosis should be based on histologic examination and requires appropriate treatment for both tumors.
  • [MeSH-major] Adenocarcinoma, Mucinous / epidemiology. Carcinoma, Endometrioid / epidemiology. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / epidemiology. Uterine Cervical Neoplasms / epidemiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / secondary. Carcinoembryonic Antigen / metabolism. Combined Modality Therapy. Female. Humans. Lung Neoplasms / secondary. Lymphatic Metastasis. Necrosis. Vulvar Neoplasms / secondary



63. Tomshine JC, Severson SR, Wigle DA, Sun Z, Beleford DA, Shridhar V, Horazdovsky BF: Cell proliferation and epidermal growth factor signaling in non-small cell lung adenocarcinoma cell lines are dependent on Rin1. J Biol Chem; 2009 Sep 25;284(39):26331-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell proliferation and epidermal growth factor signaling in non-small cell lung adenocarcinoma cell lines are dependent on Rin1.
  • In this study, we show that Rin1 is expressed at high levels in a large number of non-small cell lung adenocarcinoma cell lines, including Hop62, H650, HCC4006, HCC827, EKVX, HCC2935, and A549.
  • Rin1 depletion from A549 cells resulted in a decrease in cell proliferation that was correlated to a decrease in epidermal growth factor receptor (EGFR) signaling.
  • Expression of wild type Rin1 but not the Rab5 guanine nucleotide exchange factor-deficient Rin1 (Rin1Delta) complemented the Rin1 depletion effects, and overexpression of Rin1Delta had a dominant negative effect on cell proliferation.
  • Rin1 depletion stabilized the cell surface levels of EGFR, suggesting that internalization was necessary for robust signaling in A549 cells.
  • These data demonstrate that proper internalization and endocytic trafficking are critical for EGFR-mediated signaling in A549 cells and suggest that up-regulation of Rin1 in A549 cell lines may contribute to their proliferative nature.
  • [MeSH-major] Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor. Cell Survival. Dynamins / genetics. Dynamins / metabolism. Endocytosis. Endosomes / metabolism. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Mutation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Transfection. rab5 GTP-Binding Proteins / genetics. rab5 GTP-Binding Proteins / metabolism

  • 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] Cell. 1991 Mar 8;64(5):915-25 [1900457.001]
  • [Cites] Cell. 1990 May 18;61(4):623-34 [2344614.001]
  • [Cites] EMBO J. 1994 Mar 15;13(6):1287-96 [8137813.001]
  • [Cites] Arch Biochem Biophys. 1994 Sep;313(2):351-9 [8080283.001]
  • [Cites] Mol Cell Biol. 1995 Mar;15(3):1318-23 [7862125.001]
  • [Cites] Br J Cancer. 1995 Jul;72(1):56-64 [7599067.001]
  • [Cites] J Cell Biol. 1996 Mar;132(6):1011-23 [8601581.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2369-77 [8628304.001]
  • [Cites] Science. 1996 Dec 20;274(5295):2086-9 [8953040.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 13;94(10):4954-9 [9144171.001]
  • [Cites] Breast Cancer Res Treat. 1999 Jan;53(1):41-50 [10206071.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15284-91 [10329739.001]
  • [Cites] Genomics. 2005 Jun;85(6):704-14 [15885497.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11478-85 [16357156.001]
  • [Cites] Trends Cell Biol. 2006 Jan;16(1):27-35 [16330212.001]
  • [Cites] Exp Cell Res. 2006 Apr 15;312(7):1106-18 [16457816.001]
  • [Cites] Anticancer Res. 2006 Mar-Apr;26(2A):905-16 [16619486.001]
  • [Cites] Biochem Soc Symp. 2007;(74):47-57 [17233579.001]
  • [Cites] Oncol Rep. 2007 May;17(5):1171-5 [17390061.001]
  • [Cites] Nat Struct Mol Biol. 2007 May;14(5):406-12 [17450153.001]
  • [Cites] Endocrinology. 2007 Jun;148(6):2944-54 [17363458.001]
  • [Cites] Annu Rev Cell Dev Biol. 2007;23:519-47 [17506697.001]
  • [Cites] Cancer Res. 2007 Dec 15;67(24):11510-6 [18089779.001]
  • [Cites] Mol Cell Biol. 2008 Mar;28(5):1573-83 [18160707.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1069-75 [18948947.001]
  • [Cites] J Histochem Cytochem. 2000 Jan;48(1):21-33 [10653583.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Jun;28(2):153-63 [10825000.001]
  • [Cites] Nat Genet. 2000 Oct;26(2):216-20 [11017081.001]
  • [Cites] J Cell Biol. 2000 Oct 30;151(3):539-50 [11062256.001]
  • [Cites] Yeast. 2000 Dec;17(4):302-306 [11119307.001]
  • [Cites] J Cell Sci. 2001 Sep;114(Pt 17):3075-81 [11590234.001]
  • [Cites] Dev Cell. 2001 Jul;1(1):73-82 [11703925.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Dec;3(12):893-905 [12461556.001]
  • [Cites] Exp Cell Res. 2003 Mar 10;284(1):78-88 [12648467.001]
  • [Cites] J Biol Chem. 2003 Aug 22;278(34):32027-36 [12783862.001]
  • [Cites] Biochem Soc Trans. 2003 Dec;31(Pt 6):1178-81 [14641021.001]
  • [Cites] Acta Pharmacol Sin. 2004 Jan;25(1):61-7 [14704124.001]
  • [Cites] Cell. 2004 Sep 3;118(5):607-17 [15339665.001]
  • [Cites] Eur J Cell Biol. 2004 Jul;83(6):305-14 [15511088.001]
  • [Cites] J Cell Biol. 1976 Oct;71(1):159-71 [977646.001]
  • [Cites] J Cell Biol. 1979 May;81(2):382-95 [313931.001]
  • [Cites] J Supramol Struct. 1979;12(4):517-31 [233024.001]
  • [Cites] J Cell Biol. 1989 Dec;109(6 Pt 1):2741-9 [2592403.001]
  • [Cites] J Cell Biol. 1989 Dec;109(6 Pt 1):2751-60 [2592404.001]
  • [Cites] J Cell Sci. 1992 Oct;103 ( Pt 2):335-48 [1478937.001]
  • (PMID = 19570984.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / RIN1 protein, human; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.5.2 / rab5 GTP-Binding Proteins; EC 3.6.5.5 / Dynamins
  • [Other-IDs] NLM/ PMC2785321
  •  go-up   go-down



64. Masi T, Cekanova M, Walker K, Bernert H, Majidi M, Becker JM, Schuller HM: Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced pulmonary adenocarcinomas in Syrian golden hamsters contain beta 2-adrenergic receptor single-nucleotide polymorphisms. Genes Chromosomes Cancer; 2005 Oct;44(2):212-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced pulmonary adenocarcinomas in Syrian golden hamsters contain beta 2-adrenergic receptor single-nucleotide polymorphisms.
  • Cigarette smoking contributes to the development of lung cancer throughout the world, with cases of pulmonary adenocarcinoma (PAC) the most numerous.
  • Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which is formed from nicotine, has been demonstrated to cause mutations in genes that affect cell regulation and proliferation.
  • Here we report the cloning and sequencing of Adrb2 clones from either dissected lung tumors from NNK-injected animals or whole-lung tissue from water-injected controls.
  • Our data verified the mutagenic effects of NNK as well as demonstrated that this animal model provides an outstanding way of identifying mutations not only in the Adrb2, but also in other genes that may play essential roles in the regulation and growth of pulmonary adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinogens / toxicity. Lung Neoplasms / genetics. Nitrosamines / toxicity. Polymorphism, Single Nucleotide. Receptors, Adrenergic, beta-2 / genetics

  • 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 = 15942941.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA088809; United States / NCI NIH HHS / CA / R01CA096128
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Receptors, Adrenergic, beta-2; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
  •  go-up   go-down



65. Mangal D, Vudathala D, Park JH, Lee SH, Penning TM, Blair IA: Analysis of 7,8-dihydro-8-oxo-2'-deoxyguanosine in cellular DNA during oxidative stress. Chem Res Toxicol; 2009 May;22(5):788-97
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Similar levels were observed in human lung adenocarcinoma A549 cells, mouse hepatoma Hepa-1c1c7 cells, and human HeLa cervical epithelial adenocarcinoma cells.
  • In contrast, no 8-oxo-dGuo was observed in H358 cell DNA after treatment with MMS.
  • In keeping with this concept, inhibition of catechol-O-methyl transferase (COMT)-mediated detoxification of B[a]P-7,8-catechol with Ro 410961 caused increased 8-oxo-dGuo formation in the H358 cell DNA.

  • COS Scholar Universe. author profiles.
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Free Radic Res. 1998 Dec;29(6):601-8 [10098465.001]
  • [Cites] Electrophoresis. 1999 Jul;20(10):2133-8 [10451126.001]
  • [Cites] Free Radic Res. 2002 Jun;36(6):649-59 [12180190.001]
  • [Cites] Carcinogenesis. 2002 Nov;23(11):1911-8 [12419840.001]
  • [Cites] Carcinogenesis. 2002 Dec;23(12):2129-33 [12507938.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):361-70 [10688856.001]
  • [Cites] Chem Res Toxicol. 2000 Mar;13(3):135-60 [10725110.001]
  • [Cites] Chem Res Toxicol. 2000 Jul;13(7):541-9 [10898585.001]
  • [Cites] Nutrition. 2001 Feb;17(2):161, 163-5 [11240347.001]
  • [Cites] J Biol Chem. 2001 Feb 23;276(8):40601-4 [11246639.001]
  • [Cites] Nucleic Acids Res. 2001 May 15;29(10):2117-26 [11353081.001]
  • [Cites] Science. 2001 Jun 15;292(5524):2083-6 [11408659.001]
  • [Cites] Biochemistry. 2001 Sep 11;40(36):10901-10 [11535067.001]
  • [Cites] Trends Cardiovasc Med. 2001 Apr-May;11(3-4):148-55 [11686005.001]
  • [Cites] Rapid Commun Mass Spectrom. 2003;17(2):126-34 [12512091.001]
  • [Cites] Biochem Pharmacol. 2003 Apr 1;65(7):1035-41 [12663039.001]
  • [Cites] Free Radic Biol Med. 2003 Apr 15;34(8):1089-99 [12684094.001]
  • [Cites] FASEB J. 2003 Jul;17(10):1195-214 [12832285.001]
  • [Cites] Cell Mol Life Sci. 2003 Oct;60(10):2064-83 [14618256.001]
  • [Cites] Chem Res Toxicol. 2003 Nov;16(11):1470-6 [14615974.001]
  • [Cites] FASEB J. 2005 Jan;19(1):82-4 [15533950.001]
  • [Cites] Mol Carcinog. 2005 Mar;42(3):127-41 [15584022.001]
  • [Cites] Free Radic Biol Med. 2005 Jun 15;38(12):1543-52 [15917183.001]
  • [Cites] Chem Res Toxicol. 2005 Jun;18(6):1026-37 [15962938.001]
  • [Cites] Mutat Res. 2005 Dec 11;591(1-2):60-73 [16081110.001]
  • [Cites] Clin Chim Acta. 2006 Mar;365(1-2):30-49 [16214123.001]
  • [Cites] Toxicology. 2006 Apr 17;221(2-3):172-8 [16457930.001]
  • [Cites] Toxicology. 2006 Apr 17;221(2-3):166-71 [16490296.001]
  • [Cites] Chem Res Toxicol. 2006 May;19(5):719-28 [16696575.001]
  • [Cites] Mutagenesis. 2006 May;21(3):185-90 [16597659.001]
  • [Cites] Antioxid Redox Signal. 2006 May-Jun;8(5-6):1021-31 [16771692.001]
  • [Cites] DNA Repair (Amst). 2006 Jul 13;5(7):761-72 [16621731.001]
  • [Cites] DNA Repair (Amst). 2006 Nov 8;5(11):1337-45 [16861056.001]
  • [Cites] DNA Repair (Amst). 2007 Mar 1;6(3):274-9 [17161978.001]
  • [Cites] J Neurosci Res. 2007 Apr;85(5):919-34 [17279544.001]
  • [Cites] DNA Repair (Amst). 2007 Jun 1;6(6):760-9 [17280880.001]
  • [Cites] Mutat Res. 2007 Jul 1;620(1-2):135-44 [17403525.001]
  • [Cites] Mutat Res. 2007 Jul 1;620(1-2):71-82 [17434188.001]
  • [Cites] J Nutr Biochem. 2007 Sep;18(9):567-79 [17360173.001]
  • [Cites] J Phys Chem B. 2007 Sep 6;111(35):10453-60 [17661513.001]
  • [Cites] Mol Aspects Med. 2007 Jun-Aug;28(3-4):307-22 [17659329.001]
  • [Cites] Mol Biotechnol. 2007 Sep;37(1):48-51 [17914163.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):3-14 [18199707.001]
  • [Cites] Free Radic Biol Med. 2008 Feb 1;44(3):464-73 [17983606.001]
  • [Cites] J Neurol Sci. 2008 Mar 15;266(1-2):57-62 [17888453.001]
  • [Cites] Eur J Nutr. 2008 May;47 Suppl 2:19-28 [18458832.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 13;105(19):6846-51 [18474869.001]
  • [Cites] Chem Res Toxicol. 2008 May;21(5):1039-49 [18489080.001]
  • [Cites] Acc Chem Res. 2008 Aug;41(8):1075-83 [18666785.001]
  • [Cites] Free Radic Biol Med. 2008 Nov 1;45(9):1318-25 [18775490.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 3;95(17):1263-5 [12953074.001]
  • [Cites] Mutat Res. 2002 Jan 15;513(1-2):37-48 [11719088.001]
  • [Cites] Free Radic Res. 2002 Mar;36(3):239-45 [12071341.001]
  • [Cites] Free Radic Res. 2002 Mar;36(3):307-16 [12071350.001]
  • [Cites] J Biol Chem. 2002 Jul 5;277(27):24799-808 [11978787.001]
  • [Cites] Mutat Res. 2003 Oct 29;531(1-2):177-90 [14637254.001]
  • [Cites] Arch Biochem Biophys. 2004 Mar 1;423(1):57-65 [14989265.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2977-85 [15131033.001]
  • [Cites] Lancet Oncol. 2004 Oct;5(10):600-6 [15465463.001]
  • [Cites] J Biol Chem. 1988 Feb 5;263(4):1814-20 [3276678.001]
  • [Cites] J Environ Pathol Toxicol Oncol. 1992 May-Jun;11(3):139-43 [1625183.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7915-22 [8367443.001]
  • [Cites] Ann Rheum Dis. 1993 Sep;52(9):659-66 [8239761.001]
  • [Cites] Mol Cell Biol. 1995 Feb;15(2):989-96 [7823963.001]
  • [Cites] Environ Health Perspect. 1994 Dec;102 Suppl 10:33-6 [7705301.001]
  • [Cites] J Bacteriol. 1996 Jul;178(13):3885-92 [8682794.001]
  • [Cites] Science. 1996 Jul 5;273(5271):59-63 [8658196.001]
  • [Cites] Biotechniques. 1997 Mar;22(3):550-3 [9067036.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jan 6;95(1):288-93 [9419368.001]
  • [Cites] Chem Res Toxicol. 1998 Aug;11(8):882-7 [9705749.001]
  • [Cites] FASEB J. 1998 Oct;12(13):1397-400 [9761783.001]
  • [Cites] Nucleic Acids Res. 1998 Nov 15;26(22):5116-22 [9801308.001]
  • [Cites] Free Radic Res. 1998 Dec;29(6):541-50 [10098458.001]
  • (PMID = 19309085.001).
  • [ISSN] 1520-5010
  • [Journal-full-title] Chemical research in toxicology
  • [ISO-abbreviation] Chem. Res. Toxicol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES015857; United States / NIEHS NIH HHS / ES / U01ES016004; United States / NCI NIH HHS / CA / R01CA130038; United States / NIEHS NIH HHS / ES / R01ES015857; United States / NIEHS NIH HHS / ES / P30 ES013508; United States / NIEHS NIH HHS / ES / U01 ES016004; United States / NIEHS NIH HHS / ES / P30ES013508; United States / NCI NIH HHS / CA / R01 CA130038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
  • [Other-IDs] NLM/ PMC2684441
  •  go-up   go-down



66. Río Ramírez MT, Casado López ME, Peirón Puyal MJ, Peñas Herrero JM: [Pulmonary adenocarcinoma and Bazex syndrome (paraneoplastic acrokeratosis)]. Arch Bronconeumol; 2007 Jan;43(1):46-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pulmonary adenocarcinoma and Bazex syndrome (paraneoplastic acrokeratosis)].
  • [Transliterated title] Adenocarcinoma de pulmón y síndrome de Bazex (acroqueratosis paraneoplásica).
  • The tumors most frequently associated with Bazex syndrome are squamous cell carcinomas of the upper respiratory and digestive tracts, whereas lung cancers, particularly adenocarcinomas, are rarely associated.
  • We present a case in which both pulmonary adenocarcinoma and Bazex syndrome were present.
  • [MeSH-major] Acrodermatitis / etiology. Adenocarcinoma / complications. Keratosis / etiology. Lung Neoplasms / complications. Paraneoplastic Syndromes / etiology
  • [MeSH-minor] Aged. Fatal Outcome. Foot Dermatoses / diagnosis. Foot Dermatoses / etiology. Hand Dermatoses / diagnosis. Hand Dermatoses / etiology. Humans. Lymphatic Metastasis. Male. Nail Diseases / diagnosis. Nail Diseases / etiology. Pruritus / etiology. Pulmonary Fibrosis / complications. Respiratory Insufficiency / complications. Syndrome

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17257564.001).
  • [ISSN] 0300-2896
  • [Journal-full-title] Archivos de bronconeumología
  • [ISO-abbreviation] Arch. Bronconeumol.
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down



67. Tsutsumida H, Goto M, Kitajima S, Kubota I, Hirotsu Y, Wakimoto J, Batra SK, Imai K, Yonezawa S: MUC4 expression correlates with poor prognosis in small-sized lung adenocarcinoma. Lung Cancer; 2007 Feb;55(2):195-203
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MUC4 expression correlates with poor prognosis in small-sized lung adenocarcinoma.
  • The mortality of lung cancer remains high, despite improved diagnostic techniques that allow small lung tumors to be detected.
  • In this study, we evaluated the prognostic significance of the tracheal mucin MUC4 by immunohistochemical investigation of the expression profiles of MUC4, ErbB2, p27 and MUC1 in lung adenocarcinoma specimens (non-bronchiolo-alveolar type, < or =3cm) from 185 patients.
  • However, MUC4 expression was found to be unrelated to expression of MUC1, ErbB2 and p27 in small-sized lung adenocarcinomas.
  • In conclusion, high MUC4 expression in small-sized lung adenocarcinomas correlates with a short DFI and a poor survival rate.
  • Therefore, MUC4 expression might be a new independent factor for prediction of outcome and indication of poor prognosis in lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Lung Neoplasms / metabolism. Mucins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Mucin-4. Neoplasm Recurrence, Local. Prognosis. Proliferating Cell Nuclear Antigen / metabolism. Receptor, ErbB-2 / metabolism. Statistics, Nonparametric. Survival Rate

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 17126950.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 78590
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / MUC4 protein, human; 0 / Mucin-4; 0 / Mucins; 0 / Proliferating Cell Nuclear Antigen; 0 / p27 antigen; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down



68. Yamazaki S, Sekine I, Matsuno Y, Takei H, Yamamoto N, Kunitoh H, Ohe Y, Tamura T, Kodama T, Asamura H, Tsuchiya R, Saijo N: Clinical responses of large cell neuroendocrine carcinoma of the lung to cisplatin-based chemotherapy. Lung Cancer; 2005 Aug;49(2):217-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical responses of large cell neuroendocrine carcinoma of the lung to cisplatin-based chemotherapy.
  • BACKGROUND: The efficacy of chemotherapy in patients with large cell neuroendocrine carcinoma of the lung (LCNEC) remains unclear.
  • METHODS: Patients with LCNEC who received cisplatin-based chemotherapy were identified by reviewing 567 autopsied and 2790 surgically resected lung cancer patients.
  • The response rate did not differ between patients with the initial diagnosis of SCLC and those with the initial diagnosis of NSCLC, however, the response rate in chemo-naive patients (64%) was significantly different from that in previously treated patients (17%).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Neuroendocrine / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adult. Aged. Carcinoma, Large Cell / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Small Cell / drug therapy. Cisplatin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitomycin / administration & dosage. Neoplasm Staging. Treatment Outcome. Vindesine / administration & dosage

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • Hazardous Substances Data Bank. VINDESINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16022916.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; RSA8KO39WH / Vindesine
  •  go-up   go-down



69. Dunn GP, Sheehan KC, Old LJ, Schreiber RD: IFN unresponsiveness in LNCaP cells due to the lack of JAK1 gene expression. Cancer Res; 2005 Apr 15;65(8):3447-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We reported previously that 23% of human lung adenocarcinoma cell lines were unresponsive to IFN-gamma.
  • To extend this finding to cancer cells derived from distinct tissues of origin, we assessed IFN-gamma receptor signaling in the LNCaP human prostate adenocarcinoma cell line, which in previous experiments by others failed to induce a range of IFN-dependent biological responses.
  • These results identify the molecular basis for IFN insensitivity in the LNCaP cell line and suggest that epigenetic silencing of key immunologic signaling components may be one mechanism by which tumor cells evade immune detection and elimination.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / immunology. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Gene Expression. Histone Deacetylase Inhibitors. Humans. Interferon-alpha. Janus Kinase 1. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Recombinant Proteins. Signal Transduction. Transfection

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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 = 15833880.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA107527; United States / NCI NIH HHS / CA / CA43059
  • [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 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / interferon-alpha A-D; 82115-62-6 / Interferon-gamma; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 1
  •  go-up   go-down



70. Oh JJ, Koegel AK, Phan DT, Razfar A, Slamon DJ: The two single nucleotide polymorphisms in the H37/RBM5 tumour suppressor gene at 3p21.3 correlated with different subtypes of non-small cell lung cancers. Lung Cancer; 2007 Oct;58(1):7-14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The two single nucleotide polymorphisms in the H37/RBM5 tumour suppressor gene at 3p21.3 correlated with different subtypes of non-small cell lung cancers.
  • Allele loss and genetic alteration in chromosome 3p, particularly in 3p21.3 region, are the most frequent and the earliest genomic abnormalities found in lung cancer.
  • In the current study, in an attempt to find, if any, mutations in the H37 coding region in lung cancer cells, we compared nucleotide sequences of the entire H37 gene in tumour versus adjacent normal tissues from 17 non-small cell lung cancer (NSCLC) patients.
  • In addition, we found that specific allele types at these SNP positions are correlated with different histological subtypes of NSCLC; tumours containing heterozygous alleles (C+T) at these SNP positions are more likely to be associated with adenocarcinoma (AC), whereas, homozygous alleles (either C or T) are associated with squamous cell carcinoma (SCC) (p=0.0098).
  • We postulate that, these two silent polymorphisms may be in linkage disequilibrium (LD) with a disease causative allele in the 3p21.3 tumour suppressor region which is packed with a large number of important genes affecting lung cancer development.
  • In addition, because of prevalent loss of heterozygosity (LOH) detected at 3p21.3 which precedes lung cancer initiation, these SNPs may be developed into a marker screening for the high risk individuals.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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] Nat Biotechnol. 2000 Sep;18(9):1001-5 [10973224.001]
  • [Cites] Oncogene. 2000 Aug 3;19(33):3774-81 [10949932.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6116-33 [11085536.001]
  • [Cites] Nature. 2001 Feb 15;409(6822):928-33 [11237013.001]
  • [Cites] Oncogene. 2001 May 10;20(21):2713-9 [11420683.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8718-22 [11751390.001]
  • [Cites] J Neurosci Res. 2002 Mar 15;67(6):812-22 [11891796.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3207-13 [12036935.001]
  • [Cites] Apoptosis. 2002 Oct;7(5):421-32 [12207175.001]
  • [Cites] Otol Neurotol. 2002 Sep;23(5):736-48 [12218628.001]
  • [Cites] Genes Cells. 2003 Feb;8(2):109-19 [12581154.001]
  • [Cites] Nat Genet. 2003 Apr;33(4):457-8 [12652301.001]
  • [Cites] Hypertension. 2003 Oct;42(4):500-6 [12925562.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):1949-60 [14578194.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2716-26 [15048096.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3060-71 [15126342.001]
  • [Cites] Neurotox Res. 2004;6(1):51-6 [15184105.001]
  • [Cites] Apoptosis. 2004 Jul;9(4):475-84 [15192330.001]
  • [Cites] J Endocrinol. 2004 Sep;182(3):479-84 [15350189.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523.001]
  • [Cites] Vet Pathol. 1994 Sep;31(5):561-71 [7801434.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 17;89(18):1366-73 [9308707.001]
  • [Cites] Genes Chromosomes Cancer. 1997 Dec;20(4):399-407 [9408757.001]
  • [Cites] Cancer Res. 1998 Apr 15;58(8):1605-8 [9563468.001]
  • [Cites] Br J Cancer. 1998 Jul;78(1):73-8 [9662254.001]
  • [Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]
  • [Cites] Recent Results Cancer Res. 1999;151:3-12 [10337715.001]
  • [Cites] Int J Cancer. 1999 Nov 12;83(4):456-64 [10508479.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Future Oncol. 2005 Feb;1(1):79-92 [16555978.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3419-27 [16585163.001]
  • [Cites] Pediatr Allergy Immunol. 2006 Aug;17(5):323-8 [16846449.001]
  • [Cites] Science. 2007 Jan 26;315(5811):525-8 [17185560.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):49-54 [12469122.001]
  • [Cites] Genes Cells. 2000 Oct;5(10):849-58 [11029660.001]
  • (PMID = 17606309.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090388-01; United States / NCI NIH HHS / CA / P50 CA090388; United States / NCI NIH HHS / CA / P50 CA090388-01; United States / NCI NIH HHS / CA / P50 CA90388
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / RBM5 protein, human; 0 / RNA-Binding Proteins; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ NIHMS31518; NLM/ PMC2071930
  •  go-up   go-down



71. Takahashi F, Kumasaka T, Nagaoka T, Wakiya M, Fujii H, Shimizu K, Uchida K, Morio Y, Seyama K, Hino O, Takahashi K, Fukuchi Y: Osteopontin expression in pulmonary tumor thrombotic microangiopathy caused by gastric carcinoma. Pathol Int; 2009 Oct;59(10):752-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osteopontin expression in pulmonary tumor thrombotic microangiopathy caused by gastric carcinoma.
  • Pulmonary tumor thrombotic microangiopathy (PTTM) is characterized by fibrocellular intimal proliferation and thrombus formation in small pulmonary arteries and arterioles in patients with metastatic carcinoma.
  • Herein is described an autopsy case of gastric adenocarcinoma with severe pulmonary hypertension due to PTTM.
  • Histologically, tumor cell emboli markedly induced both fibromuscular intimal thickening and thrombosis, resulting in luminal stenosis and occlusion of small pulmonary arteries and arterioles.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Lung Neoplasms / metabolism. Osteopontin / metabolism. Stomach Neoplasms / pathology. Thrombotic Microangiopathies / metabolism
  • [MeSH-minor] Adult. Cell Proliferation. Fatal Outcome. Humans. Hypertension, Pulmonary / etiology. Male. Platelet-Derived Growth Factor / metabolism. Thrombosis / etiology. Tunica Intima / pathology. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19788622.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Platelet-Derived Growth Factor; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / platelet-derived growth factor A; 106441-73-0 / Osteopontin
  •  go-up   go-down



72. Liu S, Cheng H, Yao S, Wang C, Han G, Li X, Liu C: The clinical application value of PET/CT in adenocarcinoma with bronchioloalveolar carcinoma features. Ann Nucl Med; 2010 Aug;24(7):541-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical application value of PET/CT in adenocarcinoma with bronchioloalveolar carcinoma features.
  • OBJECTIVE: The goal of our study was to demonstrate the clinical usefulness of positron emission tomography/computed tomography (PET/CT) for adenocarcinoma with bronchioloalveolar carcinoma (BAC) features, through evaluating the relationship between the intrathoracic lymph node metastases and maximum standardized uptake value (SUVmax), tumor size of the primary tumor and the ratio of BAC component and analysing the correlation of SUVmax, tumor size and the ratio of BAC component.
  • Forty-five patients with focal peripheral lung adenocarcinoma with BAC features were included in this study and underwent the PET/CT scan.
  • The diagnosis of the lesion was made by surgical histopathology.
  • The maximum dimension of a tumor on pulmonary window setting images (pDmax, P = 0.373) had no significance.
  • CONCLUSIONS: PET/CT would be clinically useful for adenocarcinoma with BAC features, because SUVmax obtained by PET/CT can predict the incidence of intrathoracic lymph node metastases at preoperative stages and even for inoperable patients.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Adenocarcinoma, Bronchiolo-Alveolar / complications. Positron-Emission Tomography. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20614257.001).
  • [ISSN] 1864-6433
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  •  go-up   go-down



73. Yamada S, Fukuoka K, Miyake M, Miyata S, Nakajima T, Tamura K, Tabata C, Iida S, Kuribayashi K, Uesaka A, Murakami A, Yasumitsu A, Nakano T: [A case of primary lung cancer with cervical tuberculous lymphadenitis]. Nihon Kokyuki Gakkai Zasshi; 2007 Sep;45(9):720-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of primary lung cancer with cervical tuberculous lymphadenitis].
  • Partial lung resection of the right S4 was carried out by video-assisted thoracoscopic surgery and primary lung cancer was diagnosed.
  • To our knowledge, there has been no previous report of both primary lung cancer and cervical tuberculous lymphadenitis being present at the time of the first examination.
  • [MeSH-major] Adenocarcinoma / complications. Lung Neoplasms / complications. Tuberculosis, Lymph Node / complications

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Cervical cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17929476.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down



74. Khodarev NN, Pitroda SP, Beckett MA, MacDermed DM, Huang L, Kufe DW, Weichselbaum RR: MUC1-induced transcriptional programs associated with tumorigenesis predict outcome in breast and lung cancer. Cancer Res; 2009 Apr 1;69(7):2833-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MUC1-induced transcriptional programs associated with tumorigenesis predict outcome in breast and lung cancer.
  • The Mucin 1 (MUC1) oncoprotein is aberrantly overexpressed in diverse human malignancies including breast and lung cancer.
  • Although MUC1 modulates the activity of several transcription factors, there is no information regarding the effects of MUC1 on global gene expression patterns and the potential role of MUC1-induced genes in predicting outcome for cancer patients.
  • A set of experimentally derived MUC1-induced genes associated with tumorigenesis was applied to the analysis of breast and lung adenocarcinoma cancer databases.
  • A 35-gene MUC1-induced tumorigenesis signature predicts significant decreases in both disease-free and overall survival in patients with breast (n=295) and lung (n=442) cancers.
  • The data show that the MUC1 oncoprotein contributes to the regulation of genes that are highly predictive of clinical outcome in breast and lung cancer patients.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Biotechniques. 2002 Feb;32(2):316, 318, 320 [11848408.001]
  • [Cites] Genomics. 2003 Feb;81(2):202-9 [12620398.001]
  • [Cites] Oncogene. 2003 Sep 4;22(38):6107-10 [12955090.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35458-64 [12826677.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1714-9 [14755057.001]
  • [Cites] Cancer Cell. 2004 Feb;5(2):163-75 [14998492.001]
  • [Cites] J Biol Chem. 2004 May 14;279(20):20607-12 [14999001.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Oct 1;60(2):553-63 [15380592.001]
  • [Cites] Hybridoma. 1984 Fall;3(3):223-32 [6094338.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2320-3 [2895474.001]
  • [Cites] Cancer Res. 1989 Dec 15;49(24 Pt 1):6966-71 [2582438.001]
  • [Cites] J Biol Chem. 1992 Mar 25;267(9):6171-7 [1556125.001]
  • [Cites] Nature. 1998 Jul 16;394(6690):287-91 [9685160.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):167-78 [15710329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3738-43 [15701700.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3146-54 [15833844.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10413-22 [16288032.001]
  • [Cites] Nat Struct Mol Biol. 2006 Jan;13(1):71-6 [16369486.001]
  • [Cites] Mol Cell. 2006 Jan 20;21(2):295-305 [16427018.001]
  • [Cites] Trends Cell Biol. 2006 Sep;16(9):467-76 [16904320.001]
  • [Cites] BMC Cancer. 2006;6:220 [16953875.001]
  • [Cites] Int J Cancer. 2007 Jun 15;120(12):2643-9 [17294451.001]
  • [Cites] Int J Oncol. 2007 Sep;31(3):671-7 [17671696.001]
  • [Cites] Sci Signal. 2008;1(27):pe35 [18612140.001]
  • [Cites] Nat Med. 2008 Aug;14(8):822-7 [18641660.001]
  • (PMID = 19318547.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097098; United States / NCI NIH HHS / CA / R01 CA1114231; United States / NCI NIH HHS / CA / R01 CA97098; United States / NCI NIH HHS / CA / R01 CA111423-01A1; United States / NCI NIH HHS / CA / R01 CA111423; United States / NCI NIH HHS / CA / CA111423-01A1; United States / NCI NIH HHS / CA / R01 CA097098-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MUC1 protein, human; 0 / Mucin-1
  • [Other-IDs] NLM/ NIHMS263646; NLM/ PMC3034477
  •  go-up   go-down



75. Altinisik J, Balta ZB, Aydin G, Ulutin T, Buyru N: Investigation of glutathione S-transferase M1 and T1 deletions in lung cancer. Mol Biol Rep; 2010 Jan;37(1):263-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigation of glutathione S-transferase M1 and T1 deletions in lung cancer.
  • Previous studies have suggested that GST genotypes may play a role in determining susceptibility to a number of unrelated cancers, including lung cancer.
  • The GSTM1 and GSTT1 polymorphisms were determined by PCR-based analysis in 75 lung cancer patients and 55 controls.
  • The frequencies of GSTM1 and GSTT1 null genotypes were 37.3 and 22.7% in lung cancer patients and 27.3 and 16.4% in controls, respectively.
  • When analyzed by histology the GSTM1 null genotype was more prevalent in squamous-cell carcinoma and adenocarcinoma patients.
  • Whereas, GSTT1 null genotype frequency was lower in small-cell lung cancer patients than controls.
  • According to smoking status, null genotype for both gene are associated with an increase in risk for lung cancer.
  • Our results suggest that GSTM1 and GSTT1 polymorphisms may play a role in the development of lung cancer for some histological subtypes and modifies the risk of smoking-related lung cancer.
  • [MeSH-major] Gene Deletion. Glutathione Transferase / genetics. Lung Neoplasms / enzymology. Lung Neoplasms / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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] Biochem J. 1992 Sep 15;286 ( Pt 3):929-35 [1417752.001]
  • [Cites] Biochem J. 1991 Mar 1;274 ( Pt 2):409-14 [1848757.001]
  • [Cites] Ann Intern Med. 1986 Oct;105(4):607-9 [3752764.001]
  • [Cites] Cancer Lett. 1999 Mar 22;137(1):53-60 [10376794.001]
  • [Cites] Carcinogenesis. 1993 Sep;14(9):1821-4 [8403204.001]
  • [Cites] Biochem J. 1994 May 15;300 ( Pt 1):271-6 [8198545.001]
  • [Cites] Hum Genet. 1985;69(1):66-8 [3967891.001]
  • [Cites] Genomics. 1995 Jan 20;25(2):381-7 [7789971.001]
  • [Cites] Cancer Res. 1990 Mar 1;50(5):1585-90 [2302718.001]
  • [Cites] Carcinogenesis. 1986 May;7(5):751-3 [3698203.001]
  • [Cites] Pharmacol Rev. 1982 Jun;34(2):189-222 [6287505.001]
  • [Cites] CRC Crit Rev Biochem. 1988;23(3):283-337 [3069329.001]
  • [Cites] Pharmacogenetics. 1998 Dec;8(6):495-502 [9918133.001]
  • [Cites] Cancer Res. 1995 Oct 1;55(19):4237-9 [7671227.001]
  • [Cites] Lancet. 1996 Feb 3;347(8997):295-7 [8569364.001]
  • [Cites] Lung Cancer. 2004 Aug;45(2):155-60 [15246186.001]
  • [Cites] Carcinogenesis. 2000 Nov;21(11):1971-5 [11062156.001]
  • [Cites] Lung Cancer. 2004 Mar;43(3):259-66 [15165083.001]
  • [Cites] Cancer Lett. 2003 Nov 25;201(2):185-93 [14607333.001]
  • [Cites] Carcinogenesis. 2002 Aug;23(8):1343-50 [12151353.001]
  • [Cites] Cancer Lett. 2002 Jun 28;180(2):165-71 [12175548.001]
  • [Cites] Lung Cancer. 2003 Jun;40(3):247-58 [12781423.001]
  • [Cites] Carcinogenesis. 1995 May;16(5):1243-5 [7767992.001]
  • [Cites] J Natl Cancer Inst. 1993 Jul 21;85(14):1159-64 [8320745.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Aug;8(8):675-82 [10744127.001]
  • [Cites] Mutat Res. 2005 Dec 30;592(1-2):45-57 [16009381.001]
  • [Cites] Cancer Invest. 1999;17(8):661-2 [10592773.001]
  • [Cites] Arch Toxicol. 1994;68(7):423-7 [7979958.001]
  • [Cites] Cancer Lett. 2004 May 10;208(1):65-74 [15105047.001]
  • [Cites] Biochem Pharmacol. 1992 Apr 15;43(8):1671-4 [1575765.001]
  • [Cites] Pharmacology. 2000 Sep;61(3):154-66 [10971201.001]
  • [Cites] Recent Results Cancer Res. 1998;154:47-85 [10026993.001]
  • [Cites] Pharmacogenetics. 1995 Oct;5(5):332-4 [8563775.001]
  • [Cites] Carcinogenesis. 1995 Jul;16(7):1655-7 [7614702.001]
  • (PMID = 19669596.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
  •  go-up   go-down



76. Pinnarò P, Soriani A, Landoni V, Giordano C, Papale M, Marsella A, Marucci L, Arcangeli G, Strigari L: Accelerated hypofractionated radiotherapy as adjuvant regimen after conserving surgery for early breast cancer: interim report of toxicity after a minimum follow up of 3 years. J Exp Clin Cancer Res; 2010;29:9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated hypofractionated radiotherapy as adjuvant regimen after conserving surgery for early breast cancer: interim report of toxicity after a minimum follow up of 3 years.
  • METHODS: From October 2004 to March 2006, 39 consecutive patients aged over 18 years with pTis, pT1-2, pN0-1 breast adenocarcinoma who underwent conservative surgery were treated with an adjuvant accelerated hypofractionated radiotherapy schedule consisting of 34 Gy in 10 daily fractions over 2 weeks to the whole breast, followed after 1 week by an electron boost dose of 8 Gy in a single fraction to the tumour bed.
  • Skin and lung radiation toxicity was evaluated daily during therapy, once a week for one month after radiotherapy completion, every 3 months for the first year and from then on every six months.
  • In particular lung toxicity was investigated in terms of CT density evaluation, pulmonary functional tests, and clinical and radiological scoring.
  • Paired t-test, Chi-square test and non-parametric Wilcoxon test were performed.
  • None of the patients showed any clinical signs of lung toxicity, no CT-lung toxicity was denoted by radiologist on CT lung images acquired about 1 year post-radiotherapy, no variation of pulmonary density evaluated in terms of normalised Hounsfield numbers was evident.
  • [MeSH-major] Adenocarcinoma / radiotherapy. Breast Neoplasms / radiotherapy. Dose Fractionation. Radiotherapy / adverse effects
  • [MeSH-minor] Aged. Aged, 80 and over. Feasibility Studies. Female. Follow-Up Studies. Humans. Lung / radiation effects. Mastectomy, Segmental. Middle Aged. Radiotherapy, Adjuvant. Skin

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Radiation Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2002 Oct 17;347(16):1233-41 [12393820.001]
  • [Cites] Ann Oncol. 2009 Mar;20(3):437-40 [19139179.001]
  • [Cites] Radiother Oncol. 1983 Nov;1(2):187-91 [6680223.001]
  • [Cites] Br J Radiol. 1989 Aug;62(740):679-94 [2670032.001]
  • [Cites] Chest. 1990 Mar;97(3):554-61 [2106409.001]
  • [Cites] Eur Respir J Suppl. 1993 Mar;16:5-40 [8499054.001]
  • [Cites] Radiother Oncol. 1995 Apr;35(1):17-60 [7569012.001]
  • [Cites] J Natl Cancer Inst. 1996 Jul 3;88(13):918-22 [8656444.001]
  • [Cites] Radiother Oncol. 1998 Dec;49(3):245-54 [10075257.001]
  • [Cites] Oncol Rep. 1999 May-Jun;6(3):513-7 [10203583.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Sep 1;45(2):323-9 [10487552.001]
  • [Cites] Radiother Oncol. 2005 Apr;75(1):9-17 [15878095.001]
  • [Cites] Strahlenther Onkol. 2005 Sep;181(9):567-73 [16170483.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Nov 1;63(3):672-82 [15939548.001]
  • [Cites] Lancet. 2005 Dec 17;366(9503):2087-106 [16360786.001]
  • [Cites] Lancet Oncol. 2006 Jun;7(6):467-71 [16750496.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Dec 1;48(5):1307-10 [11121627.001]
  • [Cites] Ann Oncol. 2001 Jul;12(7):997-1003 [11521809.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Jan 1;52(1):144-55 [11777632.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Apr 1;52(5):1196-206 [11955730.001]
  • [Cites] J Natl Cancer Inst. 2002 Aug 7;94(15):1143-50 [12165639.001]
  • [Cites] Am J Clin Oncol. 2006 Oct;29(5):479-83 [17023783.001]
  • [Cites] Lancet. 2008 Mar 29;371(9618):1098-107 [18355913.001]
  • [Cites] Lancet Oncol. 2008 Apr;9(4):331-41 [18356109.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Oct 1;72(2):485-93 [18407434.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Nov 15;57(4):912-4 [14575821.001]
  • (PMID = 20100335.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2837631
  •  go-up   go-down



77. Satouchi M, Kotani Y, Katakami N, Shimada T, Urata Y, Yoshimura S, Funada Y, Hata A, Ando M, Negoro S: Randomized phase II study of two different schedules of gemcitabine and oral S-1 in chemo-naïve patients with advanced non-small cell lung cancer. J Thorac Oncol; 2010 May;5(5):696-701
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II study of two different schedules of gemcitabine and oral S-1 in chemo-naïve patients with advanced non-small cell lung cancer.
  • INTRODUCTION: This study was conducted to evaluate the efficacy and safety and to compare dosing schedules of gemcitabine combined with S-1 in chemo-naïve non-small cell lung cancer patients.
  • METHODS: Patients with chemo-naïve stage IIIB/IV non-small cell lung cancer were randomized into two treatment arms.
  • CONCLUSION: The combination of gemcitabine and S-1 was determined to be feasible and effective for advanced non-small cell lung cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Squamous Cell / drug therapy. Lung Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • Genetic Alliance. consumer health - Oral cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20147856.001).
  • [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] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
  •  go-up   go-down



78. Fan T, Li R, Todd NW, Qiu Q, Fang HB, Wang H, Shen J, Zhao RY, Caraway NP, Katz RL, Stass SA, Jiang F: Up-regulation of 14-3-3zeta in lung cancer and its implication as prognostic and therapeutic target. Cancer Res; 2007 Aug 15;67(16):7901-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Up-regulation of 14-3-3zeta in lung cancer and its implication as prognostic and therapeutic target.
  • A functional genomic approach integrating microarray and proteomic analyses done in our laboratory has identified 14-3-3zeta as a putative oncogene whose activation was common and driven by its genomic amplification in lung adenocarcinomas.
  • 14-3-3zeta is believed to function in cell signaling, cycle control, and apoptotic death.
  • Following our initial finding, here, we analyzed its expression in lung tumor tissues obtained from 205 patients with various histologic and stage non-small cell lung cancers (NSCLC) using immunohistochemistry and then explored the effects of specific suppression of the gene in vitro and in a xenograft model using small interfering RNA.
  • The increased 14-3-3zeta expression was positively correlated with a more advanced pathologic stage and grade of NSCLCs (P = 0.001 and P = 0.006, respectively) and was associated with overall and cancer-specific survival rates of the patients (P = 0.022 and P = 0.018, respectively).
  • Down-regulation of 14-3-3zeta in lung cancer cells led to a dose-dependent increased sensitivity to cisplatin-induced cell death, which was associated with the inhibition of cell proliferation and increased G2-M arrest and apoptosis.
  • The result was further confirmed in the animal model, which showed that the A549 lung cancer cells with reduced 14-3-3zeta grew significantly slower than the wild-type A549 cells after cisplatin treatment (P = 0.008).
  • [MeSH-major] 14-3-3 Proteins / biosynthesis. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cisplatin / pharmacology. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Middle Aged. Prognosis. RNA, Small Interfering / genetics. Transfection. Up-Regulation

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17699796.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-113707
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / RNA, Small Interfering; Q20Q21Q62J / Cisplatin
  •  go-up   go-down



79. Song SW, Lee HS, Kim MS, Lee JM, Kim JH, Nam BH, Zo JI: Preoperative serum fibrinogen level predicts postoperative pulmonary complications after lung cancer resection. Ann Thorac Surg; 2006 Jun;81(6):1974-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preoperative serum fibrinogen level predicts postoperative pulmonary complications after lung cancer resection.
  • BACKGROUND: Patients undergoing pulmonary resection are thought to be at high risk for the development of postoperative pulmonary complications (PPCs), and these complications may lead to serious morbidity.
  • The purpose of this study was to identify the factors associated with postoperative pulmonary complications in patients undergoing lung cancer resection and to determine the effect of PPCs on survival.
  • METHODS: The study involved a retrospective review of 635 patients who had undergone curative resection for lung cancer.
  • Cancer types comprised 330 squamous cell carcinomas (52.0%), 255 adenocarcinomas (40.2%) and 50 others (7.8%).
  • Univariate analysis showed that the following factors were predictors for PPCs: male sex, erythrocyte sedimentation rate, preoperative serum fibrinogen level, pulmonary function, chronic obstructive pulmonary disease, smoking, double primary cancer, and surgical duration.
  • [MeSH-minor] Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Bronchial Fistula / blood. Bronchial Fistula / epidemiology. Bronchial Fistula / etiology. Bronchial Spasm / blood. Bronchial Spasm / epidemiology. Bronchial Spasm / etiology. Carcinoma, Large Cell / surgery. Carcinoma, Squamous Cell / surgery. Empyema, Pleural / blood. Empyema, Pleural / epidemiology. Empyema, Pleural / etiology. Female. Fistula / blood. Fistula / epidemiology. Fistula / etiology. Humans. Intraoperative Period. Life Tables. Lung Neoplasms / surgery. Male. Middle Aged. Pleural Diseases / blood. Pleural Diseases / epidemiology. Pleural Diseases / etiology. Predictive Value of Tests. Pulmonary Disease, Chronic Obstructive / epidemiology. Retrospective Studies. Risk. Sex Factors. Smoking / epidemiology. Sputum. Survival Analysis. Survival Rate

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - Pneumonia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16731116.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 9001-32-5 / Fibrinogen
  •  go-up   go-down



80. Ohtsuka K, Ohnishi H, Fujiwara M, Kishino T, Matsushima S, Furuyashiki G, Takei H, Koshiishi Y, Goya T, Watanabe T: Abnormalities of epidermal growth factor receptor in lung squamous-cell carcinomas, adenosquamous carcinomas, and large-cell carcinomas: tyrosine kinase domain mutations are not rare in tumors with an adenocarcinoma component. Cancer; 2007 Feb 15;109(4):741-50
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abnormalities of epidermal growth factor receptor in lung squamous-cell carcinomas, adenosquamous carcinomas, and large-cell carcinomas: tyrosine kinase domain mutations are not rare in tumors with an adenocarcinoma component.
  • BACKGROUND: Tyrosine kinase domain (TKD) gene mutations of the epidermal growth factor receptor gene (EGFR) have proven to be clinically significant in nonsmall-cell lung cancer (NSCLC), particularly in adenocarcinoma.
  • However, TKD mutations together with deletion mutations in the extracellular domain of EGFR (EGFRvIII) have not been fully investigated in NSCLC except for adenocarcinoma.
  • METHODS: EGFR TKD mutations were investigated using direct sequencing and mutation-specific polymerase chain reaction (PCR), and EGFRvIII mutations were examined using reverse transcriptase-PCR in samples from 42 NSCLC patients and 6 NSCLC cell lines excluding adenocarcinoma.
  • RESULTS: EGFR TKD mutations were detected in 1 of 7 (14%) squamous-cell carcinomas with an adenocarcinoma component and 2 of 4 (50%) adenosquamous carcinomas.
  • In contrast, EGFR TKD mutations were not identified in 24 pure squamous-cell carcinomas without any adenocarcinoma component, 7 large-cell carcinomas, or 6 cell lines.
  • EGFRvIII was detected solely in 1 of 7 large-cell carcinomas (14%), but not in 31 squamous-cell carcinomas, 4 adenosquamous carcinomas, or 6 cell lines.
  • CONCLUSIONS: These results suggest that EGFR TKD mutations are found in NSCLCs with an adenocarcinoma element.
  • [MeSH-major] Carcinoma, Adenosquamous / genetics. Carcinoma, Large Cell / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Squamous Cell / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / genetics. Male. Middle Aged. Neoplasm Staging. Prognosis. Protein Structure, Tertiary. Protein-Tyrosine Kinases / chemistry. Survival Rate

  • 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 = 17238183.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down



81. Cadranel J, Quoix E, Baudrin L, Mourlanette P, Moro-Sibilot D, Morere JF, Souquet PJ, Soria JC, Morin F, Milleron B, IFCT-0401 Trial Group: IFCT-0401 Trial: a phase II study of gefitinib administered as first-line treatment in advanced adenocarcinoma with bronchioloalveolar carcinoma subtype. J Thorac Oncol; 2009 Sep;4(9):1126-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IFCT-0401 Trial: a phase II study of gefitinib administered as first-line treatment in advanced adenocarcinoma with bronchioloalveolar carcinoma subtype.
  • PURPOSE: Intergroupe Francophone de Cancérologie Thoracique-0401 phase II trial aimed to evaluate the efficacy and safety of gefitinib as a first-line treatment for patients with adenocarcinoma with bronchioloalveolar carcinoma subtype (ADC-BAC).
  • CONCLUSION: Results from the Intergroupe Francophone de Cancérologie Thoracique-0401 trial demonstrate that gefitinib combines efficacy with low toxicity and is, therefore, suitable as a first-line treatment of advanced ADC-BAC, particularly in patients with nonmucinous BAC subtype.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Antineoplastic Agents / therapeutic use. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Thorac Oncol. 2009 Sep;4(9):1047-8 [19704334.001]
  • (PMID = 19574932.001).
  • [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] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Investigator] Cadranel J; Mourlanette P; Quoix E; Moro-Sibilot D; Morére JF; Souquet PJ; Soria JC; Friard S; Lebeau B; Janicot H; Monnet I; Pérol M; Dansin E; Zalcman G; Vergnenégre A; Coëtmeur D; Depierre A; Oliviero G; Le Groumellec A; David P; Fraboulet G; Lemarié E; Le Treut J; Le Guen Y; Chouabe S; Masson P; Robinet G; Thiberville L; Paillotin D; Douillard JY; Gervais R; Antoine M; Lebitasy MP; Poulain S; Amour E; Rouveau R; Establier N
  •  go-up   go-down



82. Tamura K, Fukuoka M: Gefitinib in non-small cell lung cancer. Expert Opin Pharmacother; 2005 Jun;6(6):985-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib in non-small cell lung cancer.
  • Gefitinib (Iressa), an orally-active tyrosine kinase inhibitor of the epidermal growth factor receptor (EGFR), is the first approved molecular-targeted drug for the management of patients with advanced non-small cell lung cancer (NSCLC).
  • Two Phase II trials (IDEAL [Iressa Dose Evaluation in Advanced Lung Cancer]-1 and -2), evaluated the efficacy of gefitinib in advanced NSCLC patients who received < or = 2 (IDEAL1) or > or = 2 (IDEAL2) previous chemotherapy regimens.
  • Furthermore, in a recent randomised, placebo-controlled, Phase III trial (ISEL: IRESSA Survival Evaluation in Lung cancer), gefitinib failed to prolong survival compared with placebo in patients with advanced NSCLC who had failed one or more lines of chemotherapy.
  • Subgroup analysis of ISEL suggested improved survival in patients of Asian origin and non-smokers.
  • In addition, subset analyses of IDEAL and several retrospective studies have indicated that female gender, adenocarcinoma histology (especially bronchial alveolar carcinoma), non-smoker status and Asian ethnicity are factors which predict to response to gefitinib.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use



83. Singh J, Naran A, Misso NL, Rigby PJ, Thompson PJ, Bhoola KD: Expression of kallikrein-related peptidases (KRP/hK5, 7, 6, 8) in subtypes of human lung carcinoma. Int Immunopharmacol; 2008 Feb;8(2):300-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of kallikrein-related peptidases (KRP/hK5, 7, 6, 8) in subtypes of human lung carcinoma.
  • Lung cancer is currently the leading cause of cancer mortality worldwide.
  • Expression of kallikrein-related peptidases (KRP/hK/KLK) may be induced during lung carcinogenesis.
  • To test the hypothesis that KRP/hK, previously identified in the skin (KRP/hK5, 7) and brain (KRP/hK6, 8), are expressed in lung tumours, experiments were designed to investigate their localization in four malignant sub-types of human lung cancer.
  • Using specific antibodies, expression of these KRP/hK was determined in archived lung tumour sections of the four subtypes, and in normal skin, brain, lung and submandibular gland tissue sections.
  • In the squamous cell carcinoma, small cell carcinoma and carcinoid tumour, 40-90% of the malignant cells showed positive cytoplasmic labelling for KRP/hK5, 7, 6 and 8 (intensity grade 2+/3+).
  • In the adenocarcinoma there was no cytoplasmic labelling for any of the KRP/hK, but the nuclei of 20% of the tumour cells were labelled for KRP/hK5, 7 and 8 (intensity grade 2+/3+).
  • Further studies are required to determine the functional significance of the expression of KRP/hK in human lung carcinomas, and whether any of these proteins may be potential biomarkers for specific sub-types of lung cancer.
  • [MeSH-major] Kallikreins / analysis. Lung Neoplasms / enzymology
  • [MeSH-minor] Brain / enzymology. Humans. Lung / enzymology. Salivary Glands / enzymology. Skin / enzymology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18182244.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.4.21.- / KLK5 protein, human; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / KLK7 protein, human; EC 3.4.21.- / KLK8 protein, human; EC 3.4.21.- / Kallikreins
  •  go-up   go-down



84. Theoharides TC, Rozniecki JJ, Sahagian G, Jocobson S, Kempuraj D, Conti P, Kalogeromitros D: Impact of stress and mast cells on brain metastases. J Neuroimmunol; 2008 Dec 15;205(1-2):1-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma.
  • Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB).
  • Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stress.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Neuroimmunol. 2009 Apr 30;209(1-2):121-2 [19195717.001]
  • (PMID = 18977036.001).
  • [ISSN] 0165-5728
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47658; United States / NCI NIH HHS / BC / BC24430; United States / NIDDK NIH HHS / DK / DK62861; United States / NINDS NIH HHS / NS / NS38326; United States / NINDS NIH HHS / NS / NS55681
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Inflammation Mediators
  • [Number-of-references] 173
  •  go-up   go-down



85. Boland JM, Erdogan S, Vasmatzis G, Yang P, Tillmans LS, Johnson MR, Wang X, Peterson LM, Halling KC, Oliveira AM, Aubry MC, Yi ES: Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas. Hum Pathol; 2009 Aug;40(8):1152-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas.
  • Recently, the fusion gene EML4-ALK was identified in non-small cell lung carcinoma, which could be a potential therapeutic target.
  • Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry.
  • Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of anaplastic lymphoma kinase immunostaining as a screening tool.
  • Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling.
  • In the independent cohort, anaplastic lymphoma kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas.
  • In conclusion, anaplastic lymphoma kinase immunoreactivity in non-small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Lung Neoplasms / genetics. Protein-Tyrosine Kinases / genetics. Up-Regulation / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Cohort Studies. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA. Transcription, Genetic

  • Genetic Alliance. consumer health - Anaplastic Small Cell Lymphoma.
  • 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
  • [CommentIn] Hum Pathol. 2010 Apr;41(4):614-5; author reply 615-616 [20163822.001]
  • (PMID = 19386350.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  •  go-up   go-down



86. Al-Wadei HA, Schuller HM: Nicotinic receptor-associated modulation of stimulatory and inhibitory neurotransmitters in NNK-induced adenocarcinoma of the lungs and pancreas. J Pathol; 2009 Aug;218(4):437-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nicotinic receptor-associated modulation of stimulatory and inhibitory neurotransmitters in NNK-induced adenocarcinoma of the lungs and pancreas.
  • Small airway-derived pulmonary adenocarcinoma (PAC) and pancreatic ductal adenocarcinoma (PDAC) are among the most common human cancers and smoking is a risk factor for both.
  • Emerging research has identified cAMP signalling stimulated by the stress neurotransmitters adrenaline and noradrenaline as an important stimulator of adenocarcinomas, including PAC and PDAC.
  • These findings suggest that NNK-induced alterations in regulatory nAChRs may contribute to the development of smoking-associated PAC and PDAC by disturbing the balance between cancer-stimulating and -inhibiting neurotransmitters.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Smoking.
  • Hazardous Substances Data Bank. Norepinephrine .
  • Hazardous Substances Data Bank. EPINEPHRINE .
  • Hazardous Substances Data Bank. 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone .
  • 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
  • [Copyright] (c) 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4510-5 [10493497.001]
  • [Cites] Int J Cancer. 2005 Nov 1;117(2):294-9 [15900604.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Oct;131(10):639-48 [16091975.001]
  • [Cites] Oncol Rep. 2006 Feb;15(2):431-5 [16391865.001]
  • [Cites] Mol Pharmacol. 2006 Feb;69(2):618-28 [16269536.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):369-75 [16428474.001]
  • [Cites] Int J Cancer. 2006 Mar 15;118(6):1370-80 [16206275.001]
  • [Cites] Int J Cancer. 2006 Jun 1;118(11):2744-9 [16381019.001]
  • [Cites] Cancer Biol Ther. 2006 May;5(5):511-7 [16582591.001]
  • [Cites] Nat Med. 2006 Aug;12(8):939-44 [16862152.001]
  • [Cites] Int J Cancer. 2006 Oct 1;119(7):1547-52 [16671086.001]
  • [Cites] Cancer Detect Prev. 2006;30(5):403-11 [17067750.001]
  • [Cites] Toxicol Sci. 2007 Mar;96(1):21-9 [17003101.001]
  • [Cites] Toxicol Appl Pharmacol. 2007 Jun 15;221(3):261-7 [17498763.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6863-71 [17638897.001]
  • [Cites] Cancer Genomics Proteomics. 2007 Jan-Feb;4(1):35-42 [17726239.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1737-44 [17557921.001]
  • [Cites] Clin Exp Pharmacol Physiol. 2002 Mar;29(3):181-8 [11906480.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Oct;128(10):525-32 [12384795.001]
  • [Cites] J Neurobiol. 2002 Dec;53(4):606-17 [12436424.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6467-9 [12438237.001]
  • [Cites] Ann N Y Acad Sci. 2002 Dec;978:405-12 [12582069.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jul;80(1):63-70 [12889599.001]
  • [Cites] Prog Cardiovasc Dis. 2003 Jul-Aug;46(1):91-111 [12920702.001]
  • [Cites] Lung Cancer. 2004 Jul;45(1):11-8 [15196729.001]
  • [Cites] Neurosci Lett. 2004 Nov 3;370(1):80-3 [15489022.001]
  • [Cites] Biochem Pharmacol. 1989 Oct 15;38(20):3439-42 [2573356.001]
  • [Cites] Cancer Res. 1990 Mar 15;50(6):1960-5 [2306745.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 May;87(9):3294-8 [2159143.001]
  • [Cites] Mutat Res. 1990 Nov-Dec;233(1-2):105-16 [2233792.001]
  • [Cites] Neuron. 1991 Jul;7(1):91-100 [2069816.001]
  • [Cites] IARC Sci Publ. 1991;(105):54-61 [1855913.001]
  • [Cites] Cancer. 2008 Feb 15;112(4):767-78 [18098271.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3746-53 [18559592.001]
  • [Cites] Anticancer Drugs. 2008 Aug;19(7):655-71 [18594207.001]
  • [Cites] Br J Pharmacol. 2008 Aug;154(8):1558-71 [18500366.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2008 Aug;7(4):345-56 [18693168.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2008 Oct 12;363(1507):3159-68 [18640919.001]
  • [Cites] Carcinogenesis. 2008 Oct;29(10):1979-85 [18310090.001]
  • [Cites] Oncogene. 1991 Aug;6(8):1353-62 [1679529.001]
  • [Cites] Carcinogenesis. 2001 Mar;22(3):473-9 [11238189.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2866-9 [11306460.001]
  • [Cites] J Neurochem. 2001 Sep;78(6):1367-78 [11579145.001]
  • [Cites] Neurosci Lett. 2001 Oct 26;312(3):161-4 [11602335.001]
  • [Cites] Carcinogenesis. 1993 Mar;14(3):451-5 [8453721.001]
  • [Cites] Cancer Res. 1993 Jun 1;53(11):2498-501 [8495411.001]
  • [Cites] Cancer Res. 1995 Aug 15;55(16):3504-8 [7627955.001]
  • [Cites] Crit Rev Toxicol. 1996;26(2):163-81 [8688159.001]
  • [Cites] Prog Brain Res. 1996;109:125-37 [9009699.001]
  • [Cites] Cardiovasc Drugs Ther. 1997 Jan;10(6):657-65 [9110108.001]
  • [Cites] Prog Neurobiol. 1997 Oct;53(2):199-237 [9364611.001]
  • [Cites] Biochem Pharmacol. 1998 May 1;55(9):1377-84 [10076528.001]
  • [Cites] Cancer. 1999 Apr 15;85(8):1703-10 [10223563.001]
  • [Cites] Dig Dis Sci. 1999 Jul;44(7):1303-11 [10489910.001]
  • (PMID = 19274673.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA042829; United States / NCI NIH HHS / CA / R01 CA096128; United States / NCI NIH HHS / CA / R01CA042829; United States / NCI NIH HHS / CA / R01CA096128
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurotransmitter Agents; 0 / Nitrosamines; 0 / Receptors, Nicotinic; 56-12-2 / gamma-Aminobutyric Acid; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; E0399OZS9N / Cyclic AMP; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
  • [Other-IDs] NLM/ NIHMS380611; NLM/ PMC3372983
  •  go-up   go-down



87. Chen GY, Yang ZY, Hong X, Wang M, Lu L, Zhang CH: [Establishment of a multi drug-resistant human lung adenocarcinoma cell line and biological characteristics there of]. Zhonghua Yi Xue Za Zhi; 2007 Apr 3;87(13):924-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Establishment of a multi drug-resistant human lung adenocarcinoma cell line and biological characteristics there of].
  • OBJECTIVE: To establish a multidrug-resistant human lung adenocarcinoma cell line and to investigate its biologic characteristics.
  • METHODS: NBV of the terminal concentration of 0.02 mg/L was co-cultured with the human lung adenocarcinoma cells of the line Anip973.
  • Anip973 and Anip973/NVB cells were co-cultured with 10 anti-cancer drugs: NVB, cisplatin, fluorouracil, gemcitabine, paclitaxel, etoposide, irinotecan, dacarbazine, ifosfamide, and pharmorubicin of different concentrations respectively.
  • Flow cytometry was conducted to observe the cell cycle.
  • CONCLUSION: A reliable multi-drug resistant human lung adenocarcinoma cell line Anip973/NVB has been successfully established.
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Adenocarcinoma / ultrastructure. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Cisplatin / pharmacology. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Dose-Response Relationship, Drug. Flow Cytometry. Fluorouracil / pharmacology. Humans. Inhibitory Concentration 50. Lung Neoplasms / pathology. Lung Neoplasms / physiopathology. Lung Neoplasms / ultrastructure. Microscopy, Electron

  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cellosaurus - a cell line knowledge resource .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17650408.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down



88. Lyon CM, Klinge DM, Liechty KC, Gentry FD, March TH, Kang T, Gilliland FD, Adamova G, Rusinova G, Telnov V, Belinsky SA: Radiation-induced lung adenocarcinoma is associated with increased frequency of genes inactivated by promoter hypermethylation. Radiat Res; 2007 Oct;168(4):409-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation-induced lung adenocarcinoma is associated with increased frequency of genes inactivated by promoter hypermethylation.
  • Epigenetic inactivation of genes by promoter hypermethylation, a major mechanism in the initiation and progression of tobacco-induced cancer, has also been associated with lung cancer induced through environmental and occupational exposures.
  • Our previous study of gene methylation in workers from the MAYAK nuclear enterprise identified a significantly higher prevalence for methylation of the p16 gene (CDKN2A) in adenocarcinomas from workers compared to tumors from non-worker controls.
  • The purpose of this investigation was to determine whether genes in addition to p16 are "targeted" for silencing and whether overall gene methylation was more common in radiation-induced adenocarcinoma.
  • Evaluating the frequency for methylation of a five-gene panel revealed that 93% of adenocarcinomas from workers compared to 66% of tumors from controls were methylated for at least one gene.
  • Increased frequency for inactivation of genes by promoter hypermethylation and targeting of tumor suppressor genes such as GATA5 may be factors that contribute to the increased risk for lung cancer associated with radiation exposure.
  • [MeSH-major] Adenocarcinoma / etiology. DNA Methylation. Lung Neoplasms / etiology. Neoplasms, Radiation-Induced / etiology. Occupational Exposure / adverse effects. Promoter Regions, Genetic
  • [MeSH-minor] Adult. Aged. B-Cell-Specific Activator Protein / genetics. Cadherins / genetics. DNA Damage. Female. GATA5 Transcription Factor / genetics. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Occupational Health.
  • 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 = 17903034.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES08801; United States / NIEHS NIH HHS / ES / P30 ES012072
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Cadherins; 0 / GATA5 Transcription Factor; 0 / GATA5 protein, human; 0 / H-cadherin; 0 / PAX5 protein, human
  •  go-up   go-down



89. Choo MK, Sakurai H, Kim DH, Saiki I: A ginseng saponin metabolite suppresses tumor necrosis factor-alpha-promoted metastasis by suppressing nuclear factor-kappaB signaling in murine colon cancer cells. Oncol Rep; 2008 Mar;19(3):595-600
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A ginseng saponin metabolite suppresses tumor necrosis factor-alpha-promoted metastasis by suppressing nuclear factor-kappaB signaling in murine colon cancer cells.
  • SC-514, an inhibitor of IkappaB kinase beta (IKKbeta), blocked the TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB) as well as the TNF-alpha-promoted metastasis of murine colon adenocarcinoma cells.
  • The TNF-alpha-evoked increase in lung and liver metastasis of colon carcinoma was also abrogated by treatment with M1 in vitro.
  • [MeSH-minor] Animals. Cell Movement. Female. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Signal Transduction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18288389.001).
  • [ISSN] 1021-335X
  • [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, Phytogenic; 0 / Ginsenosides; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / ginsenoside M1
  •  go-up   go-down



90. De Las Heras M, Ortín A, Salvatori D, Pérez de Villareal M, Cousens C, Miguel Ferrer L, Miguel Cebrián L, García de Jalón JA, Gonzalez L, Michael Sharp J: A PCR technique for the detection of Jaagsiekte sheep retrovirus in the blood suitable for the screening of ovine pulmonary adenocarcinoma in field conditions. Res Vet Sci; 2005 Dec;79(3):259-64
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A PCR technique for the detection of Jaagsiekte sheep retrovirus in the blood suitable for the screening of ovine pulmonary adenocarcinoma in field conditions.
  • Ovine pulmonary adenocarcinoma (OPA) is a naturally occurring contagious lung neoplasia caused by jaagsiekte sheep retrovirus (JSRV).
  • [MeSH-major] Jaagsiekte sheep retrovirus / isolation & purification. Polymerase Chain Reaction / methods. Polymerase Chain Reaction / veterinary. Pulmonary Adenomatosis, Ovine / diagnosis. Pulmonary Adenomatosis, Ovine / virology. Sheep / virology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16054897.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / RNA, Viral
  •  go-up   go-down



91. Idowu MO, Powers CN: Lung cancer cytology: potential pitfalls and mimics - a review. Int J Clin Exp Pathol; 2010;3(4):367-85
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer cytology: potential pitfalls and mimics - a review.
  • Cytology is increasingly being used in the evaluation of lung lesions.
  • Familiarity with the mimics and the pitfalls is essential in avoiding a misdiagnosis because a false positive or false negative diagnosis may have significant management implications.
  • This article focuses on the main classification of primary lung carcinoma - small cell carcinoma, adenocarcinoma and squamous cell carcinoma - with potential mimics discussed under each tumor category.
  • [MeSH-major] Cytodiagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Cytological Techniques. Diagnosis, Differential. Diagnostic Errors. False Negative Reactions. False Positive Reactions. Humans

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Acta Cytol. 2005 Nov-Dec;49(6):621-6 [16450901.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):608-15 [16938658.001]
  • [Cites] J Clin Oncol. 2006 Oct 1;24(28):4539-44 [17008692.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):561-70 [17290066.001]
  • [Cites] Nat Rev Cancer. 2007 Mar;7(3):169-81 [17318210.001]
  • [Cites] Mol Cancer Ther. 2007 Apr;6(4):1223-9 [17406029.001]
  • [Cites] J Thorac Cardiovasc Surg. 2007 May;133(5):1193-200 [17467428.001]
  • [Cites] Acta Cytol. 1988 Sep-Oct;32(5):622-8 [3421009.001]
  • [Cites] Acta Cytol. 1989 Jul-Aug;33(4):511-5 [2750440.001]
  • [Cites] Diagn Cytopathol. 1989;5(2):174-80 [2776600.001]
  • [Cites] Br J Cancer. 1989 Sep;60(3):358-65 [2789942.001]
  • [Cites] Mayo Clin Proc. 1999 Nov;74(11):1129-33 [10560602.001]
  • [Cites] Cancer. 2000 Feb 25;90(1):55-60 [10692217.001]
  • [Cites] Acta Cytol. 2000 Jul-Aug;44(4):640-6 [10934959.001]
  • [Cites] Arch Pathol Lab Med. 2007 Nov;131(11):1700-8 [17979490.001]
  • [Cites] Diagn Cytopathol. 2008 Jan;36(1):13-9 [18064688.001]
  • [Cites] J Thorac Oncol. 2007 Dec;2(12):1086-90 [18090579.001]
  • [Cites] Diagn Cytopathol. 2008 Feb;36(2):89-93 [18181192.001]
  • [Cites] J Thorac Oncol. 2008 May;3(5):472-6 [18448998.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2570-8 [18451218.001]
  • [Cites] Lung Cancer. 2008 May;60(2):175-82 [18061305.001]
  • [Cites] Eur J Cardiothorac Surg. 2008 Aug;34(2):438-43; discussion 443 [18502660.001]
  • [Cites] N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Jun;1(1):39-44 [19138934.001]
  • [Cites] Hum Pathol. 2009 May;40(5):678-82 [19144385.001]
  • [Cites] Clin Neuropathol. 2009 Nov-Dec;28(6):453-9 [19919820.001]
  • [Cites] Am J Med Sci. 2010 Jan;339(1):68-76 [19996730.001]
  • [Cites] Diagn Cytopathol. 2010 Apr;38(4):297-307 [19856422.001]
  • [Cites] Cancer. 1999 Dec 25;87(6):380-9 [10603192.001]
  • [Cites] Cancer. 2001 Dec 25;93(6):364-75 [11748576.001]
  • [Cites] Ann Thorac Surg. 2002 Jun;73(6):1964-5 [12078805.001]
  • [Cites] Acta Cytol. 2003 Mar-Apr;47(2):216-20 [12685192.001]
  • [Cites] Diagn Cytopathol. 2003 Jul;29(1):8-12 [12827707.001]
  • [Cites] Hum Genet. 2003 Aug;113(3):238-43 [12802680.001]
  • [Cites] Diagn Cytopathol. 2003 Nov;29(5):297-9 [14595800.001]
  • [Cites] Diagn Cytopathol. 2004 May;30(5):359-61 [15108238.001]
  • [Cites] Curr Opin Pharmacol. 2004 Jun;4(3):241-50 [15140415.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5131-6 [15297416.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] Yale J Biol Med. 1971 Feb-Apr;43(4-5):213-22 [5578741.001]
  • [Cites] J Thorac Cardiovasc Surg. 1975 Oct;70(4):606-12 [170482.001]
  • [Cites] Acta Cytol. 1976 Jan-Feb;20(1):15-9 [1063517.001]
  • [Cites] Ann Thorac Surg. 1977 Nov;24(5):474-80 [921379.001]
  • [Cites] Acta Cytol. 1981 May-Jun;25(3):210-4 [6942610.001]
  • [Cites] Acta Cytol. 1985 Mar-Apr;29(2):162-6 [2580412.001]
  • [Cites] Acta Cytol. 1985 Sep-Oct;29(5):887-94 [2996275.001]
  • [Cites] Diagn Cytopathol. 1986 Sep;2(3):187-93 [3021409.001]
  • [Cites] Rontgenblatter. 1987 Oct;40(10):321-4 [3685839.001]
  • [Cites] Toxicol Appl Pharmacol. 1988 May;93(3):472-83 [3285521.001]
  • [Cites] Diagn Cytopathol. 1988 Mar;4(1):1-8 [2837371.001]
  • [Cites] Diagn Cytopathol. 2000 Oct;23(4):294-5 [11002375.001]
  • [Cites] Cancer. 2001 Feb 25;93(1):29-34 [11241263.001]
  • [Cites] Acta Cytol. 2001 Mar-Apr;45(2):267-70 [11284317.001]
  • [Cites] Eur J Cancer. 2001 Sep;37 Suppl 4:S9-15 [11597399.001]
  • [Cites] Respir Res. 2000;1(3):163-9 [11667981.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1405-12 [11684957.001]
  • [Cites] Diagn Cytopathol. 1990;6(5):317-22 [2292218.001]
  • [Cites] Acta Cytol. 1991 Mar-Apr;35(2):183-5 [2028691.001]
  • [Cites] Am J Clin Pathol. 1992 May;97(5):669-77 [1575213.001]
  • [Cites] Diagn Cytopathol. 1993;9(1):89-97 [8384547.001]
  • [Cites] Am J Clin Pathol. 1993 May;99(5):566-9 [8388161.001]
  • [Cites] Am J Surg Pathol. 1995 Jun;19(6):627-35 [7755149.001]
  • [Cites] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182.001]
  • [Cites] Acta Cytol. 1996 Jul-Aug;40(4):695-707 [8693889.001]
  • [Cites] Diagn Cytopathol. 1995 Dec;13(5):443-7 [8834319.001]
  • [Cites] Diagn Cytopathol. 1995 Dec;13(5):448-62 [8834320.001]
  • [Cites] Diagn Cytopathol. 1997 May;16(5):396-401 [9143840.001]
  • [Cites] Diagn Cytopathol. 1997 Dec;17(6):412-6 [9407200.001]
  • [Cites] Arch Pathol Lab Med. 2005 Jan;129(1):19-22 [15628903.001]
  • [Cites] Am J Surg Pathol. 2005 Feb;29(2):179-87 [15644774.001]
  • [Cites] Cancer. 2005 Apr 25;105(2):80-6 [15662708.001]
  • [Cites] Arch Pathol Lab Med. 2005 May;129(5):614-8 [15859631.001]
  • [Cites] Arch Pathol Lab Med. 2005 May;129(5):619-23 [15859632.001]
  • [Cites] Am J Clin Pathol. 2005 Jun;123(6):874-8 [15899778.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7568-72 [16140919.001]
  • [Cites] Nat Genet. 2005 Dec;37(12):1315-6 [16258541.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):963-9 [16152581.001]
  • (PMID = 20490328.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 86
  • [Other-IDs] NLM/ PMC2872744
  • [Keywords] NOTNLM ; Pitfalls / adenocarcinoma / clinical history / lung cancer / mimics / non-small cell carcinoma / pulmonary carcinoma / respiratory cytology / squamous cell carcinoma
  •  go-up   go-down



92. Pan W, Qu J, Chen T, Sun L, Qi J: FLIM and emission spectral analysis of caspase-3 activation inside single living cell during anticancer drug-induced cell death. Eur Biophys J; 2009 Apr;38(4):447-56