[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 2496
1. Yoshino I, Osoegawa A, Yohena T, Kameyama T, Oki E, Oda S, Maehara Y: Loss of heterozygosity (LOH) in non-small cell lung cancer: difference between adenocarcinoma and squamous cell carcinoma. Respir Med; 2005 Mar;99(3):308-12
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of heterozygosity (LOH) in non-small cell lung cancer: difference between adenocarcinoma and squamous cell carcinoma.
  • BACKGROUND: In non-small cell lung cancer, a loss of heterozygosity (LOH) is frequently observed; however, few studies have investigated the differences in the LOH status between adenocarcinoma and squamous cell carcinoma.
  • PATIENTS AND METHODS: In a consecutive series of 49 patients with adenocarcinomas and 22 patients with squamous cell carcinomas, the LOH in tumors was analyzed using polymerase chain reaction employing 5 fluorescence-labeled dinucleotide markers (D2S123, D5S107, D10S197, D11SS904, D13S175) and an autosequencer.
  • RESULTS: LOH was more frequently observed in squamous cell carcinoma (20 of 22, 90%) than in adenocarcinomas (33 of 49, 67%) (P=0.0348), and the number of LOH per patient was also higher in the patients with squamous cell carcinoma (2.2+/-1.4) than in those with adenocarcinoma (1.5+/-1.2, P=0.037).
  • In adenocarcinomas, the number of LOH per patients correlated significantly with the pack-year index, whereas the pathological stage significantly affected the number of LOH in squamous cell carcinomas.
  • CONCLUSION: The presence of LOH is relatively uncommon in adenocarcinoma of the lung; however, the incidence of LOH tends to be associated with the smoking status.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Squamous Cell / genetics. Loss of Heterozygosity / genetics. Lung Neoplasms / genetics


2. Shah SA, Spinale FG, Ikonomidis JS, Stroud RE, Chang EI, Reed CE: Differential matrix metalloproteinase levels in adenocarcinoma and squamous cell carcinoma of the lung. J Thorac Cardiovasc Surg; 2010 Apr;139(4):984-90; discussion 990
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential matrix metalloproteinase levels in adenocarcinoma and squamous cell carcinoma of the lung.
  • OBJECTIVE: The matrix metalloproteinases (MMPs) have been implicated in the aggressive course of non-small cell lung cancer (NSCLC).
  • This study tested the hypothesis that a differential MMP profile would exist between NSCLC and normal lung and that MMP patterns would differ between NSCLC histologic types.
  • METHODS: NSCLC samples and remote normal samples were obtained from patients with stage I or II NSCLC with either squamous cell (n = 22) or adenocarcinoma (n = 19) histologic characteristics.
  • For example MMP-1, -8, -9, and -12 increased by more than 4-fold in squamous cell versus adenocarcinoma (P < .05).

  • 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
  • [Copyright] Copyright 2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
  • [Cites] Cancer Metastasis Rev. 2006 Mar;25(1):45-56 [16680571.001]
  • [Cites] Br J Cancer. 2006 Apr 10;94(7):941-6 [16538215.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5448-53 [17000679.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2054-60 [17404086.001]
  • [Cites] Semin Cell Dev Biol. 2008 Feb;19(1):52-60 [17625931.001]
  • [Cites] Int J Biochem Cell Biol. 2008;40(6-7):1362-78 [18258475.001]
  • [Cites] Cancer Sci. 2008 Jun;99(6):1188-94 [18422740.001]
  • [Cites] Cancer Sci. 2008 Nov;99(11):2185-92 [18823373.001]
  • [Cites] Ann Thorac Surg. 2008 Nov;86(5):1576-83 [19049753.001]
  • [Cites] Anticancer Res. 2009 Jan;29(1):67-74 [19331134.001]
  • [Cites] Int J Cancer. 2009 Aug 15;125(4):894-901 [19480010.001]
  • [Cites] Anticancer Res. 2009 Jul;29(7):2513-7 [19596921.001]
  • [Cites] J Pathol. 2000 Feb;190(2):150-6 [10657012.001]
  • [Cites] Circulation. 2000 Oct 17;102(16):1944-9 [11034943.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):3944-8 [11051242.001]
  • [Cites] Oncol Rep. 2001 Mar-Apr;8(2):421-4 [11182067.001]
  • [Cites] Science. 2002 Mar 29;295(5564):2387-92 [11923519.001]
  • [Cites] Nat Rev Cancer. 2002 Mar;2(3):161-74 [11990853.001]
  • [Cites] J Cell Sci. 2002 Oct 1;115(Pt 19):3719-27 [12235282.001]
  • [Cites] Int J Cancer. 2003 Feb 20;103(5):647-51 [12494473.001]
  • [Cites] Circ Res. 2003 May 2;92(8):827-39 [12730128.001]
  • [Cites] Int J Cancer. 2003 Sep 20;106(5):745-51 [12866035.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):3098-104 [12912961.001]
  • [Cites] Int J Cancer. 2003 Nov 20;107(4):541-50 [14520690.001]
  • [Cites] Lung Cancer. 2004 Aug;45(2):171-9 [15246188.001]
  • [Cites] J Clin Oncol. 2004 Aug 15;22(16):3218-29 [15249585.001]
  • [Cites] Pathol Int. 1997 Jul;47(7):461-9 [9234385.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):149-53 [9918213.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):842-9 [15681529.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1086-92 [15709175.001]
  • [Cites] Circulation. 2005 Mar 8;111(9):1166-74 [15723986.001]
  • [Cites] Int J Colorectal Dis. 2005 May;20(3):245-52 [15592677.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1676-84 [15754326.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2831-9 [15837997.001]
  • [Cites] Anal Biochem. 2005 Aug 1;343(1):54-65 [15953581.001]
  • [Cites] Am J Cardiol. 2006 Feb 15;97(4):532-7 [16461051.001]
  • [Cites] Lung Cancer. 2006 Mar;51(3):313-21 [16423426.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):227-39 [16498445.001]
  • [Cites] Circulation. 2006 Jul 4;114(1 Suppl):I365-70 [16820601.001]
  • (PMID = 20304142.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL059165; United States / NHLBI NIH HHS / HL / R01 HL059165-11; United States / NHLBI NIH HHS / HL / HL59165; United States / NHLBI NIH HHS / HL / HL81691
  • [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] EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ NIHMS167053; NLM/ PMC2844342
  •  go-up   go-down


3. Koutsopoulos AV, Dambaki KI, Datseris G, Giannikaki E, Froudarakis M, Stathopoulos E: A novel combination of multiple primary carcinomas: urinary bladder transitional cell carcinoma, prostate adenocarcinoma and small cell lung carcinoma--report of a case and review of the literature. World J Surg Oncol; 2005 Jul 26;3:51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel combination of multiple primary carcinomas: urinary bladder transitional cell carcinoma, prostate adenocarcinoma and small cell lung carcinoma--report of a case and review of the literature.
  • CASE PRESENTATION: We report a case of a man in whom urinary bladder transitional cell carcinoma, metachronous prostate adenocarcinoma and small cell lung carcinoma were diagnosed within an eighteen-month period.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Dermatol. 1999 Jan;140(1):150-3 [10215787.001]
  • [Cites] J Cancer Res Clin Oncol. 1997;123(11-12):678-80 [9620229.001]
  • [Cites] Clin Exp Dermatol. 1999 Jul;24(4):281-2 [10457131.001]
  • [Cites] Eur J Dermatol. 1999 Sep;9(6):483-6 [10491509.001]
  • [Cites] Clin Exp Dermatol. 2000 Jul;25(5):381-3 [11012589.001]
  • [Cites] Oncol Rep. 2001 Jan-Feb;8(1):111-4 [11115580.001]
  • [Cites] Hinyokika Kiyo. 2003 May;49(5):261-4 [12822453.001]
  • [Cites] An Med Interna. 1992 May;9(5):257 [1324018.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 1992 Aug 21;46(1):53-6 [1330760.001]
  • [Cites] Khirurgiia (Mosk). 1991 Oct;(10):136-43 [1803082.001]
  • [Cites] Am J Clin Oncol. 1991 Feb;14(1):49-51 [1987738.001]
  • [Cites] Eur J Surg Oncol. 1991 Feb;17(1):81-3 [1995363.001]
  • [Cites] Gut. 1979 May;20(5):414-9 [223949.001]
  • [Cites] Neurol Med Chir (Tokyo). 1986 Nov;26(11):908-12 [2437485.001]
  • [Cites] Gan No Rinsho. 1987 Nov;33(14):1846-53 [2826842.001]
  • [Cites] No Shinkei Geka. 1987 Sep;15(9):1011-7 [2827047.001]
  • [Cites] Gan No Rinsho. 1988 Jul;34(8):1001-5 [3043037.001]
  • [Cites] J Surg Oncol. 1986 May;32(1):8-10 [3724193.001]
  • [Cites] Cancer. 1985 Jun 1;55(11):2566-74 [3995473.001]
  • [Cites] Arch Otorhinolaryngol. 1985;242(1):7-12 [4038153.001]
  • [Cites] J Surg Oncol. 1985 Aug;29(4):261-3 [4079408.001]
  • [Cites] J Surg Oncol. 1979;11(1):75-8 [431085.001]
  • [Cites] Cancer. 1974 Apr;33(4):1134-44 [4406171.001]
  • [Cites] Ann Otolaryngol Chir Cervicofac. 1979 Sep;96(9):619-21 [525951.001]
  • [Cites] IMJ Ill Med J. 1982 Feb;161(2):115-6 [6122671.001]
  • [Cites] Arch Pathol Lab Med. 1984 Apr;108(4):272-4 [6546663.001]
  • [Cites] Am J Med. 1983 Feb;74(2):343-8 [6572034.001]
  • [Cites] Arch Dermatol. 1980 Jun;116(6):687-9 [6892866.001]
  • [Cites] Pathol Int. 1994 Apr;44(4):325-32 [8044300.001]
  • [Cites] J Natl Med Assoc. 1994 May;86(5):387-8 [8046769.001]
  • [Cites] Cancer Lett. 1993 Sep 15;73(1):51-7 [8402598.001]
  • [Cites] Cancer Res. 1993 Feb 1;53(3):452-5 [8425176.001]
  • [Cites] Cancer Res. 1993 Mar 1;53(5):957-61 [8439970.001]
  • [Cites] Dermatology. 1995;191(4):321-2 [8573931.001]
  • [Cites] Surg Neurol. 1996 Mar;45(3):219-29 [8638217.001]
  • [Cites] Jpn J Clin Oncol. 1996 Oct;26(5):368-73 [8895679.001]
  • [Cites] J Urol. 1997 Jan;157(1):65-7 [8976217.001]
  • [Cites] Pathol Int. 1997 Jan;47(1):68-72 [9051695.001]
  • [Cites] J Urol Nephrol (Paris). 1976 Jul-Aug;82(7-8):621-6 [1034027.001]
  • (PMID = 16045793.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1226150
  •  go-up   go-down


Advertisement
4. Xu ML, Liu Y, Zhong HH, Wu BQ: [Status and clinicopathologic implication of epidermal growth factor receptor mutation in non-small cell carcinoma of lung]. Zhonghua Bing Li Xue Za Zhi; 2007 Jul;36(7):453-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Status and clinicopathologic implication of epidermal growth factor receptor mutation in non-small cell carcinoma of lung].
  • OBJECTIVE: To investigate mutations of epidermal growth factor receptor (EGFR) exon 19 and 21 in non-small cell lung carcinoma and to explore their clinicopathological correlations.
  • METHOD: DNA was extracted from the excised tumor specimens of 66 non-small cell lung carcinoma patients by traditional phenol-chloroform and ethanol precipitation.
  • Those with adenocarcinoma with bronchiolo-alveolar carcinoma (BAC) components had higher frequency of EGFR mutation (6/11) than those without non-BAC element (4/32, 12.5%).
  • CONCLUSIONS: The mutations appear to occur in highly selected subgroups of lung cancer patients: adenocarcinomas with BAC components and patients of the female gender.
  • The results may offer practical approach to the rapid identification of lung cancer patients who likely respond to EGFR inhibitor therapy.
  • [MeSH-major] Amino Acid Substitution. Carcinoma, Non-Small-Cell Lung / genetics. Gene Deletion. Lung Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons. Female. Humans. Male. Middle Aged. Mutation. Sex Factors

  • 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 = 17845757.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


5. Brooks DR, Klint A, Dickman PW, Ståhle E, Lambe M: Temporal trends in non-small cell lung cancer survival in Sweden. Br J Cancer; 2007 Feb 12;96(3):519-22
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temporal trends in non-small cell lung cancer survival in Sweden.
  • We modeled temporal trends in the 1- and 5-year survival of 32 499 patients with adenocarcinoma and squamous cell carcinoma of the lung in the Swedish Cancer Register between 1961 and 2000.
  • The 1-year relative survival for adenocarcinoma improved from 37% for patients diagnosed 1961-1965 to 45% for those diagnosed 1996-2000 and from 39 to 45% for squamous cell carcinoma.
  • The adjusted excess mortality ratios for the period 1996-2000 compared with 1961-1965 were 0.80 for adenocarcinoma and 0.81 for squamous cell carcinoma.
  • Thus, a previous report in a Dutch study of a relatively worsening prognosis for adenocarcinoma over time could not be confirmed.
  • [MeSH-major] Adenocarcinoma / mortality. Carcinoma, Non-Small-Cell Lung / mortality. Carcinoma, Squamous Cell / mortality. Lung Neoplasms / mortality

  • 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
  • [Cites] Lung Cancer. 2001 Feb-Mar;31(2-3):123-37 [11165391.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1371-5 [16452191.001]
  • [Cites] Int J Cancer. 2001 Mar 15;91(6):876-87 [11275995.001]
  • [Cites] Cancer Causes Control. 2001 Aug;12(6):539-49 [11519762.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1525-30 [11745231.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3244-50 [12036940.001]
  • [Cites] Cancer Lett. 2002 Dec 10;187(1-2):47-51 [12359350.001]
  • [Cites] Am J Epidemiol. 2002 Dec 15;156(12):1114-22 [12480656.001]
  • [Cites] Lung Cancer. 2003 Sep;41(3):245-58 [12928116.001]
  • [Cites] Stat Med. 2004 Jan 15;23(1):51-64 [14695639.001]
  • [Cites] Jpn J Clin Oncol. 1990 Sep;20(3):238-45 [2174996.001]
  • [Cites] Environ Health Perspect. 1995 Nov;103 Suppl 8:143-8 [8741774.001]
  • [Cites] Int J Epidemiol. 1997 Feb;26(1):14-23 [9126499.001]
  • [Cites] Cancer. 1997 Aug 1;80(3):382-8 [9241071.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2996-3018 [9256144.001]
  • [Cites] J Natl Cancer Inst. 1997 Nov 5;89(21):1580-6 [9362155.001]
  • [Cites] Br J Cancer. 1998 Jun;77(11):2053-7 [9667692.001]
  • [Cites] Br J Cancer. 1961 Mar;15:51-3 [13754310.001]
  • [Cites] BMC Public Health. 2005 Mar 5;5:22 [15748289.001]
  • [Cites] Epidemiology. 2001 Mar;12(2):256-8 [11246589.001]
  • (PMID = 17245337.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2360026
  •  go-up   go-down


6. Gerosa M, Nicolato A, Foroni R, Tomazzoli L, Bricolo A: Analysis of long-term outcomes and prognostic factors in patients with non-small cell lung cancer brain metastases treated by gamma knife radiosurgery. J Neurosurg; 2005 Jan;102(s_supplement):75-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of long-term outcomes and prognostic factors in patients with non-small cell lung cancer brain metastases treated by gamma knife radiosurgery.
  • OBJECT: The authors conducted a study to evaluate the long-term outcomes and prognostic factors for survival in a large series of patients treated by gamma knife surgery (GKS) for non-small cell lung cancer (NSCLC) brain metastases.
  • The most common histological types were adenocarcinoma (51%) and squamous cell carcinoma (27%).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28306429.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; brain metastasis / gamma knife surgery / non—small cell lung cancer
  •  go-up   go-down


7. Shimada A, Kano J, Ishiyama T, Okubo C, Iijima T, Morishita Y, Minami Y, Inadome Y, Shu Y, Sugita S, Takeuchi T, Noguchi M: Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development. Cancer Sci; 2005 Oct;96(10):668-75
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment of an immortalized cell line from a precancerous lesion of lung adenocarcinoma, and genes highly expressed in the early stages of lung adenocarcinoma development.
  • Atypical adenomatous hyperplasia (AAH) is classified as a precancerous lesion of lung adenocarcinoma.
  • We established an immortalized AAH cell line (PL16T) and a human non-neoplastic bronchial epithelial cell line (PL16B) from the same patient by transfection with the gene for SV40 large T antigen.
  • In normal lung tissue, both TACSTD2 and S100A2 were expressed at very low levels, but seven and five of 14 AAH were positive for TACSTD2 and S100A2, respectively.
  • The frequency of TACSTD2 positivity was increased in 16 of 22 bronchioloalveolar carcinomas (BAC) and adenocarcinoma with mixed subtype with BAC component (mixed BAC).
  • The abnormal transcription of TACSTD2 and S100A2 are thought to be unique molecular markers of the preinvasive stage of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antigens, Neoplasm / biosynthesis. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Adhesion Molecules / biosynthesis. Chemotactic Factors / biosynthesis. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. S100 Proteins / biosynthesis
  • [MeSH-minor] Female. Gene Expression Profiling. Humans. Hyperplasia. Lung / pathology. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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 = 16232198.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cell Adhesion Molecules; 0 / Chemotactic Factors; 0 / S100 Proteins; 0 / S100A2 protein, human; 0 / TACSTD2 protein, human
  •  go-up   go-down


8. Bing Z, Adegboyega PA: Metastasis of small cell carcinoma of lung into an ovarian mucinous neoplasm: immunohistochemistry as a useful ancillary technique for diagnosis and classification of rare tumors. Appl Immunohistochem Mol Morphol; 2005 Mar;13(1):104-7
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastasis of small cell carcinoma of lung into an ovarian mucinous neoplasm: immunohistochemistry as a useful ancillary technique for diagnosis and classification of rare tumors.
  • The authors report the first case of ovarian mucinous adenocarcinoma with metastasis from a synchronous small cell neuroendocrine carcinoma of the lung.
  • Bronchial brushing as well as transbronchial fine-needle aspiration was diagnostic of small cell carcinoma.
  • Microscopic examination disclosed a mucinous neoplasm with both mucinous cystadenoma and mucinous papillary adenocarcinoma components.
  • Immunohistochemistry showed that group of cells to be positive for thyroid transcription factor 1 and chromogranin, confirming them to be metastasis from the pulmonary small cell neuroendocrine carcinoma.

  • Genetic Alliance. consumer health - Ovarian small cell carcinoma.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15722802.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; EC 1.11.1.- / Peroxidases
  •  go-up   go-down


9. Lin PY, Chang YC, Chen HY, Chen CH, Tsui HC, Yang PC: Tumor size matters differently in pulmonary adenocarcinoma and squamous cell carcinoma. Lung Cancer; 2010 Mar;67(3):296-300
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor size matters differently in pulmonary adenocarcinoma and squamous cell carcinoma.
  • Little about primary tumor size and nodal/distant metastases among different cell types in non-small cell lung cancer (NSCLC) was discussed.
  • This study aimed to investigate distinct associations between tumor size and nodal/distant metastases in pulmonary adenocarcinoma and squamous cell carcinoma.
  • Our data showed that 2.5 cm was the critical cutoff size regarding increased nodal/distant metastases in adenocarcinoma (p<0.001), but not in squamous cell carcinoma (p>0.05).
  • In addition, the incidence of nodal/distant metastases reached a plateau of more than 80% in adenocarcinoma when the tumor size exceeded 2.5 cm.
  • In contrast, there was no such correlation observed in squamous cell carcinoma.
  • This study showed that tumor size mattered differently in pulmonary adenocarcinoma and squamous cell carcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Carcinoma, Non-Small-Cell Lung / secondary. Carcinoma, Squamous Cell / secondary. Lung Neoplasms / pathology

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19473720.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  •  go-up   go-down


10. Yamauchi S, Kudoh S, Kimura T, Yoshimura N, Mukohara T, Hirata K, Yoshikawa J: The association of adenocarcinoma and hemosputum in pulmonary malignancies. Respiration; 2005 Sep-Oct;72(5):499-503
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association of adenocarcinoma and hemosputum in pulmonary malignancies.
  • BACKGROUND: Hemosputum was considered one of the popular symptoms of patients with centrally located carcinoma of the lung, especially squamous cell or small cell type.
  • Recent studies reported a relative increase in adenocarcinoma compared with squamous cell carcinoma, especially in developed countries.
  • There were 66 patients with adenocarcinoma, 55 with squamous cell carcinoma, 15 with small cell carcinoma, 5 with large cell carcinoma, 3 with other cell type carcinoma and 5 with metastatic carcinoma.
  • On bronchoendoscopic examination, abnormal findings in the segmental or more proximal bronchi were found in 82 patients, including 36 with squamous cell carcinoma, 31 with adenocarcinoma, 12 with small cell carcinoma, 2 with large cell carcinoma and 1 with metastatic carcinoma.
  • On the other hand, 67 patients were diagnosed with pulmonary malignancy in the subsegmental or more distal area, including 35 with adenocarcinoma, 19 with squamous cell carcinoma, 3 with small cell carcinoma, 3 with large cell carcinoma, 3 with other cell type carcinoma and 4 with metastatic carcinoma.
  • CONCLUSIONS: The most frequent histological type of malignancy with hemosputum was adenocarcinoma.
  • The number of adenocarcinoma with hemosputum was increased in both central and peripheral regions.
  • [MeSH-major] Carcinoma / pathology. Hemoptysis / etiology. Lung Neoplasms / pathology. Sputum

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16210889.001).
  • [ISSN] 0025-7931
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


11. Tsou JA, Shen LY, Siegmund KD, Long TI, Laird PW, Seneviratne CK, Koss MN, Pass HI, Hagen JA, Laird-Offringa IA: Distinct DNA methylation profiles in malignant mesothelioma, lung adenocarcinoma, and non-tumor lung. Lung Cancer; 2005 Feb;47(2):193-204
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct DNA methylation profiles in malignant mesothelioma, lung adenocarcinoma, and non-tumor lung.
  • In particular when limited cell numbers are available, amplifyable DNA markers can provide a very sensitive tool for cancer detection and classification.
  • Malignant mesothelioma (MM), an aggressive cancer strongly associated with asbestos exposure, can be difficult to distinguish from adenocarcinoma of the lung when limited material is available.
  • In an attempt to identify molecular markers for MM and adenocarcinoma, we examined the DNA methylation status of 14 loci.
  • Analysis of methylation levels in 10 MM and 8 adenocarcinoma cell lines showed that methylation of APC was significantly elevated in adenocarcinoma compared to MM cell lines (P=0.0003), while methylation of CDH1 was higher in MM (P<0.02).
  • Subsequent examination of the methylation status of the 14 loci in 6 MM and 7 adenocarcinoma primary tumors, which yielded similar methylation profiles, supported these observations.
  • Comparison of methylation in MM cell lines and tumors versus non-tumor lung tissue indicated that APC exhibits less methylation in MM (P=0.003) while RASSF1, PGR1, ESR1, and CDH1 show more methylation in MM, the latter two showing the most significant difference between the two tissue types (P< or = 0.0001).
  • Comparison of methylation in adenocarcinoma cell lines and tumors versus non-tumor lung tissue showed methylation of ESR1, PGR1 and RASSF1 to be significantly elevated in adenocarcinoma, with RASSF1 being most significant (P=0.0002).
  • Thus, with the examination of 14 loci, we have identified 5 candidates that show potential for distinguishing between MM, adenocarcinoma and/or non-cancer lung.
  • Our observations support the strong potential of methylation markers as tools for accurate diagnosis of neoplasms in and around the lung.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Non-Small-Cell Lung / genetics. DNA Methylation. DNA, Neoplasm. Genetic Markers. Lung Neoplasms / genetics. Mesothelioma / genetics
  • [MeSH-minor] Genes, Tumor Suppressor. Humans. Lung. Sensitivity and Specificity. Tumor Cells, Cultured


12. Mitsuta K, Yokoyama A, Kondo K, Nakajima M, Arita K, Kohno N: Polymorphism of the MUC1 mucin gene is associated with susceptibility to lung adenocarcinoma and poor prognosis. Oncol Rep; 2005 Jul;14(1):185-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism of the MUC1 mucin gene is associated with susceptibility to lung adenocarcinoma and poor prognosis.
  • We hypothesize that MUC1 allele length polymorphism (variable number of tandem repeats) is associated with development of lung adenocarcinoma.
  • We evaluated MUC1 gene polymorphism using Southern blot analysis of peripheral blood from patients with non-small cell lung cancer (n=56), patients with benign respiratory disease (n=52), and healthy volunteers (n=52).
  • We found that large MUC1 allele length was significantly associated with lung adenocarcinoma but not with squamous cell carcinoma of the lung.
  • Adenocarcinoma patients with a homozygous large MUC1 genotype had a worse prognosis than patients with a heterozygous (large + small) MUC1 genotype or a homozygous small MUC1 genotype.
  • These results suggest that the large MUC1 allele is associated with susceptibility to lung adenocarcinoma and poor prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Genetic Predisposition to Disease / genetics. Lung Neoplasms / pathology. Mucin-1 / genetics. Polymorphism, Genetic
  • [MeSH-minor] Aged. Aged, 80 and over. Alleles. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. Multivariate Analysis. Prognosis. Survival Analysis

  • 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 = 15944787.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Mucin-1
  •  go-up   go-down


13. Matsuda Y, Yamamoto T, Kudo M, Kawahara K, Kawamoto M, Nakajima Y, Koizumi K, Nakazawa N, Ishiwata T, Naito Z: Expression and roles of lumican in lung adenocarcinoma and squamous cell carcinoma. Int J Oncol; 2008 Dec;33(6):1177-85
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and roles of lumican in lung adenocarcinoma and squamous cell carcinoma.
  • Lumican is a member of a small leucine-rich proteoglycan family and is highly expressed in several types of cancer cells and/or stromal tissue.
  • In this study, we examined the expression and role of lumican in lung cancer including adenocarcinoma (ADC) and squamous cell carcinoma (SqCC).
  • Immunohistochemically, lumican was weakly expressed in vascular smooth muscle cells, perivascular and peribronchial connective tissues and bronchial epithelium of normal lung tissues.
  • In lung cancer tissues, lumican was localized in the cytoplasm of cancer cells and/or stromal tissues adjacent to cancer cells.
  • In lung cancer cell lines, lumican mRNA and protein were expressed in LC-1/Sq and EBC-1 cells established from SqCC, and A549, RERF-LC-KJ and PC-3 cells from ADC.
  • The molecular weight of lumican extracted from the cytoplasm of lung cancer cells differed from that in the culture medium owing to glycosylation of the protein.
  • These findings suggest that the expression pattern and the glycosylated type of lumican in cells and stromal tissues correlate with the aggressiveness of lung SqCC and ADC.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Chondroitin Sulfate Proteoglycans / metabolism. Keratan Sulfate / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Aged. Blotting, Western. Cell Line, Tumor. Cytoplasm / metabolism. Female. Gene Expression Regulation, Neoplastic. Glycosylation. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Molecular Weight. Neoplasm Invasiveness. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / metabolism. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19020750.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chondroitin Sulfate Proteoglycans; 0 / RNA, Messenger; 0 / lumican; 9056-36-4 / Keratan Sulfate
  •  go-up   go-down


14. Novello S, Abrey LE, Grossi F, Camps C, Mazieres J, Selaru P, Patyna S, Torigoe Y, Chao R, Scagliotti G: Administration of sunitinib to patients with non-small cell lung cancer and irradiated brain metastases: A phase II trial. J Clin Oncol; 2009 May 20;27(15_suppl):8077

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Administration of sunitinib to patients with non-small cell lung cancer and irradiated brain metastases: A phase II trial.
  • : 8077 Background: Sunitinib (SU), an oral, multitargeted inhibitor of VEGFRs, PDGFRs, KIT, FLT3, CSF-1R, and RET has promising single-agent antitumor activity in refractory non-small cell lung cancer (NSCLC) (Socinski JCO 2008).
  • Safety was assessed by monitoring adverse events (AEs) and health-related quality of life was assessed using FACT/NCCN Lung Symptom Index (FLSI) and Brain Symptom Index (FBrSI).
  • RESULTS: To date, 47 pts, including 28 with adenocarcinoma and 10 with squamous cell carcinoma, received SU for a median of 2 cycles (range: 1, 9).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962653.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Meng X Jr, Yu JM, Yang GR, Zhao SQ, Sun XD: &lt;sup&gt;11&lt;/sup&gt;C-PD153035 PET/CT molecular imaging of EGFR for evaluation of advanced non-small cell lung cancer (NSCLC) to EGFR-targeted therapy. J Clin Oncol; 2009 May 20;27(15_suppl):7576

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] <sup>11</sup>C-PD153035 PET/CT molecular imaging of EGFR for evaluation of advanced non-small cell lung cancer (NSCLC) to EGFR-targeted therapy.
  • RESULTS: 12 patients (5 men, 7 women; age range, 60-79 years) have been enrolled in this study from August 2008, including 3 cases of squamous cell carcinoma, 1 case of large cell carcinoma, and the other of adenocarcinoma.
  • Tumor/lung ratio at 20 min was 4.14 ± 1.80.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963384.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Fan M, Xie L, Xu X, Zhang G, Chen J, Fu X, Zhou X, Li W, Jiang G: Phase I dose-escalation study of thoracic radiotherapy in combination with gefitinib in patients with IIIB/IV non-small cell lung cancer (NCT00497250). J Clin Oncol; 2009 May 20;27(15_suppl):e14581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I dose-escalation study of thoracic radiotherapy in combination with gefitinib in patients with IIIB/IV non-small cell lung cancer (NCT00497250).
  • However, a higher incidence of interstitial lung disease, sometimes lethal, is also found.
  • RESULTS: Since June 2007, 2 cohorts, a total of 16 patients, were enrolled and treated: 8 stage IIIB and 8 stage IV; 2 squamous-cell carcinoma and 14 adenocarcinoma; 8 smokers and 8 nonsmokers.
  • CONCLUSIONS: Thoracic radiotherapy up to 56 Gy concurrent with gefitinib 250 mg daily was well tolerated and clinically active in this group of pretreated Chinese NSCLC patients, including nonsmokers with adenocarcinoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963755.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Sorensen J, Hansen O, Vilmar A, Frank H: Prospective randomized phase III trial of triplet chemotherapy with paclitaxel + gemcitabine + cisplatin compared to standard doublet chemotherapy with vinorelbine + cisplatin in advanced non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):8034

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective randomized phase III trial of triplet chemotherapy with paclitaxel + gemcitabine + cisplatin compared to standard doublet chemotherapy with vinorelbine + cisplatin in advanced non-small cell lung cancer.
  • Overall, median age was 62 years (range 38-75 yrs), 58% were males, 11% had performance status 2, 62% stage IV disease, 46% adenocarcinoma, and 28% squamous cell carcinoma (SCC), equally distributed between the regimens.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962834.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Toyooka S, Hotta K, Nakamura H, Nakata M, Tada H, Yamashita M, Watanabe N, Sakamoto J, Aoe M, Date H: A multicenter, phase III study of carboplatin/paclitaxel versus oral uracil-tegafur as the adjuvant chemotherapy in resected non-small cell lung cancer (NSCLC): Planned interim analyses. J Clin Oncol; 2009 May 20;27(15_suppl):7560

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicenter, phase III study of carboplatin/paclitaxel versus oral uracil-tegafur as the adjuvant chemotherapy in resected non-small cell lung cancer (NSCLC): Planned interim analyses.
  • Sixty patients had adenocarcinoma, 30 had squamous cell carcinoma, and 10 had other histologies.
  • The median survival time of A and B arms combined was 4.1 year.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963337.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Yu J, Liu N, Hu M, Song X, Xie L, Meng X, Wang X, Kong L, Yang G: Further evaluation of &lt;sup&gt;11&lt;/sup&gt;C-PD153035 as a molecular imaging probe for the assessment of the epidermal growth factor receptor status in non-small cell lung cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):3590

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Further evaluation of <sup>11</sup>C-PD153035 as a molecular imaging probe for the assessment of the epidermal growth factor receptor status in non-small cell lung cancer patients.
  • Our pilot study has demonstrated that <sup>11</sup>C-PD153035, a highly EGFR selective tracer for positron emission tomography (PET), accumulated in tumor mass of non-small cell lung cancer (NSCLC) and the tracer uptake correlated with EGFR expression.
  • METHODS: Fourteen patients (45-71y, mean 59.2±9.2 y, Male: Female = 8:6, squamous carcinoma: adenocarcinoma = 9:5) with pathologically proved NSCLC were examined with PET using <sup>11</sup>C-PD153035 one week before surgery.
  • CONCLUSIONS: PET with <sup>11</sup>C-PD153035 might therefore be used to visualize EGFR pattern on tumor in NSCLC patients and for individualized planning of therapeutic strategies with EGFR targeted drugs, especially small-molecule TKIs (gefitinib and erlotinib) which targeting the intracellular EGFR tyrosine kinase domain as PD153035.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961761.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Fleischmann AM, Waser B, Reubi JC: Gastrin-releasing peptide receptors in the tumor vascular bed of various human cancers: high incidence in urinary tract cancers. J Clin Oncol; 2009 May 20;27(15_suppl):e14575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Frequent human cancers from the breast (n=134), lung (n=57), prostate (n=50), kidney (n=32), colon (n=46), urinary tract (n=26) and biliary tract (n=23) were analyzed using in vitro GRP-receptor autoradiography on tissue sections with the <sup>125</sup>I-[Tyr<sup>4</sup>]-bombesin radioligand and/or the universal radioligand <sup>125</sup>I-[D-Tyr<sup>6</sup>, ß-Ala<sup>11</sup>, Phe<sup>13</sup>, Nle<sup>14</sup>]-bombesin(6-14).
  • Different tumor-types within a given site may have divergent prevalence of vascular GRP-receptors (e.g. lung: small cell cancer: 0%; adenocarcinoma: 59%; squamous carcinoma: 83%).
  • Also the vascular score varies widely, with highest score in urinary tract cancer (1.69), moderate scores in lung (0.91), colon (0.88), kidney (0.84) and biliary tract (0.69) cancers and low scores in breast (0.39) and prostate (0.14) cancers.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963648.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. Takahashi T, Yamamoto N, Murakami H, Ohe Y, Kunitoh H, Nokihara H, Koshiji M, Tamura T: A phase I study of enzastaurin (Enz) combined with pemetrexed (Pem) in advanced non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):2572

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of enzastaurin (Enz) combined with pemetrexed (Pem) in advanced non-small cell lung cancer (NSCLC).
  • Pre-clinical data shows Enz's synergistic activity with Pem in many cancer cell lines including NSCLC.
  • This phase 1 study is to evaluate the safety, pharmacokinetics (PK), and clinical activity of two schedules of Enz combined with Pem in patients (pts) with previously treated advanced NSCLC.
  • RESULTS: 12 pts (8 males, 4 females; ECOG PS 0-1) with median age of 62 (49 - 74) were enrolled into this study and completed safety evaluation for cycle 1: 8 pts with adenocarcinoma, 3 pts with squamous cell carcinoma, and one with other.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961896.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


22. Tanaka F, Yoneda K, Hashimoto M, Takuwa T, Matsumoto S, Okumura Y, Kondo N, Hasegawa S, Fukuoka K, Nakano T: Circulating tumor cells (CTCs) and endothelial cells (CECs) in primary lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):11066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating tumor cells (CTCs) and endothelial cells (CECs) in primary lung cancer.
  • : 11066 Background: Circulating tumor cell (CTC), a surrogate of distant metastasis, and circulating endothelia cell (CEC), a surrogate of angiogenesis, are potentially useful in the diagnosis of malignant tumors, but clinical significance of CTC/CEC in primary lung cancer (LC) remains unclear.
  • RESULTS: In 42 (30.7%) of 137 LC cases, CTC in the peripheral blood was positive (CTC-count, more than 1 cell/7.5mL), and the maximum CTC-count was 62 cells.
  • In 11 (18.3%) of 145 cases with non-malignant (NM) diseases, CTC was also positive; however, in NM cases, CTC-count was 1 (cell/7.5mL) in most CTC-positive cases and the maximun CTC-count was 2.
  • Among LC cases, the incidence of case with CTC-positive (CTC-count, 1 or more) was highest in small cell carcinoma cases (7/10, 70.0%), followed by squamous cell carcinoma (9/22, 40.9%) and adenocarcinoma (23/94, 24.5%) cases; the incidence of CTC-positive case was significantly higher in stage IV cases (68.6%; p<0.001), but it should be noted that CTC was positive in 17.4% of stage I cases and 15.4% of stage II cases.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963143.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


23. Oizumi S, Akie K, Ogura S, Shinagawa N, Fukumoto S, Harada M, Kojima T, Kinoshita I, Dosaka-Akita H, Isobe H, Nishimura M: Phase II study of irinotecan plus S-1 combination for previously untreated advanced non-small cell lung cancer: Hokkaido Lung Cancer Clinical Study Group 0601. J Clin Oncol; 2009 May 20;27(15_suppl):e19012

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of irinotecan plus S-1 combination for previously untreated advanced non-small cell lung cancer: Hokkaido Lung Cancer Clinical Study Group 0601.
  • : e19012 Background: Platinum-containing therapy is a standard first-line treatment for advanced non-small cell lung cancer (NSCLC).
  • Median age was 64 years (range, 42-75); 29 patients (73%) had adenocarcinoma, and 8 patients (20%) had squamous cell carcinoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962633.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


24. Sugio K, Nagashima A, Nakanishi R, Uchiyama A, Inoue M, Osaki T, Yoshimatsu T, Takenoyama M, Hanagiri T, Yasumoto K: Randomized phase II trial of the biweekly schedule of adjuvant chemotherapy with carboplatin plus paclitaxel versus carboplatin plus gemcitabine in patients with non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):7562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II trial of the biweekly schedule of adjuvant chemotherapy with carboplatin plus paclitaxel versus carboplatin plus gemcitabine in patients with non-small cell lung cancer (NSCLC).
  • The histologic types included adenocarcinoma (n=51), squamous cell carcinoma (n=18), large cell carcinoma (n=5), and adenosquamous cell carcinoma (n=1).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963358.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


25. Laskin JJ, Pugh T, Jackson C, Sutcliffe M, Ionescu D, Melosky B, Ho C, Sun S, Murray N, Marra M: Transcriptome-wide mutation discovery in patients in a phase II clinical trial of first-line erlotinib for clinically selected patients with advanced non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):8102

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptome-wide mutation discovery in patients in a phase II clinical trial of first-line erlotinib for clinically selected patients with advanced non-small cell lung cancer.
  • Eligibility criteria included: stage IIIB/IV NSCLC; no prior chemo; ECOG ≤2; at least 2 of the following 4 criteria: women, never-smokers, Southeast Asian origin, adenocarcinoma and/or BAC.
  • Pathology: 44 ACA; 3 BAC;1 squamous carcinoma; 13 NSCLC NOS.
  • The discovery of novel mutations in multiple pts suggests patterns that may shed light on lung cancer specific behaviour.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


26. Stoehlmacher J, Goekkurt E, Hoeffken G, Zinsky R, Lynch F, Buettner H, Scheil-Bertram S, Schirren J, Ehninger G, Fisseler-Eckhoff A: Thymidylate synthase polymorphisms and immunohistochemistry in non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):11101

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thymidylate synthase polymorphisms and immunohistochemistry in non-small cell lung cancer.
  • : 11101 Background: Recently, pemetrexed has been introduced into the treatment of non-small cell lung cancer (NSCLC).
  • There's evidence that pemetrexed appears to be more efficient in non squamous NSCLC including adenocarcinoma (AC) and large cell carcinoma (LCC).
  • Distribution of histology was as follows: 50% AC, 42% squamous cell carcinoma (SCC), 3% LCC and 5% mixed or other histological subtypes.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963465.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


27. Sugarbaker DJ, Tilleman TR, Swanson SJ, Jaklitsch MT, Mentzer SJ, Mujoomdar AA, Bueno R: The role of extrapleural pneumonectomy in the management of pleural cancers. J Clin Oncol; 2009 May 20;27(15_suppl):7577

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Of these, 32 patients had mediastinoscopy negative T4 lung cancer, 11 had metastases to only one pleura from extrathoracic sites, 10 had unilateral lung sarcomas involving the pleural envelope, 8 had thymomas metastatic to a pleural space, 2 were preoperatively diagnosed as mesotheliomas but at final pathology were determined to be small cell lung cancer and sarcomatoid carcinoma, and 2 represented primary mucoepidermoid and neuroectodermal malignancies.
  • Twenty-eight patients had stage IIIB (T4-N0-1) lung adenocarcinoma representing the largest homogeneous group of patients by cell type and stage.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963385.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


28. Luttgen MS, Marrinucci D, Lazar D, Malchiodi M, Clark P, Huynh E, Bethel K, Bazhenova L, Nieva J, Kuhn P: Circulating tumor cells monitored over time in lung cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):11025

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating tumor cells monitored over time in lung cancer patients.
  • : 11025 Background: Circulating tumor cell (CTC) detection and enumeration is a valuable tool for monitoring cancer patient status and outcome.
  • While many current techniques employ immunomagnetic-enrichment based protocols focused on the importance of a particular CTC number as the indicator of patient status or outcome, we employ a cytometric, enrichment free approach using an immunofluorescent protocol to monitor CTC counts in patients with non-small cell lung cancer (NSCLC) over the course of treatment.
  • The histological subtypes in the 42 cases for which the data was available included adenocarcinoma (22/42), squamous cell carcinoma (6/42), large cell undifferentiated carcinoma (3/42), and non-small cell lung carcinoma not further described, poorly differentiated, or with a mixed pattern (11/42).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963968.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


29. Saji H, Tsuboi M, Miyajima K, Shimada Y, Ohira T, Ikeda N: Impact of number of resected and involved lymph nodes (LN) at the time of surgical resection on the survival of non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):7514

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of number of resected and involved lymph nodes (LN) at the time of surgical resection on the survival of non-small cell lung cancer (NSCLC).
  • RESULTS: Demographics are as follows: median age: 65.0 (22-87yrs), sex: 547 males and 381 females, median follow-up time: 2.5 yrs, clinical stage: 765 stage I, 84 stage II and 76 stage III, histology: 684 adenocarcinoma, 182 squamous cell carcinoma, and 62 others, operation: 870 lobectomy, 42 bilobectomy and 16 pneumonectomy, mean number of resected LN: 15 (1-49), mean number of involved LN: 0.9 (0-22).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963485.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


30. Ou SI, Zell JA: Frequency of carcinoma not otherwise specified (NOS) as a histologic diagnosis among non-small cell lung cancer (NSCLC) cases between 1989 to 2006: An epidemiologic study from the California Cancer Registry. J Clin Oncol; 2009 May 20;27(15_suppl):e19049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of carcinoma not otherwise specified (NOS) as a histologic diagnosis among non-small cell lung cancer (NSCLC) cases between 1989 to 2006: An epidemiologic study from the California Cancer Registry.
  • We investigated the distribution of carcinoma NOS (not otherwise specified) among NSCLC cases in California.
  • RESULTS: Carcinoma NOS accounted for 22.2% of all NSCLC patients, was most commonly diagnosed cytologically (36.7%) and had the worst 5-year survival estimates (5.8%) and median OS (5 months) compared to other major histologies.
  • The proportion of carcinoma NOS was highest among stage 4 disease and increased significantly from 1989 to 2006 among all patients, both males and females, all 4 major ethnicities (Caucasian, African-American, Hispanic, and Asian), all age- categories, and all AJCC stages.
  • The percentage of the very elderly (80+) increased from 10.8% to 17.1% among all NSCLC patients and they had the highest percentages of carcinoma NOS and cytologically-diagnosed NSCLC among all age categories.
  • Among stage 4 patients, carcinoma NOS patients derived less survival benefit from chemotherapy than adenocarcinoma patients during the most recent period of diagnosis and Cox proportional hazards analysis indicated carcinoma NOS (vs. adenocarcinoma; HR = 1.061, 95% CI: 1.040- 1.083) and cytologically-diagnosed NSCLC (vs. histologically-diagnosed NSCLC, HR = 1.043, 95% CI: 1.024-1.062) were independent unfavorable prognostic factors for OS.
  • CONCLUSIONS: Carcinoma NOS was a common histologic diagnosis and was increasing in proportion among NSCLC in California from 1989 to 2006.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962101.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


31. Iliopoulou EG, Kountourakis P, Karamouzis MV, Doufexis D, Ardavanis A, Baxevanis CN, Rigatos G, Papamichail M, Perez SA: A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):3001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC).
  • Preclinical studies revealed that activated NK cells massively infiltrate lung tissue and improve recipient survival, suggesting a potential role in lung cancer therapeutics.
  • Pts characteristics: M/F 12/4; histology: adenocarcinoma/squamous cell carcinoma 13/3; stage IIIb/IV 2/14; 1<sup>st</sup>/2<sup>nd</sup> line treatment 13/3; median age 64 years (range, 50-71).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962051.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


32. Seki N, Eguchi K, Kaneko M, Ohmatsu H, Kakinuma R, Matsui E, Kusumoto M, Tsuchida T, Nishiyama H, Moriyama N: Stage-size relationship in long-term repeated CT screening for lung cancer: Anti-Lung Cancer Association project. J Clin Oncol; 2009 May 20;27(15_suppl):1540

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stage-size relationship in long-term repeated CT screening for lung cancer: Anti-Lung Cancer Association project.
  • : 1540 Background: We have investigated the individualized benefit of CT screening as Anti-Lung Cancer Association projects (presented at ASCO 2006-2008).
  • However, there has not been enough information about the relationship of lung cancer stage to tumor size in repeated CT screening.
  • Therefore, we evaluated the stage-size relationship of these asymptomatic lung cancer cases diagnosed by long-term repeated screening with low-dose helical CT.
  • Histology for the categories 15 mm or less was localized bronchioloalveolar carcinoma in 13 cases, adenocarcinoma with mixed subtype in 11 cases, invasive adenocarcinoma in five cases, other non-small cell carcinoma in 10 cases, and small cell carcinoma in one case.
  • CONCLUSIONS: These results provide direct evidence of a stage-size relationship in long-term repeated CT screening for lung cancer.
  • Furthermore, early detection of lung cancer of 15 mm or less in diameter leads to the detection of early-stage (N0M0) lung cancer in repeated CT screening.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964081.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


33. Quesenberry PJ, Del Tatto M, Berz D, Miner T, Ng T, Winer ES, Aliotta J, Colvin G, Dooner M, Dooner G, Fontaine JP: Marrow cell genetic phenotype change induced by human lung cancer cells. J Clin Oncol; 2009 May 20;27(15_suppl):11108

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963460.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


34. Tojo T, Tojo T, Naito H, Kimura M, Takasawa S, Dohi Y, Nagata Y, Taniguchi S: Regenerating gene 1α (REG 1α) expression and new treatment strategies in early non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e22178

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regenerating gene 1α (REG 1α) expression and new treatment strategies in early non-small cell lung cancer.
  • In the present study, to elucidate roles for REG Iα in non-small cell lung cancer (NSCLC), we investigated REG Iα expression in NSCLCs, focusing especially on its relationship with prognosis.
  • METHODS: We enrolled 70 NSCLCs (adenocarcinoma (AC)(n=48) and squamous cell carcinoma (SCC)(n=22)) who received surgery at Nara Medical University Hospital.
  • Total RNA was extracted from each tumor tissue and corresponding normal lung tissue (NL)(n=70), cDNA was then reverse-transcribed from total RNA, and quantitative real-time reverse transcriptase-polymerase chain reaction was then carried out.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963718.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


35. Davidson JA, Wong V, Fraser R, Hirsh V: Comparison of primary tumor maximal standardized uptake value (SUV&lt;sub&gt;max&lt;/sub&gt;) on preoperative [18F]fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) and histological subtype in patients with non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):7571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of primary tumor maximal standardized uptake value (SUV<sub>max</sub>) on preoperative [18F]fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) and histological subtype in patients with non-small cell lung cancer (NSCLC).
  • Only patients with Adenocarcinoma (AC), Squamous Cell carcinoma (SC), or Large Cell carcinoma (LC), and definitive pathological staging, were included.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963356.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


36. Johnson K, Berger A, Watkins T, Cheadle C, Casciola-Rosen L, Levine SM: Gene set enrichment analysis to evaluate expression of autoantigens in lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e22048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene set enrichment analysis to evaluate expression of autoantigens in lung cancer.
  • METHODS: Tumor tissue from ten lung cancer biopsies (adenocarcinoma (4), carcinoid (4), and squamous cell carcinoma (2)) and normal lung from the same patients were obtained.
  • RESULTS: Single-linkage hierarchical clustering analysis reveals groups of autoantigens that are differentially expressed between normal lung tissue, carcinoid tumors, and adenocarcinomas.
  • Adenocarcinoma tumor samples were significantly enriched for myositis (nominal p-value <0.001, false discovery rate (FDR) q-value 0.009) and SLE autoantigens (p-value 0.004, FDR 0.029).
  • While autoantigens comprise only a small fraction of the total transcriptome, they are disproportionately expressed in tumors known to associate with autoimmunity, supporting the hyporthesis that autoimmunity to these proteins may arise via nascent anti-tumor responses.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963230.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


37. Grilley-Olson JE, Hayes DN, Qaqish BF, Moore DT, Socinski MA, Yin X, Wilkerson MD, Leslie KO, Travis WD, Funkhouser WK Jr, VOILA Group: Validation of Inter-Observer Agreement in Lung Cancer Assessment: Diagnostic reproducibility of squamous cell carcinoma (SC) in the era of histology-directed non-small cell lung cancer (NSCLC) chemotherapy: A large prospective study. J Clin Oncol; 2009 May 20;27(15_suppl):8008

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic reproducibility of squamous cell carcinoma (SC) in the era of histology-directed non-small cell lung cancer (NSCLC) chemotherapy: A large prospective study.
  • METHODS: Pathologists (P) assigned WHOC diagnoses to virtual H&E slides from an incident surgical cohort of 96 primary lung tumors.
  • RESULTS: 12 self-identified "lung experts" (E) and 12 community (C) P scored slides based on the 44 possible WHOC DC totaling 222 pathologist-pairs and 7130 slides-pairs.
  • Distribution of DC included SC 30% and adenocarcinoma 36%.
  • Although this model tests the reproducibility of the WHOC, not clinical lung cancer diagnoses, it shows that reproducible diagnosis of SC based on H&E morphology alone is inadequate.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962788.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


38. Scagliotti G, Monica V, Ceppi P, Righi L, Cambieri A, Volante M, Novello S, Cappelletto E, Papotti M: Baseline thymidylate synthase expression according to histological subtypes of non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):7521

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Baseline thymidylate synthase expression according to histological subtypes of non-small cell lung cancer.
  • : 7521 Background: In non-small cell lung cancer (NSCLC) baseline thymidilate synthase (TS) levels are higher in squamous cell carcinoma (SCC) compared to adenocarcinoma (AC) and randomized clinical trials have shown a selective benefit for patients with non-squamous histology treated with pemetrexed, a TS-inhibiting agent.
  • TS expression in undifferentiated large cell carcinoma (LCC) is unknown.
  • c) in all histotypes TS protein level with desmocollin-3 (DSC-3) immunostaining, a marker of squamous cell differentiation.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963288.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


39. Zhang J, Jin X, Fang S, Wang R, Li Y, Wang N, Guo W, Wang Y, Wen D, Wei L, Dong Z, Kuang G: The functional polymorphism in the matrix metalloproteinase-7 promoter increases susceptibility to esophageal squamous cell carcinoma, gastric cardiac adenocarcinoma and non-small cell lung carcinoma. Carcinogenesis; 2005 Oct;26(10):1748-53
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The functional polymorphism in the matrix metalloproteinase-7 promoter increases susceptibility to esophageal squamous cell carcinoma, gastric cardiac adenocarcinoma and non-small cell lung carcinoma.
  • To assess the effects of the functional single nucleotide polymorphism on cancer susceptibility and progression, the MMP-7 -181A/G genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism analysis among 258 patients with esophageal squamous cell carcinoma (ESCC), 201 patients with gastric cardiac carcinoma (GCA), 243 patients with non-small cell lung carcinoma (NSCLC) and 350 healthy individuals without cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Matrix Metalloproteinase 7 / genetics. Polymorphism, Single Nucleotide. Promoter Regions, Genetic
  • [MeSH-minor] Adenocarcinoma / genetics. Carcinoma, Squamous Cell / genetics. Esophageal Neoplasms / genetics. Genetic Predisposition to Disease. Heart Neoplasms / genetics. Humans. Stomach Neoplasms / genetics

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15930031.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.23 / Matrix Metalloproteinase 7
  •  go-up   go-down


40. Muehlenbein CE, Klein RW, Liepa AM, Babineaux SM, Wielage RC, Schwartzberg LS: The importance of histology when evaluating the cost-effectiveness of pemetrexed plus cisplatin as first-line therapy for advanced non-small cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e17533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The importance of histology when evaluating the cost-effectiveness of pemetrexed plus cisplatin as first-line therapy for advanced non-small cell lung cancer.
  • : e17533 Background: A recent randomized phase III study was the first to report survival differences between first-line platinum doublets based on non-small cell lung cancer (NSCLC) histology (Scagliotti et al, J Clin Oncol. 2008).
  • Nonsquamous histology subgroups explored were adenocarcinoma, large cell and not otherwise specified (NOS).
  • In the subset of patients with nonsquamous NSCLC (adenocarcinoma, large cell, or NOS), the incremental cost per LYG was $83,537 vs. Cis/Gem and $178,613 vs. Carb/Pac.
  • Further specifying the population to include only those with adenocarcinoma or large cell NSCLC yielded an incremental cost per LYG of $72,325 vs. Cis/Gem and $132,547 vs. Carb/Pac.
  • CONCLUSIONS: In an unselected advanced NSCLC population, Cis/Pem may not be considered cost-effective for first-line therapy; however, in its licensed indication of nonsquamous NSCLC, it can be considered cost-effective and even more so for patients with adenocarcinoma or large cell carcinoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963793.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


41. Qiu Y, Song B, Zhao G, Deng B, Makino T, Tomita Y, Wang J, Luo W, Doki Y, Aozasa K, Morii E: Expression level of Pre B cell leukemia homeobox 2 correlates with poor prognosis of gastric adenocarcinoma and esophageal squamous cell carcinoma. Int J Oncol; 2010 Mar;36(3):651-63
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression level of Pre B cell leukemia homeobox 2 correlates with poor prognosis of gastric adenocarcinoma and esophageal squamous cell carcinoma.
  • Pre B cell leukemia homeobox 2 (PBX2), a member of PBX family, acts as a co-factor of homeobox proteins to regulate proliferation and differentiation of tumor cells.
  • Our recent study revealed prognostic significance of PBX2 expression in non-small cell lung carcinoma.
  • The significance of PBX2 expression was examined in cases with gastric cancer (GC) and esophageal squamous cell carcinoma (ESCC), and the role of PBX2 in tumor behavior was evaluated in GC and ESCC cell lines of knocked-down PBX2 expression.
  • Knocked-down expression of PBX2 in GC and ESCC cell lines resulted in decrease of in vitro colony formation and in vivo tumorigenic activities, but proliferative and invasive activities did not change.
  • Under serum depletion, apoptotic cell proportion was higher in PBX2 knocked-down cells than in control cells.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis. Cell Differentiation. Cell Proliferation. Female. Humans. Male. Middle Aged. Prognosis

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20126986.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / PBX2 protein, human; 0 / Proto-Oncogene Proteins
  •  go-up   go-down


42. Casal J, Vázquez S, León L, Lázaro M, Fírvida JL, Amenedo M, Alonso G, Santomé L, Afonso FJ: Erlotinib as maintenance therapy after concurrent chemoradiotherapy in patients (p) with stage III non-small cell lung cancer (NSCLC): A Galician Lung Cancer Group phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):7537

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Erlotinib as maintenance therapy after concurrent chemoradiotherapy in patients (p) with stage III non-small cell lung cancer (NSCLC): A Galician Lung Cancer Group phase II study.
  • Baseline characteristics: median age 62 years (range 41-76); male 94.6%; caucasian 100%; smokers/never smokers (%) 97.3/2.7; ECOG PS 0/1/2 (%) 18.9/75.7/2.7; adenocarcinoma/squamous cell carcinoma/large cell carcinoma (%) 16.2/75.7/5.4; stage IIIA/IIIB (%) 16.2/83.8.
  • In spite of the majority of patients are caucasian, males, smokers with squamous cell carcinoma, maintenance with single agent erlotinib reached a promising median OS of 18.7 months.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963306.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


43. Parshin VD, Grigor'eva SP, Mirzoian OS, Fedorov DN: [Surgical treatment of bronchiolo-alveolar cancer]. Khirurgiia (Mosk); 2009;(12):4-12
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bronchioloalveolar cancer (BAC) belongs to a high- grade differentiated lung adenocarcinoma, localizes in peripheral parts of the lung and demonstrates an intraalveolar growth.
  • It comprised 0,5% of the whole amount of patients operated on lung cancer.
  • Long-term treatment results are somewhat better then of other forms of non-small cell carcinoma of lung: of 21 radically operated patients, 11 are alive.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / surgery. Lung Neoplasms / surgery. Pneumonectomy / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20037505.001).
  • [ISSN] 0023-1207
  • [Journal-full-title] Khirurgiia
  • [ISO-abbreviation] Khirurgiia (Mosk)
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


44. Reshetov AV, Iablonskiĭ PK, Orlova RV, Markin FM, Pishchik VG: [The possibility and prognostic value of secondary lymphatic cancer spread in intrapulmonic metastases of solid tumors]. Vestn Khir Im I I Grek; 2008;167(3):36-42
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the period from 1996 to 2007 operations were fulfilled in 120 patients with isolated pulmonary metastases of solid tumors (68 men and 52 women aged from 22 through 77 years): 46 patients with metastases of colorectal cancer, 28 - with cancer of the kidney, 23 - with non-small cell carcinoma of lung, 7 - with breast cancer, 9 - with endometrium cancer, 7 - with melanoma.
  • In most cases (21 patients) they were lesions of lymph nodes of the lung root and intrapulmonary lymph nodes.
  • In 93% of cases (27 patients) localization of the lesion coincided with anatomical pathways of lymph outflow from the affected part of the lung.
  • A conclusion is made of possible secondary lymphatic cancer spread from intrapulmonary metastases of solid tumors and its negative influence on results of treatment that allows recommendation of revision of the lymphatic system of the lungs and mediastinum in all cases of surgical treatment of intrapulmonary metastases, and in a number of cases recommendation of anatomical resections of the lung tissue as operation of choice.
  • [MeSH-major] Adenocarcinoma / secondary. Breast Neoplasms / secondary. Colorectal Neoplasms / secondary. Endometrial Neoplasms / secondary. Kidney Neoplasms / secondary. Neoplasms / pathology. Skin Neoplasms / secondary

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18652211.001).
  • [ISSN] 0042-4625
  • [Journal-full-title] Vestnik khirurgii imeni I. I. Grekova
  • [ISO-abbreviation] Vestn. Khir. Im. I. I. Grek.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


45. Karoubi G, Gugger M, Schmid R, Dutly A: OCT4 expression in human non-small cell lung cancer: implications for therapeutic intervention. Interact Cardiovasc Thorac Surg; 2009 Apr;8(4):393-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] OCT4 expression in human non-small cell lung cancer: implications for therapeutic intervention.
  • Here we investigate the expression of OCT4 human lung adenocarcinoma and bronchioloalveolar carcinoma (BAC) tumor biopsies and tumor-derived primary cell cultures.
  • We assessed the presence of OCT4 in clinical tumor samples of both adenocarcinoma and BAC at the cellular and transcriptional levels, respectively.
  • Furthermore, we evaluated tumor-derived cell cultures for potential differences in OCT4 expression.
  • Immunohistochemical analysis depicted OCT4 in 2 of 8 adenocarcinoma tumor samples and 3 of 5 BAC tumor samples, with no apparent difference in the degree of expression among the sections examined.
  • Flow cytometric assessment of 11 adenocarcinoma-derived cell cultures and 3 BAC-derived cell cultures revealed significantly higher OCT4 expression in adenocarcinoma tumors compared to their normal counterparts.
  • Comparative studies of OCT4 in adenocarcinoma and BAC tumor cell cultures demonstrated a dramatically higher expression in the former.
  • The expression of OCT4 may represent a specific and effective target for therapeutic intervention in adenocarcinoma and BAC.
  • In addition, the aberrant expression and distribution of OCT4 may indicate important parameters concerning the differences between adenocarcinoma and BAC.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Octamer Transcription Factor-3 / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19126554.001).
  • [ISSN] 1569-9285
  • [Journal-full-title] Interactive cardiovascular and thoracic surgery
  • [ISO-abbreviation] Interact Cardiovasc Thorac Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / RNA, Messenger
  •  go-up   go-down


46. Uchihara T, Okubo C, Tanaka R, Minami Y, Inadome Y, Iijima T, Morishita Y, Fujita J, Noguchi M: Neuronatin expression and its clinicopathological significance in pulmonary non-small cell carcinoma. J Thorac Oncol; 2007 Sep;2(9):796-801
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuronatin expression and its clinicopathological significance in pulmonary non-small cell carcinoma.
  • The purpose of this study was to clarify the significance of neuronatin expression in pulmonary non-small cell carcinoma.
  • METHODS: We determined the frequency of neuronatin expression in surgically resected samples from non-small cell lung carcinoma (51 adenocarcinoma and 41 squamous cell carcinoma) by immunohistochemical staining, and investigated the correlations between expression level and various clinicopathological features.
  • RESULTS: Expression of neuronatin was observed more frequently in squamous cell carcinoma (63%) than in adenocarcinoma (25%).
  • In most cases, nontumorous lung tissue did not react with the antibody against neuronatin.
  • In both adenocarcinoma and squamous cell carcinoma, less differentiated tumors expressed neuronatin more frequently than did differentiated tumors.
  • In adenocarcinoma, but not squamous cell carcinoma, the prognosis of neuronatin-positive cases was significantly worse than that of neuronatin-negative cases.
  • CONCLUSION: Neuronatin expression is specific for tumor tissue and was detected in both pulmonary adenocarcinoma and squamous cell carcinoma at high frequency, particularly in less differentiated tumors.
  • Neuronatin expression is associated with poor prognosis in patients with adenocarcinoma, and may be useful as a prognostic marker for lung adenocarcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung. Gene Expression Regulation, Neoplastic. Lung Neoplasms. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics. RNA, Neoplasm / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17805055.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Neoplasm
  •  go-up   go-down


47. Vereczkei A, Horvath OP, Varga G, Molnar TF: Gastroesophageal reflux disease and non-small cell lung cancer. Results of a pilot study. Dis Esophagus; 2008;21(5):457-60
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastroesophageal reflux disease and non-small cell lung cancer. Results of a pilot study.
  • The sharp rise in the frequency of adenocarcinoma and relative decrease of squamous cell carcinoma of the respiratory and digestive systems, raises suspicion of a common element in their carcinogenetic cascade, which could result in similar trends in cell-type distribution changes of esophageal and lung cancers.
  • The possible role of chemical irritation caused by gastroesophageal reflux disease (GERD) in non-small cell lung cancer (NSCLC) patients was investigated.
  • There was no significant difference between the adenocarcinoma and the squamous cell carcinoma groups, neither in the composite DeMeester scores nor in any of the separate parameters of the complex score investigated.


48. Abe M, Hamada J, Takahashi O, Takahashi Y, Tada M, Miyamoto M, Morikawa T, Kondo S, Moriuchi T: Disordered expression of HOX genes in human non-small cell lung cancer. Oncol Rep; 2006 Apr;15(4):797-802
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disordered expression of HOX genes in human non-small cell lung cancer.
  • In this study, we quantified the expression levels of 39 HOX genes in 41 human non-small cell lung cancer (non-SCLC) and non-cancerous lung tissues by a comprehensive analysis system based on the real-time RT-PCR method.
  • We found that the expression levels of HOXA1, A5, A10 and C6 in squamous cell carcinoma tissues (and HOXA5 and A10 in adenocarcinoma tissues) were significantly higher than those in the non-cancerous tissues.
  • Comparison of HOX gene expressions between adenocarcinoma and squamous cell carcinoma tissues showed higher expressions of HOXA1, D9, D10 and D11 in squamous cell carcinoma tissues than in adenocarcinoma tissues.
  • Immunohistochemical analysis revealed that HOXA5 and A10 proteins were localized in the cytoplasm of tumor cells in both adenocarcinoma and squamous cell carcinoma tissues.
  • These results suggest that the disordered patterns of HOX gene expressions were involved not only in the development of non-SCLC but also in the histologically aberrant diversity such as adenocarcinoma and squamous cell carcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Homeodomain Proteins / genetics. 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 = 16525661.001).
  • [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 / Homeodomain Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 157907-48-7 / HoxA protein
  •  go-up   go-down


49. Tonon G, Wong KK, Maulik G, Brennan C, Feng B, Zhang Y, Khatry DB, Protopopov A, You MJ, Aguirre AJ, Martin ES, Yang Z, Ji H, Chin L, Depinho RA: High-resolution genomic profiles of human lung cancer. Proc Natl Acad Sci U S A; 2005 Jul 5;102(27):9625-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genomic profiles of human lung cancer.
  • Lung cancer is the leading cause of cancer mortality worldwide, yet there exists a limited view of the genetic lesions driving this disease.
  • In this study, an integrated high-resolution survey of regional amplifications and deletions, coupled with gene-expression profiling of non-small-cell lung cancer subtypes, adenocarcinoma and squamous-cell carcinoma (SCC), identified 93 focal copy-number alterations, of which 21 span <0.5 megabases and contain a median of five genes.
  • Whereas all known lung cancer genes/loci are contained in the dataset, most of these recurrent copy-number alterations are previously uncharacterized and include high-amplitude amplifications and homozygous deletions.
  • Notably, despite their distinct histopathological phenotypes, adenocarcinoma and SCC genomic profiles showed a nearly complete overlap, with only one clear SCC-specific amplicon.
  • Among the few genes residing within this amplicon and showing consistent overexpression in SCC is p63, a known regulator of squamous-cell differentiation.
  • Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Nature Publishing Group. commentaries/discussion - Highlights from Nature Reviews Cancer .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Genes Dev. 2004 Mar 1;18(5):465-9 [15037544.001]
  • [Cites] Genomics. 2001 May 15;74(1):79-88 [11374904.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Jul;31(3):282-7 [11391799.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1264-7 [11493482.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • [Cites] Blood. 2002 May 15;99(10):3857-60 [11986249.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jun;34(2):224-33 [11979556.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):49-52 [12086887.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3636-40 [12097266.001]
  • [Cites] Trends Biochem Sci. 2002 Aug;27(8):396-402 [12151224.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12963-8 [12297621.001]
  • [Cites] Oncogene. 2002 Oct 7;21(45):6877-83 [12362270.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]
  • [Cites] Carcinogenesis. 2004 Jun;25(6):857-64 [15033906.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9067-72 [15199222.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4744-8 [15256441.001]
  • [Cites] Science. 2004 Jul 23;305(5683):525-8 [15273396.001]
  • [Cites] Genes Chromosomes Cancer. 1994 Aug;10(4):231-43 [7522536.001]
  • [Cites] Histol Histopathol. 1997 Apr;12(2):319-36 [9151120.001]
  • [Cites] Cancer Res. 1997 Jun 15;57(12):2331-5 [9192802.001]
  • [Cites] Genes Chromosomes Cancer. 1998 May;22(1):79-82 [9591638.001]
  • [Cites] Hum Mol Genet. 1998 Jul;7(7):1071-82 [9618163.001]
  • [Cites] Genomics. 1999 Oct 1;61(1):5-14 [10512675.001]
  • [Cites] J Clin Oncol. 2005 Apr 10;23(11):2556-68 [15767641.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4514-9 [11389083.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Hum Mol Genet. 2003 Oct 15;12 Spec No 2:R145-52 [12915456.001]
  • [Cites] Br J Cancer. 2003 Nov 3;89(9):1714-21 [14583775.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7113-21 [14612504.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):40-7 [14729606.001]
  • [Cites] Genes Dev. 2004 Jan 15;18(2):126-31 [14729569.001]
  • [Cites] Nat Rev Cancer. 2004 Mar;4(3):177-83 [14993899.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Mar;125(2):87-99 [11369051.001]
  • (PMID = 15983384.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084313; United States / NCI NIH HHS / CA / R01 CA099041; United States / NCI NIH HHS / CA / U01-CA084313-07; United States / NCI NIH HHS / CA / R01 CA084628-12; United States / NCI NIH HHS / CA / R01 CA084628; United States / NIA NIH HHS / AG / K08AG 2400401
  • [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 / Carrier Proteins; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / TP63 protein, human; 0 / TPX2 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / WHSC1L1 protein, human
  • [Other-IDs] NLM/ PMC1160520
  •  go-up   go-down


50. Gencer M, Ceylan E, Aksoy N, Uzun K: Association of serum reactive oxygen metabolite levels with different histopathological types of lung cancer. Respiration; 2006;73(4):520-4
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of serum reactive oxygen metabolite levels with different histopathological types of lung cancer.
  • Additionally, they may have a role in the pathogenesis of lung cancer with different histopathological types.
  • OBJECTIVES: In this study, we aimed to investigate the degree of oxidative stress in different types of carcinoma such as small cell carcinoma and non-small cell carcinoma, including epidermoid carcinoma and adenocarcinoma, and to find out whether the degree of oxidative stress shows any difference among them and whether it can be used as an index for their differential diagnosis.
  • METHODS: Thirty-eight patients with lung cancer and 26 healthy persons were included in the study.
  • Of the patients with lung cancer, 14 had epidermoid carcinoma, 12 adenocarcinoma and 12 small cell carcinoma.
  • Although all subtypes had significantly high ROM levels compared with the controls, the highest significance was found in the small cell carcinoma (p<0.001), and then in the adenocarcinoma and epidermoid carcinoma (p<0.01 and p<0.01, respectively).
  • CONCLUSIONS: In the light of these data, it might be possible to conclude that the serum ROM levels increase in patients with different types of lung cancers and may be an index parameter for lung cancer.
  • It could be thought that this increase, particularly in small cell carcinoma, may contribute to its poor progression.
  • [MeSH-major] Biomarkers, Tumor / blood. Lung Neoplasms / blood. Lung Neoplasms / pathology. Reactive Oxygen Species / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / pathology. Adult. Aged. Carcinoma / blood. Carcinoma / classification. Carcinoma / pathology. Carcinoma, Small Cell / blood. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Reference Values. Smoking / epidemiology

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16432293.001).
  • [ISSN] 0025-7931
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Reactive Oxygen Species
  •  go-up   go-down


51. Trani L, Myerson J, Ashley S, Young K, Sheri A, Hubner R, Puglisi M, Popat S, O'Brien ME: Histology classification is not a predictor of clinical outcomes in advanced non-small cell lung cancer (NSCLC) treated with vinorelbine or gemcitabine combinations. Lung Cancer; 2010 Nov;70(2):200-4
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histology classification is not a predictor of clinical outcomes in advanced non-small cell lung cancer (NSCLC) treated with vinorelbine or gemcitabine combinations.
  • We have categorised patients treated with vinorelbine and gemcitabine based first line chemotherapy regimes for advanced NSCLC as either squamous or non-squamous, and also as either adenocarcinoma and non-adenocarcinoma, and compared outcome.
  • RESULTS: Neither univariate nor multivariate analysis suggested that there was a significant difference in the response rates for adenocarcinoma vs. non-adenocarcinoma or between squamous and non-squamous pathology.
  • There was no difference in PFS between adenocarcinoma and non-adenocarcinoma pathologies until 8 months (p = 0.98), and there was a statistically significant advantage in PFS for squamous vs. non-squamous pathologies (p = 0.04).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Non-Small-Cell Lung / drug therapy. Deoxycytidine / analogs & derivatives. Lung Neoplasms / diagnosis. Lung Neoplasms / drug therapy. Vinblastine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis. Survival Analysis. Treatment Outcome

  • 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. VINORELBINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20227784.001).
  • [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
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; B76N6SBZ8R / gemcitabine; Q6C979R91Y / vinorelbine
  •  go-up   go-down


52. Idowu MO, Powers CN: Lung cancer cytology: potential pitfalls and mimics - a review. Int J Clin Exp Pathol; 2010;3(4):367-85
COS Scholar Universe. author profiles.

  • [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.
  • 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

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] 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


53. Hammerer V: [Diagnosis and treatment of carcinomatous meningitis in lung cancer]. Rev Mal Respir; 2007 Oct;24(8 Pt 2):6S222-5
MedlinePlus Health Information. consumer health - Meningitis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and treatment of carcinomatous meningitis in lung cancer].
  • Carcinomatous meningitis occurs in approximately 5 to 18% of bronchial carcinoma, particularly in adenocarcinoma and small cell lung cancer.
  • [MeSH-major] Lung Neoplasms / complications. Meningitis / diagnosis. Meningitis / therapy

  • 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 = 18235418.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 18
  •  go-up   go-down


54. Chou R, Chen A, Lau D: Complete response of brain metastases to irinotecan-based chemotherapy. J Clin Neurosci; 2005 Apr;12(3):242-5
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this article, we report complete responses to irinotecan-based chemotherapy in three patients with brain metastases from parotid adenocarcinoma, esophageal adenocarcinoma and small cell lung cancer.
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / surgery. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Female. Humans. Lung Neoplasms / pathology. Lung Neoplasms / surgery. Magnetic Resonance Imaging. Male. Middle Aged. Parotid Neoplasms / pathology. Parotid Neoplasms / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15851073.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


55. Toffalorio F, Giovannetti E, De Pas T, Radice D, Pelosi G, Manzotti M, Minocci D, Spaggiari L, Spitaleri G, Noberasco C, Catania C, Boselli S, Danesi R, de Braud F: Expression of gemcitabine- and cisplatin-related genes in non-small-cell lung cancer. Pharmacogenomics J; 2010 Jun;10(3):180-90
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of gemcitabine- and cisplatin-related genes in non-small-cell lung cancer.
  • The aim of this study was to investigate the influence of histology and site of analysis (primary tumor versus lymph node) on the expression of genes involved in gemcitabine and cisplatin activity in non-small-cell lung cancer (NSCLC).
  • No difference was observed between primary tumor and lymph node metastasis, as well as in adenocarcinoma and squamous-cell carcinoma specimens, while we found a correlation between the CDA-A79C polymorphism and gene expression levels.
  • These data suggest a similar genetic susceptibility to gemcitabine-cisplatin regimens for squamous cell and adenocarcinoma and support the use of both lymph node and primary tumor for the expression profiling of NSCLC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Cisplatin / metabolism. Cytidine Deaminase / genetics. Deoxycytidine / analogs & derivatives
  • [MeSH-minor] 5'-Nucleotidase / genetics. Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / genetics. Cell Line, Tumor. DNA-Binding Proteins / genetics. Deoxycytidine Kinase / genetics. Endonucleases / genetics. Equilibrative Nucleoside Transporter 1 / genetics. Female. Gene Expression Profiling. Humans. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Lymphatic Metastasis / genetics. Male. Polymorphism, Single Nucleotide. RNA, Small Interfering / pharmacology. Ribonucleoside Diphosphate Reductase / genetics. Tumor Suppressor Proteins / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827857255 for PMID:19901957 [PharmGKB] .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19901957.001).
  • [ISSN] 1473-1150
  • [Journal-full-title] The pharmacogenomics journal
  • [ISO-abbreviation] Pharmacogenomics J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Small Interfering; 0 / RRM1 protein, human; 0 / SLC29A1 protein, human; 0 / Tumor Suppressor Proteins; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / ribonucleotide reductase M2; EC 1.17.4.1 / Ribonucleoside Diphosphate Reductase; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases; EC 3.1.3.5 / 5'-Nucleotidase; EC 3.5.4.5 / Cytidine Deaminase; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


56. Bugalho P, Chorão M, Fontoura P: Miliary brain metastases from primary gastric small cell carcinoma: illustrating the seed and soil hypothesis. J Neurooncol; 2005 May;73(1):53-6
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Miliary brain metastases from primary gastric small cell carcinoma: illustrating the seed and soil hypothesis.
  • Miliary metastases are a very rare condition usually found in the context of primary lung tumor (small cell and adenocarcinoma), and refer to the existence of numerous tumor nodules in widespread areas of the brain.
  • Besides pulmonary neoplasia, pancreatic adenocarcinoma and malignant melanoma have also been implicated in some cases of miliary metastases.
  • We present the first case of miliary metastases originating in a primary small cell gastric carcinoma (PSCGC), a rare type of neuroendocrine gastric tumor.
  • The pathological resemblance of PSCGC with small cell lung carcinoma may correspond to an underlying similarity in biological behavior, which accounts for this particular pattern of metastatic spreading, as proposed in the seed and soil hypothesis.
  • [MeSH-major] Brain Neoplasms / secondary. Carcinoma, Neuroendocrine / pathology. Carcinoma, Small Cell / secondary. Stomach Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. STREPTOZOTOCIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15933819.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 5W494URQ81 / Streptozocin; U3P01618RT / Fluorouracil
  •  go-up   go-down


57. Hsiao HH, Tsai HJ, Liu YC, Tseng YT, Tseng SB, Chai CY, Lin SF: A rare case of combined small-cell lung cancer with unusual soft tissue metastasis. Kaohsiung J Med Sci; 2006 Jul;22(7):352-6
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare case of combined small-cell lung cancer with unusual soft tissue metastasis.
  • Combined small-cell lung carcinoma (SCLC) is a rare tumor.
  • We report a case of combined SCLC of the lung, including adenocarcinoma and spindle-shaped cell tumor, with an unusual initial presentation.
  • A lung nodule was noted later after complete examination.
  • The diagnosis turned out to be combined cell carcinoma with three different components (small-cell carcinoma, adenocarcinoma, and spindle-shaped cell tumor) after examination upon total removal of the lung nodule by lobectomy.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma / pathology. Carcinoma, Small Cell / pathology. Lung Neoplasms / pathology. Soft Tissue Neoplasms / secondary

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16849104.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  •  go-up   go-down


58. Hanagiri T, Oka S, Takenaka S, Baba T, Yasuda M, Ono K, So T, Uramoto H, Takenoyama M, Yasumoto K: Results of surgical resection for patients with large cell carcinoma of the lung. Int J Surg; 2010;8(5):391-4
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of surgical resection for patients with large cell carcinoma of the lung.
  • PURPOSE: The clinical features of large cell carcinoma (LCC) of the lung have remained unclear due to the low incidence of the disease.
  • SUBJECTS: This study clinicopathologically evaluated 975 patients who had undergone a resection for non-small cell carcinoma between 1994 and 2007.
  • RESULTS: The LCC patients included 49 males and 8 females and included 9 patients with large cell neuroendocrine carcinoma.
  • The mean smoking pack-year index was 49.9 in the patients with LCC, 27.1 in 625 patients with adenocarcinoma, and 52.5 in 266 patients with squamous cell carcinoma, and this was significantly higher in the patients with LCC than in those with adenocarcinoma.
  • The mean tumor diameter was 38 mm for LCC, 28 mm for adenocarcinoma, and 39 mm for squamous cell carcinoma.
  • The post-operative 5-year survival rate was 60.5% for LCC, 64.3% for large cell neuroendocrine carcinoma, 67.0% for adenocarcinoma, and 50.1% for squamous cell carcinoma.
  • CONCLUSION: The tumor diameter was significantly larger for LCC than for adenocarcinoma at the time of diagnosis.
  • The proportion of smokers and the smoking pack-year index in patients with LCC were significantly higher than those of adenocarcinoma.
  • The surgical results were similar between LCC and other non-small cell lung carcinomas.
  • [MeSH-major] Carcinoma, Large Cell / surgery. Lung Neoplasms / surgery. Pneumonectomy / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20547250.001).
  • [ISSN] 1743-9159
  • [Journal-full-title] International journal of surgery (London, England)
  • [ISO-abbreviation] Int J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  •  go-up   go-down


59. Fontinele e Silva J, Barbosa Mde P, Viegas CL: Small cell carcinoma in Pancoast syndrome. J Bras Pneumol; 2009 Feb;35(2):190-3
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell carcinoma in Pancoast syndrome.
  • The majority of cases of Pancoast syndrome are caused by bronchogenic carcinoma.
  • The most commonly found histologic subtypes are adenocarcinoma and epidermoid carcinoma.
  • There have been very few reports of small cell lung carcinoma in the genesis of Pancoast syndrome.
  • We describe the case of a patient with Pancoast syndrome caused by small cell lung carcinoma and discuss the aspects related to the diagnosis and treatment.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Lung / pathology. Pancoast Syndrome / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19287924.001).
  • [ISSN] 1806-3756
  • [Journal-full-title] Jornal brasileiro de pneumologia : publicaça̋o oficial da Sociedade Brasileira de Pneumologia e Tisilogia
  • [ISO-abbreviation] J Bras Pneumol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  •  go-up   go-down


60. Gazdar AF: Should we continue to use the term non-small-cell lung cancer? Ann Oncol; 2010 Oct;21 Suppl 7:vii225-9
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Should we continue to use the term non-small-cell lung cancer?
  • Until recently the major clinical question was 'Is it small-cell or non small-cell cancer'.
  • Identification of the major non-small-cell lung cancer (NSCLC) types (adenocarcinoma and squamous carcinoma) are important for a number of predictive and prognostic reasons, including pemetrexed treatment, anti-angiogenic therapy and administration of tyrosine kinase inhibitors.
  • Fortunately, advances in pathology of lung cancer have kept abreast, with newer, simplified methods to identify the major NSCLC types in small diagnostic samples, and modifications of the pathological classification of adenocarcinomas reflecting changing clinical and molecular concepts.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20943619.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA070907
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4542692
  •  go-up   go-down


61. Galetta D, Rossi A, Pisconti S, Millaku A, Colucci G: Maintenance or non-maintenance therapy in the treatment of advanced non-small cell lung cancer: that is the question. Cancer Treat Rev; 2010 Nov;36 Suppl 3:S30-3
Hazardous Substances Data Bank. GUANINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maintenance or non-maintenance therapy in the treatment of advanced non-small cell lung cancer: that is the question.
  • Lung cancer is the most common cancer worldwide with non-small cell lung cancer (NSCLC), including squamous carcinoma, adenocarcinoma and large cell carcinoma, accounting for about 85% of all lung cancer types with most of the patients presenting with advanced disease at the time of diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Glutamates / administration & dosage. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy. Molecular Targeted Therapy. Quinazolines / administration & dosage. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vascular Endothelial Growth Factor A / antagonists & inhibitors

  • 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. PEMETREXED .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21129607.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glutamates; 0 / Quinazolines; 0 / Vascular Endothelial Growth Factor A; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


62. Mendiola C, Vaz MA: Is capecitabine a new choice of treatment for lung adenocarcinoma? A case report involving partial response in second line of treatment and hypothesis of the biological basis. Clin Transl Oncol; 2009 Aug;11(8):554-7
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is capecitabine a new choice of treatment for lung adenocarcinoma? A case report involving partial response in second line of treatment and hypothesis of the biological basis.
  • In lung cancer different histologies have different biologies.
  • Active agents in non-small-cell lung cancer (NSCLC) include platinums, paclitaxel, docetaxel, gemcitabine, erlotinib, pemetrexed and vinorelbine.
  • We report a case of a patient with metastatic lung adenocarcinoma with high levels of LDH and CEA with clear partial response to capecitabine after several lines of chemotherapy.
  • More research is needed to try to explain the striking activity of capecitabine in this patient with lung adenocarcinoma and high levels of CEA and to find molecular targets to predict the response to this agent.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / therapeutic use. Deoxycytidine / analogs & derivatives. Fluorouracil / analogs & derivatives. Lung Neoplasms / drug therapy
  • [MeSH-minor] Capecitabine. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CAPECITABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19661033.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
  •  go-up   go-down


63. Pu R, Li WM, Liu D, Mo XM, Tang Y, Liu LX, Chen BJ: [The expression and clinical significance of AKT2, phosphorylated AKT2 in non-small cell lung cancer]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2010 Jul;41(4):586-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The expression and clinical significance of AKT2, phosphorylated AKT2 in non-small cell lung cancer].
  • OBJECTIVE: To study the expression and clinical significance of AKT2, phosphorylated AKT2 (p-AKT2) in non-small cell lung cancer (NSCLC).
  • The statistic analysis was carried on to study the correlation of AKT2, p-AKT2 expression to the type of lung cancer, TNM stage, pathological grading.
  • RESULTS: The positive rates of AKT2 in lung adenocarcinoma and squamous carcinoma were 60.5% and 54.1% respectively (P > 0.05).
  • While the positive rates of p-AKT2 in lung adenocarcinoma and squamous carcinoma were 68.4% and 47.5% (P < 0.05).
  • The expressions of AKT2 and p-AKT2 were not correlated with age, gender, TNM stage and cell differentiation degree.
  • CONCLUSION: The positive expression of p-AKT2 in lung adenocarcinoma was higher than that in lung squamous carcinomas. p-AKT2 may be a prognostic factor for non-small cell lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adenocarcinoma / enzymology. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / enzymology. Female. Humans. Male. Middle Aged. Phosphorylation. Prognosis

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell 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 = 20848774.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.11.1 / AKT2 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


64. Hammar SP: Approach to the diagnosis of neuroendocrine lung neoplasms: variabilities and pitfalls. Semin Thorac Cardiovasc Surg; 2006;18(3):183-90
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Approach to the diagnosis of neuroendocrine lung neoplasms: variabilities and pitfalls.
  • With the publication of the spectrum of neuroendocrine proliferations and neoplasms and the features and criteria for diagnosing neuroendocrine lung neoplasms, there is more agreement in making a specific pathologic diagnosis of a neuroendocrine lung neoplasm.
  • However, problems exist, especially in diagnosing well-differentiated neuroendocrine carcinomas (atypical carcinoids), large-cell neuroendocrine carcinomas, and even some small-cell lung cancers.
  • Nonneuroendocrine small-cell carcinomas exist and include small-cell squamous cell carcinoma, small cell adenocarcinoma, and basaloid carcinoma.
  • Nonneuroendocrine lung cancers, especially large-cell undifferentiated carcinoma and poorly differentiated adenocarcinoma, not infrequently express neuroendocrine markers immunohistochemically.
  • [MeSH-major] Lung Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Humans. Immunohistochemistry

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17185177.001).
  • [ISSN] 1043-0679
  • [Journal-full-title] Seminars in thoracic and cardiovascular surgery
  • [ISO-abbreviation] Semin. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 26
  •  go-up   go-down


65. Gu AQ, Wang HM, Shi CL, Xiong LW, Gao ZQ, Han BH: [Clinical observation of gefitinib for the treatment of 125 cases with advanced non-small cell lung cancer]. Zhonghua Zhong Liu Za Zhi; 2010 Jan;32(1):71-4
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical observation of gefitinib for the treatment of 125 cases with advanced non-small cell lung cancer].
  • OBJECTIVE: To evaluate the efficacy and safety of gefitinib for the treatment of advanced non-small cell lung cancer (NSCLC).
  • The response rate was significantly higher in females, adenocarcinoma and nonsmokers than that in males, non-adenocarcinoma and smokers (P < 0.05).
  • The median survival time was significantly longer in adenocarcinoma, nonsmokers and gefitinib effective patients than that in non-adenocarcinoma, smokers and gefitinib ineffective patients (P < 0.05).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Diarrhea / chemically induced. Disease-Free Survival. Exanthema / chemically induced. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20211075.001).
  • [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] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
  •  go-up   go-down


66. Pan Y, Li WX, Li JM, Zhu JQ, Liang YQ, Guo AL: [Correlation of DNA-dependent protein kinase catalytic subunit expression to radiosensitivity of non-small cell lung cancer cell lines]. Ai Zheng; 2009 Jul;28(7):714-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Correlation of DNA-dependent protein kinase catalytic subunit expression to radiosensitivity of non-small cell lung cancer cell lines].
  • This study was to detect the expression of DNA-PKcs in different non-small cell lung cancer (NSCLC) cell lines and evaluate its correlation to radiosensitivity.
  • METHODS: The content and activity of DNA-PKcs in five NSCLC cell lines A549, H1299, L78, PGCL3 and H460 were measured by Western blot and the DNA-PK activity assay.
  • Cell survival was analyzed using clonogenic formation assay.
  • RESULTS: The radiosensitivities of five NSCLC cell lines were different.
  • In adenocarcinoma and large cell carcinoma cell lines, SF2 were correlated to DNA-PKcs content (P<0.05, r=0.95) and activity (P=0.03, r=0.98).
  • CONCLUSION: DNA-PKcs is an important factor to predict the radiosensitivity in adenocarcinoma and large cell lung cancer cell lines.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Cell Survival / radiation effects. DNA-Activated Protein Kinase / metabolism. Lung Neoplasms / pathology. Radiation Tolerance
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Catalytic Domain. Cell Line, Tumor. Enzyme Activation / radiation effects. Humans. Particle Accelerators

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19624897.001).
  • [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] EC 2.7.11.1 / DNA-Activated Protein Kinase
  •  go-up   go-down


67. Mencoboni M, Bergaglio M, Serra M, Ivaldi GP, Tredici S, Racchi O, Rebella L, Galbusera V, Grosso M, Faravelli B: Maintenance therapy with gefitinib after first-line chemotherapy in patients affected by advanced non-small cell lung cancer. Anticancer Res; 2007 Nov-Dec;27(6C):4425-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maintenance therapy with gefitinib after first-line chemotherapy in patients affected by advanced non-small cell lung cancer.
  • BACKGROUND: Chemotherapy extends life for patients with advanced non-small cell lung cancer (NSCLC).
  • One molecular target for lung cancer is the epidermal growth factor receptor (EGFR).
  • TTP for adenocarcinoma and non-adenocarcinoma patients was 10 months and 3.2 months, respectively.
  • OS for adenocarcinoma and non-adenocarcinoma patients were 15 and 5.9 months, respectively.
  • CONCLUSION: Gefitinib could be an ideal second-line therapy for adenocarcinoma patients responding to first-line chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use


68. Hanibuchi M, Yano S, Tomimoto H, Sone S: [Differences in the therapeutic strategies for lung cancer between Europe/United States and Japan]. Gan To Kagaku Ryoho; 2007 May;34(5):705-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Differences in the therapeutic strategies for lung cancer between Europe/United States and Japan].
  • Lung cancer is a leading cause of malignancy-related death worldwide.
  • Recently, therapeutic strategies for lung cancer have dramatically progressed, and attempts have been made to standardize the therapy for lung cancer.
  • Because the disease prevalence and the susceptibility to the drugs differ with the circumstances, such as lifestyle, and genetic background, and ethnicity, the standard therapeutic strategies for lung cancer may differ with the individual country or region.
  • Actually, the EGFR tyrosine kinase inhibitor, gefitinib, is well known to be significantly effective for oriental people, including Japanese, female, adenocarcinoma and never-smoker, suggesting an inherited difference.
  • Here we describe not only the standard therapeutic strategies but also the difference in therapeutic strategies for lung cancer between Europe/United States and Japan.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / therapy. Lung Neoplasms / therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / therapy. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Small Cell / surgery. Carcinoma, Small Cell / therapy. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Europe. Female. Humans. Japan. Tegafur / administration & dosage. United States. Uracil / administration & dosage

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17496441.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; Q20Q21Q62J / Cisplatin; S65743JHBS / gefitinib; FP protocol
  •  go-up   go-down


69. Hammerer V, Pauli G, Quoix E: [Retrospective study of a series of 26 carcinomatous meningitis secondary to lung cancer]. Bull Cancer; 2005 Nov;92(11):989-94
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Retrospective study of a series of 26 carcinomatous meningitis secondary to lung cancer].
  • Carcinomatous meningitis occur in approximately 5 to 18% of bronchial carcinoma.
  • We report here the analysis of a retrospective study of 26 cases of carcinomatous meningitis secondary to a bronchial carcinoma.
  • The most frequently involved histological types are adenocarcinoma and small cell lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / secondary. Carcinoma, Small Cell / secondary. Lung Neoplasms / pathology. Meningeal Neoplasms / secondary
  • [MeSH-minor] Adenocarcinoma / cerebrospinal fluid. Adenocarcinoma / diagnosis. Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Adult. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / cerebrospinal fluid. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Cerebrospinal Fluid / cytology. Cohort Studies. Female. Humans. Injections, Spinal. Male. Methotrexate / administration & dosage. Methotrexate / therapeutic use. Middle Aged. Prognosis. Retrospective Studies

  • 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 = 16316833.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


70. Zhao YY, Zhang Y, Zhao HY, Wu JX, Jiang W, Xue C, Zhang L: [Predictive factors for response and survival of gefitinib-treated locally advanced or metastatic non-small cell lung cancer patients: a retrospective analysis of two phase II clinical trials]. Ai Zheng; 2009 Jun;28(6):626-31
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Predictive factors for response and survival of gefitinib-treated locally advanced or metastatic non-small cell lung cancer patients: a retrospective analysis of two phase II clinical trials].
  • BACKGROUND AND OBJECTIVE: Clinical factors and molecular markers can be used to predict the prognosis of gefitinib-treated locally advanced or metastatic non-small cell lung cancer (NSCLC).
  • Adenocarcinoma and skin rash were associated with better response.
  • CONCLUSIONS: Adenocarcinoma and skin rash are predictors of better response to gefitinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Clinical Trials, Phase II as Topic. Disease Progression. Exanthema / chemically induced. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Remission Induction. Retrospective Studies. Survival Rate. Young Adult


71. Kenfield SA, Wei EK, Stampfer MJ, Rosner BA, Colditz GA: Comparison of aspects of smoking among the four histological types of lung cancer. Tob Control; 2008 Jun;17(3):198-204
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of aspects of smoking among the four histological types of lung cancer.
  • BACKGROUND: The magnitude of the link between cigarette smoking and lung cancer may vary by histological type.
  • RESULTS: From 1976 to 2002, we identified 1062 cases of lung cancer: squamous cell (n = 201), small cell (n = 236), adenocarcinoma (n = 543) and large cell carcinoma (n = 82), among 65 560 current or former smokers.
  • Risk reduction after quitting ranged from an 8% reduction (relative risk (RR): 0.92, 95% CI 0.91 to 0.94) to a 17% reduction (RR: 0.83, 95% CI 0.80 to 0.86) per year for adenocarcinoma and small cell carcinoma, respectively, with a 9% reduction observed for large cell carcinoma and an 11% reduction observed for squamous cell carcinoma.
  • The risk of adenocarcinoma increased by 6% per year of smoking, compared to 7% for large cell, 10% for squamous cell and 12% for small cell.
  • The 6% difference between adenocarcinoma and small cell carcinoma is equivalent to a 3.2 to 9.7-fold increase in risk for 20 years of smoking.
  • CONCLUSIONS: The effects of the number of cigarettes smoked per day and years since quitting smoking are different across the major types of lung cancer, which are fully appreciated at long durations of smoking and smoking cessation.
  • Smoking prevention and cessation should continue to be the focus of public health efforts to reduce lung cancer incidence and mortality.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Smoking.
  • MedlinePlus Health Information. consumer health - Smoking and Youth.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6556-62 [14559851.001]
  • [Cites] J Womens Health. 1997 Feb;6(1):49-62 [9065374.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 2;96(11):826-34 [15173266.001]
  • [Cites] J Natl Cancer Inst. 2004 Jul 21;96(14):1105-7 [15265973.001]
  • [Cites] J Epidemiol Community Health. 1978 Dec;32(4):303-13 [744822.001]
  • [Cites] Stat Med. 1985 Jul-Sep;4(3):337-44 [4059720.001]
  • [Cites] Chest. 2001 Nov;120(5):1577-83 [11713137.001]
  • [Cites] Tob Control. 2001;10 Suppl 1:i4-11 [11740038.001]
  • [Cites] Int J Cancer. 2002 May 10;99(2):245-51 [11979440.001]
  • [Cites] J Clin Oncol. 2003 Mar 1;21(5):921-6 [12610194.001]
  • [Cites] Am J Epidemiol. 1989 Oct;130(4):688-95 [2549787.001]
  • [Cites] Cancer. 1991 Nov 1;68(9):2074-8 [1655236.001]
  • [Cites] Epidemiology. 1992 Jan;3(1):61-4 [1313311.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):336-44 [8381164.001]
  • [Cites] Int J Cancer. 1993 Apr 22;54(1):44-8 [8386708.001]
  • [Cites] Am J Epidemiol. 1994 Dec 1;140(11):1016-9 [7985649.001]
  • [Cites] J Toxicol Environ Health. 1997 Mar;50(4):307-64 [9120872.001]
  • [Cites] Epidemiology. 1998 Jan;9(1):79-83 [9430273.001]
  • [Cites] N Engl J Med. 1999 Jan 28;340(4):265-71 [9920950.001]
  • [Cites] J Natl Cancer Inst. 1999 Jul 21;91(14):1194-210 [10413421.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2125-30 [16172220.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):806-13 [8622028.001]
  • [Cites] Cancer Causes Control. 1996 May;7(3):366-76 [8734831.001]
  • [Cites] J Clin Epidemiol. 2004 Feb;57(2):113-22 [15125620.001]
  • (PMID = 18390646.001).
  • [ISSN] 1468-3318
  • [Journal-full-title] Tobacco control
  • [ISO-abbreviation] Tob Control
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA087969; United States / NCI NIH HHS / CA / CA87969; United States / NCI NIH HHS / CA / T32 CA009001; United States / NCI NIH HHS / CA / P01 CA087969-12; United States / NCI NIH HHS / CA / T32CA09001
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS262473; NLM/ PMC3044470
  •  go-up   go-down


72. Song P, Spindel ER: Basic and clinical aspects of non-neuronal acetylcholine: expression of non-neuronal acetylcholine in lung cancer provides a new target for cancer therapy. J Pharmacol Sci; 2008 Feb;106(2):180-5
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Basic and clinical aspects of non-neuronal acetylcholine: expression of non-neuronal acetylcholine in lung cancer provides a new target for cancer therapy.
  • Lung cancer is the leading cause of cancer death worldwide and new treatment strategies are clearly needed.
  • The recent discovery that lung and other cancers synthesize and secrete acetylcholine (ACh) which acts as an autocrine growth factor suggests that this cholinergic autocrine loop may present new therapeutic targets.
  • In normal bronchial epithelium, small airway epithelium and pulmonary neuroendocrine cells synthesize Ach; and in squamous cell lung carcinoma, adenocarcinoma, and small cell lung carcinoma, the respective lung cancers that derive from those cell types similarly synthesize ACh.
  • ACh secreted by those cancers stimulates growth of the tumors by binding to nicotinic and muscarinic receptors expressed on lung cancers.
  • Thus antagonists to nicotinic and muscarinic receptors can inhibit lung cancer growth.
  • The muscarinic receptor (mAChR) subtype utilized for cell proliferation is the M(3) subtype and consistent with this M(3) mAChR antagonists inhibit growth of SCLC and squamous cell carcinomas.
  • As multiple other cancer types besides lung carcinomas express both M(3) mAChR and acetylcholine, other cancer types besides lung carcinoma may respond to M(3) mAChR antagonists.
  • [MeSH-major] Acetylcholine / metabolism. Lung Neoplasms / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18285655.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Muscarinic Antagonists; 0 / Receptor, Muscarinic M3; N9YNS0M02X / Acetylcholine
  • [Number-of-references] 21
  •  go-up   go-down


73. Joh J, Jenson AB, Moore GD, Rezazedeh A, Slone SP, Ghim SJ, Kloecker GH: Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV) in non small cell lung cancer. Exp Mol Pathol; 2010 Dec;89(3):222-6
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV) in non small cell lung cancer.
  • A meta-analysis of the literature suggests that HPV is also associated with 20%-25% of non small cell lung carcinoma (NSCLC).
  • Merkel cell Polyomavirus (MCPyV) causes most Merkel cell carcinomas in immunocompromised hosts, and is associated with some squamous carcinomas of skin in immunocompetent individuals.
  • Since both oncogenic viruses appear to involve the tonsils and, therefore, have clear access to the lungs, we examined that the possible association of HPV and MCPyV infections with lung cancers, especially, NSCLC.
  • DNAs were extracted from 51 frozen tissues from 30 lung cancer patients, and examined for the presence of HPV and MCPyV by PCR and DNA sequencing analysis.
  • HPVs were only detected in 5 adenocarcinomas (16.7% of all lung cancers examined).
  • Three of the 5 were identified in squamous carcinomas, 1 in adenocarcinoma, and 1 in an unspecified NSCLC.
  • Two additional samples were positive for MCPyV DNA within benign adjacent lung tissue only.
  • In one adenocarcinoma, HPV-11 was identified in an adenocarcinoma, and MCPyV DNA was detected in the adjacent "benign" tissue.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / virology. Lung Neoplasms / virology. Papillomavirus Infections / complications. Polyomavirus Infections / complications

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Merkel cell cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010. Published by Elsevier Inc.
  • (PMID = 20699096.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
  •  go-up   go-down


74. Wu YL, Zhong WZ, Li LY, Zhang XT, Zhang L, Zhou CC, Liu W, Jiang B, Mu XL, Lin JY, Zhou Q, Xu CR, Wang Z, Zhang GC, Mok T: Epidermal growth factor receptor mutations and their correlation with gefitinib therapy in patients with non-small cell lung cancer: a meta-analysis based on updated individual patient data from six medical centers in mainland China. J Thorac Oncol; 2007 May;2(5):430-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor mutations and their correlation with gefitinib therapy in patients with non-small cell lung cancer: a meta-analysis based on updated individual patient data from six medical centers in mainland China.
  • BACKGROUND: Convincing data on epidermal growth factor receptor (EGFR) mutations in Chinese patients with non-small-cell lung cancer (NSCLC) remain limited.
  • Patients with adenocarcinoma had a higher mutation rate than those with non-adenocarcinoma (44.1% vs 9.2%; p < 0.00001).
  • Multivariate analysis showed that "adenocarcinoma" and "non-smoker" were independent predictors of EGFR mutations.
  • "EGFR mutation", "adenocarcinoma," and "non-smoker" were independent predictors of response.
  • "Adenocarcinoma status" was an independent prognostic factor for survival.
  • CONCLUSIONS: In mainland China, "adenocarcinoma" and "non-smoker" are independent predictors for EGFR mutations.
  • The clinical selected populations for gefitinib are non-smokers with adenocarcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / drug therapy. Lung Neoplasms / genetics. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics


75. Dong QG, Han BH, Huang JS, Yang LM, Huang J, Zhao CY, Lu LQ: [Analysis of EGFR mutations in 176 cases of non-small cell lung cancer]. Zhonghua Zhong Liu Za Zhi; 2006 Sep;28(9):686-90
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of EGFR mutations in 176 cases of non-small cell lung cancer].
  • OBJECTIVE: To analyze the incidence and profile of mutations in epidermal growth factor receptor (EGFR) in Chinese patients with non-small cell lung cancer (NSCLC).
  • METHODS: A total of 176 cases of NSCLC tissue was enrolled in this study, among which 123 normal lung samples were also included.
  • RESULTS: The EGFR gene in exon 19-21 was of wild type in all normal lung tissues detected.
  • Mutations were found in 57 cases of 176 lung cancer samples, with an incidence of 32. 4%.
  • The EGFR mutations were more frequent in female patients than male ones, in adenocarcinoma and adenosquamous cell carcinoma versus cancer of other histologies.
  • These mutations are more frequently detected in female, adenocarcinoma and adenosquamous cell carcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adult. Aged. Amino Acid Sequence. Base Sequence. Carcinoma, Squamous Cell / genetics. Codon. DNA Mutational Analysis. Exons. Female. Gene Deletion. Humans. Male. Middle Aged. Mutation, Missense. Sex Factors

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell 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 = 17274376.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Codon; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


76. Nakagawa K, Noguchi Y, Uenaka A, Sato S, Okumura H, Tanaka M, Shimono M, Ali Eldib AM, Ono T, Ohara N, Yoshino T, Yamashita K, Tsunoda T, Aoe M, Shimizu N, Nakayama E: XAGE-1 expression in non-small cell lung cancer and antibody response in patients. Clin Cancer Res; 2005 Aug 1;11(15):5496-503
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] XAGE-1 expression in non-small cell lung cancer and antibody response in patients.
  • We recently identified XAGE-1b as a dominant antigen recognized by sera from lung adenocarcinoma patients.
  • We here investigated the mRNA expression of four XAGE-1 variants and XAGE-1 protein expression in non-small cell lung cancer (NSCLC).
  • RESULTS: XAGE-1b and XAGE-1d mRNA were detected in 15 and 6 of 49 lung cancer specimens, respectively.
  • XAGE-1b mRNA expression was observed in 14 of 31 (45%) adenocarcinoma and 1 of 18 (6%) lung cancer with other histologic types.
  • Seropositivity was observed in 5 of 56 patients with adenocarcinoma, whereas none of 18 patients with other histologic types produced XAGE-1b antibody.
  • CONCLUSION: XAGE-1b is highly and strongly expressed in lung adenocarcinoma and immunogenic in patients, suggesting that XAGE-1b is a promising antigen for immunotherapy against lung adenocarcinoma.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Antibodies, Monoclonal / chemistry. Blotting, Western. DNA Primers / chemistry. DNA, Complementary / metabolism. Databases as Topic. Enzyme-Linked Immunosorbent Assay. Expressed Sequence Tags. Genetic Vectors. Humans. Immunohistochemistry. Immunotherapy / methods. Plasmids / metabolism. Protein Structure, Tertiary. RNA, Messenger / metabolism. Recombinant Proteins / chemistry. Recombinant Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

  • 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.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Clin Cancer Res. 2005 Aug 1;11(15):5331-2 [16061843.001]
  • (PMID = 16061866.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / DNA Primers; 0 / DNA, Complementary; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / XAGE1A protein, human
  •  go-up   go-down


77. Bai XY, Shen H: [Quantitative analysis of thyroid transcription factor-1 mRNA expressions in primary lung cancer and its metastatic foci]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Jan;28(1):20-5
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Quantitative analysis of thyroid transcription factor-1 mRNA expressions in primary lung cancer and its metastatic foci].
  • OBJECTIVE: To observe the expression of thyroid transcription factor-1 (TTF-1) mRNA in human normal adult type II alveolar epithelial cells, embryonic alveolar epithelial cells, and primary lung carcinoma and lymph nodes, thereby exploring the role of TTF-1 mRNA expression in the tumorigenesis, development and metastasis of lung carcinoma.
  • RESULTS: TTF-1 mRNA expression was significantly less intense in embryonic lung than in normal adult lung tissues (P= 0.000), and the two tissues both had significantly greater expression than lung adenocarcinoma, squamous cell carcinoma, small cell carcinoma and large cell carcinoma (P=0.000).
  • Lung adenocarcinoma and small cell carcinoma, with similar expression intensity (P= 0.068), showed stronger expression than squamous cell carcinoma and large cell carcinoma (P=0.000), and squamous cell carcinoma showed stronger expression than large cell carcinoma (P=0.018).
  • In lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma, the intensity of TTF-1 mRNA expression was stronger in lymph node metastases than in the primary foci (P=0.003, P=0.000, P=0.019, respectively).
  • The lymph node metastases had more intense expression than the primary foci of small cell lung carcinoma (P=0.078).
  • The intensity of TTF-1 mRNA expression was greater in primary lung carcinomas with lymph node metastases than in those without metastases (P=0.026).
  • CONCLUSION: The amount of TTF-1 mRNA expression lowers in the order of normal adult lung, embryonic lung and lung carcinoma tissues.
  • In lung carcinomas, TTF-1 mRNA expression differs between the histological types, high in lung adenocarcinoma and small cell carcinoma and rather low in squamous cell carcinoma and large cell carcinoma.
  • Strong expression of TTF-1 mRNA often indicates high likeliness of lung carcinoma metastasis, and highlights the high metastatic potentials of lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Lung Neoplasms / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Female. Humans. In Situ Hybridization. Lymphatic Metastasis. Male. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Thyroid Gland / metabolism. Tissue Array Analysis / methods

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Thyroid Cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18227018.001).
  • [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 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
  •  go-up   go-down


78. Han SW, Kim TY, Lee KH, Hwang PG, Jeon YK, Oh DY, Lee SH, Kim DW, Im SA, Chung DH, Heo DS, Bang YJ: Clinical predictors versus epidermal growth factor receptor mutation in gefitinib-treated non-small-cell lung cancer patients. Lung Cancer; 2006 Nov;54(2):201-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical predictors versus epidermal growth factor receptor mutation in gefitinib-treated non-small-cell lung cancer patients.
  • BACKGROUND: Clinical predictors including Asian, female, adenocarcinoma and never-smoker and epidermal growth factor mutation are associated with gefitinib responsiveness in non-small-cell lung cancer.
  • Patients were grouped according to the number of clinical predictors (female, adenocarcinoma and never-smoker).
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Squamous Cell / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics


79. Tatematsu A, Shimizu J, Murakami Y, Horio Y, Nakamura S, Hida T, Mitsudomi T, Yatabe Y: Epidermal growth factor receptor mutations in small cell lung cancer. Clin Cancer Res; 2008 Oct 1;14(19):6092-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor mutations in small cell lung cancer.
  • PURPOSE: The vast majority of epidermal growth factor receptor (EGFR) mutations occur in lung adenocarcinoma, and even rare cases of other subtypes with this mutation, such as adenosquamous cell carcinoma, are associated with adenocarcinoma histology.
  • According to this adenocarcinoma-specific nature of EGFR mutation, analysis of EGFR mutations with small cell lung cancers (SCLC) may provide a clue to its histogenesis.
  • The patients were mainly in the light smoker and histologic combined subtype.
  • Notably, in three tumors of the combined SCLC subtype, both components of adenocarcinoma and SCLC harbored an EGFR mutation, whereas gene amplification was detected only in the adenocarcinoma component.
  • CONCLUSIONS: Although EGFR mutations are rare in SCLC, a combined subtype of SCLC with adenocarcinoma in light smokers may have a chance of harboring EGFR mutations.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, erbB-1. Lung Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / physiology. Small Cell Lung Carcinoma / genetics

  • 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 = 18829487.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


80. Malhotra S, Lam S, Man SF, Gan WQ, Sin DD: The relationship between stage 1 and 2 non-small cell lung cancer and lung function in men and women. BMC Pulm Med; 2006;6:2
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The relationship between stage 1 and 2 non-small cell lung cancer and lung function in men and women.
  • BACKGROUND: Reduced forced expiratory volume in one second (FEV1) has been linked to non small cell lung cancer (NSCLC).
  • We divided the cohort into quartiles of predicted FEV1 and using both logistic and linear regression modeling techniques determined whether FEV1 was related to the occurrence of adeno or squamous cell carcinoma in men and women.
  • On average, women were more likely to have adenocarcinoma than were men (72% of all cases of NSCLC in women versus 40% in men; p < 0.001).
  • In men, however, there was an inverse relationship between the risk of adenocarcinoma and FEV1 such that the lowest quartile of FEV1 was 47% less likely to have adenocarcinoma compared with the highest FEV1 quartile (adjusted odds ratio, 0.52; 0.28 to 0.98; p for trend, 0.028).
  • The reverse was observed for squamous cell carcinoma.
  • CONCLUSION: In individuals undergoing lung resection for NSCLC, the risk of adenocarcinoma and squamous cell carcinoma of the lung varies as a function of FEV1, independent of smoking intensity in men but not in women.
  • CLINICAL IMPLICATIONS: These data indicate that women are much more susceptible to adenocarcinoma than are men especially when they have normal or near normal lung function.
  • It may thus be useful to conduct periodic surveillance chest radiographs in asymptomatic female smokers (or ex-smokers) to ascertain peripheral nodules or masses before distant metastases occur since adenocarcinomas tend to metastasize earlier in the disease course than squamous cell carcinomas.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / etiology. Lung / physiology. Lung Neoplasms / etiology. Neoplasm Staging

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 1996 Oct;17(10):2201-5 [8895489.001]
  • [Cites] N Engl J Med. 1995 Dec 28;333(26):1757-63 [7491141.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3317-20 [10416585.001]
  • [Cites] Thorax. 2005 Jul;60(7):570-5 [15994265.001]
  • [Cites] Exp Lung Res. 2000 Dec;26(8):731-42 [11195467.001]
  • [Cites] Ann Surg. 2002 Mar;235(3):440-3 [11882767.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2002 May;282(5):L1122-34 [11943679.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2002 Oct 1;22(10):1631-6 [12377741.001]
  • [Cites] Chest. 2003 Jan;123(1 Suppl):21S-49S [12527563.001]
  • [Cites] Clin Cancer Res. 2003 May;9(5):1604-10 [12738712.001]
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Integr Cancer Ther. 2003 Sep;2(3):238-46 [15035887.001]
  • [Cites] Thorax. 2004 Aug;59(8):679-81 [15282388.001]
  • [Cites] J Allergy Clin Immunol. 2004 Aug;114(2):248-53 [15316498.001]
  • [Cites] Am Rev Respir Dis. 1981 Jun;123(6):659-64 [7271065.001]
  • [Cites] Ann Intern Med. 1986 Oct;105(4):503-7 [3752756.001]
  • [Cites] Ann Intern Med. 1987 Apr;106(4):512-8 [3826952.001]
  • [Cites] Am Rev Respir Dis. 1990 Mar;141(3):613-7 [2310094.001]
  • [Cites] J Natl Cancer Inst. 1990 Aug 15;82(16):1333-9 [2380990.001]
  • [Cites] Am Rev Respir Dis. 1991 Nov;144(5):1202-18 [1952453.001]
  • [Cites] Clin Cancer Res. 1999 May;5(5):1001-5 [10353732.001]
  • (PMID = 16451726.001).
  • [ISSN] 1471-2466
  • [Journal-full-title] BMC pulmonary medicine
  • [ISO-abbreviation] BMC Pulm Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1373665
  •  go-up   go-down


81. Landi MT, Zhao Y, Rotunno M, Koshiol J, Liu H, Bergen AW, Rubagotti M, Goldstein AM, Linnoila I, Marincola FM, Tucker MA, Bertazzi PA, Pesatori AC, Caporaso NE, McShane LM, Wang E: MicroRNA expression differentiates histology and predicts survival of lung cancer. Clin Cancer Res; 2010 Jan 15;16(2):430-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression differentiates histology and predicts survival of lung cancer.
  • PURPOSE: The molecular drivers that determine histology in lung cancer are largely unknown.
  • We investigated whether microRNA (miR) expression profiles can differentiate histologic subtypes and predict survival for non-small cell lung cancer.
  • EXPERIMENTAL DESIGN: We analyzed miR expression in 165 adenocarcinoma and 125 squamous cell carcinoma (SQ) tissue samples from the Environment And Genetics in Lung cancer Etiology (EAGLE) study using a custom oligo array with 440 human mature antisense miRs.
  • RESULTS: MiR expression profiles strongly differed between adenocarcinoma and SQ (P(global) < 0.0001), particularly in the early stages, and included miRs located on chromosome loci most often altered in lung cancer (e.g., 3p21-22).
  • Major findings were confirmed by quantitative real time-polymerase chain reaction (qRT-PCR) in EAGLE samples and in an independent set of lung cancer cases.
  • CONCLUSIONS: We identified a miR expression profile that strongly differentiated adenocarcinoma from SQ and had prognostic implications.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / mortality. Carcinoma, Squamous Cell / pathology. Case-Control Studies. Diagnosis, Differential. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / physiology. Humans. Male. Middle Aged. Neoplasm Staging / methods. Oligonucleotide Array Sequence Analysis. Prognosis. Smoking / epidemiology. Survival Analysis

  • 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] J Natl Cancer Inst. 2007 Jun 6;99(11):847-57 [17551145.001]
  • [Cites] Carcinogenesis. 2009 Nov;30(11):1903-9 [19736307.001]
  • [Cites] RNA. 2007 Oct;13(10):1668-74 [17698639.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):857-65 [15681531.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 [15741570.001]
  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):257-62 [16231326.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D140-4 [16381832.001]
  • [Cites] Genes Dev. 2006 Mar 1;20(5):515-24 [16510870.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):189-98 [16530703.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Respirology. 2006 Sep;11(5):533-8 [16916324.001]
  • [Cites] Lung. 2006 Nov-Dec;184(6):355-62 [17086460.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6116-33 [11085536.001]
  • [Cites] Int J Cancer. 2002 Aug 10;100(5):534-41 [12124802.001]
  • [Cites] Genome Biol. 2003;4(4):R28 [12702209.001]
  • [Cites] PLoS Biol. 2004 Apr;2(4):E108 [15094809.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3753-6 [15172979.001]
  • [Cites] Cancer Res. 1992 May 1;52(9 Suppl):2665s-2669s [1562997.001]
  • [Cites] Clin Cancer Res. 1996 Jul;2(7):1185-9 [9816286.001]
  • [Cites] Cell. 2005 Jan 14;120(1):15-20 [15652477.001]
  • [Cites] Lung Cancer. 2007 Jan;55(1):43-51 [17109992.001]
  • [Cites] J Natl Cancer Inst. 2007 Jan 17;99(2):147-57 [17227998.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(5):1859-67 [17194750.001]
  • [Cites] J Thorac Oncol. 2006 Jul;1(6):520-5 [17409911.001]
  • [Cites] Oncogene. 2007 Apr 26;26(19):2799-803 [17072344.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5763-8 [17908966.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]
  • [Cites] Mol Hum Reprod. 2007 Nov;13(11):797-806 [17766684.001]
  • [Cites] Cancer Res. 2007 Dec 1;67(23):11099-101 [18056431.001]
  • [Cites] Cancer Res. 2007 Dec 15;67(24):11612-20 [18089790.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):43-50 [18066065.001]
  • [Cites] PLoS One. 2008;3(2):e1651 [18297132.001]
  • [Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3903-8 [18308936.001]
  • [Cites] Cell Cycle. 2008 Mar 1;7(5):570-2 [18256538.001]
  • [Cites] BMC Public Health. 2008;8:203 [18538025.001]
  • [Cites] J Clin Oncol. 2008 Jul 20;26(21):3543-51 [18506025.001]
  • [Cites] J Transl Med. 2008;6:39 [18647411.001]
  • [Cites] Clin Chem. 2008 Oct;54(10):1696-704 [18719201.001]
  • [Cites] Trends Cell Biol. 2008 Oct;18(10):505-16 [18774294.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Dec 12;377(2):668-73 [18948085.001]
  • [Cites] J Thorac Oncol. 2008 Dec;3(12):1468-81 [19057275.001]
  • [Cites] Nat Struct Mol Biol. 2009 Jan;16(1):23-9 [19079265.001]
  • [Cites] Eur Respir J. 2009 Feb;33(2):352-9 [19010987.001]
  • [Cites] Clin Cancer Res. 2009 Feb 15;15(4):1177-83 [19228723.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2824-8 [19196983.001]
  • [Cites] FASEB J. 2009 Mar;23(3):806-12 [18952709.001]
  • [Cites] J Transl Med. 2009;7:20 [19309508.001]
  • [Cites] Mol Oncol. 2008 Apr;1(4):395-405 [19383313.001]
  • [Cites] Int J Cancer. 2009 Jul 1;125(1):146-52 [19350630.001]
  • [Cites] Cancer Res. 2009 Jul 15;69(14):5776-83 [19584273.001]
  • [Cites] Cancer Cell. 2008 Jan;13(1):48-57 [18167339.001]
  • [Cites] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):778-90 [17882278.001]
  • (PMID = 20068076.001).
  • [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
  • [Grant] United States / Intramural NIH HHS / / ZIA CP005803-16
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS160630; NLM/ PMC3163170
  •  go-up   go-down


82. Siegfried JM, Hershberger PA, Stabile LP: Estrogen receptor signaling in lung cancer. Semin Oncol; 2009 Dec;36(6):524-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen receptor signaling in lung cancer.
  • Lung cancer has long been thought of as a cancer that mainly affects men, but over the past several decades, because of the high increase in tobacco use by women, there has been a corresponding dramatic increase in lung cancer among women.
  • Since 1998, lung cancer deaths in women have surpassed those caused by breast cancer in the United States.
  • Annual lung cancer deaths among US women currently surpass those caused by breast, ovarian, and cervical cancers combined.
  • Women are more likely than men to be diagnosed with adenocarcinoma and small cell carcinoma of the lung compared to squamous cell carcinoma, and never-smokers diagnosed with lung cancer are almost three times more likely to be female than male.
  • These observations in the population, coupled to the findings that both estrogen receptors (ERs) and aromatase, the enzyme that synthesizes 17beta-estradiol, are expressed by lung tumors, suggest a role for female steroid hormones in control of lung cancer growth.
  • Preclinical data and clinical data are increasingly emerging to support this concept, and to suggest that a local production of estrogen and expression of ERs occurs in lung tumors that arise in men as well as in women.
  • An additional protein that recognizes 17beta-estradiol with high affinity, GPR30, also is expressed in lung tumors at high levels and may be responsible for some of the proliferation signals induced by estrogen.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1995 Dec 1;270(5241):1491-4 [7491495.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5925-30 [8650195.001]
  • [Cites] FEBS Lett. 1996 Aug 19;392(1):49-53 [8769313.001]
  • [Cites] Nature. 1997 Oct 16;389(6652):753-8 [9338790.001]
  • [Cites] J Natl Cancer Inst. 1998 Sep 16;90(18):1371-88 [9747868.001]
  • [Cites] Cell. 1998 Dec 23;95(7):927-37 [9875847.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3317-20 [10416585.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1459-70 [15735034.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1598-605 [15735050.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Chest. 2005 Mar;127(3):768-77 [15764756.001]
  • [Cites] Steroids. 2005 May-Jun;70(5-7):372-81 [15862820.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6450-8 [16024650.001]
  • [Cites] J Thorac Cardiovasc Surg. 2005 Oct;130(4):979-86 [16214508.001]
  • [Cites] Clin Cancer Res. 2005 Oct 15;11(20):7280-7 [16243798.001]
  • [Cites] Anticancer Res. 2005 Nov-Dec;25(6C):4693-8 [16334162.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11287-91 [16357134.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):59-63 [16314616.001]
  • [Cites] Int J Oncol. 2006 Feb;28(2):337-44 [16391787.001]
  • [Cites] Mol Biol Cell. 2006 May;17(5):2125-37 [16495339.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7165-9 [16636272.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):472-8 [17290054.001]
  • [Cites] Steroids. 2007 Feb;72(2):135-43 [17276470.001]
  • [Cites] Gynecol Endocrinol. 2007 Mar;23(3):131-7 [17454165.001]
  • [Cites] Cancer Res. 2007 Nov 1;67(21):10484-90 [17974992.001]
  • [Cites] J Clin Oncol. 2007 Dec 20;25(36):5785-92 [18089876.001]
  • [Cites] Lung Cancer. 2008 Jan;59(1):88-94 [17905466.001]
  • [Cites] Mol Endocrinol. 2008 Mar;22(3):609-22 [18048642.001]
  • [Cites] Cancer. 2008 Feb 1;112(3 Suppl):700-9 [18072256.001]
  • [Cites] Cancer Treat Rev. 2008 Apr;34(2):157-74 [18164821.001]
  • [Cites] Endocr Relat Cancer. 2008 Jun;15(2):475-83 [18509000.001]
  • [Cites] Oncology. 2007;73(5-6):305-10 [18493157.001]
  • [Cites] Clin Cancer Res. 2008 Jul 15;14(14):4417-26 [18579664.001]
  • [Cites] Mol Cell Endocrinol. 2008 Aug 13;290(1-2):51-9 [18571833.001]
  • [Cites] J Cell Biochem. 2008 Dec 15;105(6):1342-51 [18846505.001]
  • [Cites] Mol Endocrinol. 2009 Feb;23(2):146-56 [19106194.001]
  • [Cites] Endocrinology. 2009 Mar;150(3):1112-21 [19008315.001]
  • [Cites] Ann N Y Acad Sci. 2009 Feb;1155:194-205 [19250205.001]
  • [Cites] Lung Cancer. 2009 Apr;64(1):51-9 [18701186.001]
  • [Cites] J Biol Chem. 2009 Apr 3;284(14):9540-8 [19189968.001]
  • [Cites] Steroids. 2009 Jun;74(6):489-97 [19428437.001]
  • [Cites] J Steroid Biochem Mol Biol. 2009 Aug;116(1-2):102-9 [19460433.001]
  • [Cites] Lancet. 2009 Oct 10;374(9697):1243-51 [19767090.001]
  • [Cites] Jpn J Clin Oncol. 2009 Dec;39(12):829-32 [19692419.001]
  • [Cites] J Endocrinol. 2010 Feb;204(2):105-14 [19767412.001]
  • [Cites] Cancer Res. 2000 Jun 15;60(12):3175-82 [10866308.001]
  • [Cites] Mol Pharmacol. 2000 Sep;58(3):584-90 [10953052.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 1;92(21):1764-72 [11058619.001]
  • [Cites] Mol Endocrinol. 2001 Jul;15(7):1104-13 [11435611.001]
  • [Cites] Science. 2002 Mar 29;295(5564):2465-8 [11923541.001]
  • [Cites] Cancer Res. 2002 Apr 1;62(7):2141-50 [11929836.001]
  • [Cites] Endocrinology. 2003 Oct;144(10):4562-74 [12959972.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(23):8542-52 [14612399.001]
  • [Cites] N Engl J Med. 2004 Mar 11;350(11):1081-92 [15014181.001]
  • [Cites] Exp Eye Res. 2004 Apr;78(4):861-71 [15037120.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4130-5 [15024130.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2004 Jun;286(6):E1011-22 [14736707.001]
  • [Cites] J Mol Endocrinol. 2004 Jun;32(3):689-701 [15171709.001]
  • [Cites] J Cell Biochem. 2004 Oct 1;93(2):358-73 [15368362.001]
  • [Cites] Cancer. 1980 Dec 15;46(12 Suppl):2884-8 [7448733.001]
  • [Cites] Cancer Res. 1987 Nov 15;47(22):6126-33 [3664512.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Apr;74(4):879-83 [1548354.001]
  • [Cites] Genes Dev. 1993 Dec;7(12A):2431-45 [8253388.001]
  • [Cites] Cancer Res. 1994 Nov 15;54(22):5801-3 [7954403.001]
  • [Cites] Mol Cell Endocrinol. 1994 Aug;104(1):103-11 [7821701.001]
  • [Cites] Cancer Lett. 1995 Jan 6;88(1):1-5 [7850764.001]
  • (PMID = 19995644.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090440-09; United States / NCI NIH HHS / CA / P50 CA090440; United States / NCI NIH HHS / CA / CA090440-09S10006; United States / NCI NIH HHS / CA / P50 CA090440-09S10006; United States / NCI NIH HHS / CA / CA090440-09
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GPER protein, human; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 4TI98Z838E / Estradiol; EC 1.14.14.1 / Aromatase
  • [Other-IDs] NLM/ NIHMS167495; NLM/ PMC2818861
  •  go-up   go-down


83. Truong T, Hung RJ, Amos CI, Wu X, Bickeböller H, Rosenberger A, Sauter W, Illig T, Wichmann HE, Risch A, Dienemann H, Kaaks R, Yang P, Jiang R, Wiencke JK, Wrensch M, Hansen H, Kelsey KT, Matsuo K, Tajima K, Schwartz AG, Wenzlaff A, Seow A, Ying C, Staratschek-Jox A, Nürnberg P, Stoelben E, Wolf J, Lazarus P, Muscat JE, Gallagher CJ, Zienolddiny S, Haugen A, van der Heijden HF, Kiemeney LA, Isla D, Mayordomo JI, Rafnar T, Stefansson K, Zhang ZF, Chang SC, Kim JH, Hong YC, Duell EJ, Andrew AS, Lejbkowicz F, Rennert G, Müller H, Brenner H, Le Marchand L, Benhamou S, Bouchardy C, Teare MD, Xue X, McLaughlin J, Liu G, McKay JD, Brennan P, Spitz MR: Replication of lung cancer susceptibility loci at chromosomes 15q25, 5p15, and 6p21: a pooled analysis from the International Lung Cancer Consortium. J Natl Cancer Inst; 2010 Jul 7;102(13):959-71
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Replication of lung cancer susceptibility loci at chromosomes 15q25, 5p15, and 6p21: a pooled analysis from the International Lung Cancer Consortium.
  • BACKGROUND: Genome-wide association studies have identified three chromosomal regions at 15q25, 5p15, and 6p21 as being associated with the risk of lung cancer.
  • To confirm these associations in independent studies and investigate heterogeneity of these associations within specific subgroups, we conducted a coordinated genotyping study within the International Lung Cancer Consortium based on independent studies that were not included in previous genome-wide association studies.
  • METHODS: Genotype data for single-nucleotide polymorphisms at chromosomes 15q25 (rs16969968, rs8034191), 5p15 (rs2736100, rs402710), and 6p21 (rs2256543, rs4324798) from 21 case-control studies for 11 645 lung cancer case patients and 14 954 control subjects, of whom 85% were white and 15% were Asian, were pooled.
  • Associations between the variants and the risk of lung cancer were estimated by logistic regression models.
  • RESULTS: Associations between 15q25 and the risk of lung cancer were replicated in white ever-smokers (rs16969968: odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.21 to 1.32, P(trend) = 2 x 10(-26)), and this association was stronger for those diagnosed at younger ages.
  • There was no association in never-smokers or in Asians between either of the 15q25 variants and the risk of lung cancer.
  • The associations between the 5p15 variants and lung cancer differed by histology; odds ratios for rs2736100 were highest in adenocarcinoma and for rs402710 were highest in adenocarcinoma and squamous cell carcinomas.
  • Neither of the two variants on chromosome 6p21 was associated with the risk of lung cancer.
  • CONCLUSIONS: In this international genetic association study of lung cancer, previous associations found in white populations were replicated and new associations were identified in Asian populations.
  • Future genetic studies of lung cancer should include detailed stratification by histology.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Smoking.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hepatology. 2009 Mar;49(3):802-8 [19152425.001]
  • [Cites] PLoS One. 2009;4(2):e4653 [19247474.001]
  • [Cites] Carcinogenesis. 2009 Jun;30(6):987-90 [19369581.001]
  • [Cites] Cancer Res. 2009 Jun 15;69(12):5065-72 [19491260.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):905-8 [19578366.001]
  • [Cites] Nat Genet. 2009 Aug;41(8):899-904 [19578367.001]
  • [Cites] Environ Health Perspect. 2009 Nov;117(11):1718-23 [20049123.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2009 Jun 5;150B(4):453-66 [19259974.001]
  • [Cites] Ann Nutr Metab. 1999;43(4):195-204 [10592368.001]
  • [Cites] Lung Cancer. 2003 Aug;41(2):163-9 [12871779.001]
  • [Cites] J Natl Cancer Inst. 2003 Aug 20;95(16):1211-8 [12928346.001]
  • [Cites] FEBS Lett. 2004 Apr 23;564(1-2):9-13 [15094035.001]
  • [Cites] Int J Cancer. 2005 Jan 1;113(1):141-7 [15386428.001]
  • [Cites] Health Phys. 2005 Jan;88(1):71-9 [15596992.001]
  • [Cites] Gesundheitswesen. 2005 Aug;67 Suppl 1:S26-30 [16032514.001]
  • [Cites] Int J Cancer. 2006 Feb 1;118(3):714-20 [16094634.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):560-7 [16195237.001]
  • [Cites] Hum Mol Genet. 2006 Apr 1;15(7):1181-6 [16497724.001]
  • [Cites] Br J Cancer. 2006 May 22;94(10):1452-9 [16641908.001]
  • [Cites] Front Biosci. 2007;12:905-11 [17127347.001]
  • [Cites] Clin Chem. 2007 Jan;53(1):53-61 [17130181.001]
  • [Cites] Hum Mol Genet. 2007 Jan 1;16(1):36-49 [17135278.001]
  • [Cites] Hum Mol Genet. 2007 Jan 1;16(1):24-35 [17158188.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):1835-41 [17311257.001]
  • [Cites] Genes Dev. 2007 Apr 1;21(7):848-61 [17403783.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):823-8 [17416778.001]
  • [Cites] Exp Hematol. 2007 Jun;35(6):939-46 [17533048.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5538-44 [17545637.001]
  • [Cites] Carcinogenesis. 2007 Aug;28(8):1718-25 [17468511.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2649-55 [18086770.001]
  • [Cites] Mol Psychiatry. 2008 Apr;13(4):368-73 [18227835.001]
  • [Cites] Nature. 2008 Apr 3;452(7187):633-7 [18385738.001]
  • [Cites] Nature. 2008 Apr 3;452(7187):638-42 [18385739.001]
  • [Cites] Nat Genet. 2008 May;40(5):616-22 [18385676.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1127-35 [18483334.001]
  • [Cites] PLoS Genet. 2008 Jul;4(7):e1000125 [18618000.001]
  • [Cites] J Med Genet. 2008 Oct;45(10):654-6 [18835860.001]
  • [Cites] J Natl Cancer Inst. 2008 Nov 5;100(21):1552-6 [18957677.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3081-9 [18990748.001]
  • [Cites] Cancer Res. 2008 Nov 15;68(22):9137-40 [19010884.001]
  • [Cites] Nat Genet. 2008 Dec;40(12):1407-9 [18978787.001]
  • [Cites] Nat Genet. 2008 Dec;40(12):1404-6 [18978790.001]
  • [Cites] J Invest Dermatol. 2009 Feb;129(2):415-21 [18668136.001]
  • [Cites] Carcinogenesis. 2009 Jan;30(1):65-70 [19005185.001]
  • [Cites] Nat Genet. 2009 Feb;41(2):221-7 [19151717.001]
  • [CommentIn] J Natl Cancer Inst. 2010 Jul 7;102(13):920-3 [20548020.001]
  • (PMID = 20548021.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA104231; United States / NCI NIH HHS / CA / CA55769; United States / NIEHS NIH HHS / ES / ES06717; United States / NCI NIH HHS / CA / CA127219; United States / NCI NIH HHS / CA / R01 CA127219; United States / NCI NIH HHS / CA / CA121197; United States / NCRR NIH HHS / RR / P20RR018787; United States / NCI NIH HHS / CA / CA55874; United States / NIDA NIH HHS / DA / DA11386; United States / NCI NIH HHS / CA / P01 CA68384; United States / NCI NIH HHS / CA / CA127219-04; United States / NCI NIH HHS / CA / CA85997; United States / NCI NIH HHS / CA / CA133996; United States / NCI NIH HHS / CA / R01 CA092039; United States / NCI NIH HHS / CA / CA77118; United States / NIEHS NIH HHS / ES / ES011667; United States / NCI NIH HHS / CA / K99CA131477; United States / NCI NIH HHS / CA / CA90833; United States / NCI NIH HHS / CA / CA84354; United States / NCI NIH HHS / CA / R03 CA133939-01; United States / NCI NIH HHS / CA / R01 CA127219-04; United States / NCI NIH HHS / CA / CA80127; United States / NCI NIH HHS / CA / CA09142
  • [Publication-type] Journal Article; Meta-Analysis; 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
  • [Other-IDs] NLM/ PMC2897877
  •  go-up   go-down


84. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung cancer risk and cigarette smoking, lung tuberculosis according to histologic type and gender in a population based case-control study.
  • 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.
  • [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


85. Al-Zahrani IH: The value of immunohistochemical expression of TTF-1, CK7 and CK20 in the diagnosis of primary and secondary lung carcinomas. Saudi Med J; 2008 Jul;29(7):957-61
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The value of immunohistochemical expression of TTF-1, CK7 and CK20 in the diagnosis of primary and secondary lung carcinomas.
  • METHODS: Forty-three cases of lung carcinoma, 14 squamous cell carcinoma, 12 adenocarcinoma, 8 small cell carcinoma, 3 mesothelioma, and 6 metastatic tumors, were collected from the files of the Pathology Department, King Abdul-Aziz University Hospital, Jeddah, Saudi Arabia between 2004 and 2006.
  • RESULTS: Immunohistochemical staining of 43 cases of lung carcinoma revealed nuclear immunoreactivity for TTF-1 in all primary adenocarcinoma, and small cell carcinoma, while cases of squamous cell carcinoma were negative.
  • Cytokeratin 7 was positively expressed in primary tumors of lung, as well as metastatic tumors from the thyroid and breast.
  • Cytokeratin 20 was negative in all primary lung tumors, while positive in metastatic carcinomas from the colon.
  • CONCLUSION: Thyroid transcription factor-1 is a sensitive marker for diagnosis of primary pulmonary adenocarcinoma, and differentiation between poorly differentiated squamous cell carcinoma and small cell carcinoma and adenocarcinoma.
  • Cytokeratin 20 could be a marker for metastatic tumors from the colon to the lung since it was negative in all primary lung tumors.
  • [MeSH-major] Carcinoma / diagnosis. Keratin-20 / metabolism. Keratin-7 / metabolism. Lung Neoplasms / diagnosis. Nuclear Proteins / metabolism. Transcription Factors / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18626520.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Keratin-20; 0 / Keratin-7; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
  •  go-up   go-down


86. Buys TP, Aviel-Ronen S, Waddell TK, Lam WL, Tsao MS: Defining genomic alteration boundaries for a combined small cell and non-small cell lung carcinoma. J Thorac Oncol; 2009 Feb;4(2):227-39
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defining genomic alteration boundaries for a combined small cell and non-small cell lung carcinoma.
  • In the rare case of a male patient presenting with a combined small cell lung carcinoma (SCLC), large cell neuroendocrine carcinoma and adenocarcinoma, we used whole genome analysis by tiling-path array comparative genomic hybridization to evaluate the clonal relationship between nodules.
  • The absence of shared genome alteration features for the adenocarcinoma and large cell neuroendocrine carcinoma components suggested that these tumors evolved independently from the SCLC.
  • Taken together, the array comparative genomic hybridization data demonstrate the development and evolution of three independent primary lung cancers in close proximity to each other to form a combined carcinoma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Chromosome Aberrations. Genome, Human. Lung Neoplasms / genetics. Neoplasms, Multiple Primary / genetics. Small Cell Lung Carcinoma / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Neuroendocrine / genetics. Carcinoma, Neuroendocrine / metabolism. Carcinoma, Neuroendocrine / pathology. Comparative Genomic Hybridization. Humans. Immunophenotyping. Male. Microarray Analysis. Middle Aged

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19179901.001).
  • [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 / Biomarkers, Tumor
  •  go-up   go-down


87. Alam N, Gustafson KS, Ladanyi M, Zakowski MF, Kapoor A, Truskinovsky AM, Dudek AZ: Small-cell carcinoma with an epidermal growth factor receptor mutation in a never-smoker with gefitinib-responsive adenocarcinoma of the lung. Clin Lung Cancer; 2010 Sep 1;11(5):E1-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small-cell carcinoma with an epidermal growth factor receptor mutation in a never-smoker with gefitinib-responsive adenocarcinoma of the lung.
  • Activating mutations in the epidermal growth factor receptor (EGFR) gene are extremely rare in small-cell lung cancer (SCLC).
  • Here, we present a case of an EGFR-mutant gefitinib-responsive non-small-cell lung cancer (NSCLC) of adenocarcinoma histology occurring in a never-smoker followed by subsequent diagnosis of metastatic SCLC carrying an EGFR mutation.
  • Epidermal growth factor receptor mutation analysis revealed that the exon 21 L858R activating mutation was present in both the original lung adenocarcinoma and the metastatic SCLC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Small Cell / genetics. Lung Neoplasms / genetics. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Aged. Female. Humans. Liver Neoplasms / secondary. Mutation

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • 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 = 20837450.001).
  • [ISSN] 1938-0690
  • [Journal-full-title] Clinical lung cancer
  • [ISO-abbreviation] Clin Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  •  go-up   go-down


88. Hassan KA, Chen G, Kalemkerian GP, Wicha MS, Beer DG: An embryonic stem cell-like signature identifies poorly differentiated lung adenocarcinoma but not squamous cell carcinoma. Clin Cancer Res; 2009 Oct 15;15(20):6386-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An embryonic stem cell-like signature identifies poorly differentiated lung adenocarcinoma but not squamous cell carcinoma.
  • PURPOSE: An embryonic stem cell (ESC) profile correlates with poorly differentiated breast, bladder, and glioma cancers.
  • In this article, we assess the correlation between the ESC profile and clinical variables in lung cancer.
  • EXPERIMENTAL DESIGN: Microarray gene expression analysis was done using Affymetrix Human Genome U133A on 443 samples of human lung adenocarcinoma and 130 samples of squamous cell carcinoma (SCC).
  • RESULTS: Our analysis showed that an increased expression of the ESC gene set and a decreased expression of the Polycomb target gene set identified poorly differentiated lung adenocarcinoma.
  • In addition, this gene expression signature was associated with markers of poor prognosis and worse overall survival in lung adenocarcinoma.
  • However, there was no correlation between this ESC gene signature and any histologic or clinical variable assessed in lung SCC.
  • CONCLUSIONS: This work suggests that not all poorly differentiated non-small cell lung cancers exhibit a gene expression profile similar to that of ESC, and that other characteristics may play a more important role in the determination of differentiation and survival in SCC of the lung.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Squamous Cell / genetics. Lung Neoplasms / genetics

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • 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 Genet. 2000 Apr;24(4):372-6 [10742100.001]
  • [Cites] Mol Cancer Res. 2009 Mar;7(3):330-8 [19276181.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Nat Med. 2002 Aug;8(8):816-24 [12118244.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Cell. 2003 May 30;113(5):643-55 [12787505.001]
  • [Cites] Neuron. 2003 Aug 28;39(5):749-65 [12948443.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):895-902 [14737120.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2922-7 [15131026.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Science. 1998 Nov 6;282(5391):1145-7 [9804556.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9328-37 [16230395.001]
  • [Cites] Oncogene. 2006 Mar 16;25(12):1696-708 [16449977.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3344-54 [16740756.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7466-72 [16885343.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • [Cites] PLoS One. 2007;2(2):e243 [17327908.001]
  • [Cites] Stem Cells. 2007 Apr;25(4):961-73 [17204602.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4827-33 [17510412.001]
  • [Cites] Cell Death Differ. 2008 Mar;15(3):504-14 [18049477.001]
  • [Cites] Nat Genet. 2008 May;40(5):499-507 [18443585.001]
  • [Cites] Nat Med. 2008 Aug;14(8):822-7 [18641660.001]
  • [Cites] Mol Cell Biol. 2001 Jul;21(13):4330-6 [11390661.001]
  • (PMID = 19808871.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / K08 CA158425; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / P30 CA046592-14; United States / NCI NIH HHS / CA / 5P30 CA46592
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS143924; NLM/ PMC2787085
  •  go-up   go-down


89. Wislez M, Gounant V, Cadranel J: [Bronchioloalveolar carcinoma]. Rev Mal Respir; 2005 Dec;22(6 Pt 2):8S70-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Bronchioloalveolar carcinoma].
  • Bronchioloalveolar carcinoma is one of the four histological subtypes of adenocarcinoma and its incidence is increasing.
  • For other types high-resolution lung CT-scan is necessary to evaluate pulmonary involvement because of the high frequency of multifocal disease at initial presentation and because of the presence of ground glass opacities, which can be one of the first manifestations of CBA on CT.
  • Therapeutic management does not differ from non-small cell lung cancer.
  • However, the recent discovery of the particular sensitivity of this form of adenocarcinoma to EGFR (Epidermal Growth Factor Receptor) tyrosine kinase inhibitors offers new possibilities for management.
  • [MeSH-major] Adenocarcinoma. Bronchial Neoplasms. Lung Neoplasms. Pulmonary Alveoli

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16340839.001).
  • [ISSN] 0761-8425
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 32
  •  go-up   go-down


90. Kitazaki T, Soda H, Doi S, Nakano H, Nakamura Y, Kohno S: Gefitinib inhibits MUC5AC synthesis in mucin-secreting non-small cell lung cancer cells. Lung Cancer; 2005 Oct;50(1):19-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib inhibits MUC5AC synthesis in mucin-secreting non-small cell lung cancer cells.
  • Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is an active agent in non-small cell lung cancer, and rapidly relieves bronchorrhea in patients with bronchioloalveolar carcinoma before the improvement of radiological findings.
  • The present study was designed to clarify whether gefitinib modifies mucin production in lung cancer cell lines apart from its anti-proliferative effects, using A549 adenocarcinoma and NCI-H292 mucoepidermoid carcinoma cells expressing EGFR and MUC5AC mRNA.
  • Thus, gefitinib inhibits mucin production, which is encouraging for trials involving its use against bronchorrhea in patients with lung cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / pathology. Mucins / biosynthesis. Quinazolines / pharmacology
  • [MeSH-minor] Adenocarcinoma / pathology. Blotting, Western. Enzyme-Linked Immunosorbent Assay. Humans. Mitogen-Activated Protein Kinase Kinases / metabolism. Mucin 5AC. Oncogene Protein v-akt / metabolism. Phosphorylation. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16009452.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucins; 0 / Quinazolines; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; S65743JHBS / gefitinib
  •  go-up   go-down


91. Yoon MY, Song CS, Seo MH, Kim MJ, Oh TY, Jang UH, Kwag HJ, Kim HS, Lim SY, Lim SY, Lee SS: A case of metachronous metastasis to the breast from non-small cell lung carcinoma. Cancer Res Treat; 2010 Sep;42(3):172-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of metachronous metastasis to the breast from non-small cell lung carcinoma.
  • We report here on a case of a 42-year-old female with metastasis of non-small cell lung cancer to the breast, and she is now being followed up on an outpatient basis.
  • In 2004, she presented with a solitary pulmonary nodule in the left lung, and this lesion had been noted to have gradually increased in size over time.
  • The final pathological diagnosis was adenocarcinoma, and the diagnosis was made by performing percutaneous needle aspiration and lobectomy of the left upper lobe.
  • Unfortunately, a nodule in the left breast was noted three years later, and metastatic non-small-cell lung cancer to the breast was diagnosed by excisional biopsy.
  • Making the correct diagnosis to distinguish a primary breast carcinoma from a metastatic one is important, because the therapeutic plan and outcome for these two types of cancer are quite different.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20948923.001).
  • [ISSN] 2005-9256
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2953781
  • [Keywords] NOTNLM ; Adenocarcinoma / Metachronous breast metastasis / Non-small cell lung carcinoma
  •  go-up   go-down


92. Konishi J, Yamazaki K, Kinoshita I, Isobe H, Ogura S, Sekine S, Ishida T, Takashima R, Nakadate M, Nishikawa S, Hattori T, Asahina H, Imura M, Kikuchi E, Kikuchi J, Shinagawa N, Yokouchi H, Munakata M, Dosaka-Akita H, Nishimura M: Analysis of the response and toxicity to gefitinib of non-small cell lung cancer. Anticancer Res; 2005 Jan-Feb;25(1B):435-41
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the response and toxicity to gefitinib of non-small cell lung cancer.
  • BACKGROUND: Gefitinib is an oral agent that inhibits the tyrosine kinase of epidermal growth factor receptor (EGFR), which had antitumor activity in patients with previously treated non-small cell lung cancer (NSCLC).
  • Significant variables associated with improved survival included good performance status (PS), female, adenocarcinoma and never smoked status, while never smoked status and good PS were independent prognostic factors in multivariate analysis.
  • CONCLUSION: Gefitinib showed favorable anti-tumor activity in females, never smokers and adenocarcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use
  • [MeSH-minor] Adenocarcinoma / metabolism. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Multivariate Analysis. Proportional Hazards Models. Retrospective Studies. Sex Factors. Smoking. Time Factors. Treatment Outcome


93. Chen XJ, Xiao W, Qu X, Zhou SY: NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma through up-regulation of p21WAF1 and p27KIP1 protein. Neoplasma; 2008;55(3):200-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma through up-regulation of p21WAF1 and p27KIP1 protein.
  • Gemcitabine is a chemotherapeutic drug widely used in the treatment of non-small cell lung carcinoma, especially in advanced lung adenocarcinoma.
  • However, many patients with advanced lung adenocarcinoma show a resistance to gemcitabine.
  • Overexpression of COX-2 has been found in human non-small cell lung cancer tissues and itA s cell lines.
  • However, It is unknown whether COX-2 inhibitor can augment the efficacy of gemcitabine against lung adenocarcinoma.
  • The cell viability was examined by MTT assay.
  • The cell cycle distribution and apoptotic ratio were tested by flow cytometry.
  • It can be concluded that NS-398 enhances the efficacy of gemcitabine against lung adenocarcinoma and the efficacy is associated with up-regulation of p21WAF1 and p27KIP1protein.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. Deoxycytidine / analogs & derivatives. Lung Neoplasms / drug therapy. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Drug Synergism. Humans. Up-Regulation

  • 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 = 18348652.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 0W860991D6 / Deoxycytidine; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; B76N6SBZ8R / gemcitabine
  •  go-up   go-down


94. Li Q, Yang H, Deng Y, Xiao C: [Comparative study of expressions of P16 protein in patients suffered from non-small-cell-lung-cancer of Xuanwei and Kunming district]. Wei Sheng Yan Jiu; 2010 Nov;39(6):701-4
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Comparative study of expressions of P16 protein in patients suffered from non-small-cell-lung-cancer of Xuanwei and Kunming district].
  • OBJECTIVE: To study the effect and function of P16 protein during the development of lung cancer, in order to explore the differences of expression of P16 protein in non-small cell lung cancer (NSCLC) between Xuanwei and Kunming district.
  • Immunohistochemical staining were used to analyze the expressions of P16 protein in paraffin-embedded tissues from these 90 residing patients with lung cancer.
  • RESULTS: 45 cases with lung cancer were negative for P16 protein expression, total loss expression rates were 41.7% (45/108).
  • In comparition the loss expression of P16 protein in clinicopathologic characteristics between the two groups, there were some statistically significant differences in the loss expression rate of P16 (P < 0.05): the loss expression rate of P16 in cases with stage I, adenocarcinoma and stage T2 in Xuanwei were more higher than those in Kunming; the loss expression rates of P16 in Xuanwei and Kungming were more higher than those in pneumatocele respectively.
  • CONCLUSION: Loss expression rates of P16 protein in the early stage and adenocarcinoma in Xuanwei lung cancer group were significant difference compared with in Kunming lung cancer group.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Lung Neoplasms / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21351635.001).
  • [ISSN] 1000-8020
  • [Journal-full-title] Wei sheng yan jiu = Journal of hygiene research
  • [ISO-abbreviation] Wei Sheng Yan Jiu
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
  •  go-up   go-down


95. Langer CJ, Besse B, Gualberto A, Brambilla E, Soria JC: The evolving role of histology in the management of advanced non-small-cell lung cancer. J Clin Oncol; 2010 Dec 20;28(36):5311-20
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The evolving role of histology in the management of advanced non-small-cell lung cancer.
  • Until recently, non-small-cell lung cancer (NSCLC) was treated as a single disease despite recognition of its histologic and molecular heterogeneity.
  • For example, the labeling of the licensed agents bevacizumab and pemetrexed is restricted to patients with nonsquamous cell NSCLC.
  • For bevacizumab, this restriction is due to an apparent association between squamous cell histology and severe pulmonary hemorrhage, whereas for pemetrexed, superior treatment effects have been observed in patients with nonsquamous cell histology.
  • Given fewer agents are both active and tolerable in patients with squamous cell carcinoma compared with adenocarcinoma, and the nature of this particular phenotype of NSCLC, new drugs are needed for this histology.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology


96. Momozane T, Higashiyama M, Maeda J, Okami J, Oda K, Imamura F, Yoneda K, Takenaka A, Kodama K: [Surgical treatment for the second double lung cancers following chemotherapy for small cell lung cancer]. Kyobu Geka; 2009 Feb;62(2):117-21
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment for the second double lung cancers following chemotherapy for small cell lung cancer].
  • We report a case with surgery for the 2nd primary double lung cancers-adenocarcinoma and squamous cell carcinoma which developed in the right upper lobe after 5 years successful control by chemotherapy for small cell lung cancer in the left upper lobe.
  • Long term survivors with small cell lung cancer have recently increased as a result of progress of chemotherapy.
  • Therefore, 2nd primary lung cancer is not rare after the treatment for the initial small cell lung cancer.
  • Although several causes have been proposed on the development of 2nd primary lung cancer after small cell lung cancer treatment, smoking history was strongly suggested as a cause in this case.
  • Careful follow-up especially focusing on 2nd primary lung cancer development is necessary for patients after successful treatment for small cell lung cancer.
  • [MeSH-major] Adenocarcinoma / surgery. Carcinoma, Squamous Cell / surgery. Lung Neoplasms / drug therapy. Lung Neoplasms / surgery. Neoplasms, Second Primary. Small Cell Lung Carcinoma / drug therapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19202930.001).
  • [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


97. Teixeira E, Sotto-Mayor R, Macedo R, Todo-Bom F, de Almeida AB: Treatment of non-small cell lung cancer, advanced disease, with erlotinib in 2(nd) and 3(rd) lines. Two cases report. Rev Port Pneumol; 2008 Oct;14 Suppl 3:S53-60
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of non-small cell lung cancer, advanced disease, with erlotinib in 2(nd) and 3(rd) lines. Two cases report.
  • [Transliterated title] Tratamento do carcinoma pulmonar de não pequenas células, doença avançada, com erlotinib em segunda e terceira linhas. A propósito de dois casos clínicos.
  • Agents that inhibit the activity of cell membrane receptor tyrosine kinases, such as the human epidermal growth factor receptor (EGFR) have been an attractive target because EGFR is expressed by 80% of NSCLC.
  • Women, Asiens, patients with Adenocarcinoma and never smokers, were more likely than other patients to have a response to erlotinib.

  • 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
  • [Copyright] © 2008 Sociedade Portuguesa de Pneumologia/SPP.
  • (PMID = 25967688.001).
  • [ISSN] 0873-2159
  • [Journal-full-title] Revista portuguesa de pneumologia
  • [ISO-abbreviation] Rev Port Pneumol
  • [Language] eng; por
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Keywords] NOTNLM ; Carcinoma pulmonar de não pequenas células / EGFR inhibitors / Non-small cell lung cancer / erlotinib / inibidores do EGFR / terapêutica / treatment
  •  go-up   go-down


98. Yang CJ, Hwang JJ, Kang WY, Chong IW, Wang TH, Sheu CC, Tsai JR, Huang MS: Gastro-intestinal metastasis of primary lung carcinoma: clinical presentations and outcome. Lung Cancer; 2006 Dec;54(3):319-23
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastro-intestinal metastasis of primary lung carcinoma: clinical presentations and outcome.
  • Symptomatic gastro-intestinal (GI) metastasis in lung carcinomas is extremely rare and only a few case reports have been published.
  • Here we review all of the cases of lung cancer from January 2003 to April 2005 in a tertiary teaching hospital in Taiwan.
  • A total of six patients (1.77%, 6/339) with primary lung cancer demonstrated symptomatic gastro-intestinal metastasis.
  • Three patients had squamous cell carcinoma, one had adenocarcinoma, and two had small cell carcinoma.
  • Two patients with small bowel perforation and intussusception were diagnosed via laparotomy.
  • [MeSH-major] Carcinoma / diagnosis. Intestinal Neoplasms / diagnosis. Lung Neoplasms / pathology. Stomach Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Lung Cancer. 2007 Aug;57(2):247-8 [17602784.001]
  • (PMID = 17010474.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
  •  go-up   go-down


99. El Mezni F, Mrabet N, Ismaïl O: [Pathological profile of lung carcinoma in Tunisia. About 869 cases]. Tunis Med; 2005 Mar;83(3):157-62
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathological profile of lung carcinoma in Tunisia. About 869 cases].
  • To establish the pathologic profile of broncho-pulmonary carcinoma, 869 cases were retrospectively collected.
  • This sex-ratio was less than one recorded in 1994 (11, 5 M / 1F), and then the question is: did the womanly broncho-pulmonary carcinoma on the increase, in Tunisia?
  • In histological data, we noted that adenocarcinoma is actually more frequent than epidermoid carcinoma.
  • Its ratio increased from 15, 3 % in 1994 to 30, 3 % in 2003, whereas, epidermoid carcinoma's ratio decreased from 42, 8 % to 29, 5 %.
  • The relationship tobacco- different histological type of broncho-pulmonary carcinoma was clearly observed, varying between 90, 6% (adenocarcinoma) and 100 % (large cell carcinoma).
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Large Cell / pathology. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Biopsy. Data Interpretation, Statistical. Female. Humans. Lung / pathology. Male. Middle Aged. Retrospective Studies. Sex Factors. Smoking / adverse effects. Tunisia / epidemiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15929445.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Tunisia
  •  go-up   go-down


100. Chen QL, Zheng WL, Yao WJ, Nie LW, Cheng SH, Ma WL: Analysis of SOX4 gene mutation in non-small cell lung cancer tissues. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Oct;24(5):505-9
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of SOX4 gene mutation in non-small cell lung cancer tissues.
  • OBJECTIVE: To investigate the mutation of SOX4 gene in the different tumor tissues with pathological stages and types of non-small cell lung cancer (NSCLC), and to explore its roles in the progression of lung carcinoma.
  • METHODS: The SOX4 gene HMG-box of lung cancer tissues and paracancerous tissues were amplified by PCR, 20 cases shown difference by single strand conformation polymorphyism analysis were sequenced.
  • Seven were detected from squamous cell carcinoma, five from adenocarcinoma and six from adeno-squamous.
  • The results indicate that the SOX4 gene mutations might be related in the lung carcinogenesis and tumor metastasis.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mutation. SOXC Transcription Factors / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17922414.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / SOX4 protein, human; 0 / SOXC Transcription Factors
  •  go-up   go-down






Advertisement