BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fall in diffusing capacity associated with induction therapy for lung cancer: a predictor of postoperative complication?

However, the impact of induction therapy on the pulmonary toxicity and associated pulmonary complications has not been fully investigated in the setting of lung cancer surgery.

The diffusing capacity of lung for carbon monoxide (D(LCO)) was decreased significantly by 21% (from 90.3% +/- 18.3% to 71.1% +/- 12.5%; p < 0.0005).

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / physiopathology. Lung Neoplasms / physiopathology. Pneumonectomy. Postoperative Complications / epidemiology. Pulmonary Diffusing Capacity

[MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / physiopathology. Adenocarcinoma / radiotherapy. Adenocarcinoma / surgery. Aged. Anoxia / etiology. Carbon Monoxide / analysis. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / physiopathology. Carcinoma, Large Cell / radiotherapy. Carcinoma, Large Cell / surgery. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / physiopathology. Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / surgery. Cisplatin / administration & dosage. Combined Modality Therapy. Empyema, Pleural / etiology. Female. Forced Expiratory Volume. Forecasting. Humans. Male. Middle Aged. Mitomycin / administration & dosage. Pneumonia / etiology. Predictive Value of Tests. Pulmonary Atelectasis / etiology. Pulmonary Embolism / etiology. Pulmonary Embolism / mortality. Pulmonary Gas Exchange. Radiotherapy / adverse effects. Remission Induction. Respiratory Distress Syndrome, Adult / etiology. Respiratory Distress Syndrome, Adult / mortality. Respiratory Insufficiency / etiology. Retrospective Studies. Risk Factors. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives. Vindesine / administration & dosage. Vital Capacity

Genetic Alliance. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - After Surgery.

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

Hazardous Substances Data Bank. MITOMYCIN C .

Hazardous Substances Data Bank. VINDESINE .

Hazardous Substances Data Bank. Carbon monoxide .

Hazardous Substances Data Bank. VINORELBINE .

Hazardous Substances Data Bank. VINBLASTINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16798220.001).

[ISSN] 1552-6259

[Journal-full-title] The Annals of thoracic surgery

[ISO-abbreviation] Ann. Thorac. Surg.

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 50SG953SK6 / Mitomycin; 5V9KLZ54CY / Vinblastine; 7U1EE4V452 / Carbon Monoxide; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine; RSA8KO39WH / Vindesine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase II trial of a 2-h infusion of gemcitabine plus carboplatin as first-line chemotherapy for advanced non-small-cell lung cancer.

PURPOSE: To evaluate the efficacy and safety of the combination of using gemcitabine as a rate infusion of 10 mg/m(2) per min with carboplatin in front-line chemonaive patients with advanced non-small-cell lung cancer (NSCLC).

Thirty-two (59%) patients had adenocarcinoma, 13 (24%) squamous cell, 1 (2%) large cell carcinoma and 8 (15%) others.

CONCLUSIONS: Prolonged gemcitabine infusion combined with carboplatin is manageable and tolerated, and its efficacy is similar to that of other chemotherapeutic schemes used for NSCLC treatment.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. CARBOPLATIN .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16614849.001).

[ISSN] 0344-5704

[Journal-full-title] Cancer chemotherapy and pharmacology

[ISO-abbreviation] Cancer Chemother. Pharmacol.

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.

BACKGROUND: Lung adenocarcinomas from patients who respond to the tyrosine kinase inhibitors gefitinib (Iressa) or erlotinib (Tarceva) usually harbor somatic gain-of-function mutations in exons encoding the kinase domain of the epidermal growth factor receptor (EGFR).

Biochemical analyses of transfected cells and growth inhibition studies with lung cancer cell lines demonstrate that the T790M mutation confers resistance to EGFR mutants usually sensitive to either gefitinib or erlotinib.

This observation should help guide the search for more effective therapy against a specific subset of lung cancers.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Rev Drug Discov. 2004 Dec;3(12):1001-10 [15573099.001]

[Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]

[Cites] Curr Opin Hematol. 2002 Jul;9(4):303-7 [12042704.001]

[Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]

[Cites] J Biol Chem. 2002 Nov 29;277(48):46265-72 [12196540.001]

[Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]

[Cites] Cancer Res. 2004 Sep 1;64(17):5913-9 [15342366.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]

[Cites] Cancer Res. 2004 Sep 15;64(18):6652-9 [15374980.001]

[Cites] Blood. 2004 Oct 15;104(8):2532-9 [15256422.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7241-4 [15492241.001]

[Cites] J Neurosci Methods. 1993 Nov;50(2):205-16 [8107502.001]

[Cites] Nature. 2004 Nov 18;432(7015):294-7 [15549090.001]

[Cites] Science. 2004 Aug 20;305(5687):1163-7 [15284455.001]

[Cites] Cancer Res. 2004 Dec 15;64(24):8919-23 [15604253.001]

[Cites] Clin Cancer Res. 2004 Dec 15;10(24):8195-203 [15623594.001]

[Cites] Blood. 2005 Apr 1;105(7):2640-53 [15618470.001]

[Cites] PLoS Med. 2005 Jan;2(1):e17 [15696205.001]

[Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]

[Cites] J Biol Chem. 2003 Apr 25;278(17):15435-40 [12594213.001]

[Cites] Ann Hematol. 2003 May;82(5):284-9 [12692682.001]

[Cites] Hematol J. 2004;5(1):55-60 [14745431.001]

[Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]

[Cites] Chem Biol. 2004 May;11(5):691-701 [15157880.001]

[Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]

[Cites] Gastroenterology. 2004 Jul;127(1):294-9 [15236194.001]

[CommentIn] PLoS Med. 2005 Mar;2(3):e75 [15736989.001]

[CommentIn] PLoS Med. 2005 Sep;2(9):e269 [16173832.001]

(PMID = 15737014.001).

[ISSN] 1549-1676

[Journal-full-title] PLoS medicine

[ISO-abbreviation] PLoS Med.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / T32 CA009207; United States / NCI NIH HHS / CA / T32 CA 09207

[Publication-type] Case Reports; 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 / Antineoplastic Agents; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib

[Other-IDs] NLM/ PMC549606

   

Advertisement

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Gefitinib therapy for non-small cell lung cancer.

Gefitinib is a small molecule that specifically inhibits the tyrosine kinase activity of the epidermal growth factor receptor (EGFR) type 1 by interfering with the adenosine triphosphate (ATP) binding site.

An infrequent but serious side effect of gefitinib is interstitial lung disease (ILD).

The Iressa dose evaluation for advanced lung cancer phase II trials (IDEAL 1 and IDEAL 2) of single agent gefitinib, 250 or 500 mg orally per day in pretreated patients with non-small cell lung cancer (NSCLC), found about 20% of patients on IDEAL-1 and 10% of patients on IDEAL-2 had major objective responses and improvement of symptoms.

Although there have been no direct comparisons, the small molecule inhibitors of EGFR gefitinib and erlotinib appear to have similar efficacy.

Nonsmokers, women, and patients with adenocarcinoma, are more likely to have major objective responses than other patients.

Bronchioalveolar lung cancer is a subtype of NSCLC that is more likely to respond to gefitinib.

[MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Clinical Trials as Topic. Combined Modality Therapy. Dose-Response Relationship, Drug. Humans. Survival Analysis

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Lung Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 2004 Mar 1;22(5):777-84 [14990632.001]

[Cites] Exp Cell Res. 2003 Mar 10;284(1):122-30 [12648471.001]

[Cites] J Clin Oncol. 2003 Jun 15;21(12):2237-46 [12748244.001]

[Cites] J Clin Oncol. 2004 Mar 15;22(6):1103-9 [15020612.001]

[Cites] J Clin Oncol. 2002 Nov 1;20(21):4292-302 [12409327.001]

[Cites] Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):27-38 [15142632.001]

[Cites] J Clin Oncol. 2004 Mar 1;22(5):785-94 [14990633.001]

[Cites] Lancet. 2003 Jan 11;361(9352):137-9 [12531582.001]

(PMID = 15610717.001).

[ISSN] 1527-2729

[Journal-full-title] Current treatment options in oncology

[ISO-abbreviation] Curr Treat Options Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib

[Number-of-references] 25

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] First- and second-line treatment of advanced metastatic non-small-cell lung cancer: a global view.

Treatment of non-small-cell lung cancer is dependent on disease stage.

This review discusses therapeutic options for first- and second-line treatment in patients with advanced non-small-cell lung cancer.

According to current data, the combination of two cytotoxic agents is the optimum first-line treatment for patients with non-small-cell lung cancer and performance status of 0-1.

There are currently three drugs approved for second-line treatment of patients with advanced non-small-cell lung cancer after failure of first-line chemotherapy.

Analysis of data from different subgroups included in the BR.21 trial show that overall survival is similar among women and men, among patients with adenocarcinoma and epidermoid carcinoma or Asian patients compared with other ethnicities.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Support Oncol. 2005 Mar-Apr;3(2):149-54 [15796447.001]

[Cites] J Clin Oncol. 2005 May 1;23(13):3125-37 [15860872.001]

[Cites] Int J Cancer. 1999 Sep 24;83(1):18-29 [10449602.001]

[Cites] J Natl Cancer Inst. 1999 Jan 6;91(1):66-72 [9890172.001]

[Cites] BMJ. 1998 Sep 19;317(7161):771-5 [9740561.001]

[Cites] J Clin Oncol. 1991 Sep;9(9):1618-26 [1651993.001]

[Cites] J Clin Oncol. 2004 May 1;22(9):1589-97 [15117980.001]

[Cites] Expert Rev Anticancer Ther. 2003 Aug;3(4):435-42 [12934656.001]

[Cites] J Natl Cancer Inst. 2003 Mar 5;95(5):362-72 [12618501.001]

[Cites] Lung Cancer. 2003 Jan;39(1):55-61 [12499095.001]

[Cites] N Engl J Med. 2002 Jan 10;346(2):92-8 [11784875.001]

[Cites] J Clin Oncol. 2001 Jul 1;19(13):3210-8 [11432888.001]

[Cites] Cancer Control. 2000 Nov-Dec;7(6):539-47 [11088062.001]

[Cites] Eur J Cancer. 2000 Sep;36(14):1741-54 [10974621.001]

[Cites] J Clin Oncol. 2000 May;18(10):2095-103 [10811675.001]

[Cites] Oncologist. 2008;13 Suppl 1:14-20 [18263770.001]

[Cites] Oncologist. 2008;13 Suppl 1:5-13 [18263769.001]

[Cites] J Clin Oncol. 2007 Oct 20;25(30):4743-50 [17909199.001]

[Cites] Clin Cancer Res. 2007 Jul 1;13(13):3913-21 [17606725.001]

[Cites] J Clin Oncol. 2007 Mar 1;25(7):760-6 [17228019.001]

[Cites] J Clin Oncol. 2007 Mar 1;25(7):751-3 [17228017.001]

[Cites] Ann Oncol. 2007 Feb;18(2):317-23 [17079694.001]

[Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6049-55 [17062680.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3831-7 [16921034.001]

[Cites] Clin Lung Cancer. 2006 May;7(6):389-94 [16800964.001]

[Cites] Oncologist. 2006 Jun;11(6):655-65 [16794244.001]

[Cites] N Engl J Med. 2005 Jul 14;353(2):133-44 [16014883.001]

[Cites] N Engl J Med. 2005 Jul 14;353(2):123-32 [16014882.001]

[Cites] Intern Med. 2005 Feb;44(2):107-13 [15750269.001]

(PMID = 18831719.001).

[ISSN] 1753-6561

[Journal-full-title] BMC proceedings

[ISO-abbreviation] BMC Proc

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2559799

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Integrin alpha 11 regulates IGF2 expression in fibroblasts to enhance tumorigenicity of human non-small-cell lung cancer cells.

Integrin alpha11 (ITGA11/alpha11) is localized to stromal fibroblasts and commonly overexpressed in non-small-cell lung carcinoma (NSCLC).

SV40 immortalized mouse embryonic fibroblasts established from wild-type (WT) and Itga11-deficient [knockout (KO)] mice were tested for their tumorigenicity in immune-deficient mice when implanted alone or coimplanted with the A549 human lung adenocarcinoma cells.

A549 coimplanted with the fibroblasts showed a markedly enhanced tumor growth rate compared with A549, WT, or KO, which alone formed only small tumors.

These findings were validated in two other NSCLC cell lines, NCI-H460 and NCI-H520.

The results indicate that alpha11 is an important stromal factor in NSCLC and propose a paradigm for carcinoma-stromal interaction indirectly through interaction between the matrix collagen and stromal fibroblasts to stimulate cancer cell growth.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Fibroblasts / metabolism. Gene Expression Regulation, Neoplastic / physiology. Growth Substances / physiology. Integrin alpha Chains / physiology. Lung Neoplasms / metabolism. Proteins / genetics. Proteins / metabolism

[MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Line, Transformed. Cell Line, Tumor. Collagen / metabolism. Extracellular Matrix / genetics. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Humans. Insulin-Like Growth Factor II. Male. Mice. Mice, Knockout. Mice, SCID. Stromal Cells / metabolism. Stromal Cells / pathology

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Proc Soc Exp Biol Med. 1999 Nov;222(2):124-38 [10564536.001]

[Cites] J Cell Biochem. 2004 Jan 1;91(1):41-6 [14689580.001]

[Cites] Cancer Res. 2004 Feb 15;64(4):1331-7 [14973050.001]

[Cites] Clin Cancer Res. 2004 Mar 15;10(6):1984-91 [15041716.001]

[Cites] Gastroenterology. 2004 Apr;126(4):1190-3 [15057757.001]

[Cites] Dev Biol. 2004 Jun 15;270(2):427-42 [15183724.001]

[Cites] Mol Cells. 2004 Apr 30;17(2):188-202 [15179030.001]

[Cites] Exp Oncol. 2004 Jun;26(2):106-10 [15273661.001]

[Cites] J Cell Biol. 2004 Aug 2;166(3):407-18 [15289498.001]

[Cites] Nat Rev Mol Cell Biol. 2004 Oct;5(10):816-26 [15459662.001]

[Cites] Cancer Res. 1991 Jul 15;51(14):3753-61 [1712249.001]

[Cites] Exp Cell Res. 1995 Sep;220(1):112-23 [7545126.001]

[Cites] J Biol Chem. 1996 May 10;271(19):11477-83 [8626706.001]

[Cites] J Clin Endocrinol Metab. 1996 Oct;81(10):3774-82 [8855837.001]

[Cites] Cell. 1996 Nov 15;87(4):733-43 [8929541.001]

[Cites] Int J Cancer. 1996 Nov 15;68(4):441-6 [8945613.001]

[Cites] FASEB J. 1997 Jan;11(1):60-7 [9034167.001]

[Cites] Cancer Res. 1997 Aug 1;57(15):3305-13 [9242465.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13612-7 [9391074.001]

[Cites] J Anim Sci. 1998 Apr;76(4):1216-31 [9581947.001]

[Cites] J Biol Chem. 1999 Sep 3;274(36):25735-42 [10464311.001]

[Cites] Cancer Res. 1999 Oct 1;59(19):5002-11 [10519415.001]

[Cites] Nat Rev Cancer. 2004 Nov;4(11):839-49 [15516957.001]

[Cites] Lung Cancer. 2004 Aug;45 Suppl 2:S163-75 [15552797.001]

[Cites] J Biol Chem. 2004 Dec 3;279(49):51677-87 [15383545.001]

[Cites] Cell. 2005 May 6;121(3):335-48 [15882617.001]

[Cites] Cancer Res. 2005 Dec 15;65(24):11236-40 [16357124.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):331-42 [16397247.001]

[Cites] Exp Cell Res. 2006 Mar 10;312(5):651-8 [16325811.001]

[Cites] Nat Rev Cancer. 2006 May;6(5):392-401 [16572188.001]

[Cites] Cancer Res. 2006 May 15;66(10):5330-7 [16707459.001]

[Cites] Mol Cell Biol. 2007 Jun;27(12):4306-16 [17420280.001]

[Cites] J Cell Sci. 1999 Dec;112 ( Pt 24):4751-61 [10574722.001]

[Cites] Cancer Res. 2000 Jan 15;60(2):269-72 [10667574.001]

[Cites] Cancer Res. 2000 Mar 1;60(5):1254-60 [10728684.001]

[Cites] J Biol Chem. 2000 Nov 24;275(47):36532-40 [10976102.001]

[Cites] Cell Tissue Res. 2001 Sep;305(3):285-98 [11572082.001]

[Cites] Cell Tissue Res. 2001 Oct;306(1):107-16 [11683172.001]

[Cites] Cancer Res. 2001 Nov 15;61(22):8135-42 [11719442.001]

[Cites] J Biol Chem. 2001 Dec 21;276(51):48206-12 [11572855.001]

[Cites] Am J Pathol. 2002 Jan;160(1):195-204 [11786413.001]

[Cites] Genes Dev. 2002 Apr 15;16(8):948-58 [11959843.001]

[Cites] Cell. 2002 Sep 20;110(6):673-87 [12297042.001]

[Cites] Oncogene. 2002 Oct 24;21(49):7598-604 [12386823.001]

[Cites] Dev Cell. 2002 Dec;3(6):877-87 [12479812.001]

[Cites] FEBS Lett. 2003 Jun 19;545(2-3):203-8 [12804776.001]

[Cites] Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25 [14685170.001]

[Cites] Science. 2004 Feb 6;303(5659):848-51 [14764882.001]

(PMID = 17600088.001).

[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

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Growth Substances; 0 / IGF2 protein, human; 0 / ITGA11 protein, human; 0 / Integrin alpha Chains; 0 / Proteins; 67763-97-7 / Insulin-Like Growth Factor II; 9007-34-5 / Collagen

[Other-IDs] NLM/ PMC1913903

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] ANLN plays a critical role in human lung carcinogenesis through the activation of RHOA and by involvement in the phosphoinositide 3-kinase/AKT pathway.

Gene expression profile analysis of non-small cell lung cancers (NSCLC) and subsequent functional analyses revealed that human ANLN, a homologue of anillin, an actin-binding protein in Drosophila, was transactivated in lung cancer cells and seemed to play a significant role in pulmonary carcinogenesis.

Induction of small interfering RNAs against ANLN in NSCLC cells suppressed its expression and resulted in growth suppression; moreover, treatment with small interfering RNA yielded cells with larger morphology and multiple nuclei, which subsequently died.

On the other hand, induction of exogenous expression of ANLN enhanced the migrating ability of mammalian cells by interacting with RHOA, a small guanosine triphosphatase, and inducing actin stress fibers.

Immunohistochemical staining of nuclear ANLN on lung cancer tissue microarrays was associated with the poor survival of NSCLC patients, indicating that this molecule might serve as a prognostic indicator.

Our data imply that up-regulation of ANLN is a common feature of the carcinogenetic process in lung tissue, and suggests that selective suppression of ANLN could be a promising approach for developing a new strategy to treat lung cancers.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Contractile Proteins / metabolism. Lung Neoplasms / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. rhoA GTP-Binding Protein / metabolism

[MeSH-minor] Actins / metabolism. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Adenosquamous / genetics. Carcinoma, Adenosquamous / metabolism. Carcinoma, Adenosquamous / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Movement. Enzyme Activation. Female. Flow Cytometry. Humans. Lung / metabolism. Lung / pathology. Male. Middle Aged. Prognosis. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Survival Rate. Tissue Array Analysis. Tumor Cells, Cultured. Wound Healing

MedlinePlus Health Information. consumer health - Lung Cancer.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16357138.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Actins; 0 / Contractile Proteins; 0 / RNA, Small Interfering; 0 / anillin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / rhoA GTP-Binding Protein

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Epidermal growth factor receptor inhibition and non-small cell lung cancer.

The majority of non-small cell (NSC) lung cancers express epidermal growth factor receptor (EGFR).

Many studies have evaluated the clinical effect from targeted therapy achieved by blocking EGFR in patients with NSC lung cancer.

Treatment of biologically unselected patients with NSC lung cancer with two reversible quinazole EGFR inhibitors, gefitinib and erlotinib, gave negative results in all controlled trials but one.

Ten percent to 20% of patients with NSC lung cancers have somatic mutations in EGFR, and these patients have a significantly higher response rate (73%) to treatment with EGFR inhibitors than patients with wild-type EGFR (10%).

Patients with Asian background, women, non-smokers, and patients with adenocarcinoma had higher response rates than other patients, and the differences may be due to an association between the clinical characteristics and EGFR mutations.

Further studies are needed to fully evaluate the effect of EGFR inhibitor-treatment for subgroups of patients with NSC lung cancer with favorable biological and clinical characteristics.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / 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. CETUXIMAB .

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 = 16769595.001).

[ISSN] 1040-8363

[Journal-full-title] Critical reviews in clinical laboratory sciences

[ISO-abbreviation] Crit Rev Clin Lab Sci

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab; S65743JHBS / gefitinib

[Number-of-references] 215

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Multicentre randomised phase III study comparing the same dose and schedule of cisplatin plus the same schedule of vinorelbine or gemcitabine in advanced non-small cell lung cancer.

This study compares two cytotoxic regimens comprising the same dose and schedule of cisplatin (CP) plus vinorelbine (VNR) or gemcitabine (GEM) administered under the same schedule to patients with advanced non-small cell lung cancers (NSCLC).

Their main characteristics were: male/female ratio 214/58; median age 63 (range 32-77) years; median Karnofsky Performance Status (PS) 80 (range 70-100); stage IIIB 34%, stage IV 61%, recurrent disease 5%; histology - epidermoid 29%, adenocarcinoma 53%, other NSCLC 18%.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Deoxycytidine / analogs & derivatives. Lung Neoplasms / drug therapy. Vinblastine / analogs & derivatives

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. CIS-DIAMINEDICHLOROPLATINUM .

Hazardous Substances Data Bank. VINORELBINE .

Hazardous Substances Data Bank. VINBLASTINE .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Eur J Cancer. 2005 Jul;41(11):1655; author reply 1656-7 [15951165.001]

(PMID = 15617993.001).

[ISSN] 0959-8049

[Journal-full-title] European journal of cancer (Oxford, England : 1990)

[ISO-abbreviation] Eur. J. Cancer

[Language] eng

[Publication-type] Clinical Trial; Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] High-grade neuroendocrine carcinoma of the ampulla of vater: a clinicopathologic and immunohistochemical analysis of 14 cases.

We describe the clinical and pathologic features of 14 cases of high-grade neuroendocrine carcinoma (HGNEC) of the ampulla of Vater classified according to WHO classification of lung tumors into small cell carcinoma (SCC, 6 cases) and large cell neuroendocrine carcinoma (LCNEC, 8 cases) types.

Two HGNECs were combined with a conventional adenocarcinoma and another with a squamous cell carcinoma component.

The association with adenoma and or conventional adenocarcinoma components may suggest a common pathway in the initial carcinogenesis of these two types of tumors.

Thus, there are differences in the molecular phenotypes of these two types of ampullary carcinoma, supporting the distinction of poorly differentiated carcinomas with a neuroendocrine phenotype from those without.

[MeSH-major] Ampulla of Vater / pathology. Carcinoma, Neuroendocrine / pathology. Common Bile Duct Neoplasms / pathology

[MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Survival Rate

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15832081.001).

[ISSN] 0147-5185

[Journal-full-title] The American journal of surgical pathology

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Polymorphisms of vitamin D receptor and survival in early-stage non-small cell lung cancer patients.

Our previous analysis suggested that surgery season in the summer time and high vitamin D intake are associated with improved survival in early-stage non-small cell lung cancer (NSCLC) patients.

There was no association between VDR polymorphisms and survival, overall or among adenocarcinoma patients.

Among squamous cell carcinoma (SCC) patients, the G/A+A/A genotype group of the Cdx-2 polymorphism was associated with better OS: the 5-year OS rates were 41% [95% confidence interval (95% CI), 28-53] for the G/G and 55% (95% CI, 39-71) for the G/A+A/A genotypes, respectively (P = 0.04, log-rank test), with the adjusted hazard ratio of 0.56 (95% CI, 0.33-0.95) for G/A+A/A versus G/G.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / mortality. Lung Neoplasms / genetics. Lung Neoplasms / mortality. Polymorphism, Genetic. Receptors, Calcitriol / genetics

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17119052.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA074386; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / CA092824; United States / NCI NIH HHS / CA / CA119650-01A1; United States / NCI NIH HHS / CA / ES/CA 06409; United States / NIEHS NIH HHS / ES / ES00002

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Topoisomerase II alpha expression and the benefit of adjuvant chemotherapy for postoperative patients with non-small cell lung cancer.

BACKGROUND: Adjuvant chemotherapy has been shown to improve survival rates of postoperative patients with non-small cell lung cancer (NSCLC).

Univariate survival analysis showed that male sex (P = 0.036), non-adenocarcinoma (P = 0.004), earlier pathological TNM stage (P = 0.001) or pathological N stage (P < 0.001), and high expression of TopIIα (P = 0.012) were correlated with better DFS, whereas age, smoking history, different chemotherapy regimens, T stage and expression level of Ki67 were of no prognostic significance.

[MeSH-major] Antigens, Neoplasm / biosynthesis. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / surgery. Chemotherapy, Adjuvant / methods. DNA Topoisomerases, Type II / biosynthesis. DNA-Binding Proteins / biosynthesis. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Lung Neoplasms / surgery

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] Ann Oncol. 1999;10 Suppl 5:S83-6 [10582146.001]

[Cites] J Cancer Res Clin Oncol. 2010 Jul;136(7):1029-37 [20052594.001]

[Cites] Lung Cancer. 2001 May;32(2):117-28 [11325482.001]

[Cites] Anticancer Res. 2001 Mar-Apr;21(2A):905-10 [11396183.001]

[Cites] Clin Cancer Res. 2002 Apr;8(4):1061-7 [11948114.001]

[Cites] Lancet Oncol. 2002 Apr;3(4):235-43 [12067686.001]

[Cites] Int J Oncol. 2004 Jan;24(1):201-9 [14654958.001]

[Cites] Anticancer Res. 2003 Sep-Oct;23(5A):3965-70 [14666704.001]

[Cites] N Engl J Med. 2004 Jan 22;350(4):351-60 [14736927.001]

[Cites] J Clin Oncol. 2004 Oct 1;22(19):3860-7 [15326194.001]

[Cites] Cancer Res. 1987 Oct 15;47(20):5455-60 [2888532.001]

[Cites] J Natl Cancer Inst. 1992 Jan 15;84(2):113-8 [1310509.001]

[Cites] Cancer Res. 1992 Apr 1;52(7):1666-74 [1312895.001]

[Cites] Br J Cancer. 1993 Mar;67(3):456-63 [8382508.001]

[Cites] Biochim Biophys Acta. 1995 Dec 27;1264(3):337-46 [8547322.001]

[Cites] Br J Cancer. 1996 Dec;74(12):1869-76 [8980384.001]

[Cites] Breast Cancer Res Treat. 1999 May;55(1):61-71 [10472780.001]

[Cites] J Clin Oncol. 2005 May 10;23(14):3270-8 [15886314.001]

[Cites] N Engl J Med. 2005 Jun 23;352(25):2589-97 [15972865.001]

[Cites] Breast Cancer Res. 2005;7(3):R374-84 [15987433.001]

[Cites] Mol Pharmacol. 2005 Sep;68(3):625-34 [15942022.001]

[Cites] Lancet Oncol. 2006 Sep;7(9):719-27 [16945766.001]

[Cites] Clin Cancer Res. 2007 Feb 1;13(3):994-9 [17289895.001]

[Cites] Cancer Res. 2007 Mar 15;67(6):2893-8 [17363613.001]

[Cites] J Clin Oncol. 2008 Feb 10;26(5):736-44 [18258981.001]

[Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]

[Cites] BMC Cancer. 2009;9:72 [19250538.001]

[Cites] Lancet Oncol. 2009 Oct;10(10):1001-10 [19796752.001]

[Cites] Ann Surg Oncol. 2010 May;17(5):1392-7 [20217261.001]

[Cites] Future Oncol. 2010 May;6(5):741-67 [20465389.001]

[Cites] Pathobiology. 2000 May-Jun;68(3):137-43 [11174071.001]

(PMID = 21067592.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha

[Other-IDs] NLM/ PMC2988758

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Mutation in the epidermal growth factor receptor (EGFR) is frequently seen in non-small cell lung cancers (NSCLCs), especially in Asian females with adenocarcinoma.

For fresh cases a portion of samples isolated to establish the diagnosis of lung cancer was used.

The EGFR mutation was significantly associated with adenocarcinoma (p = 0.006) and light-smoking (p < 0.0001), but not gender.

Our result suggests that the female predominance in the EGFR mutation rate is a reflection of a higher frequency of adenocarcinoma in females.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. DNA Mutational Analysis. Genes, erbB-1. Lung Neoplasms / genetics. Neoplasm Proteins / genetics

[MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / epidemiology. Adenocarcinoma / genetics. Adult. Aged. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / genetics. DNA, Neoplasm / genetics. Exons / genetics. Female. Gene Frequency. Humans. Japan / epidemiology. Male. Middle Aged. Point Mutation. Polymerase Chain Reaction / methods. Sequence Deletion. Sex Factors. Smoking / genetics

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 .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19609951.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [The role of thyroid transcription factor-1 DNA binding activity in lung cancer.].

BACKGROUND: TTF-1 is a homeodomain transcriptional regulator of both structural organization of the lung and differentiation of highly specialized epithelial cell types such as alveolar typeII cells.

This study is to investigate the Thyroid transcription factor-1 (TTF-1) DNA binding activity in lung cancer tissue and its significance with lung cancer pathologic type and differentiation level.

METHODS: The TTF-1 DNA binding activity was detected in lung cancer tissue by Electrophoretic mobility shift assay (EMSA), autoradiography and photo densitometry.

RESULTS: The optical density of TTF-1 DNA binding activity in adenocarcinoma tissue was 172+/-23.2 and it was remarkably higher than that in other pathological types, including 141+/-16.3 of small cell carcinomas and 122+/-13.6 of squamous carcinoma (P <0.05).

The optical density of TTF-1 DNA binding activity in highly differentiated lung cancer tissues was significantly higher than that in poor-differentiated lung cancer (P <0.05).

CONCLUSIONS: TTF-1 DNA binding activity is a potential predictor of lung cancer metastasis and survival.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20716405.001).

[ISSN] 1999-6187

[Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer

[ISO-abbreviation] Zhongguo Fei Ai Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Detection of epidermal growth factor receptor mutations in non-small cell lung cancer by real-time PCR using TaqMan-MGB probes].

OBJECTIVE: To investigate mutations of EGFR TK gene in non-small cell lung cancer (NSCLC) and the diagnostic value of the mutations assayed by real-time PCR using TaqMan-MGB probes.

Real-time PCR with TagMan MGB probes could detect EGFR mutation in as rare as 50 EGFR mutant cells and in a proportion of 10% of mutant cells in a cell population.

The mutations were significantly higher in the adenocarcinoma than in non-adenocarcinoma (16/38 vs. 5/42, chi2 = 9.702, P <0.01), in the female patients than in the male patients (14/29 vs. 7/51, chi2 = 11.4, P <0.01) and in non-smokers than in smokers (16/40 vs. 5/40, chi2 = 7.812, P < 0.01).

CONCLUSION: Somatic mutations of EGFR gene develop in NSCLC and are more common in female, non-smoker and adenocarcinoma patients.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Mutation. Polymerase Chain Reaction / methods. Receptor, Epidermal Growth Factor / genetics

[MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Base Sequence. Cell Line, Tumor. Chi-Square Distribution. Codon. DNA Mutational Analysis. DNA Probes / genetics. Exons. Female. Gene Deletion. Humans. Male. Middle Aged. Neoplasm Staging. Sex Factors. Smoking

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 = 17645848.001).

[ISSN] 0253-3766

[Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]

[ISO-abbreviation] Zhonghua Zhong Liu Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Codon; 0 / DNA Probes; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

RESULTS: The system has been tested with a total of 896 lung cancer cases that include the diagnoses groups: cohort (1) normal lung--cancer; cancer subdivided: cohort (2) small cell lung cancer--non small cell lung cancer; non small cell lung cancer subdivided: cohort (3) squamous cell carcinoma--adenocarcinoma--large cell carcinoma.

CONCLUSION: The developed system is a fast and reliable procedure to fulfill all requirements for an automated "pre-screening" of virtual slides in lung pathology.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Pathol. 2001 Nov;195(4):508-14 [11745684.001]

[Cites] Telemed J E Health. 2000 Winter;6(4):373-7 [11242544.001]

[Cites] Cell Tissue Res. 1999 Jun;296(3):443-55 [10370131.001]

[Cites] Anal Quant Cytol Histol. 1998 Oct;20(5):443-60 [9801763.001]

[Cites] Cancer. 1992 Mar 15;69(6 Suppl):1636-8 [1540904.001]

[Cites] Anal Cell Pathol. 1997;15(2):73-83 [9413593.001]

[Cites] J Pathol. 1997 May;182(1):68-75 [9227344.001]

[Cites] Pathologica. 1995 Jun;87(3):255-62 [8570286.001]

[Cites] J Microsc. 1986 Jul;143(Pt 1):3-45 [3761363.001]

[Cites] Anal Quant Cytol Histol. 1988 Aug;10(4):299-306 [3166674.001]

[Cites] Eur Urol. 1999;35(5-6):484-91 [10325510.001]

[Cites] Anal Quant Cytol Histol. 1998 Aug;20(4):313-20 [9739414.001]

(PMID = 16764733.001).

[ISSN] 1746-1596

[Journal-full-title] Diagnostic pathology

[ISO-abbreviation] Diagn Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC1524814

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of kallikrein-related peptidases (KRP/hK5, 7, 6, 8) in subtypes of human lung carcinoma.

Lung cancer is currently the leading cause of cancer mortality worldwide.

Expression of kallikrein-related peptidases (KRP/hK/KLK) may be induced during lung carcinogenesis.

To test the hypothesis that KRP/hK, previously identified in the skin (KRP/hK5, 7) and brain (KRP/hK6, 8), are expressed in lung tumours, experiments were designed to investigate their localization in four malignant sub-types of human lung cancer.

Using specific antibodies, expression of these KRP/hK was determined in archived lung tumour sections of the four subtypes, and in normal skin, brain, lung and submandibular gland tissue sections.

In the squamous cell carcinoma, small cell carcinoma and carcinoid tumour, 40-90% of the malignant cells showed positive cytoplasmic labelling for KRP/hK5, 7, 6 and 8 (intensity grade 2+/3+).

In the adenocarcinoma there was no cytoplasmic labelling for any of the KRP/hK, but the nuclei of 20% of the tumour cells were labelled for KRP/hK5, 7 and 8 (intensity grade 2+/3+).

Further studies are required to determine the functional significance of the expression of KRP/hK in human lung carcinomas, and whether any of these proteins may be potential biomarkers for specific sub-types of lung cancer.

[MeSH-major] Kallikreins / analysis. Lung Neoplasms / enzymology

[MeSH-minor] Brain / enzymology. Humans. Lung / enzymology. Salivary Glands / enzymology. Skin / enzymology

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18182244.001).

[ISSN] 1567-5769

[Journal-full-title] International immunopharmacology

[ISO-abbreviation] Int. Immunopharmacol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] EC 3.4.21.- / KLK5 protein, human; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / KLK7 protein, human; EC 3.4.21.- / KLK8 protein, human; EC 3.4.21.- / Kallikreins

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cystic bronchioloalveolar cell carcinoma.

Bronchioloalveolar cell carcinomas (BACs), a subset of primary lung adenocarcinomas, are uncommon.

Similar to other non-small cell lung cancers, patients with BAC are usually 40-70 years of age.

Distinguishing features relative to other non-small cell lung cancers include occurrence in young patients, a higher relative predominance in women, and weaker association with smoking.

[MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / diagnosis. Lung Neoplasms / diagnosis. Tomography, X-Ray Computed / methods

[MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle / methods. Cough / etiology. Diagnosis, Differential. Female. Humans. Lung / pathology. Lung / radiography. Male. Middle Aged

MedlinePlus Health Information. consumer health - CT Scans.

MedlinePlus Health Information. consumer health - Lung Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15818211.001).

[ISSN] 0883-5993

[Journal-full-title] Journal of thoracic imaging

[ISO-abbreviation] J Thorac Imaging

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Radiosensitivity of tumor cell lines after pretreatment with the EGFR tyrosine kinase inhibitor ZD1839 (Iressa).

MATERIAL AND METHODS: Three tumor cell lines (A549, H596, FaDu) were exposed to ionizing radiation, treatment with ZD1839, and combined treatment.

Clonogenic cell survival was determined by colony assays, EGFR and transforming growth factor-(TGF-)alpha expression by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), cell cycle distribution and apoptosis by flow cytometry.

Both cell lines expressed moderate amounts of EGFR mRNA and very low levels of TGF-alpha mRNA.

FaDu cells expressed relatively high amounts of EGFR and TGF-alpha transcripts and showed marked inhibition of clonogenic growth, reduction of S-phase cells, and induction of apoptosis after treatment with 1 microM ZD1839 and combined treatment.

CONCLUSION: The sensitivity to ZD1839 correlated with the EGFR expression level, an inhibition of cell proliferation, and induction of apoptosis in the cell lines analyzed.

[MeSH-minor] Adenocarcinoma. Carcinoma, Non-Small-Cell Lung. Carcinoma, Squamous Cell. Cell Line, Tumor. Humans. Lung Neoplasms

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 = 15756525.001).

[ISSN] 0179-7158

[Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]

[ISO-abbreviation] Strahlenther Onkol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Response to erlotinib in first-line treatment of non-small-cell lung cancer in a white male smoker with squamous-cell histology.

Erlotinib, a potent inhibitor of the tyrosine-kinase (TK) activity of human epidermal growth factor receptor (HER1/EGFR), produces significant survival and quality of life benefits in patients with previously treated advanced-stage non-small-cell lung cancer.

Although the survival benefit from erlotinib was observed in varied subgroups of patients, the radiographic responses were more common in certain patient subgroups, such as women, never-smokers, patients with adenocarcinoma histology, patients of Asian ethnicity, and patients with presence of HER1/EGFR TK domain mutations.

Herein, we describe a white male former smoker with advancedstage squamous cell non-small-cell lung cancer, who responded to first-line erlotinib.

[MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Lung Cancer.

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 = 17239298.001).

[ISSN] 1525-7304

[Journal-full-title] Clinical lung cancer

[ISO-abbreviation] Clin Lung Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression and its significance of TSG101 in lung cancer tissue and lung cancer cell lines.].

BACKGROUND: It has been proven that TSG101 is a candidate tumor suppressor gene whose deletion in NIH3T3 cells leads to spontaneous lung metastases in nude mice.

To investigate the possible role of TSG101 and aberrant transcripts of TSG101 in lung cancer, we performed transcript analysis and protein analysis in lung cancer cell lines and lung cancer tissue.

METHODS: Immunohistochemical method (S-P method) was used to detect the expression of TSG101 in 79 human squamous carcinoma and adenocarcinoma cases with the neighboring noncancerous tissue.

RT-PCR was adopted to detect a common shortened TSG101 transcript because of aberrant alternative splicing and the wild-type transcript in lung cancer lines.

Western Blot method was adopted to detect the expression of TSG101 protein in lung cell cells.

Reverse transcriptase RT-PCR analysis detected a common shortened TSG101 transcript because of aberrant alternative splicing, which was co-expressed with the wild-type transcript in seven lung cancer lines.

Although shortened transcript was detected in all of lung cell cells being involved in our experiment, there is more aberrant transcipts in small cell lung cancer (SCLC) lines .Western blot analysis have detected the same differences in protein level.

CONCLUSIONS: TSG101 is a candidate tumor suppressor in non small cell lung cancer.

However the common TSG101 aberrant transcript may be associated with types of lung cancer, and can be used as valuable biomarkers to evaluate lung cancer poor prognosis.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20731896.001).

[ISSN] 1999-6187

[Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer

[ISO-abbreviation] Zhongguo Fei Ai Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A phase II, open-label, randomized study to assess the efficacy and safety of AZD6244 (ARRY-142886) versus pemetrexed in patients with non-small cell lung cancer who have failed one or two prior chemotherapeutic regimens.

This study aimed to evaluate the efficacy and safety of AZD6244 versus pemetrexed as second- or third-line treatment in patients with advanced non-small cell lung cancer (NSCLC).

[MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / therapeutic use. Benzimidazoles / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Glutamates / therapeutic use. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy. Salvage Therapy

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. PEMETREXED .

Hazardous Substances Data Bank. GUANINE .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20802351.001).

[ISSN] 1556-1380

[Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

[ISO-abbreviation] J Thorac Oncol

[Language] eng

[Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / AZD 6244; 0 / Antimetabolites, Antineoplastic; 0 / Benzimidazoles; 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

However, there is limited data on the effects of combination therapies on the development of bone metastasis in animal models of lung cancer.

The purpose of this study was to establish a human lung adenocarcinoma cell line with high bone metastatic potential in an immunodeficient mouse model and to evaluate the synergistic inhibitory activity of zoledronate and paclitaxel (P) on bone metastasis in nude mice.

A human lung adenocarcinoma cell line with high bone metastatic potential (SPC-A1-BM) was established by 10 rounds of in vivo selection.

The results of this study indicated that zoledronate enhanced the efficacy of paclitaxel synergistically, by reducing the incidence of bone metastasis from lung cancer and prolonging survival in a mouse model of non-small cell lung cancer with a high potential for metastasis to bone.

[MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Paclitaxel / therapeutic use

[MeSH-minor] Animals. Collagen Type I / blood. Drug Therapy, Combination. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Incidence. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Mice. Mice, Nude. Peptides / blood. Proto-Oncogene Proteins c-bcl-2 / metabolism. Survival Rate. Tumor Cells, Cultured. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism

MedlinePlus Health Information. consumer health - Bone Cancer.

Hazardous Substances Data Bank. TAXOL .

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 = 18695909.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Bcl2l1 protein, mouse; 0 / Bone Density Conservation Agents; 0 / Collagen Type I; 0 / Diphosphonates; 0 / Imidazoles; 0 / Peptides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 0 / collagen type I trimeric cross-linked peptide; 6XC1PAD3KF / zoledronic acid; P88XT4IS4D / Paclitaxel

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The expression of RNA-binding protein HuR in non-small cell lung cancer correlates with vascular endothelial growth factor-C expression and lymph node metastasis.

The expression levels of the RNA-binding protein Hu antigen (HuR) and vascular endothelial growth factor-C (VEGF-C) were examined immunohistochemically in 81 non-small cell lung cancers (NSCLC) and 15 benign human lung tissues.

Cytoplasmic immunoreactivity for HuR was observed in 45.7% (37/81) of NSCLC, while only nuclear expression of HuR was observed in 13.3% (2/15) of benign lung tissues.

In vitro, HuR showed a predominantly nuclear staining in Lewis lung cancer cells, as seen by confocal microscopy.

When lung cancer cells were treated with siRNA targeted against HuR, expression levels of the HuR and VEGF-C proteins were significantly reduced, as seen by Western blotting.

[MeSH-major] Antigens, Surface / biosynthesis. Carcinoma, Non-Small-Cell Lung / metabolism. Gene Expression Regulation, Neoplastic. Lung Neoplasms / metabolism. Lymphatic Metastasis. RNA-Binding Proteins / biosynthesis. Vascular Endothelial Growth Factor C / biosynthesis

[MeSH-minor] Adenocarcinoma / metabolism. Aged. Carcinoma, Squamous Cell / metabolism. ELAV Proteins. ELAV-Like Protein 1. Female. Humans. Male. Microscopy, Confocal. Middle Aged

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 .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2009 S. Karger AG, Basel.

(PMID = 19420963.001).

[ISSN] 1423-0232

[Journal-full-title] Oncology

[ISO-abbreviation] Oncology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antigens, Surface; 0 / ELAV Proteins; 0 / ELAV-Like Protein 1; 0 / ELAVL1 protein, human; 0 / RNA-Binding Proteins; 0 / Vascular Endothelial Growth Factor C

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here we analyzed the effects of TrxR1 targeting in the human A549 lung carcinoma cell line, having a very high basal TrxR1 expression.

Knocking down TrxR1 by approx 90% using siRNA gave only a slight effect on cell growth, irrespective of concurrent glutathione depletion (> or = 98% decrease), and no increase in cell death or distorted cell cycle phase distributions.

[MeSH-major] Adenocarcinoma / drug therapy. Lung Neoplasms / drug therapy. Thioredoxin Reductase 1 / metabolism

[MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Auranofin / pharmacology. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Growth Processes / drug effects. Cell Growth Processes / genetics. Cell Line, Tumor. Cisplatin / pharmacology. Dinitrochlorobenzene / pharmacology. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Humans. Naphthoquinones / pharmacology. RNA, Small Interfering / genetics. Vitamin K 3 / pharmacology

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

Hazardous Substances Data Bank. AURANOFIN .

Hazardous Substances Data Bank. MENADIONE .

Hazardous Substances Data Bank. 1-CHLORO-2,4-DINITROBENZENE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19766715.001).

[ISSN] 1873-4596

[Journal-full-title] Free radical biology & medicine

[ISO-abbreviation] Free Radic. Biol. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Naphthoquinones; 0 / RNA, Small Interfering; 3H04W2810V / Auranofin; 723JX6CXY5 / Vitamin K 3; EC 1.8.1.9 / Thioredoxin Reductase 1; GE3IBT7BMN / Dinitrochlorobenzene; Q20Q21Q62J / Cisplatin; W6Q80SK9L6 / juglone

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: The Ras-dependent ERK1/2 MAP kinase signaling pathway plays a central role in cell proliferation control and is frequently activated in human colorectal cancer.

Small-molecule inhibitors of MEK1/MEK2 are therefore viewed as attractive drug candidates for the targeted therapy of this malignancy.

METHODS: Wild type and constitutively active forms of MEK1 and MEK2 were ectopically expressed by retroviral gene transfer in the normal intestinal epithelial cell line IEC-6.

We studied the impact of MEK1 and MEK2 activation on cellular morphology, cell proliferation, survival, migration, invasiveness, and tumorigenesis in mice.

RESULTS: We found that expression of activated MEK1 or MEK2 is sufficient to morphologically transform intestinal epithelial cells, dysregulate cell proliferation and induce the formation of high-grade adenocarcinomas after orthotopic transplantation in mice.

A large proportion of these intestinal tumors metastasize to the liver and lung.

Importantly, we show that silencing of MEK2 expression completely suppresses the proliferation of human colon carcinoma cell lines, whereas inactivation of MEK1 has a much weaker effect.

[MeSH-major] Adenocarcinoma / secondary. Cell Transformation, Neoplastic. Intestinal Mucosa / pathology. Intestinal Neoplasms / pathology. MAP Kinase Kinase 1 / metabolism. MAP Kinase Kinase 2 / metabolism

[MeSH-minor] Animals. Anoikis. Cell Line, Tumor. Colorectal Neoplasms / enzymology. Colorectal Neoplasms / pathology. Humans. Matrix Metalloproteinases / metabolism. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Transplantation. Oligonucleotide Array Sequence Analysis. Protein Isoforms / metabolism. RNA Interference. Rats

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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] Oncogene. 2007 May 14;26(22):3227-39 [17496918.001]

[Cites] Nat Rev Cancer. 2007 Apr;7(4):295-308 [17384584.001]

[Cites] Int J Exp Pathol. 2008 Feb;89(1):1-12 [18081801.001]

[Cites] J Cell Biol. 2000 Feb 7;148(3):543-56 [10662779.001]

[Cites] Oncogene. 2000 Mar 23;19(13):1665-75 [10763823.001]

[Cites] Endocr Rev. 2001 Apr;22(2):153-83 [11294822.001]

[Cites] J Biol Chem. 2001 Jan 26;276(4):2686-92 [11031257.001]

[Cites] Br J Cancer. 2001 Sep 1;85(5):692-6 [11531254.001]

[Cites] Cancer Cell. 2002 Apr;1(3):233-6 [12086859.001]

[Cites] Nature. 2002 Jun 27;417(6892):949-54 [12068308.001]

[Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]

[Cites] Mol Cell Biol. 2002 Sep;22(17):6023-33 [12167697.001]

[Cites] Cancer Res. 2002 Aug 15;62(16):4781-90 [12183438.001]

[Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]

[Cites] Nat Rev Mol Cell Biol. 2002 Dec;3(12):932-43 [12461559.001]

[Cites] Int J Oncol. 2003 Mar;22(3):469-80 [12579299.001]

[Cites] J Biol Chem. 2003 Mar 7;278(10):8118-25 [12506122.001]

[Cites] Nat Rev Cancer. 2003 Jun;3(6):459-65 [12778136.001]

[Cites] Cancer Metastasis Rev. 2003 Dec;22(4):395-403 [12884914.001]

[Cites] Nat Cell Biol. 2003 Aug;5(8):733-40 [12844146.001]

[Cites] Nat Rev Mol Cell Biol. 2003 Aug;4(8):657-65 [12923528.001]

[Cites] Cancer Res. 2003 Sep 15;63(18):5669-73 [14522881.001]

[Cites] Oncogene. 2003 Oct 2;22(43):6785-93 [14555991.001]

[Cites] J Biol Chem. 2003 Oct 24;278(43):42615-24 [12915405.001]

[Cites] Oncogene. 2004 Jan 22;23(3):763-76 [14737111.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2004 May;286(5):G736-46 [14701721.001]

[Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):355-66 [15122349.001]

[Cites] J Invest Dermatol. 2004 Sep;123(3):503-15 [15304090.001]

[Cites] Cancer Res. 2004 Sep 1;64(17):6035-40 [15342384.001]

[Cites] J Natl Cancer Inst. 1974 Sep;53(3):661-74 [4412247.001]

[Cites] Cancer Res. 1976 Dec;36(12):4562-9 [1000501.001]

[Cites] J Natl Cancer Inst. 1977 Jul;59(1):221-6 [327080.001]

[Cites] J Cell Biol. 1979 Feb;80(2):248-65 [88453.001]

[Cites] Br J Cancer. 1983 Mar;47(3):373-81 [6830688.001]

[Cites] Cancer Res. 1988 Dec 1;48(23):6863-71 [2846163.001]

[Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]

[Cites] Cell. 1994 Jun 17;77(6):841-52 [7911739.001]

[Cites] Science. 1994 Aug 12;265(5174):966-70 [8052857.001]

[Cites] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Aug 15;92(17):7686-9 [7644477.001]

[Cites] J Biol Chem. 1996 Feb 9;271(6):3265-71 [8621729.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):6924-8 [8692920.001]

[Cites] J Biol Chem. 1997 Apr 25;272(17):11426-33 [9111053.001]

[Cites] Mol Endocrinol. 1997 Oct;11(11):1618-25 [9328344.001]

[Cites] Gastroenterology. 1997 Nov;113(5):1589-98 [9352861.001]

[Cites] J Cell Physiol. 1998 Jan;174(1):35-47 [9397154.001]

[Cites] Curr Opin Oncol. 1999 Jan;11(1):68-75 [9914881.001]

[Cites] Nucleic Acids Res. 1999 May 15;27(10):2086-90 [10219080.001]

[Cites] Cell Growth Differ. 1999 May;10(5):317-32 [10359013.001]

[Cites] Nat Med. 1999 Jul;5(7):810-6 [10395327.001]

[Cites] Virology. 1964 Jun;23:291-4 [14187925.001]

[Cites] Nature. 2004 Nov 18;432(7015):298-306 [15549091.001]

[Cites] Nat Rev Cancer. 2004 Dec;4(12):937-47 [15573115.001]

[Cites] J Cell Biol. 2005 Jan 3;168(1):55-66 [15631990.001]

[Cites] Lancet Oncol. 2005 May;6(5):322-7 [15863380.001]

[Cites] Gastroenterology. 2005 Aug;129(2):577-90 [16083714.001]

[Cites] Front Biosci. 2006;11:479-91 [16146745.001]

[Cites] Biochim Biophys Acta. 2005 Nov 25;1756(2):103-14 [16098678.001]

[Cites] Mol Cancer. 2006;5:63 [17112382.001]

[Cites] N Engl J Med. 2007 Nov 15;357(20):2040-8 [18003960.001]

(PMID = 19014680.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Protein Isoforms; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.1.- / MAP2K2 protein, human; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 2.7.12.2 / MAP Kinase Kinase 2; EC 3.4.24.- / Matrix Metalloproteinases

[Other-IDs] NLM/ PMC2596176

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Correlation between SUV of (18)F-FDG PET-CT and the expression of GLUT1, MVD and Ki67 in non-small cell lung cancer].

OBJECTIVE: To investigate the correlation between 18F-FDG standard uptake value (SUV) and expression of GLUT1, MVD and Ki67 in non-small cell lung cancer (NSCLC).

METHODS: Thirty-three patients with non-small cell lung cancer received preoperative 18F-FDG PET-CT examination and underwent surgery.

Positive expression of GLUT1 was found in 22 cases (66.7%, 12 adenocarcinomas and 10 squamous cell carcinomas), and negative expression in 11 cases (10 adenocarcinomas and 1 squamous cell carcinoma).

Twenty-four patients (72.7%) showed positive expression of Ki67 (13 adenocarcinomas and 11 squamous cell carcinomas), and other 9 (adenocarcinomas) had negative expression.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Fluorodeoxyglucose F18 / pharmacokinetics. Glucose Transporter Type 1 / metabolism. Ki-67 Antigen / metabolism. Lung Neoplasms / metabolism

[MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / radionuclide imaging. Adult. Aged. Antigens, CD34 / metabolism. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Female. Humans. Lymphatic Metastasis. Male. Microvessels / radionuclide imaging. Middle Aged. Neoplasm Staging. Positron-Emission Tomography. Radiopharmaceuticals / pharmacokinetics. Tomography, X-Ray Computed. Tumor Burden

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 = 19173807.001).

[ISSN] 0253-3766

[Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]

[ISO-abbreviation] Zhonghua Zhong Liu Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Glucose Transporter Type 1; 0 / Ki-67 Antigen; 0 / Radiopharmaceuticals; 0 / SLC2A1 protein, human; 0Z5B2CJX4D / Fluorodeoxyglucose F18

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Deregulated expression of hnRNP A/B proteins in human non-small cell lung cancer: parallel assessment of protein and mRNA levels in paired tumour/non-tumour tissues.

The altered expression pattern of hnRNP A2/B1 and/or splicing variant B1 alone in human lung cancer and their potential to serve as molecular markers for early diagnosis remain issues of intense investigation.

The main objective of the present study was to use paired tumour/non-tumour biopsies from patients with non-small cell lung cancer (NSCLC) to investigate the expression profiles of hnRNP A1, A2/B1 and A3 in conjunction with ASF/SF2.

METHODS: We combined western blotting of tissue homogenates with immunohistochemical examination of fixed tissue sections and quantification of mRNA expression levels in tumour versus adjacent normal-looking areas of the lung in the same patient.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Heterogeneous-Nuclear Ribonucleoprotein Group A-B / metabolism. Lung / metabolism. RNA, Messenger / genetics

[MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / metabolism. Adenocarcinoma, Bronchiolo-Alveolar / secondary. Aged. Blotting, Western. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / secondary. Female. Humans. Immunoenzyme Techniques. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. RNA-Binding Proteins / genetics. RNA-Binding Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine-Arginine Splicing Factors. Survival Rate. Treatment Outcome

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Int J Oncol. 2000 Apr;16(4):763-7 [10717246.001]

[Cites] Clin Cancer Res. 1999 Dec;5(12):4048-52 [10632338.001]

[Cites] Cancer Res. 2001 Mar 1;61(5):1896-902 [11280744.001]

[Cites] Anticancer Res. 2001 Mar-Apr;21(2A):979-84 [11396191.001]

[Cites] Lung Cancer. 2001 Dec;34(3):341-50 [11714531.001]

[Cites] Nat Rev Mol Cell Biol. 2002 Mar;3(3):195-205 [11994740.001]

[Cites] Cancer Lett. 2002 Sep 26;183(2):215-20 [12065097.001]

[Cites] Lung Cancer. 2003 Apr;40(1):45-53 [12660006.001]

[Cites] J Pathol. 2003 May;200(1):88-94 [12692846.001]

[Cites] Lung Cancer. 2003 Aug;41(2):131-43 [12871776.001]

[Cites] Lung Cancer. 2003 Aug;41(2):179-86 [12871781.001]

[Cites] Br J Cancer. 2003 Oct 20;89(8):1493-501 [14562022.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7679-88 [14633690.001]

[Cites] Mol Carcinog. 2004 Dec;41(4):187-96 [15390079.001]

[Cites] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9788-92 [2557628.001]

[Cites] Annu Rev Biochem. 1993;62:289-321 [8352591.001]

[Cites] Science. 1994 Jul 29;265(5172):615-21 [8036511.001]

[Cites] Genomics. 1995 Jan 20;25(2):365-71 [7789969.001]

[Cites] Exp Cell Res. 1995 Nov;221(1):187-96 [7589244.001]

[Cites] J Biol Chem. 1996 May 3;271(18):10760-6 [8631886.001]

[Cites] RNA. 1998 Apr;4(4):430-44 [9630249.001]

[Cites] Clin Cancer Res. 1998 Jul;4(7):1631-40 [9676837.001]

[Cites] Am J Respir Cell Mol Biol. 1998 Oct;19(4):554-62 [9761751.001]

[Cites] Cancer Res. 1998 Dec 15;58(24):5818-24 [9865741.001]

[Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2237-46 [9815620.001]

[Cites] Exp Cell Res. 1999 Feb 1;246(2):399-411 [9925756.001]

[Cites] Mol Cell Biol. 1999 Mar;19(3):1720-30 [10022859.001]

[Cites] Cancer Res. 1999 Apr 1;59(7):1404-7 [10197602.001]

[Cites] Curr Opin Cell Biol. 1999 Jun;11(3):363-71 [10395553.001]

[Cites] Int J Oncol. 2005 Mar;26(3):635-40 [15703818.001]

[Cites] Genes Dev. 2005 Mar 15;19(6):643-64 [15769940.001]

[Cites] Biochem Biophys Res Commun. 2005 Aug 5;333(3):888-95 [15964549.001]

[Cites] J Cell Sci. 2005 Jul 15;118(Pt 14):3173-83 [16014382.001]

[Cites] Biochim Biophys Acta. 2006 Apr;1765(2):85-100 [16378690.001]

[Cites] Cancer Detect Prev. 2006;30(5):395-402 [17067748.001]

[Cites] Clin Cancer Res. 2007 Mar 15;13(6):1638-42 [17363515.001]

[Cites] Cancer Genomics Proteomics. 2007 May-Jun;4(3):233-9 [17878526.001]

[Cites] Mol Carcinog. 2007 Nov;46(11):887-900 [17477362.001]

[Cites] FEBS Lett. 2008 Jun 18;582(14):1977-86 [18342629.001]

[Cites] Curr Med Chem. 2009;16(9):1047-61 [19275611.001]

[Cites] Anticancer Res. 2009 Apr;29(4):1373-82 [19414390.001]

[Cites] Am J Respir Cell Mol Biol. 2000 Nov;23(5):636-45 [11062142.001]

(PMID = 20716340.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / HNRNPA3 protein, human; 0 / Heterogeneous-Nuclear Ribonucleoprotein Group A-B; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; 0 / hnRNP A1; 170974-22-8 / Serine-Arginine Splicing Factors

[Other-IDs] NLM/ PMC2933625

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] High expression of nuclear factor of activated T cells in Chinese primary non-small cell lung cancer tissues.

PURPOSE: Nuclear factor of activated T cells (NFAT) has been reported to be involved in the development of various types of cancer including adenocarcinoma of the breast.

This research was the first to investigate NFAT protein expression in primary non-small cell lung cancer (NSCLC) tissues from Chinese patients.

CONCLUSION: Our results revealed that high NFAT expression was present in Chinese NSCLCs and that NFAT expression might be involved in the process of human lung cancer development.

[MeSH-major] Biomarkers, Tumor / biosynthesis. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. NFATC Transcription Factors / biosynthesis

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 = 17922467.001).

[ISSN] 0393-6155

[Journal-full-title] The International journal of biological markers

[ISO-abbreviation] Int. J. Biol. Markers

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 094964; United States / NCI NIH HHS / CA / CA 103180; United States / NCI NIH HHS / CA / CA 112557; United States / NIEHS NIH HHS / ES / ES 012451

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NFATC Transcription Factors

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase II randomized controlled trial of an epidermal growth factor vaccine in advanced non-small-cell lung cancer.

PURPOSE: We show the result of a randomized phase II clinical trial with an epidermal growth factor (EGF)-based cancer vaccine in advanced non-small-cell lung cancer (NSCLC) patients, evaluating immunogenicity, safety, and effect on survival.

[MeSH-major] Cancer Vaccines / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / immunology. Epidermal Growth Factor / therapeutic use. Lung Neoplasms / drug therapy. Lung Neoplasms / immunology

[MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / immunology. Adult. Aged. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / immunology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / immunology. Female. Humans. Immunotherapy, Active / methods. Male. Middle Aged. Neoplasm Staging. Receptor, Epidermal Growth Factor / metabolism. Survival Analysis. Treatment Outcome

Genetic Alliance. consumer health - Factor II Deficiency.

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

[CommentIn] J Clin Oncol. 2008 Mar 20;26(9):1402-3 [18349390.001]

(PMID = 18349395.001).

[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] Clinical Trial, Phase II; Comparative Study; Journal Article; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Cancer Vaccines; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears.

OBJECTIVES: A diagnosis in pulmonary onco-cytopathology primarily necessitates distinguishing small cell carcinoma (SCLC) from non-small cell carcinoma (NSCLC), which includes squamous cell carcinoma and adenocarcinoma.

Lately, p63 antibody has been used for distinguishing squamous cell carcinoma from SCLC and adenocarcinoma.

RESULTS: Out of 100 cases, 21 were cytologically diagnosed as squamous cell carcinoma.

Twenty of these showed 2+ or 3+ p63 positivity, whereas one, which was adenocarcinoma on histology, showed 1+ staining.

Of seven cases cytologically diagnosed as adenocarcinoma, six showed no p63 staining, whereas one, which was squamous cell carcinoma on histology, showed 1+ staining.

The former three were found to be SCLC on histology while the latter was squamous cell carcinoma.

The former eight were adenocarcinoma on histology and the latter two were squamous cell carcinoma.

The 10 cases that showed 1+ p63 staining were adenocarcinomas (n = 5), squamous cell carcinoma (n = 4) and NSCLC, not otherwise specified (n = 1).

Overall sensitivity of p63 for squamous cell carcinoma was 100% and specificity was 90.4%.

CONCLUSIONS: p63 immunostaining on processed cytology smears can be used to help identify squamous cell carcinoma.

Its diffuse expression was specific for squamous cell carcinoma while focal staining was also seen in adenocarcinoma.

[MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Trans-Activators / metabolism. Tumor Suppressor Proteins / metabolism

[MeSH-minor] Adenocarcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Bronchoalveolar Lavage / methods. Bronchoalveolar Lavage Fluid / cytology. Carcinoma, Non-Small-Cell Lung / diagnosis. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Transcription Factors

MedlinePlus Health Information. consumer health - Lung Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19744186.001).

[ISSN] 1365-2303

[Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology

[ISO-abbreviation] Cytopathology

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [A randomized, prospective, multi-centre clinical trial of NP regimen (vinorelbine+cisplatin) plus Gensing Rg3 in the treatment of advanced non-small cell lung cancer patients].

The aim of this study is to observe the clinical anticancer effect of Rg3 in combination with chemotherapy regimen NP (vinorelbine+cisplatin) in advanced non-small cell lung cancer (NSCLC).

Types of pathology: adenocarcinoma, 71; squamous cell carcinoma, 29; adenosquamous carcinoma, 8; others, 7.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21172156.001).

[ISSN] 1009-3419

[Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer

[ISO-abbreviation] Zhongguo Fei Ai Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Approval summary: pemetrexed maintenance therapy of advanced/metastatic nonsquamous, non-small cell lung cancer (NSCLC).

Food and Drug Administration approved pemetrexed injection (Alimta® Injection; Eli Lilly and Company, Indianapolis, IN) for maintenance treatment of patients with locally advanced or metastatic nonsquamous non-small cell lung cancer whose disease has not progressed after four cycles of platinum-based doublet induction chemotherapy.

[MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Drug Approval. Glutamates / therapeutic use. Guanine / analogs & derivatives. Lung Neoplasms / drug therapy

[MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / pathology. Double-Blind Method. Female. Humans. Male. Middle Aged. Neoplasm Staging. Pemetrexed. Placebos. Thymidylate Synthase / antagonists & inhibitors. Treatment Outcome. United States. United States Food and Drug Administration

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

Genetic Alliance. consumer health - Metastatic cancer.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. PEMETREXED .

Hazardous Substances Data Bank. GUANINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer. 2006 Oct 1;107(7):1589-96 [16955506.001]

[Cites] Lung Cancer. 2006 May;52(2):155-63 [16569462.001]

[Cites] Oncologist. 2007 Apr;12(4):451-64 [17470688.001]

[Cites] J Natl Cancer Inst Monogr. 2007;(37):27-30 [17951228.001]

[Cites] J Clin Oncol. 2007 Nov 10;25(32):5133-40 [17991933.001]

[Cites] J Clin Oncol. 2008 Jul 20;26(21):3543-51 [18506025.001]

[Cites] Oncologist. 2009 Mar;14(3):253-63 [19221167.001]

[Cites] Oncologist. 2009 Sep;14(9):930-5 [19737998.001]

[Cites] Oncology (Williston Park). 2009 Nov 30;23(13):1133-40 [20043461.001]

[Cites] Oncologist. 2010;15(1):3-5 [20086166.001]

[Cites] J Clin Oncol. 2001 Mar 1;19(5):1336-43 [11230476.001]

[Cites] J Clin Oncol. 2002 Mar 1;20(5):1335-43 [11870177.001]

[Cites] J Clin Oncol. 2002 Nov 1;20(21):4285-91 [12409326.001]

[Cites] Biochem Pharmacol. 2003 Aug 1;66(3):431-8 [12907242.001]

[Cites] J Clin Oncol. 2004 Jan 15;22(2):330-53 [14691125.001]

[Cites] J Clin Oncol. 2004 May 1;22(9):1589-97 [15117980.001]

[Cites] Cancer Treat Rep. 1982 Mar;66(3):439-49 [7060033.001]

[Cites] Lung Cancer. 2005 Feb;47(2):253-9 [15639724.001]

[Cites] Oncologist. 2005 Jun-Jul;10(6):363-8 [15967829.001]

[Cites] Cancer. 2006 Apr 1;106(7):1595-601 [16489621.001]

[Cites] Ann Oncol. 2006 Mar;17 Suppl 2:ii67-70 [16608989.001]

[Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]

(PMID = 21148615.001).

[ISSN] 1549-490X

[Journal-full-title] The oncologist

[ISO-abbreviation] Oncologist

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glutamates; 0 / Placebos; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; EC 2.1.1.45 / Thymidylate Synthase

[Other-IDs] NLM/ PMC3227931

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

INTRODUCTION: The lung cancers are among the five most frequent cancers (and incidence continues to increase in men and females), with the highest percentage of mortality and an obvious stagnation of surviving rates, in spite of therapeutic improvements.

STATE OF ART: The lung cancers constitute a more mixed group than expected, with unpredictable behaviours and sensitivities to treatments.

The detection of early small lesions allowing a drastic surgery and an adjuvant chemotherapy improve the prognostic, if we can differentiate precisely and effectively the resectable tumors from the others.

PERSPECTIVES: The analysis of the earliest radio-clinical, histological and surgical studies associated with the most recent technical evolutions of multidetector CT scan and PET scan, among others, improve our understanding and organization of screenings, radio-clinic and histologic diagnostics, as well as the evaluation of the tumoral extension of non small cell lung carcinomas (NSCLC).

CONCLUSION: Notably, the WHO histological classification of lung cancer, the diagnostic algorithms of solitary nodules, the mediastinal lymph nodes mapping and the TNM staging are so redefined to achieve effective improvements on the prognosis of such cancers.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Lung Neoplasms / diagnosis

[MeSH-minor] Adenocarcinoma / diagnosis. Humans. Lymphatic Metastasis. Mediastinum. Neoplasm Staging

MedlinePlus Health Information. consumer health - Lung Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18971827.001).

[ISSN] 0761-8425

[Journal-full-title] Revue des maladies respiratoires

[ISO-abbreviation] Rev Mal Respir

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Microvessel density and expression of thrombospondin-1 in non-small cell lung cancer and their correlation with clinicopathological features.

Microvessel density and thrombospondin-1 (TSP-1) expression were analysed in 42 non-small cell lung cancer (NSCLC) specimens and 40 normal lung tissue specimens using immunohistochemistry.

A statistically significant inverse correlation was observed between TSP-1 expression and microvessel density in squamous cell carcinoma but not in adenocarcinoma.

The lack of correlation between microvessel density and TSP-1 expression in adenocarcinoma suggests that the mechanism of tumour inhibition by TSP-1 varies according to histological type.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / blood supply. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / blood supply. Lung Neoplasms / metabolism. Microvessels / pathology. Thrombospondin 1 / metabolism

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 = 19383251.001).

[ISSN] 0300-0605

[Journal-full-title] The Journal of international medical research

[ISO-abbreviation] J. Int. Med. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Thrombospondin 1

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A phase II study of concurrent carboplatin and paclitaxel and thoracic radiotherapy for completely resected stage II and IIIA non-small cell lung cancer.

BACKGROUND: To determine the feasibility of combining concurrent carboplatin/paclitaxel and thoracic radiotherapy (TRT) for completely resected stage II and IIIA non-small cell lung cancer.

METHODS: Eligibility stipulated gross total resections with involved lymph nodes (N1 or N2), pathologic stage II or IIIA non-small cell lung cancer.

Patients with adenocarcinoma had a 5-year overall survival of 28% versus 68% for all other cell types.

CONCLUSIONS: Our results support the Radiation Therapy Oncology Group 97-05 findings and suggest that with new and better tolerated chemotherapy regimens the strategy of concurrent TRT and chemotherapy after completely resected stage II and IIIA non-small cell lung cancer should be further explored.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / radiotherapy. Lung Neoplasms / drug therapy. Lung Neoplasms / radiotherapy. Neoplasm Invasiveness / pathology

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. TAXOL .

Hazardous Substances Data Bank. CARBOPLATIN .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17409799.001).

[ISSN] 1556-1380

[Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

[ISO-abbreviation] J Thorac Oncol

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article

[Publication-country] United States

[Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analysis of host- and tumor-derived proteinases using a custom dual species microarray reveals a protective role for stromal matrix metalloproteinase-12 in non-small cell lung cancer.

We used a customized Affymetrix protease microarray (Hu/Mu ProtIn chip) designed to distinguish human and mouse genes to analyze the expression of proteases and protease inhibitors in lung cancer.

Using an orthotopic lung cancer model, we showed that murine matrix metalloproteinase (MMP)-12, MMP-13, and cathepsin K were up-regulated in tumor tissue compared with normal mouse lung.

To determine the relevance of stromal proteases detected using this model system, we compared the results to an analysis of human lung adenocarcinoma specimens using the U133 Plus 2.0 Affymetrix microarray.

MMP-12, MMP-13, and cathepsin K showed an increase in expression in human tumors compared with normal lung similar to that seen in the orthotopic model.

Immunohistochemical analysis confirmed MMP-12 expression in the stroma of human lung tumor samples.

To determine the biological relevance of stromal MMP-12, murine Lewis lung carcinoma cells were injected into the tail vein of syngeneic wild-type (WT) and MMP-12-null mice.

MMP-12-null and WT mice developed equivalent numbers of lung tumors; however, there was a 2-fold increase in the number of tumors that reached >2 mm in diameter in MMP-12-null mice compared with WT controls.

These results show a protective role for stromal MMP-12 in lung tumor growth.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Lung Neoplasms / genetics. Matrix Metalloproteinase 12 / genetics. Oligonucleotide Array Sequence Analysis

[MeSH-minor] Animals. DNA Primers. DNA-Binding Proteins / deficiency. Genes, Reporter. Humans. Lung / enzymology. Mice. Mice, Inbred C57BL. Mice, Knockout. Polymerase Chain Reaction. Stromal Cells / enzymology. Stromal Cells / pathology

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16912171.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NHLBI NIH HHS / HL / 1 P01 HL6744-01; United States / NCI NIH HHS / CA / P30 CA68485; United States / NIDDK NIH HHS / DK / P30 DK58404; United States / NCI NIH HHS / CA / P50 CA90949; United States / NIDDK NIH HHS / DK / P60 DK20593; United States / NCI NIH HHS / CA / T32 CA009385

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Rag2 protein, mouse; EC 3.4.24.65 / Matrix Metalloproteinase 12

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Efficacy of gefitinib on advanced non-small cell lung cancer in expanded access program (EAP)].

BACKGROUND & OBJECTIVE: Gefitinib is a selective inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, and has been used in treating advanced non-small cell lung cancer (NSCLC).

[MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use

[MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Alanine Transaminase / blood. Diarrhea / chemically induced. Exanthema / chemically induced. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Survival Rate. Young Adult

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Lung Cancer.

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 = 17166387.001).

[Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer

[ISO-abbreviation] Ai Zheng

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.6.1.2 / Alanine Transaminase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: Effusion samples were collected from 62 patients with malignant PE caused by lung cancer and from 64 patients with tuberculous pleurisy.

[MeSH-minor] Adenocarcinoma / complications. Adult. Aged. Carcinoma, Small Cell / complications. Diagnosis, Differential. Female. Humans. Lung Neoplasms / complications. Male. Middle Aged. Pleural Effusion / microbiology. ROC Curve. Sensitivity and Specificity. Tuberculosis, Pulmonary / complications

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19275801.001).

[ISSN] 1027-3719

[Journal-full-title] The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease

[ISO-abbreviation] Int. J. Tuberc. Lung Dis.

[Language] eng

[Publication-type] Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Endostatins; 0 / Vascular Endothelial Growth Factor A

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Frequent inactivation of RAMP2, EFEMP1 and Dutt1 in lung cancer by promoter hypermethylation.

PURPOSE: The goal of this study is to identify novel genes frequently silenced by promoter hypermethylation in lung cancer.

EXPERIMENTAL DESIGNS: Bioinformatic analysis was done to identify candidate genes significantly down-regulated in lung cancer.

Methylation-specific PCR was developed and used to analyze DNA methylation in cell lines and clinical specimen.

Pathologic and functional analyses were done to study the role of one candidate gene, receptor activity-modifying protein 2 (RAMP2), in suppressing lung cancer cell growth.

RESULTS: Among 54 candidate genes down-regulated in lung cancer, 31 were found to contain CpG islands in their promoters.

Six of these 31 genes could be reactivated by 5-aza-2'-deoxycytidine in at least four of six lung cancer cell lines analyzed.

Promoter hypermethylation of RAMP2, epidermal growth factor-containing fibulin-like extracellular matrix protein 1, and deleted in U Twenty Twenty cells was detected in 36% to 77% of 22 lung cancer cell lines and in 38% to 50% of 32 primary lung tumors, whereas hypermethylathion of these genes was rarely found in the matched normal samples.

The methylation frequencies of these genes in lung cancer were similar to those of commonly used methylation markers, such as RAS association domain family protein 1A, p16, and methylguanine-DNA methyltransferase.

Immunohistochemistry showed that RAMP2 was down-regulated in a majority of lung tumors, and RAMP2 down-regulation was correlated with high tumor grade.

Ectopic expression of RAMP2 inhibited lung cancer cell growth and caused apoptotic cell death.

Knockdown of RAMP2 by RNA interference stimulated cell proliferation.

CONCLUSIONS: Studying the newly identified genes may provide new insight into lung tumorigenesis.

These genes might be useful as molecular markers of lung cancer.

Genetic Alliance. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. AZACITIDINE .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17671114.001).

[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 / R01 CA106348; United States / NCI NIH HHS / CA / CA106348; United States / NCI NIH HHS / CA / CA90440

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / EFEMP1 protein, human; 0 / Extracellular Matrix Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / RAMP2 protein, human; 0 / Receptor Activity-Modifying Protein 2; 0 / Receptor Activity-Modifying Proteins; 0 / Receptors, Immunologic; 0 / roundabout protein; M801H13NRU / Azacitidine

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

One hundred and fifty-six primary lung cancers undergone for surgical resection were examined.

Overall reactivity for SCGB3A2 was observed in 116 (74.4%) of 156 primary lung cancers.

SCGB3A2 was predominantly expressed in adenocarcinomas (86.5%), compared with squamous cell carcinomas (50.0%) and small cell carcinomas (42.9%).

[MeSH-major] Adenocarcinoma / chemistry. Carcinoma, Small Cell / chemistry. Carcinoma, Squamous Cell / chemistry. Lung Neoplasms / chemistry. Uteroglobin / analysis

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Respir Crit Care Med. 2006 May 1;173(9):958-64 [16456148.001]

[Cites] J Biol Chem. 2004 Dec 24;279(52):54358-68 [15485815.001]

[Cites] Mod Pathol. 1999 Mar;12(3):318-24 [10102618.001]

[Cites] Ann N Y Acad Sci. 2000;923:193-201 [11193757.001]

[Cites] Ann N Y Acad Sci. 2000;923:234-48 [11193760.001]

[Cites] Ann N Y Acad Sci. 2000;923:249-67 [11193761.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9796-801 [11481438.001]

[Cites] Mol Endocrinol. 2001 Nov;15(11):2021-36 [11682631.001]

[Cites] Am J Hum Genet. 2002 Mar;70(3):718-25 [11813133.001]

[Cites] Appl Immunohistochem Mol Morphol. 2002 Jun;10(2):103-9 [12051626.001]

[Cites] Mech Dev. 2002 Jun;114(1-2):201-4 [12175512.001]

[Cites] Mod Pathol. 2002 Oct;15(10):1058-67 [12379752.001]

[Cites] Cytogenet Genome Res. 2002;97(1-2):120-7 [12438750.001]

[Cites] Am J Respir Crit Care Med. 2002 Dec 1;166(11):1498-509 [12406855.001]

[Cites] Hum Pathol. 2003 Jun;34(6):597-604 [12827614.001]

[Cites] J Immunol. 2003 Jul 15;171(2):924-30 [12847263.001]

[Cites] Int Arch Allergy Immunol. 2003 Aug;131(4):291-5 [12915772.001]

[Cites] Mol Cell Biol. 1994 Sep;14(9):5671-81 [8065304.001]

[Cites] J Biol Chem. 1995 Mar 24;270(12):6531-6 [7896788.001]

[Cites] Genes Dev. 1996 Jan 1;10(1):60-9 [8557195.001]

[Cites] Mol Cell Biol. 1996 May;16(5):2056-64 [8628271.001]

[Cites] J Biol Chem. 1996 Mar 22;271(12):6881-8 [8636114.001]

[Cites] Mod Pathol. 1996 Apr;9(4):445-52 [8729987.001]

[Cites] J Clin Pathol. 1997 Jan;50(1):30-2 [9059352.001]

[Cites] Cell Growth Differ. 1998 Jun;9(6):475-85 [9663466.001]

[Cites] J Neurooncol. 1998 Dec;40(3):227-31 [10066094.001]

[Cites] Am J Physiol Lung Cell Mol Physiol. 2004 Dec;287(6):L1193-8 [15531759.001]

[Cites] Cancer Res. 2005 Nov 1;65(21):9659-69 [16266985.001]

[Cites] Immunol Lett. 2005 Feb 15;97(1):123-9 [15626484.001]

[Cites] Ann Oncol. 2006 Nov;17(11):1673-6 [16980598.001]

(PMID = 19418968.001).

[ISSN] 0016-2590

[Journal-full-title] Fukushima journal of medical science

[ISO-abbreviation] Fukushima J Med Sci

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z01 BC010449-06; United States / Intramural NIH HHS / / Z99 CA999999

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Nuclear Proteins; 0 / SCGB3A2 protein, human; 0 / Secretoglobins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; 9060-09-7 / Uteroglobin

[Other-IDs] NLM/ NIHMS102164; NLM/ PMC2743607

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: In vitro proliferation assays, and in vivo model studies in metastatic pancreatic carcinoma and subcutaneous xenograft melanoma and small-cell lung carcinoma models.

RESULTS: 17-DMAG emerged from screening studies as a potent geldanamycin analog, with the average concentration inhibiting the growth of the NCI anticancer cell line drug screen by 50% being 0.053 microM.

"Head to head" comparison with 17-allylamino-17-demethoxygeldanamycin (17-AAG, NSC 330507) revealed 17-DMAG to possess potent activity against certain cell types, e.g., MDA-MB-231 breast carcinoma and HL60-TB leukemia which were relatively insensitive to 17-AAG.

17-DMAG inhibited the growth of the AsPC-1 pancreatic carcinoma xenografts growing as intrahepatic metastases at doses of 6.7-10 mg/kg twice daily for 5 days administered orally under conditions where 17-AAG was without activity.

17-DMAG in an aqueous vehicle at 7.5-15 mg/kg per day for 3 days on days 1-3, 8-10 and 13-17, or 1-5 and 8-12 showed evidence of antitumor activity by the parenteral and oral routes in the MEXF 276 and MEXF 989 melanomas and by the parenteral route in the LXFA 629 and LXFS 650 adenocarcinoma and small-cell carcinoma models.

[MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / pathology. Melanoma / pathology. Quinones / pharmacology. Skin Neoplasms / pathology

[MeSH-minor] Animals. Benzoquinones. Cell Proliferation. Drug Screening Assays, Antitumor. Lactams, Macrocyclic. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / veterinary. Male. Mice. Mice, Nude. Solubility. Transplantation, Heterologous. Tumor Cells, Cultured

MedlinePlus Health Information. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - Melanoma.

MedlinePlus Health Information. consumer health - Skin Cancer.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15791458.001).

[ISSN] 0344-5704

[Journal-full-title] Cancer chemotherapy and pharmacology

[ISO-abbreviation] Cancer Chemother. Pharmacol.

[Language] eng

[Grant] United States / NCI NIH HHS / CM / N01-CM-270; United States / NCI NIH HHS / CM / N01-CM-97017; United States / NCI NIH HHS / CO / N01-CO 12400

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] Germany

[Chemical-registry-number] 0 / Benzoquinones; 0 / Lactams, Macrocyclic; 0 / Quinones; 001L2FE0M3 / 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection of oncogenic virus genomes and gene products in lung carcinoma.

We investigated a series of 122 cases of small cell lung carcinomas and non-small cell lung carcinomas for the presence of several viruses that are known to be oncogenic in humans.

None of the cases displayed a single positive tumour cell for all the viruses tested whatever the technique applied.

Taken together, our data strongly suggest that the conventional human oncogenic viruses (HPV, EBV, HCMV, HHV-8 and SV40) are unlikely to play some role in the development of lung carcinomas..

[MeSH-major] Genome, Viral. Lung Neoplasms / virology. Oncogenic Viruses / genetics. Viral Proteins / isolation & purification

[MeSH-minor] Adenocarcinoma / virology. Antibodies, Viral / analysis. Carcinoid Tumor / virology. Carcinoma, Large Cell / virology. Carcinoma, Neuroendocrine / virology. Carcinoma, Non-Small-Cell Lung / virology. Carcinoma, Small Cell / virology. Carcinoma, Squamous Cell / virology. Cytomegalovirus / genetics. DNA, Viral / isolation & purification. Herpesvirus 4, Human / genetics. Herpesvirus 8, Human / genetics. Humans. Immunohistochemistry. In Situ Hybridization. Papillomaviridae / genetics. Polymerase Chain Reaction. RNA, Viral / isolation & purification. Simian virus 40 / genetics

MedlinePlus Health Information. consumer health - Lung Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Lab Invest. 1992 Oct;67(4):457-64 [1331609.001]

[Cites] N Engl J Med. 1992 Apr 9;326(15):988-93 [1312224.001]

[Cites] Blood. 1994 Oct 15;84(8):2447-51 [7919364.001]

[Cites] Cancer Res. 1996 Oct 15;56(20):4820-5 [8841004.001]

[Cites] J Virol. 1997 Mar;71(3):2547-9 [9032398.001]

[Cites] Nat Med. 1997 Aug;3(8):908-12 [9256284.001]

[Cites] Cell. 1997 Oct 17;91(2):157-60 [9346233.001]

[Cites] Dev Biol Stand. 1998;94:147-52 [9776236.001]

[Cites] J Natl Cancer Inst. 1999 Jan 20;91(2):119-34 [9923853.001]

[Cites] Thorax. 1999 Aug;54(8):750-1 [10490415.001]

[Cites] Br J Cancer. 2005 Feb 28;92(4):747-50 [15700045.001]

[Cites] Int J Oncol. 2003 Jul;23(1):97-103 [12792781.001]

[Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]

[Cites] Oncogene. 2003 Aug 11;22(33):5173-80 [12910254.001]

[Cites] J Urol. 2003 Sep;170(3):998-1002 [12913758.001]

[Cites] Cancer Res. 2004 Feb 15;64(4):1359-68 [14973079.001]

[Cites] EMBO J. 2004 Jun 2;23(11):2269-80 [15141169.001]

[Cites] Diagn Cytopathol. 2004 Sep;31(3):196-7 [15349994.001]

[Cites] Lancet. 2004 Sep 25-Oct 1;364(9440):1157-66 [15451223.001]

[Cites] Lung. 1989;167(1):33-42 [2537916.001]

[Cites] J Natl Cancer Inst. 2000 May 3;92(9):690-8 [10793105.001]

[Cites] J Clin Pathol. 2000 Sep;53(9):676-84 [11041057.001]

[Cites] Hum Pathol. 2001 Jan;32(1):95-100 [11172301.001]

[Cites] Cancer Res. 2001 Apr 1;61(7):2799-803 [11306446.001]

[Cites] Cancer Res. 2002 Jun 15;62(12):3347-50 [12067971.001]

[Cites] Cancer Res. 2002 Sep 1;62(17):4876-8 [12208733.001]

[Cites] J Clin Virol. 2002 Aug;25 Suppl 2:S123-36 [12361763.001]

[Cites] Lancet. 2002 Nov 16;360(9345):1557-63 [12443594.001]

[Cites] Nat Rev Cancer. 2002 Dec;2(12):957-64 [12459734.001]

[Cites] J Clin Pathol. 2002 Dec;55(12):885-91 [12461047.001]

[Cites] Transplantation. 2002 Dec 15;74(11):1497-504 [12490781.001]

[Cites] Chest. 2003 Jan;123(1 Suppl):21S-49S [12527563.001]

[Cites] Lancet Infect Dis. 2003 Mar;3(3):131-40 [12614729.001]

[Cites] Exp Cell Res. 1993 Mar;205(1):91-100 [7681009.001]

(PMID = 15700034.001).

[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

[Chemical-registry-number] 0 / Antibodies, Viral; 0 / DNA, Viral; 0 / RNA, Viral; 0 / Viral Proteins

[Other-IDs] NLM/ PMC2361883

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Japanese Lung Cancer Registry Study: first prospective enrollment of a large number of surgical and nonsurgical cases in 2002.

PURPOSE: To investigate prognoses of lung cancer patients prospectively enrolled in the Japan Lung Cancer Registry Study.

METHODS: Patients newly diagnosed as having lung cancer exclusively in 2002 were enrolled.

The most frequent histology was adenocarcinoma (n = 8325, 56.7%), followed by squamous cell carcinoma (n = 3778, 26%) and small cell carcinoma (n = 1345, 9.2%).

The 5-year survival rates were 44.3% for all patients, 46.8% for those with non-small cell lung cancer, and 14.7% for those with small cell lung cancer.

According to the clinical stage of non-small cell lung cancer and small cell lung cancer, the 5-year survival rates were 79.4 and 52.7% for stage IA, 56.9 and 39.3% for IB, 49.0 and 31.7% for IIA, 42.3 and 29.9% for IIB, 30.9 and 17.2% for IIIA, 16.7 and 12.4% for IIIB, and 5.8 and 3.8% for IV, respectively.

[MeSH-major] Adenocarcinoma / pathology. Carcinoma, Large Cell / pathology. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Patient Participation. Small Cell Lung Carcinoma / pathology

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cohort Studies. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Prospective Studies. Registries. Survival Rate. Young Adult

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 = 20683209.001).

[ISSN] 1556-1380

[Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

[ISO-abbreviation] J Thorac Oncol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The results of concomitant and sequential chemoradiotherapy with cisplatin and etoposide in patients with locally advanced non-small cell lung cancer.

PURPOSE: To report on the treatment results and demographic characteristics of patients with locally advanced non small cell lung carcinoma (NSCLC) who were treated with concomitant or sequential chemoradiotherapy.

Histopathological diagnosis was epidermoid carcinoma in 96 (73%) patients, adenocarcinoma in 33 (25%) patients and large cell carcinoma in 3 (2%) patients.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17343331.001).

[ISSN] 1107-0625

[Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology

[ISO-abbreviation] J BUON

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.

PURPOSE: The EML4-ALK fusion oncogene represents a novel molecular target in a small subset of non-small-cell lung cancers (NSCLC).

PATIENTS AND METHODS: Patients with NSCLC were selected for genetic screening on the basis of two or more of the following characteristics: female sex, Asian ethnicity, never/light smoking history, and adenocarcinoma histology.

Eighteen of the 19 EML4-ALK tumors were adenocarcinomas, predominantly the signet ring cell subtype.

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.

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]

[Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]

[Cites] N Engl J Med. 2002 Jan 10;346(2):92-8 [11784875.001]

[Cites] BMC Cancer. 2002 Dec 26;2:37 [12502432.001]

[Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]

[Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]

[Cites] J Natl Cancer Inst. 2005 Mar 2;97(5):339-46 [15741570.001]

[Cites] Semin Roentgenol. 2005 Apr;40(2):90-7 [15898407.001]

[Cites] PLoS Med. 2005 Jan;2(1):e17 [15696205.001]

[Cites] N Engl J Med. 2005 Jul 14;353(2):133-44 [16014883.001]

[Cites] J Clin Oncol. 2005 Sep 1;23(25):5900-9 [16043828.001]

[Cites] Clin Cancer Res. 2006 Mar 1;12(5):1647-53 [16533793.001]

[Cites] J Clin Oncol. 2006 Jul 20;24(21):3340-6 [16785471.001]

[Cites] Br J Cancer. 2006 Oct 23;95(8):998-1004 [17047648.001]

[Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]

[Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]

[Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]

[Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]

[Cites] Nat Rev Cancer. 2008 Jan;8(1):11-23 [18097461.001]

[Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]

[Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]

[Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]

[Cites] Br J Cancer. 2008 May 6;98(9):1536-9 [18414414.001]

[Cites] J Clin Oncol. 2008 May 20;26(15):2442-9 [18458038.001]

[Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]

[Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]

[Cites] Clin Cancer Res. 2008 Oct 15;14(20):6618-24 [18927303.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]

[CommentIn] J Clin Oncol. 2009 Sep 10;27(26):4232-5 [19667260.001]

(PMID = 19667264.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / CA090578

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / anaplastic lymphoma kinase; S65743JHBS / gefitinib

[Other-IDs] NLM/ PMC2744268

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Effect of adenomatous polyposis coli(APC) promoter methylation on gene transcription in lung cancer cell lines].

In previous research, we detected APC promoter methylation in 47% lung tumor tissues.

This study was to analyze the effect of APC promoter methylation on the gene transcription in 3 lung cancer cell lines.

METHODS: The methylation status of APC promoter 1A in lung adenocarcinoma cell line SPCA1, small cell lung cancer cell line NCI-H446, and big cell lung cancer cell line NCI-H460 was detected by methylation-specific polymerase chain reaction (MSP) and microarray methylated cord blood DNA served as positive control, and unmethylated cord blood DNA served as negative control.

[MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. DNA Methylation. Genes, APC. Lung Neoplasms / metabolism. Transcription, Genetic

[MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Cell Line, Tumor. CpG Islands / genetics. Humans. Promoter Regions, Genetic. Small Cell Lung Carcinoma / metabolism. Small Cell Lung Carcinoma / pathology

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

Genetic Alliance. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

Hazardous Substances Data Bank. AZACITIDINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17562260.001).

[Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer

[ISO-abbreviation] Ai Zheng

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Quantitative analysis of DNA methylation profiles in lung cancer identifies aberrant DNA methylation of specific genes and its association with gender and cancer risk factors.

The global increase in lung cancer burden, together with its poor survival and resistance to classical chemotherapy, underscores the need for identification of critical molecular events involved in lung carcinogenesis.

Here, we have applied quantitative profiling of DNA methylation states in a panel of five cancer-associated genes (CDH1, CDKN2A, GSTP1, MTHFR, and RASSF1A) to a large case-control study of lung cancer.

Our analyses revealed a high frequency of aberrant hypermethylation of MTHFR, RASSF1A, and CDKN2A in lung tumors as compared with control blood samples, whereas no significant increase in methylation levels of GSTP1 and CDH1 was observed, consistent with the notion that aberrant DNA methylation occurs in a tumor-specific and gene-specific manner.

We observed a strong association between MTHFR hypermethylation in lung cancer and tobacco smoking, whereas methylation levels of CDH1, CDKN2A, GSTP1, and RASSF1A were not associated with smoking, indicating that tobacco smoke targets specific genes for hypermethylation.

Together, this study identifies aberrant DNA methylation patterns in lung cancer and thus exemplifies the mechanism by which environmental factors may interact with key genes involved in tumor suppression and contribute to lung cancer.

Genetic Alliance. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Rev Cancer. 2004 Sep;4(9):707-17 [15343277.001]

[Cites] Clin Cancer Res. 2003 Feb;9(2):743-8 [12576444.001]

[Cites] J Natl Cancer Inst. 1995 Feb 15;87(4):265-73 [7707417.001]

[Cites] Mol Cell Biol. 1996 Aug;16(8):4555-65 [8754856.001]

[Cites] Cancer Res. 1996 Nov 1;56(21):4862-4 [8895734.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11891-6 [9751761.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1999 Jun;8(6):513-8 [10385141.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):825-9 [10498402.001]

[Cites] Oncogene. 2004 Nov 18;23(54):8841-6 [15480421.001]

[Cites] Nat Rev Cancer. 2004 Dec;4(12):988-93 [15573120.001]

[Cites] J Natl Cancer Inst. 2005 Apr 20;97(8):567-76 [15840879.001]

[Cites] Biochemistry (Mosc). 2005 May;70(5):576-83 [15948711.001]

[Cites] Hum Genet. 2005 Aug;117(4):402-3 [15928902.001]

[Cites] Nat Rev Genet. 2006 Jan;7(1):21-33 [16369569.001]

[Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):989-95 [16467114.001]

[Cites] Cancer. 2006 Apr 15;106(8):1751-8 [16534787.001]

[Cites] Nat Genet. 2006 Dec;38(12):1378-85 [17072317.001]

[Cites] Mutagenesis. 2007 Mar;22(2):91-103 [17284773.001]

[Cites] Nat Rev Genet. 2007 Apr;8(4):286-98 [17339880.001]

[Cites] Carcinogenesis. 2007 Mar;28(3):507-18 [17183062.001]

[Cites] PLoS One. 2007;2(5):e399 [17476321.001]

[Cites] Hum Mol Genet. 2007 May 1;16(9):1072-7 [17350979.001]

[Cites] Nat Rev Cancer. 2003 Apr;3(4):253-66 [12671664.001]

[Cites] Cancer Res. 2003 Jun 15;63(12):3133-7 [12810640.001]

[Cites] Cancer Res. 2003 Jul 1;63(13):3743-6 [12839968.001]

[Cites] Biotechniques. 2003 Jul;35(1):152-6 [12866415.001]

[Cites] Int J Cancer. 2003 Oct 10;106(6):913-8 [12918069.001]

[Cites] Clin Cancer Res. 2003 Dec 1;9(16 Pt 1):5860-5 [14676107.001]

[Cites] Nat Rev Cancer. 2004 Feb;4(2):143-53 [14732866.001]

[Cites] Nucleic Acids Res. 2004;32(3):e38 [14973332.001]

[Cites] Carcinogenesis. 2004 Jun;25(6):1063-7 [14742312.001]

[Cites] IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438 [15285078.001]

[Cites] Biochim Biophys Acta. 2007 Sep;1776(1):58-85 [17692468.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):330-8 [18268116.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):645-54 [18349282.001]

[Cites] Nature. 2008 Apr 3;452(7187):633-7 [18385738.001]

[Cites] Nature. 2008 Apr 3;452(7187):638-42 [18385739.001]

[Cites] Int J Cancer. 2008 Jul 1;123(1):1-7 [18425819.001]

[Cites] Mutat Res. 2008 Jul-Aug;659(1-2):40-8 [18407786.001]

[Cites] Carcinogenesis. 2007 Jun;28(6):1334-40 [17389614.001]

[Cites] J Natl Cancer Inst. 2000 May 17;92(10):803-11 [10814675.001]

[Cites] Nat Genet. 2000 Jul;25(3):315-9 [10888881.001]

[Cites] J Clin Oncol. 2000 Sep 15;18(18):3221-9 [10986054.001]

[Cites] Cancer Res. 2000 Nov 1;60(21):5954-8 [11085511.001]

[Cites] Hum Mol Genet. 2001 Mar 1;10(5):433-43 [11181567.001]

[Cites] Cancer Res. 2001 Apr 1;61(7):3105-9 [11306494.001]

[Cites] Cancer Res. 2001 Apr 15;61(8):3419-24 [11309302.001]

[Cites] Cancer Res. 2001 Oct 1;61(19):7110-7 [11585742.001]

[Cites] Eur J Cancer. 2001 Oct;37 Suppl 8:S4-66 [11602373.001]

[Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]

[Cites] Cancer Res. 2002 Aug 1;62(15):4519-24 [12154064.001]

[Cites] Int J Cancer. 2003 Jan 10;103(2):153-60 [12455028.001]

[Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1827-31 [1542678.001]

(PMID = 19118009.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA122396-01; United States / NCI NIH HHS / CA / R03 CA122396-02; United States / NCI NIH HHS / CA / R03 CA122396-01

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CDH1 protein, human; 0 / Cadherins; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi

[Other-IDs] NLM/ NIHMS77570; NLM/ PMC2613548