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1
adenocarcinoma and small cell lung carcinoma 2005:2010[pubdate] *count=100
2490 results
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adenocarcinoma and small cell lung carcinoma
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Items 1 to 100 of about 2490
1.
Takeda S, Funakoshi Y, Kadota Y, Koma M, Maeda H, Kawamura S, Matsubara Y:
Fall in diffusing capacity associated with induction therapy for lung cancer: a predictor of postoperative complication?
Ann Thorac Surg
; 2006 Jul;82(1):232-6
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[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
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consumer health - After Surgery
.
MedlinePlus Health Information.
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.
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
.
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(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
2.
Xu N, Shen P, Zhang XC, Yu LF, Bao HY, Shi GM, Huang S, Chen J, Mou HB, Fang WJ:
Phase II trial of a 2-h infusion of gemcitabine plus carboplatin as first-line chemotherapy for advanced non-small-cell lung cancer.
Cancer Chemother Pharmacol
; 2007 Jan;59(1):1-7
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[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.
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.
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.
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CARBOPLATIN
.
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(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
3.
Pao W, Miller VA, Politi KA, Riely GJ, Somwar R, Zakowski MF, Kris MG, Varmus H:
Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.
PLoS Med
; 2005 Mar;2(3):e73
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[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.
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.
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.
NCI CPTAC Assay Portal.
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.
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[Cites]
Nat Rev Drug Discov. 2004 Dec;3(12):1001-10
[
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(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
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4.
Birnbaum A, Ready N:
Gefitinib therapy for non-small cell lung cancer.
Curr Treat Options Oncol
; 2005 Jan;6(1):75-81
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[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
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[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]
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[
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]
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]
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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
5.
Oremek GM, Sauer-Eppel H, Bruzdziak TH:
Value of tumour and inflammatory markers in lung cancer.
Anticancer Res
; 2007 Jul-Aug;27(4A):1911-5
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[Title]
Value of tumour and inflammatory markers in
lung
cancer.
Serum samples were also obtained from 20 patients suffering from bronchitis, 20 with
lung
fibrosis and 30 with sarcoidosis.
Moreover, serum marker levels were analyzed in 139 patients with different pulmonary malignancies: 29 patients with
adenocarcinoma
, 30 patients with squamous
cell carcinoma
, 80 patients with
small cell lung
cancer (SCLC).
In conclusion, when serum tumour markers are abnormally elevated in patients with
lung
cancer, CEA, CYFRA 21-1, NSE and ProGRP are useful clinical markers, good indicators of disease extent and may have important prognostic value.
[MeSH-major]
Biomarkers, Tumor / blood. Inflammation / blood.
Lung
Neoplasms / diagnosis
[MeSH-minor]
Antigens, Neoplasm / blood. Area Under Curve. C-Reactive Protein / analysis. Carcinoembryonic Antigen / blood.
Carcinoma
, Non-
Small
-
Cell Lung
/ blood.
Carcinoma
, Non-
Small
-
Cell Lung
/ diagnosis.
Carcinoma
,
Small Cell
/ blood.
Carcinoma
,
Small Cell
/ diagnosis.
Carcinoma
, Squamous
Cell
/ blood.
Carcinoma
, Squamous
Cell
/ diagnosis. Humans. Immunoassay. Keratin-19. Keratins / blood.
Lung
Diseases / blood.
Lung
Diseases / diagnosis. Peptide Fragments / blood. Peptides / blood. Phosphopyruvate Hydratase / blood. ROC Curve. Recombinant Proteins / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / blood
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(PMID = 17649794.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / antigen CYFRA21.1; 0 / pro-gastrin-releasing peptide (31-98); 68238-35-7 / Keratins; 9007-41-4 / C-Reactive Protein; EC 4.2.1.11 / Phosphopyruvate Hydratase
6.
Thatcher N:
First- and second-line treatment of advanced metastatic non-small-cell lung cancer: a global view.
BMC Proc
; 2008;2 Suppl 2:S3
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[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.
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[Cites]
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[
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
7.
Zhu CQ, Popova SN, Brown ER, Barsyte-Lovejoy D, Navab R, Shih W, Li M, Lu M, Jurisica I, Penn LZ, Gullberg D, Tsao MS:
Integrin alpha 11 regulates IGF2 expression in fibroblasts to enhance tumorigenicity of human non-small-cell lung cancer cells.
Proc Natl Acad Sci U S A
; 2007 Jul 10;104(28):11754-9
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[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
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(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
8.
Suzuki C, Daigo Y, Ishikawa N, Kato T, Hayama S, Ito T, Tsuchiya E, Nakamura Y:
ANLN plays a critical role in human lung carcinogenesis through the activation of RHOA and by involvement in the phosphoinositide 3-kinase/AKT pathway.
Cancer Res
; 2005 Dec 15;65(24):11314-25
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[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
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(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
9.
von Eyben FE:
Epidermal growth factor receptor inhibition and non-small cell lung cancer.
Crit Rev Clin Lab Sci
; 2006;43(4):291-323
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[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
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(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
10.
Martoni A, Marino A, Sperandi F, Giaquinta S, Di Fabio F, Melotti B, Guaraldi M, Palomba G, Preti P, Petralia A, Artioli F, Picece V, Farris A, Mantovani L:
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.
Eur J Cancer
; 2005 Jan;41(1):81-92
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[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
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.
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VINBLASTINE
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[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
11.
Nassar H, Albores-Saavedra J, Klimstra DS:
High-grade neuroendocrine carcinoma of the ampulla of vater: a clinicopathologic and immunohistochemical analysis of 14 cases.
Am J Surg Pathol
; 2005 May;29(5):588-94
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[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
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(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
12.
Tsurutani J, Fukuoka J, Tsurutani H, Shih JH, Hewitt SM, Travis WD, Jen J, Dennis PA:
Evaluation of two phosphorylation sites improves the prognostic significance of Akt activation in non-small-cell lung cancer tumors.
J Clin Oncol
; 2006 Jan 10;24(2):306-14
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[Title]
Evaluation of two phosphorylation sites improves the prognostic significance of Akt activation in non-
small
-
cell lung
cancer tumors.
PURPOSE: Akt is a serine/threonine kinase that has been implicated in
lung
tumorigenesis
and lung
cancer therapeutic resistance.
Full activation of Akt requires two phosphorylation events, but only one site of phosphorylation (S473) has been evaluated thus far in clinical non-
small
-
cell lung
cancer (NSCLC) specimens, which has resulted in conflicting results regarding the prognostic significance of Akt activation in NSCLC.
PATIENTS AND METHODS: Phosphospecific antibodies against T308 and S473 were validated and used in an immunohistochemical analysis of tissue microarray slides containing NSCLC specimens (n = 300) and surrounding
lung
tissue specimens (n = 100).
When Akt activation was defined by using both sites of phosphorylation, Akt activation was specific for NSCLC tumors versus surrounding tissue (73.4% v 0%; P < .05), was higher in
adenocarcinoma
than in squamous
cell carcinoma
(78.1% v 68.5%; P = .040), and was associated with shorter overall survival for all stages of disease (log-rank P = .041).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism.
Lung
Neoplasms / metabolism. Proto-Oncogene Proteins c-akt / metabolism
[MeSH-minor]
Adenocarcinoma
/ metabolism. Adult. Aged. Aged, 80 and over.
Carcinoma
, Squamous
Cell
/ metabolism.
Cell
Line, Tumor. Female. Humans. Male. Middle Aged. Phosphorylation. Prognosis
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(PMID = 16330671.001).
[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 / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
13.
Zhou W, Heist RS, Liu G, Neuberg DS, Asomaning K, Su L, Wain JC, Lynch TJ, Giovannucci E, Christiani DC:
Polymorphisms of vitamin D receptor and survival in early-stage non-small cell lung cancer patients.
Cancer Epidemiol Biomarkers Prev
; 2006 Nov;15(11):2239-45
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[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
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(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
14.
Yan S, Shun-Chang J, Li C, Jie L, Ya-Li L, Ling-Xiong W:
Topoisomerase II alpha expression and the benefit of adjuvant chemotherapy for postoperative patients with non-small cell lung cancer.
BMC Cancer
; 2010;10:621
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[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
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Ann Oncol. 1999;10 Suppl 5:S83-6
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10582146.001
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]
(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
15.
Tanaka T, Matsuoka M, Sutani A, Gemma A, Maemondo M, Inoue A, Okinaga S, Nagashima M, Oizumi S, Uematsu K, Nagai Y, Moriyama G, Miyazawa H, Ikebuchi K, Morita S, Kobayashi K, Hagiwara K:
Frequency of and variables associated with the EGFR mutation and its subtypes.
Int J Cancer
; 2010 Feb 1;126(3):651-5
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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
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(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
16.
Gao Z, Guo C, Jin X:
[The role of thyroid transcription factor-1 DNA binding activity in lung cancer.].
Zhongguo Fei Ai Za Zhi
; 2009 Feb 20;12(2):127-30
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[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.
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(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
17.
Zhou CC, Zhou SW, Pan H, Su B, Gao ZQ:
[Detection of epidermal growth factor receptor mutations in non-small cell lung cancer by real-time PCR using TaqMan-MGB probes].
Zhonghua Zhong Liu Za Zhi
; 2007 Feb;29(2):119-23
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[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
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(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
18.
Kayser K, Radziszowski D, Bzdyl P, Sommer R, Kayser G:
Towards an automated virtual slide screening: theoretical considerations and practical experiences of automated tissue-based virtual diagnosis to be implemented in the Internet.
Diagn Pathol
; 2006;1:10
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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.
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9739414.001
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(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
19.
Rena O, Massera F, Robustellini M, Papalia E, Delfanti R, Lisi E, Pirondini E, Turello D, Casadio C:
Use of the proposals of the international association for the study of lung cancer in the forthcoming edition of lung cancer staging system to predict long-term prognosis of operated patients.
Cancer J
; 2010 Mar-Apr;16(2):176-81
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[Title]
Use of the proposals of the international association for the study of
lung
cancer in the forthcoming edition of
lung
cancer staging system to predict long-term prognosis of operated patients.
PURPOSE: To evaluate the utility of the proposals of the International Association for the Study of
Lung
Cancer (IASLC) in the forthcoming 7th edition of
lung
cancer staging system to classify patients submitted to radical surgical resection of non-
small cell lung
cancer and to compare their value in predicting long-term prognosis with the existing 6th edition of the American Joint Committee on Cancer (AJCC)/Union Internationale Contre le Cancer (UICC) TNM classification.
METHODS: Nine hundred twenty-one patients received an anatomic resection and hilar-mediastinal dissection for primary non-
small cell lung
cancer during the period 1990 to 2005.
DISCUSSION: The proposals of IASLC in the forthcoming 7th edition of the
lung
cancer staging system are demonstrated to be better able to separate prognostically distinct groups of patients operated for non-
small cell lung
cancer than the accepted existing 6th AJCC/UICC TNM classification.
[MeSH-major]
Adenocarcinoma
/ pathology.
Carcinoma
, Large
Cell
/ pathology.
Carcinoma
, Non-
Small
-
Cell Lung
/ pathology.
Carcinoma
, Squamous
Cell
/ pathology.
Lung
Neoplasms / pathology
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over.
Carcinoma
, Bronchogenic / classification.
Carcinoma
, Bronchogenic / pathology.
Carcinoma
, Bronchogenic / surgery. Female. Follow-Up Studies. Humans. International Cooperation. Male. Middle Aged. Neoplasm Staging. Prognosis. Young Adult
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(PMID = 20404615.001).
[ISSN]
1540-336X
[Journal-full-title]
Cancer journal (Sudbury, Mass.)
[ISO-abbreviation]
Cancer J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
20.
Singh J, Naran A, Misso NL, Rigby PJ, Thompson PJ, Bhoola KD:
Expression of kallikrein-related peptidases (KRP/hK5, 7, 6, 8) in subtypes of human lung carcinoma.
Int Immunopharmacol
; 2008 Feb;8(2):300-6
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[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
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(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
21.
Sabloff BS, Wistuba II, Erasmus JJ:
Cystic bronchioloalveolar cell carcinoma.
J Thorac Imaging
; 2005 May;20(2):110-4
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[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
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(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
22.
Meniga IN, Tiljak MK, Ivankovic D, Aleric I, Zekan M, Hrabac P, Mazuranic I, Puljic I:
Prognostic value of computed tomography morphologic characteristics in stage I non-small-cell lung cancer.
Clin Lung Cancer
; 2010 Mar 1;11(2):98-104
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[Title]
Prognostic value of computed tomography morphologic characteristics in stage I non-
small
-
cell lung
cancer.
PATIENTS AND METHODS: All patients underwent surgery because of stage IA or IB non-
small
-
cell lung carcinoma
(NSCLC).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ radiography.
Lung
Neoplasms / radiography
[MeSH-minor]
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ radiography.
Adenocarcinoma
/ surgery.
Adenocarcinoma
, Bronchiolo-Alveolar / pathology.
Adenocarcinoma
, Bronchiolo-Alveolar / radiography.
Adenocarcinoma
, Bronchiolo-Alveolar / surgery.
Carcinoma
, Squamous
Cell
/ pathology.
Carcinoma
, Squamous
Cell
/ radiography.
Carcinoma
, Squamous
Cell
/ surgery. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome
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(PMID = 20199975.001).
[ISSN]
1938-0690
[Journal-full-title]
Clinical lung cancer
[ISO-abbreviation]
Clin Lung Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
23.
Teng XD:
[World Health Organization classification of tumours, pathology and genetics of tumours of the lung].
Zhonghua Bing Li Xue Za Zhi
; 2005 Aug;34(8):544-6
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[Title]
[World Health Organization classification of tumours, pathology and genetics of tumours of the
lung
].
[MeSH-major]
Lung
Neoplasms / classification.
Lung
Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
/ pathology.
Carcinoma
,
Small Cell
/ pathology.
Carcinoma
, Squamous
Cell
/ pathology. Diagnosis, Differential. Humans. World Health Organization
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(PMID = 16383307.001).
[ISSN]
0529-5807
[Journal-full-title]
Zhonghua bing li xue za zhi = Chinese journal of pathology
[ISO-abbreviation]
Zhonghua Bing Li Xue Za Zhi
[Language]
chi
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
China
24.
Burdak-Rothkamm S, Rübe CE, Nguyen TP, Ludwig D, Feldmann K, Wiegel T, Rübe C:
Radiosensitivity of tumor cell lines after pretreatment with the EGFR tyrosine kinase inhibitor ZD1839 (Iressa).
Strahlenther Onkol
; 2005 Mar;181(3):197-204
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[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
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(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
25.
Achille M, Gallegos-Ruiz M, Giaccone G, Soria JC:
Response to erlotinib in first-line treatment of non-small-cell lung cancer in a white male smoker with squamous-cell histology.
Clin Lung Cancer
; 2006 Nov;8(3):214-6
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[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
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(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
26.
Cai C, Zhang D, Lu P, Gao Y, Chang J:
[Expression and its significance of TSG101 in lung cancer tissue and lung cancer cell lines.].
Zhongguo Fei Ai Za Zhi
; 2008 Apr 20;11(2):172-7
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[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.
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(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
27.
Hainsworth JD, Cebotaru CL, Kanarev V, Ciuleanu TE, Damyanov D, Stella P, Ganchev H, Pover G, Morris C, Tzekova V:
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.
J Thorac Oncol
; 2010 Oct;5(10):1630-6
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[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
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(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
28.
Lu S, Zhang J, Zhou Z, Liao ML, He WZ, Zhou XY, Li ZM, Xiang JQ, Wang JJ, Chen HQ:
Synergistic inhibitory activity of zoledronate and paclitaxel on bone metastasis in nude mice.
Oncol Rep
; 2008 Sep;20(3):581-7
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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
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(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
29.
Wang J, Zhao W, Guo Y, Zhang B, Xie Q, Xiang D, Gao J, Wang B, Chen Z:
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.
Oncology
; 2009;76(6):420-9
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[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
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[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
30.
Lee NS, Park HS, Won JH, Hong DS, Uh ST, Lee SJ, Kim JH, Kim SK, Ahn MJ, Choi JH, Yang SC, Lee JA, Lee KS, Yim CY, Lee YC, Kim CS, Lee MH, Jung KD, Moon H, Lee YS:
Randomized, multi-center phase II trial of docetaxel plus cisplatin versus etoposide plus cisplatin as the first-line therapy for patients with advanced non-small cell lung cancer.
Cancer Res Treat
; 2005 Dec;37(6):332-8
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[Title]
Randomized, multi-center phase II trial of docetaxel plus cisplatin versus etoposide plus cisplatin as the first-line therapy for patients with advanced non-
small cell lung
cancer.
PURPOSE: We prospectively conducted a multi-center, open-label, randomized phase II trial to compare the efficacy and safety of docetaxel plus cisplatin (DC) and etoposide plus cisplatin (EC) for treating advanced stage non-
small cell lung
cancer (NSCLC).
The prognostic factors for longer survival were an earlier disease stage (stage III, p=0.0095), the responders to DC (p=0.0174) and the
adenocarcinoma
histology (p=0.0454).
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(PMID = 19956368.001).
[ISSN]
2005-9256
[Journal-full-title]
Cancer research and treatment : official journal of Korean Cancer Association
[ISO-abbreviation]
Cancer Res Treat
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2785933
[Keywords]
NOTNLM ; Cisplatin / Docetaxel / Etoposide / Non-small-cell lung carcinoma
31.
Eriksson SE, Prast-Nielsen S, Flaberg E, Szekely L, Arnér ES:
High levels of thioredoxin reductase 1 modulate drug-specific cytotoxic efficacy.
Free Radic Biol Med
; 2009 Dec 1;47(11):1661-71
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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.
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CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
AURANOFIN
.
Hazardous Substances Data Bank.
MENADIONE
.
Hazardous Substances Data Bank.
1-CHLORO-2,4-DINITROBENZENE
.
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(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
32.
Massard C, Tran Ba Loc P, Haddad V, Pignon JP, Girard P, Monnet I, Trédaniel J, Besse B, Soria JC:
Use of adjuvant chemotherapy in non-small cell lung cancer in routine practice.
J Thorac Oncol
; 2009 Dec;4(12):1504-10
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[Title]
Use of adjuvant chemotherapy in non-
small cell lung
cancer in routine practice.
BACKGROUND: For many years, surgery has been the standard treatment for patients with early-stage non-
small cell lung
cancer (NSCLC).
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic
Combined
Chemotherapy Protocols / therapeutic use.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Carcinoma
, Squamous
Cell
/ drug therapy.
Lung
Neoplasms / drug therapy
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(PMID = 19745763.001).
[ISSN]
1556-1380
[Journal-full-title]
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
[ISO-abbreviation]
J Thorac Oncol
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
33.
Voisin L, Julien C, Duhamel S, Gopalbhai K, Claveau I, Saba-El-Leil MK, Rodrigue-Gervais IG, Gaboury L, Lamarre D, Basik M, Meloche S:
Activation of MEK1 or MEK2 isoform is sufficient to fully transform intestinal epithelial cells and induce the formation of metastatic tumors.
BMC Cancer
; 2008;8:337
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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
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(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
34.
Duan Y, Yu LJ, Lu PO, Wang WZ:
[Correlation between SUV of (18)F-FDG PET-CT and the expression of GLUT1, MVD and Ki67 in non-small cell lung cancer].
Zhonghua Zhong Liu Za Zhi
; 2008 Oct;30(10):764-7
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[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
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(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
35.
Boukakis G, Patrinou-Georgoula M, Lekarakou M, Valavanis C, Guialis A:
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.
BMC Cancer
; 2010;10:434
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[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
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]
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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
36.
Zhang K, Li N, Chen Z, Shao K, Zhou F, Zhang C, Mu X, Wan J, Li B, Feng X, Shi S, Xiong M, Cao K, Wang X, Huang C, He J:
High expression of nuclear factor of activated T cells in Chinese primary non-small cell lung cancer tissues.
Int J Biol Markers
; 2007 Jul-Sep;22(3):221-5
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[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
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(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
37.
Neninger Vinageras E, de la Torre A, Osorio Rodríguez M, Catalá Ferrer M, Bravo I, Mendoza del Pino M, Abreu Abreu D, Acosta Brooks S, Rives R, del Castillo Carrillo C, González Dueñas M, Viada C, García Verdecia B, Crombet Ramos T, González Marinello G, Lage Dávila A:
Phase II randomized controlled trial of an epidermal growth factor vaccine in advanced non-small-cell lung cancer.
J Clin Oncol
; 2008 Mar 20;26(9):1452-8
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[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
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[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
38.
Luo L, Wang H, Ma H, Zou H, Li D, Zhou Y:
[Analysis of 41 cases of primary hypervascular non-small cell lung cancer treated with embolization of emulsion of chemotherapeutics and iodized oil].
Zhongguo Fei Ai Za Zhi
; 2010 May;13(5):540-3
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[Title]
[Analysis of 41 cases of primary hypervascular non-
small cell lung
cancer treated with embolization of emulsion of chemotherapeutics and iodized oil].
BACKGROUND AND OBJECTIVE: Transcatheter arterial chemotherapy and embolization is the main method in the treatment of
lung
cancer, but most of the reports do not study individually to
small cell lung
cancer (SCLC), non-
small cell lung
cancer (NSCLC), hypovascular and hypervascular
lung
cancer.
Suqamous
carcinoma
21 cases,
adenocarcinoma
15 cases and squamoadenocarcinoma 5 cases.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ therapy. Chemoembolization, Therapeutic. Iodized Oil / administration & dosage.
Lung
Neoplasms / therapy
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(PMID = 20677656.001).
[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
[Chemical-registry-number]
0 / Emulsions; 8001-40-9 / Iodized Oil
39.
Uke M, Rekhi B, Ajit D, Jambhekar NA:
The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears.
Cytopathology
; 2010 Feb;21(1):56-63
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[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
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(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
40.
Sun Y, Lin H, Zhu Y, Feng J, Chen Z, Li G, Zhang X, Zhang Z, Tang J, Shi M, Hao X, Han H:
[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].
Zhongguo Fei Ai Za Zhi
; 2006 Jun 20;9(3):254-8
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[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.
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(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
41.
Cohen MH, Cortazar P, Justice R, Pazdur R:
Approval summary: pemetrexed maintenance therapy of advanced/metastatic nonsquamous, non-small cell lung cancer (NSCLC).
Oncologist
; 2010;15(12):1352-8
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[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
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PEMETREXED
.
Hazardous Substances Data Bank.
GUANINE
.
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[Cites]
N Engl J Med. 2006 Dec 14;355(24):2542-50
[
17167137.001
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(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
42.
Alard S:
[NSCLC of early stage. Imaging exploration of the mediastinum].
Rev Mal Respir
; 2008 Oct;25(8 Pt 2):3S55-66
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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
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(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
43.
Chen ZJ, Le HB, Zhang YK, Qian LY, Li WD:
Microvessel density and expression of thrombospondin-1 in non-small cell lung cancer and their correlation with clinicopathological features.
J Int Med Res
; 2009 Mar-Apr;37(2):551-6
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[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
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(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
44.
Feigenberg SJ, Hanlon AL, Langer C, Goldberg M, Nicolaou N, Millenson M, Coia LR, Lanciano R, Movsas B:
A phase II study of concurrent carboplatin and paclitaxel and thoracic radiotherapy for completely resected stage II and IIIA non-small cell lung cancer.
J Thorac Oncol
; 2007 Apr;2(4):287-92
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[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
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.
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CARBOPLATIN
.
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(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
45.
Lockwood WW, Chari R, Coe BP, Thu KL, Garnis C, Malloff CA, Campbell J, Williams AC, Hwang D, Zhu CQ, Buys TP, Yee J, English JC, Macaulay C, Tsao MS, Gazdar AF, Minna JD, Lam S, Lam WL:
Integrative genomic analyses identify BRF2 as a novel lineage-specific oncogene in lung squamous cell carcinoma.
PLoS Med
; 2010 Jul 27;7(7):e1000315
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[Title]
Integrative genomic analyses identify BRF2 as a novel lineage-specific oncogene in
lung
squamous
cell carcinoma
.
BACKGROUND: Traditionally, non-
small cell lung
cancer is treated as a single disease entity in terms of systemic therapy.
Emerging evidence suggests the major subtypes--
adenocarcinoma
(AC) and squamous
cell carcinoma
(SqCC)--respond differently to therapy.
METHODS AND FINDINGS: We used an integrative genomics approach, combing high-resolution comparative genomic hybridization and gene expression microarray profiles, to compare AC and SqCC tumors in order to uncover alterations at the DNA level, with corresponding gene transcription changes, which are selected for during development of
lung
cancer subtypes.
Through the analysis of multiple independent cohorts of clinical tumor samples (>330), normal
lung
tissues and bronchial epithelial cells obtained by bronchial brushing in smokers without
lung
cancer, we identified the overexpression of BRF2, a gene on Chromosome 8p12, which is specific for development of SqCC of
lung
.
Genetic activation of BRF2, which encodes a RNA polymerase III (Pol III) transcription initiation factor, was found to be associated with increased expression of
small
nuclear RNAs (snRNAs) that are involved in processes essential for
cell
growth, such as RNA splicing.
Frequent activation of BRF2 in >35% preinvasive bronchial
carcinoma
in situ, as well as in dysplastic lesions, provides evidence that BRF2 expression is an early event in cancer development of this
cell
lineage.
CONCLUSIONS: This is the first study, to our knowledge, to show that the focal amplification of a gene in Chromosome 8p12, plays a key role in squamous
cell
lineage specificity of the disease.
Our data suggest that genetic activation of BRF2 represents a unique mechanism of SqCC
lung
tumorigenesis through the increase of Pol III-mediated transcription.
It can serve as a marker for
lung
SqCC and may provide a novel target for therapy.
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(PMID = 20668658.001).
[ISSN]
1549-1676
[Journal-full-title]
PLoS medicine
[ISO-abbreviation]
PLoS Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA070907; Canada / Canadian Institutes of Health Research / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / BRF2 protein, human; 0 / Biomarkers, Tumor; 0 / Transcription Factor TFIIIB
[Other-IDs]
NLM/ PMC2910599
46.
Acuff HB, Sinnamon M, Fingleton B, Boone B, Levy SE, Chen X, Pozzi A, Carbone DP, Schwartz DR, Moin K, Sloane BF, Matrisian LM:
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.
Cancer Res
; 2006 Aug 15;66(16):7968-75
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[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
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(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
47.
Zhang Y, Zhang L, Xu F, Wang ZQ, Zhao HY, Guan ZZ, Xu GC, Pan ZK:
[Efficacy of gefitinib on advanced non-small cell lung cancer in expanded access program (EAP)].
Ai Zheng
; 2006 Dec;25(12):1561-4
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[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
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(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
48.
Zhou WB, Bai M, Jin Y:
Diagnostic value of vascular endothelial growth factor and endostatin in malignant pleural effusions.
Int J Tuberc Lung Dis
; 2009 Mar;13(3):381-6
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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
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(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
49.
Yue W, Dacic S, Sun Q, Landreneau R, Guo M, Zhou W, Siegfried JM, Yu J, Zhang L:
Frequent inactivation of RAMP2, EFEMP1 and Dutt1 in lung cancer by promoter hypermethylation.
Clin Cancer Res
; 2007 Aug 1;13(15 Pt 1):4336-44
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[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.
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(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
50.
Tachihara-Yoshikawa M, Ishida T, Watanabe K, Sugawara A, Kanazawa K, Kanno R, Suzuki T, Niimi T, Kimura S, Munakata M:
Expression of secretoglobin3A2 (SCGB3A2) in primary pulmonary carcinomas.
Fukushima J Med Sci
; 2008 Dec;54(2):61-72
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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
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(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
51.
Hollingshead M, Alley M, Burger AM, Borgel S, Pacula-Cox C, Fiebig HH, Sausville EA:
In vivo antitumor efficacy of 17-DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin hydrochloride), a water-soluble geldanamycin derivative.
Cancer Chemother Pharmacol
; 2005 Aug;56(2):115-25
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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
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(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
52.
Brouchet L, Valmary S, Dahan M, Didier A, Galateau-Salle F, Brousset P, Degano B:
Detection of oncogenic virus genomes and gene products in lung carcinoma.
Br J Cancer
; 2005 Feb 28;92(4):743-6
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[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
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[Cites]
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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
53.
Sawabata N, Asamura H, Goya T, Mori M, Nakanishi Y, Eguchi K, Koshiishi Y, Okumura M, Miyaoka E, Fujii Y, Japanese Joint Committee for Lung Cancer Registry:
Japanese Lung Cancer Registry Study: first prospective enrollment of a large number of surgical and nonsurgical cases in 2002.
J Thorac Oncol
; 2010 Sep;5(9):1369-75
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[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
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(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
54.
Monego G, Lauriola L, Ramella S, D'Angelillo RM, Lanza P, Granone P, Ranelletti FO:
Parathyroid hormone-related peptide and parathyroid hormone-related peptide receptor type 1 expression in human lung adenocarcinoma.
Chest
; 2010 Apr;137(4):898-908
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[Title]
Parathyroid hormone-related peptide and parathyroid hormone-related peptide receptor type 1 expression in human
lung adenocarcinoma
.
In non-
small cell lung carcinoma
the clinical relevance of the expression of PTH1R remains to be investigated.
METHODS: Fifty-four
lung
adenocarcinomas of mixed histologic type from patients with stage I and II cancer were assayed by quantitative immunohistochemistry for the expression of PTHrP and PTH1R.
CONCLUSION: The paracrine/autocrine signaling through PTHrP/PTH1R could be important in early-stage
lung adenocarcinoma
progression.
[MeSH-major]
Adenocarcinoma
/ metabolism.
Lung
Neoplasms / metabolism. Parathyroid Hormone-Related Protein / metabolism. Receptor, Parathyroid Hormone, Type 1 / metabolism
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(PMID = 19952062.001).
[ISSN]
1931-3543
[Journal-full-title]
Chest
[ISO-abbreviation]
Chest
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Parathyroid Hormone-Related Protein; 0 / Receptor, Parathyroid Hormone, Type 1
55.
Saynak M, Aksu G, Fayda M, Kaytan E, Oral E, Gurocak S, Kizir A, Karadeniz A:
The results of concomitant and sequential chemoradiotherapy with cisplatin and etoposide in patients with locally advanced non-small cell lung cancer.
J BUON
; 2005 Apr-Jun;10(2):213-8
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[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.
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(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
56.
Shaw AT, Yeap BY, Mino-Kenudson M, Digumarthy SR, Costa DB, Heist RS, Solomon B, Stubbs H, Admane S, McDermott U, Settleman J, Kobayashi S, Mark EJ, Rodig SJ, Chirieac LR, Kwak EL, Lynch TJ, Iafrate AJ:
Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.
J Clin Oncol
; 2009 Sep 10;27(26):4247-53
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[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.
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Cancer. 2009 Apr 15;115(8):1723-33
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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
57.
Misthos P, Sepsas E, Kokotsakis J, Skottis I, Lioulias A:
Prognosis of stage pIIIA non small cell lung cancer after mediastinal lymph node dissection or sampling.
J BUON
; 2009 Jan-Mar;14(1):45-9
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[Title]
Prognosis of stage pIIIA non
small cell lung
cancer after mediastinal lymph node dissection or sampling.
PURPOSE: The aim of this study was to define the impact of systematic mediastinal lymph node dissection (MLD) and mediastinal lymph node sampling (MLS) on the long-term results of patients suffering from non-
small cell lung
cancer (NSCLC) with N2 disease (pIIIA/N2).
[MeSH-major]
Adenocarcinoma
/ surgery.
Carcinoma
, Non-
Small
-
Cell Lung
/ surgery.
Carcinoma
, Squamous
Cell
/ surgery.
Lung
Neoplasms / surgery. Lymph Node Excision
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(PMID = 19373946.001).
[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]
Comparative Study; Journal Article
[Publication-country]
Greece
58.
Zhang LX, Pan SY, Chen D, Xie EF, Gao L, Shu YQ, Lu ZH, Cheng L, Yang D, Zhang JN:
[Effect of adenomatous polyposis coli(APC) promoter methylation on gene transcription in lung cancer cell lines].
Ai Zheng
; 2007 Jun;26(6):576-80
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[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
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AZACITIDINE
.
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(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
59.
Vaissière T, Hung RJ, Zaridze D, Moukeria A, Cuenin C, Fasolo V, Ferro G, Paliwal A, Hainaut P, Brennan P, Tost J, Boffetta P, Herceg Z:
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.
Cancer Res
; 2009 Jan 1;69(1):243-52
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[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.
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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
60.
Kimura H, Kasahara K, Shibata K, Sone T, Yoshimoto A, Kita T, Ichikawa Y, Waseda Y, Watanabe K, Shiarasaki H, Ishiura Y, Mizuguchi M, Nakatsumi Y, Kashii T, Kobayashi M, Kunitoh H, Tamura T, Nishio K, Fujimura M, Nakao S:
EGFR mutation of tumor and serum in gefitinib-treated patients with chemotherapy-naive non-small cell lung cancer.
J Thorac Oncol
; 2006 Mar;1(3):260-7
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[Title]
EGFR mutation of tumor and serum in gefitinib-treated patients with chemotherapy-naive non-
small cell lung
cancer.
BACKGROUND: The authors evaluate the efficacy and safety of gefitinib monotherapy in chemotherapy-naive patients with advanced non-
small
-
cell lung
cancer (NSCLC).
[MeSH-major]
Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / blood.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy. DNA / blood.
Lung
Neoplasms / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics
[MeSH-minor]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ genetics. Adult. Aged. Aged, 80 and over.
Carcinoma
, Large
Cell
/ drug therapy.
Carcinoma
, Large
Cell
/ genetics.
Carcinoma
, Squamous
Cell
/ drug therapy.
Carcinoma
, Squamous
Cell
/ genetics. Exons. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Polymerase Chain Reaction
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[CommentIn]
J Thorac Oncol. 2006 Mar;1(3):199-200
[
17409855.001
]
(PMID = 17409866.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinazolines; 9007-49-2 / DNA; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
61.
Ak G, Metintas M, Metintas S, Yildirim H, Erginel S, Alatas F:
Lung cancer in individuals less than 50 years of age.
Lung
; 2007 Sep-Oct;185(5):279-286
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[Title]
Lung
cancer in individuals less than 50 years of age.
The aim of this study was to compare the epidemiologic, clinical, and laboratory characteristics and survival rates of younger and older patients with
lung
cancer.
We studied 1340 patients who were histopathologically diagnosed as having
lung
cancer from 1990 to 2005.
In the younger group, exposure to occupational risk factors was a risk factor for
lung
cancer, while in the older group, smoking was a risk factor.
The incidence of
adenocarcinoma and small
-
cell carcinoma
was greater in the younger group, while squamous
cell carcinoma
was more common in the older group.
These data indicate that
lung
cancer had different etiopathogenetic characteristics in younger patients, which may have clinical implications.
[MeSH-major]
Adenocarcinoma
/ epidemiology.
Carcinoma
,
Small Cell
/ epidemiology.
Carcinoma
, Squamous
Cell
/ epidemiology.
Lung
Neoplasms / epidemiology
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Lung Cancer. 2001 Jun;32(3):255-64
[
11390007.001
]
(PMID = 17705064.001).
[ISSN]
0341-2040
[Journal-full-title]
Lung
[ISO-abbreviation]
Lung
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
62.
Bhatia P, Srinivasan R, Rajwanshi A, Nijhawan R, Khandelwal N, Wig J, Vasishtha RK:
5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions.
Acta Cytol
; 2008 Sep-Oct;52(5):523-9
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Of the 142 malignant aspirates, the cytodiagnosis was
adenocarcinoma
in 126, neuroendocrine/carcinoid tumor in 7, papillary solid epithelial neoplasm in 2, mucinous cystadenocarcinoma in 2, acinar
cell carcinoma
in 1 and metastatic
small cell carcinoma
in
lung
in 4 cases.
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[CommentIn]
Acta Cytol. 2008 Sep-Oct;52(5):521-2
[
18833811.001
]
(PMID = 18833812.001).
[ISSN]
0001-5547
[Journal-full-title]
Acta cytologica
[ISO-abbreviation]
Acta Cytol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
63.
Hamada C, Tanaka F, Ohta M, Fujimura S, Kodama K, Imaizumi M, Wada H:
Meta-analysis of postoperative adjuvant chemotherapy with tegafur-uracil in non-small-cell lung cancer.
J Clin Oncol
; 2005 Aug 1;23(22):4999-5006
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[Title]
Meta-analysis of postoperative adjuvant chemotherapy with tegafur-uracil in non-
small
-
cell lung
cancer.
PURPOSE: Recent clinical trials have shown the efficacy of platinum-based adjuvant chemotherapy for completely resected non-
small
-
cell lung
cancer (NSCLC).
RESULTS: Of 2,003 eligible patients, most (98.8%) had squamous
cell carcinoma
or
adenocarcinoma
, and most had stage I disease; the tumor classification was T1 in 1,308 (65.3%), T2 in 674 (33.6%), and the nodal status was N0 in 1,923 (96.0%).
CONCLUSION: This meta-analysis showed that postoperative adjuvant chemotherapy with UFT was associated with improved 5- and 7-year survival in a Japanese patient population composed primarily of stage I
adenocarcinoma
patients.
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ surgery. Antimetabolites, Antineoplastic / therapeutic use.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Carcinoma
, Non-
Small
-
Cell Lung
/ surgery.
Carcinoma
, Squamous
Cell
/ drug therapy.
Carcinoma
, Squamous
Cell
/ surgery.
Lung
Neoplasms / drug therapy.
Lung
Neoplasms / surgery. Tegafur / therapeutic use
[MeSH-minor]
Chemotherapy, Adjuvant.
Combined
Modality Therapy. Humans. Survival Analysis
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(PMID = 16051951.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 1548R74NSZ / Tegafur
64.
Kuemmel A, Single K, Bittinger F, Faldum A, Schmidt LH, Sebastian M, Taube C, Buhl R, Wiewrodt R:
The prognostic impact of blood group-related antigen Lewis Y and the ABH blood groups in resected non-small cell lung cancer.
Tumour Biol
; 2007;28(6):340-9
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[Title]
The prognostic impact of blood group-related antigen Lewis Y and the ABH blood groups in resected non-
small cell lung
cancer.
Eighty-three paraffin-embedded tissue sections of non-
small cell lung
cancer (NSCLC) patients in stage I-IIIa, who underwent surgical resection of the primary tumor (73% male; 43%
adenocarcinoma
), were stained with a new, highly specific monoclonal antibody against Lewis Y (clone A70-C/C8).
[MeSH-major]
ABO Blood-Group System / metabolism. Antigens, Neoplasm / metabolism.
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism. Lewis Blood-Group System / metabolism.
Lung
Neoplasms / metabolism
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[Copyright]
(c) 2008 S. Karger AG, Basel.
(PMID = 18391551.001).
[ISSN]
1423-0380
[Journal-full-title]
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
[ISO-abbreviation]
Tumour Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ABO Blood-Group System; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lewis Blood-Group System; 0 / Lewis Y antigen
65.
Yano T, Morodomi Y, Ito K, Yoshida T, Haro A, Shoji F, Koga T, Maehara Y:
Verification of the newly proposed T category (seventh edition of the tumor, node, and metastasis classification) from a clinicopathological viewpoint in non-small cell lung cancer-special reference to tumor size.
J Thorac Oncol
; 2010 Jan;5(1):45-8
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[Title]
Verification of the newly proposed T category (seventh edition of the tumor, node, and metastasis classification) from a clinicopathological viewpoint in non-
small cell lung
cancer-special reference to tumor size.
INTRODUCTION: This study first verified the T classification, which is the major point of the revision regarding the seventh Tumor, Node, and Metastasis classification, from a viewpoint of the clinicopathological findings at the primary tumor site in non-
small cell lung
cancer.
METHODS: The medical records of 1393 patients with non-
small cell lung
cancer who underwent a complete resection at this hospital from 1974 to 2003 were thoroughly reviewed for pathologic findings and survival.
[MeSH-major]
Adenocarcinoma
/ pathology.
Carcinoma
, Non-
Small
-
Cell Lung
/ classification.
Carcinoma
, Non-
Small
-
Cell Lung
/ pathology.
Carcinoma
, Squamous
Cell
/ pathology.
Lung
Neoplasms / pathology
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(PMID = 19884855.001).
[ISSN]
1556-1380
[Journal-full-title]
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
[ISO-abbreviation]
J Thorac Oncol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
66.
Suemitsu R, Takeo S, Matsuzawa H, Yamaguchi M, Momosaki S, Uesugi N:
Can a thoracic surgeon identify lymph node metastases during surgery based on their size? Analysis of 844 metastatic and 10,462 nonmetastatic lymph nodes.
J Thorac Oncol
; 2010 Mar;5(3):349-53
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METHODS: The size of dissected lymph node was quantified in a total of 848 nodes with metastasis and 10,462 nodes without metastasis from 454 patients with
lung
cancer who underwent a pulmonary resection with lymph node dissection.
The smaller the lymph node, the less frequently the lymph nodes were metastatic; however, the ratios of nodes smaller than the fifth largest lymph node with metastasis of
adenocarcinoma and
squamous
cell carcinoma
were 21.8 to 26.2%, respectively.
When the hilar and mediastinal lymph node stations were examined, 1.14 to 4.00% of the
lung
cancer patients had lymph node metastasis in
small
lymph node despite having no metastases in the largest and second largest lymph nodes.
CONCLUSIONS: The
small
lymph nodes in the hilar or mediastinal stations frequently had metastases of
carcinoma
even though largest and second largest lymph nodes were negative for metastases, especially in
adenocarcinoma
cases.
Surgical oncologists should, therefore, perform systemic lymph node dissection, and not sampling, during a pulmonary resection of
lung
cancer.
[MeSH-major]
Carcinoma
, Large
Cell
/ surgery.
Carcinoma
, Non-
Small
-
Cell Lung
/ secondary.
Lung
Neoplasms / pathology. Lymph Nodes / pathology.
Small Cell Lung Carcinoma
/ secondary
[MeSH-minor]
Adenocarcinoma
/ secondary.
Adenocarcinoma
/ surgery.
Adenocarcinoma
, Bronchiolo-Alveolar / secondary.
Adenocarcinoma
, Bronchiolo-Alveolar / surgery. Adult. Aged. Aged, 80 and over.
Carcinoma
, Squamous
Cell
/ secondary.
Carcinoma
, Squamous
Cell
/ surgery. Female. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Mediastinal Neoplasms / secondary. Mediastinal Neoplasms / surgery. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate
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(PMID = 20009772.001).
[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
67.
Lee YC, Wu CT, Kuo SW, Tseng YT, Chang YL:
Significance of extranodal extension of regional lymph nodes in surgically resected non-small cell lung cancer.
Chest
; 2007 Apr;131(4):993-9
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[Title]
Significance of extranodal extension of regional lymph nodes in surgically resected non-
small cell lung
cancer.
STUDY OBJECTIVES: Regional lymph node (LN) involvement affects the prognosis of patients with surgically resected non-
small cell lung
cancer (NSCLC).
Histologic examinations including tumor
cell
type, grade of differentiation, vascular invasion, regional LN metastasis emphasizing the number and station of LN involvement, the presence or absence of extranodal extension, and the immunohistochemistry of p53 expression were obtained.
RESULTS: Extranodal extension was significantly higher in women,
adenocarcinoma
, advanced stage, tumors with vascular invasion, or p53 overexpression.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ surgery.
Lung
Neoplasms / surgery. Lymph Node Excision / methods
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[CommentIn]
Chest. 2007 Apr;131(4):948-9
[
17426192.001
]
[CommentIn]
Chest. 2007 Dec;132(6):2058-9; author reply 2059-60
[
18079250.001
]
(PMID = 17426201.001).
[ISSN]
0012-3692
[Journal-full-title]
Chest
[ISO-abbreviation]
Chest
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
68.
Bishop JA, Benjamin H, Cholakh H, Chajut A, Clark DP, Westra WH:
Accurate classification of non-small cell lung carcinoma using a novel microRNA-based approach.
Clin Cancer Res
; 2010 Jan 15;16(2):610-9
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[Title]
Accurate classification of non-
small cell lung carcinoma
using a novel microRNA-based approach.
PURPOSE: Advances in targeted
lung
cancer therapy now demand accurate classification of non-
small cell lung
cancer (NSCLC).
For example, hsa-miR-205 is a miRNA that is highly expressed in
lung
squamous
cell
carcinomas (SqCC) but not in
lung
adenocarcinomas.
EXPERIMENTAL DESIGN: One hundred and two resected NSCLCs were classified as SqCC or
adenocarcinoma
based on their histologic features and immunohistochemical profiles.
A quantitative reverse transcription-PCR diagnostic assay that measures the expression level of hsa-miR-205 was used to classify the carcinomas as SqCC or
adenocarcinoma
based solely on expression levels.
RESULTS: Using standard pathologic methods of classification (i.e., microscopy and immunohistochemistry), 52 resected
lung
carcinomas were classified as SqCCs and 50 as adenocarcinomas.
Indeed, classification is consistently accurate even in
small
biopsies/aspirates of poorly differentiated tumors.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ classification.
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics.
Lung
Neoplasms / classification.
Lung
Neoplasms / genetics. MicroRNAs / analysis
[MeSH-minor]
Adenocarcinoma
/ diagnosis.
Adenocarcinoma
/ pathology.
Carcinoma
, Squamous
Cell
/ diagnosis.
Carcinoma
, Squamous
Cell
/ pathology. Diagnosis, Differential. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Neoplasm Staging / methods. Nuclear Proteins / metabolism. Sensitivity and Specificity. Transcription Factors / metabolism
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(PMID = 20068099.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1
69.
Dillman RO, Zusman DR, McClure SE:
Surgical resection and long-term survival for octogenarians who undergo surgery for non-small-cell lung cancer.
Clin Lung Cancer
; 2009 Mar;10(2):130-4
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[Title]
Surgical resection and long-term survival for octogenarians who undergo surgery for non-
small
-
cell lung
cancer.
PURPOSE: An increasing proportion of newly diagnosed non-
small
-
cell lung
cancer (NSCLC) patients are octogenarians.
It has been questioned whether older patients benefit from surgical resection of
lung
cancer to the same extent as younger patients.
PATIENTS AND METHODS: We conducted a single-institution, retrospective analysis of patients newly diagnosed with NSCLC from 2000-2006, who underwent surgical resection of their
lung
cancer in Hoag Hospital.
CONCLUSION: Non-
small
-
cell lung
cancer patients < 80 years of age were less likely to undergo potentially curative surgery, but survival for octogenarians who did undergo surgical resection was comparable to younger age groups.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ mortality.
Carcinoma
, Non-
Small
-
Cell Lung
/ surgery.
Lung
Neoplasms / mortality.
Lung
Neoplasms / surgery
[MeSH-minor]
Adenocarcinoma
/ mortality.
Adenocarcinoma
/ secondary.
Adenocarcinoma
/ surgery.
Adenocarcinoma
, Bronchiolo-Alveolar / mortality.
Adenocarcinoma
, Bronchiolo-Alveolar / secondary.
Adenocarcinoma
, Bronchiolo-Alveolar / surgery. Age Factors. Aged. Aged, 80 and over.
Carcinoma
, Squamous
Cell
/ mortality.
Carcinoma
, Squamous
Cell
/ secondary.
Carcinoma
, Squamous
Cell
/ surgery. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome
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(PMID = 19362957.001).
[ISSN]
1525-7304
[Journal-full-title]
Clinical lung cancer
[ISO-abbreviation]
Clin Lung Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
70.
Domagała-Kulawik J, Górnicka B, Krenke R, Mich S, Chazan R:
The value of cytological diagnosis of small cell lung carcinoma.
Pneumonol Alergol Pol
; 2010;78(3):203-10
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[Title]
The value of cytological diagnosis of
small cell lung carcinoma
.
INTRODUCTION:
Small cell lung carcinoma
(SCLC) is a very aggressive neoplasm.
The morphology of SCLC cells was not uniform, and often a mixture of non-
small
atypical cells and bronchial epithelial cells with signs of metaplasia was observed.
There were four cases
of combined
cell
type with large
cell carcinoma
and two with
adenocarcinoma
.
The main diagnostic problem was to distinguish
small cell lung carcinoma
from lymphomas, and from cancer consisting of
small
cells with the cytological features of non-
small cell carcinoma
.
In the differential diagnosis, other tumours of
small
cells have to be taken into account.
[MeSH-major]
Lung
Neoplasms / pathology.
Small Cell Lung Carcinoma
/ pathology
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(PMID = 20461688.001).
[ISSN]
0867-7077
[Journal-full-title]
Pneumonologia i alergologia polska
[ISO-abbreviation]
Pneumonol Alergol Pol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
0 / Biomarkers, Tumor
71.
Omuro AM, Kris MG, Miller VA, Franceschi E, Shah N, Milton DT, Abrey LE:
High incidence of disease recurrence in the brain and leptomeninges in patients with nonsmall cell lung carcinoma after response to gefitinib.
Cancer
; 2005 Jun 1;103(11):2344-8
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[Title]
High incidence of disease recurrence in the brain and leptomeninges in patients with nonsmall
cell lung carcinoma
after response to gefitinib.
BACKGROUND: Gefitinib is an epidermal growth factor receptor tyrosine kinase inhibitor that induces an early and dramatic response in 10% of patients with advanced nonsmall
cell lung carcinoma
(NSCLC).
All responders had
adenocarcinoma
.
In 9 (43%) patients, the initial site of disease recurrence was the
lung and
in 1 it was the liver and bone.
Four (57%) of the patients with disease recurrence in the CNS had
lung
disease under control.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Brain Neoplasms / secondary.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Carcinoma
, Non-
Small
-
Cell Lung
/ secondary.
Lung
Neoplasms / drug therapy. Meningeal Neoplasms / secondary. Quinazolines / therapeutic use
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(PMID = 15844174.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
72.
Liang ZY, Zeng X, Zhang J, Wu SF, Gao J, Liu TH:
[Status of gene mutation and copy number of EGFR in 290 cases of non-small cell lung carcinoma].
Zhonghua Bing Li Xue Za Zhi
; 2008 Oct;37(10):654-9
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[Title]
[Status of gene mutation and copy number of EGFR in 290 cases of non-
small cell lung carcinoma
].
OBJECTIVE: To investigate EGFR mutations and gene copy number status in non-
small cell lung
carcinomas in the Chinese patients.
METHODS: Using formalin fixed and paraffin embedded tissue samples, EGFR mutations were investigated in 290 cases of non-
small cell lung
carcinomas by microdissection and scorpions amplification refractory mutation system.
Furthermore, the relationship between EGFR mutations and gene copy number, and the relationship between EGFR gene status and clinicopathological variables of non-
small cell lung carcinoma
were analyzed.
The mutation rates in
adenocarcinoma
, large
cell carcinoma
and squamous
carcinoma
were 48.4%, 16.7% and 0, respectively.
FISH positive rates in
adenocarcinoma
, large
cell carcinoma
and squamous
carcinoma
were 52.1%, 75.0% and 11.1%, respectively.
Therefore, EGFR mutations mainly occurred in the
adenocarcinoma
, and was significantly correlated with EGFR high copy number.
CONCLUSIONS: There are higher EGFR mutation rate and FISH positive rate in non-
small cell lung carcinoma
in Chinese patients.
Combined
analysis of EGFR mutation and gene copy number by FISH may provide a superior approach in selecting patients who may benefit anti-EGFR target therapy.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics. Gene Dosage. Genes, erbB-1. Genetic Diseases, Inborn.
Lung
Neoplasms / genetics. Mutation. Receptor, Epidermal Growth Factor / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over.
Carcinoma
, Squamous
Cell
/ genetics. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged
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(PMID = 19094482.001).
[ISSN]
0529-5807
[Journal-full-title]
Zhonghua bing li xue za zhi = Chinese journal of pathology
[ISO-abbreviation]
Zhonghua Bing Li Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.10.1 / Receptor, Epidermal Growth Factor
73.
Iezumi K, Masunaga A, Kadofuku T, Iwamoto S, Masuda M, Suzuki S, Suzuki T, Miyazaki A, Mitsuya T:
Combined small cell carcinoma with pulmonary blastoma and adenocarcinoma: case report and clonality analysis.
Pathol Res Pract
; 2006;202(12):895-9
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[Title]
Combined
small cell carcinoma
with pulmonary blastoma
and adenocarcinoma
: case report and clonality analysis.
Histologic examination revealed papillary
adenocarcinoma
in
small cell carcinoma
, and chondrosarcoma.
Also, the blastemal cells were located between the
small cell carcinoma and
the chondrosarcoma, and intermingled with both components.
In blastemal cells, some glands resembled a well-differentiated fetal
adenocarcinoma
.
The tumor was diagnosed as
combined
small cell carcinoma
with pulmonary blastoma and papillary
adenocarcinoma
according to the 2004 WHO classification.
Immunohistochemically, the
small cell carcinoma
expressed TTF-1, pancytokeratin, CD56, synaptophysin, and S100 protein, while blastemal cells expressed vimentin, desmin, smooth muscle actin, CD56, and S100 protein.
These results indicate that the tumor was clonal and arose from a relatively primitive
cell
, and that p53 mutation occurred before histologic metamorphosis or differentiation.
[MeSH-major]
Carcinoma
,
Small Cell
/ secondary.
Lung
Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Pulmonary Blastoma / secondary
[MeSH-minor]
Aged. Biomarkers, Tumor / analysis. Clone Cells.
Combined
Modality Therapy. DNA Mutational Analysis. DNA, Neoplasm / analysis. Humans. Male. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / genetics
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(PMID = 17046168.001).
[ISSN]
0344-0338
[Journal-full-title]
Pathology, research and practice
[ISO-abbreviation]
Pathol. Res. Pract.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53
74.
Bugalho P, Chorão M, Fontoura P:
Miliary brain metastases from primary gastric small cell carcinoma: illustrating the seed and soil hypothesis.
J Neurooncol
; 2005 May;73(1):53-6
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[Title]
Miliary brain metastases from primary gastric
small cell carcinoma
: illustrating the seed and soil hypothesis.
Miliary metastases are a very rare condition usually found in the context of primary
lung
tumor (
small cell and adenocarcinoma
), and refer to the existence of numerous tumor nodules in widespread areas of the brain.
Besides pulmonary neoplasia, pancreatic
adenocarcinoma and
malignant melanoma have also been implicated in some cases of miliary metastases.
We present the first case of miliary metastases originating in a primary
small cell
gastric
carcinoma
(PSCGC), a rare type of neuroendocrine gastric tumor.
The pathological resemblance of PSCGC with
small cell lung carcinoma
may correspond to an underlying similarity in biological behavior, which accounts for this particular pattern of metastatic spreading, as proposed in the seed and soil hypothesis.
[MeSH-major]
Brain Neoplasms / secondary.
Carcinoma
, Neuroendocrine / pathology.
Carcinoma
,
Small Cell
/ secondary. Stomach Neoplasms / pathology
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FLUOROURACIL
.
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J. Neurooncol.
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eng
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Case Reports; Journal Article
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0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 5W494URQ81 / Streptozocin; U3P01618RT / Fluorouracil
75.
Goldoni S, Seidler DG, Heath J, Fassan M, Baffa R, Thakur ML, Owens RT, McQuillan DJ, Iozzo RV:
An antimetastatic role for decorin in breast cancer.
Am J Pathol
; 2008 Sep;173(3):844-55
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Decorin, a member of the
small
leucine-rich proteoglycan gene family, down-regulates members of the ErbB receptor tyrosine kinase family and attenuates their signaling, leading to growth inhibition.
We investigated the effects of decorin on the growth of ErbB2-overexpressing mammary
carcinoma
cells in comparison with AG879, an established ErbB2 kinase inhibitor.
Cell
proliferation and anchorage-independent growth assays showed that decorin was a potent inhibitor of breast cancer
cell
growth and a pro-apoptotic agent.
Active recombinant human decorin protein core, AG879, or a combination of both was administered systemically to mice bearing orthotopic mammary
carcinoma
xenografts.
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(PMID = 18688028.001).
[ISSN]
1525-2191
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA039481; United States / NCI NIH HHS / CA / R01 CA120975; United States / NCI NIH HHS / CA / R01 CA047282; United States / NCI NIH HHS / CA / R01 CA47282; United States / NCI NIH HHS / CA / R01 CA39481
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / DCN protein, human; 0 / Dcn protein, mouse; 0 / Dcn protein, rat; 0 / Decorin; 0 / Enzyme Inhibitors; 0 / Erbb2 protein, rat; 0 / Extracellular Matrix Proteins; 0 / Glycoproteins; 0 / Proteoglycans; EC 2.7.10.1 / Receptor, ErbB-2
[Other-IDs]
NLM/ PMC2527080
76.
Leinonen T, Pirinen R, Böhm J, Johansson R, Kosma VM:
Increased expression of matrix metalloproteinase-2 (MMP-2) predicts tumour recurrence and unfavourable outcome in non-small cell lung cancer.
Histol Histopathol
; 2008 06;23(6):693-700
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[Title]
Increased expression of matrix metalloproteinase-2 (MMP-2) predicts tumour recurrence and unfavourable outcome in non-
small cell lung
cancer.
The purpose of this study was to analyse the expression of matrix metalloproteinase-2 (MMP-2) and its extracellular matrix metalloproteinase inducer (EMMPRIN) in non-
small cell lung
cancer (NSCLC), and to evaluate their significance to predict tumour behaviour.
Adenocarcinomas showed more often high expression of MMP-2 as compared with squamous
cell
or large
cell
carcinomas (p=0.001).
High cancer
cell
associated MMP-2 expression was associated with increased tumour recurrence (p=0.001).
The high stromal MMP-2 expression was noticed more often among large
cell
carcinomas as compared with other histological types (p=0.007).
High cancer
cell
associated EMMPRIN expression was found in 115 (61%) cases and was associated only with high MMP-2 expression in tumour cells (p=0.006).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ enzymology.
Lung
Neoplasms / enzymology. Matrix Metalloproteinase 2 / metabolism. Neoplasm Recurrence, Local
[MeSH-minor]
Adenocarcinoma
/ enzymology.
Adenocarcinoma
/ mortality.
Adenocarcinoma
/ secondary. Adult. Aged. Antigens, CD147 / metabolism. Biomarkers, Tumor / metabolism.
Carcinoma
, Large
Cell
/ enzymology.
Carcinoma
, Large
Cell
/ mortality.
Carcinoma
, Large
Cell
/ secondary.
Carcinoma
, Squamous
Cell
/ enzymology.
Carcinoma
, Squamous
Cell
/ mortality.
Carcinoma
, Squamous
Cell
/ secondary. Disease-Free Survival. Finland / epidemiology. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Survival Rate
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(PMID = 18366007.001).
[ISSN]
1699-5848
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / BSG protein, human; 0 / Biomarkers, Tumor; 136894-56-9 / Antigens, CD147; EC 3.4.24.24 / Matrix Metalloproteinase 2
77.
Wood LD, Calhoun ES, Silliman N, Ptak J, Szabo S, Powell SM, Riggins GJ, Wang TL, Yan H, Gazdar A, Kern SE, Pennacchio L, Kinzler KW, Vogelstein B, Velculescu VE:
Somatic mutations of GUCY2F, EPHA3, and NTRK3 in human cancers.
Hum Mutat
; 2006 Oct;27(10):1060-1
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We identified somatic mutations in GUCY2F, EPHA3, and NTRK3 in breast,
lung
, and pancreatic cancers.
[MeSH-major]
Guanylate Cyclase / genetics. Mutation / genetics. Neoplasms / genetics. Receptor Protein-Tyrosine Kinases / genetics. Receptor, trkC / genetics. Receptors,
Cell
Surface / genetics
[MeSH-minor]
Adenocarcinoma
/ genetics. Base Sequence. Breast Neoplasms / genetics.
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics.
Carcinoma
,
Small Cell
/ genetics.
Carcinoma
, Squamous
Cell
/ genetics. DNA Mutational Analysis. Female. Humans.
Lung
Neoplasms / genetics. Pancreatic Neoplasms / genetics. Polymerase Chain Reaction
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(PMID = 16941478.001).
[ISSN]
1098-1004
[Journal-full-title]
Human mutation
[ISO-abbreviation]
Hum. Mutat.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA057345; United States / NCI NIH HHS / CA / CA062924; United States / NCI NIH HHS / CA / CA121113
[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 / Receptors, Cell Surface; EC 2.7.10.1 / EPHA3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, trkC; EC 4.6.1.2 / GUCY2F protein, human; EC 4.6.1.2 / Guanylate Cyclase
78.
Strazisar M, Mlakar V, Glavac D:
The expression of COX-2, hTERT, MDM2, LATS2 and S100A2 in different types of non-small cell lung cancer (NSCLC).
Cell Mol Biol Lett
; 2009;14(3):442-56
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[Title]
The expression of COX-2, hTERT, MDM2, LATS2 and S100A2 in different types of non-
small cell lung
cancer (NSCLC).
We investigated 65 stage I-III NSCLC tumours: 32 adenocarcinomas (ADC), 26 squamous
cell
carcinomas (SCC) and 7 large
cell
carcinomas (LCC).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism. Chemotactic Factors / metabolism. Cyclooxygenase 2 / metabolism.
Lung
Neoplasms / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-mdm2 / metabolism. S100 Proteins / metabolism. Telomerase / metabolism. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Adenocarcinoma
/ enzymology.
Adenocarcinoma
/ genetics.
Adenocarcinoma
/ metabolism. Aged.
Carcinoma
, Large
Cell
/ enzymology.
Carcinoma
, Large
Cell
/ genetics.
Carcinoma
, Large
Cell
/ metabolism.
Carcinoma
, Squamous
Cell
/ enzymology.
Carcinoma
, Squamous
Cell
/ genetics.
Carcinoma
, Squamous
Cell
/ metabolism. Female. Humans. Male. Middle Aged. Neoplasm Staging
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(PMID = 19238334.001).
[ISSN]
1689-1392
[Journal-full-title]
Cellular & molecular biology letters
[ISO-abbreviation]
Cell. Mol. Biol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
[Chemical-registry-number]
0 / Chemotactic Factors; 0 / S100 Proteins; 0 / S100A2 protein, human; 0 / Tumor Suppressor Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.1.11 / LATS2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
79.
Mao C, Qiu LX, Liao RY, Du FB, Ding H, Yang WC, Li J, Chen Q:
KRAS mutations and resistance to EGFR-TKIs treatment in patients with non-small cell lung cancer: a meta-analysis of 22 studies.
Lung Cancer
; 2010 Sep;69(3):272-8
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[Title]
KRAS mutations and resistance to EGFR-TKIs treatment in patients with non-
small cell lung
cancer: a meta-analysis of 22 studies.
Epidemiologic studies have evaluated the association between KRAS mutations and resistance to the treatment of epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs) in patients with non-
small cell lung
cancer (NSCLC).
Mutations were more common among
adenocarcinoma
than other histologies (26% versus 16%; OR=1.98; P<0.01).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ diagnosis.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Lung
Neoplasms / diagnosis.
Lung
Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use
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[Copyright]
Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
(PMID = 20022659.001).
[ISSN]
1872-8332
[Journal-full-title]
Lung cancer (Amsterdam, Netherlands)
[ISO-abbreviation]
Lung Cancer
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
80.
Castillo A, Aguayo F, Koriyama C, Shuyama K, Akiba S, Herrera-Goepfert R, Carrascal E, Klinge G, Sánchez J, Eizuru Y:
Human papillomavirus in lung carcinomas among three Latin American countries.
Oncol Rep
; 2006 Apr;15(4):883-8
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[Title]
Human papillomavirus in
lung
carcinomas among three Latin American countries.
The presence of human papillomavirus (HPV) genome in
lung
carcinomas has been reported worldwide but its frequency varies from country to country.
We examined HPV genome in 36
lung
carcinomas, consisting of 14 squamous
cell
carcinomas, 13 adenocarcinomas, and 9
small cell
carcinomas, collected from Colombia, Mexico and Peru.
PCR analysis using GP5+/GP6+ primers,
combined
with Southern blot hybridization, found the presence of HPV genome in 10 (28%) of 36 cases.
This percentage is similar to the value of 22% reported by Syrjänen, who conducted a meta-analysis of nearly 2500
lung
carcinomas examined to date.
HPV-16 was more frequently found among female than male cases (P=0.008) but was not detected in any
adenocarcinoma
cases.
The presence of HPV tended to be more frequent in well-differentiated tumors when squamous
cell
carcinomas and adenocarcinomas were
combined
.
Neither p16 nor p53 expression in
carcinoma
cells was related to the proportion of HPV-positive cases.
In conclusion, high-risk HPV DNA was detected in 28% of
lung
carcinomas.
[MeSH-major]
Lung
Neoplasms / virology. Papillomaviridae / genetics. Papillomavirus Infections / virology
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ virology. Aged. Blotting, Southern.
Carcinoma
,
Small Cell
/ metabolism.
Carcinoma
,
Small Cell
/ pathology.
Carcinoma
,
Small Cell
/ virology.
Carcinoma
, Squamous
Cell
/ metabolism.
Carcinoma
, Squamous
Cell
/ pathology.
Carcinoma
, Squamous
Cell
/ virology. Colombia. Cyclin-Dependent Kinase Inhibitor p16 / analysis. DNA, Viral / chemistry. DNA, Viral / genetics. DNA, Viral / isolation & purification. Female. Genome, Viral. Genotype. Human papillomavirus 16 / genetics. Human papillomavirus 18 / genetics. Humans. Immunohistochemistry. Male. Mexico. Middle Aged. Peru. Sequence Analysis, DNA. Sex Factors. Tumor Suppressor Protein p53 / analysis
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(PMID = 16525675.001).
[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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Viral; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
81.
Ichiki Y, Hanagiri T, Takenoyama M, Baba T, Fukuyama T, Nagata Y, Mizukami M, So T, Sugaya M, Yasuda M, So T, Sugio K, Yasumoto K:
Tumor specific expression of survivin-2B in lung cancer as a novel target of immunotherapy.
Lung Cancer
; 2005 May;48(2):281-9
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[Title]
Tumor specific expression of survivin-2B in
lung
cancer as a novel target of immunotherapy.
In this study, we evaluated whether survivin-2B could be a novel vaccine target against
lung
cancer. METHOD:.
(1) The differences in the survivin-2B expression between 15 sets of
lung
cancer tissues and normal
lung
tissues were investigated using RT-PCR. (2) The expression of survivin-2B was further examined in 42
lung
cancer tissues, and the relationship between the expression and clinicopathologic factors was analyzed. (3) To compare the frequency of precursor CTL between survivin-2B positive and negative
lung
cancer patients, surivivin-2B(80-88) peptide-specific CTL were induced from regional lymph node lymphocytes (LNL) of four HLA-A24 (+)
lung
cancer patients, in whom two showed a positive survivin-2B expression of
lung
cancer while another two were negative, after stimulation with surivivin-2B(80-88).
RESULTS: Survivin-2B was specifically expressed in
lung
cancer tissues, and was expressed in 17 of 42
lung
cancer tissues (42.9%).
Histologically, it was significantly more frequently expressed in squamous
cell carcinoma
than in
adenocarcinoma
(p=0.014).
The frequency of precursor CTL in LNL was approximately one in 2.0 x 10(7) in patients with survivin-2B expression (-)
lung
cancer, however, it was one in 5.0 x 10(6) to 6.0 x 10(6) in those with survivin-2B expression (+)
lung
cancer.
CONCLUSIONS: Survivin-2B was specifically expressed in
lung
cancer tissue, and found to specifically elicit a cellular immune response in
lung
cancer patients and therefore it may be a novel candidate for peptide vaccination.
[MeSH-major]
Cancer Vaccines.
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics.
Carcinoma
, Non-
Small
-
Cell Lung
/ therapy. Immunity, Cellular.
Lung
Neoplasms / genetics.
Lung
Neoplasms / therapy. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / immunology
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(PMID = 15829330.001).
[ISSN]
0169-5002
[Journal-full-title]
Lung cancer (Amsterdam, Netherlands)
[ISO-abbreviation]
Lung Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / BIRC5 protein, human; 0 / Biomarkers; 0 / Cancer Vaccines; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
82.
Laskin JJ, Sandler AB, Johnson DH:
Redefining bronchioloalveolar carcinoma.
Semin Oncol
; 2005 Jun;32(3):329-35
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[Title]
Redefining bronchioloalveolar
carcinoma
.
Bronchioloalveolar
carcinoma
(BAC) is a subtype of non-
small cell lung
cancer (NSCLC) with distinct clinical and pathologic features.
Although BAC appears to be on a pathologic continuum with
adenocarcinoma
, the most recent World Health Organization (WHO) classification system has set stringent criteria for the diagnosis.
[MeSH-major]
Adenocarcinoma
, Bronchiolo-Alveolar.
Lung
Neoplasms
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(PMID = 15988687.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
49
83.
Wu DW, Cheng YW, Wang J, Chen CY, Lee H:
Paxillin predicts survival and relapse in non-small cell lung cancer by microRNA-218 targeting.
Cancer Res
; 2010 Dec 15;70(24):10392-401
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[Title]
Paxillin predicts survival and relapse in non-
small cell lung
cancer by microRNA-218 targeting.
Paxillin (PXN) gene mutations are associated with
lung adenocarcinoma
progression and PXN is known to be a target gene of microRNA-218 (miR-218).
On this basis, we hypothesized that PXN overexpression via miR-218 suppression may promote tumor progression and metastasis and that PXN may predict survival and relapse in non-
small cell lung
cancer (NSCLC).
Expression of miR-218 and PXN in 124 surgically resected
lung
tumors were evaluated by real-time PCR and immunohistochemical analysis.
The prognostic value of miR-218 and PXN expression on overall survival (OS) and relapse-free survival (RFS) was analyzed by the Kaplan-Meier test and Cox regression analysis. miR-218 expression in
lung
tumors was negatively associated with PXN expression.
Moreover, patients with low miR-218
combined
with PXN-positive had the worst OS and RFS among the 4 combinations.
In a
cell
model, PXN was negatively regulated by miR-218
and cell
proliferation, invasion, and soft agar colony formation were enhanced by PXN overexpression induced by miR-218 suppression.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics.
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism.
Lung
Neoplasms / genetics.
Lung
Neoplasms / metabolism. MicroRNAs / antagonists & inhibitors. MicroRNAs / biosynthesis. Paxillin / biosynthesis
[MeSH-minor]
Cell
Line, Tumor. Female. Gene Knockdown Techniques. Humans. Male. Molecular Targeted Therapy / methods. Neoplasm Invasiveness. Oncogene Proteins, Viral / genetics. Oncogene Proteins, Viral / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Repressor Proteins / genetics. Repressor Proteins / metabolism. Transcription, Genetic. Up-Regulation
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[Copyright]
©2010 AACR.
(PMID = 21159652.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / E6 protein, Human papillomavirus type 16; 0 / MIRN218 microRNA, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Viral; 0 / Paxillin; 0 / RNA, Messenger; 0 / Repressor Proteins
84.
Kasprzyk M, Dyszkiewicz W, Zwaruń D, Leśniewska K, Wiktorowicz K:
[The assessment of acute phase proteins as prognostic factors in patients surgically treated for non-small cell lung cancer].
Pneumonol Alergol Pol
; 2008;76(5):321-6
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[Title]
[The assessment of acute phase proteins as prognostic factors in patients surgically treated for non-
small cell lung
cancer].
INTRODUCTION: The aim of the study was to assess quantitative changes of the acute phase protein (APP) serum level in patients with non-
small cell lung
cancer (NSCLC) who underwent a radical resection.
The most frequent histological types of cancer were: squamous
cell lung
cancer (24 patients)
and adenocarcinoma
(17 patients).
RESULTS: The level of AT was significantly higher in patients with
adenocarcinoma
, as compared to other histological types of cancer.
In the case of patients with squamous
cell lung
cancer, significantly higher M and Cp.
CONCLUSIONS: The serum concentration of some APP may correlate with the more aggressive clinical behavior of
lung
cancer.
The patients with N1 or N2 stage of
adenocarcinoma
have significantly higher serum level of AT and the preoperative concentration of AGP and Hp correlates with the overall survival.
[MeSH-major]
Acute-Phase Proteins / analysis.
Adenocarcinoma
/ blood. Biomarkers, Tumor / blood.
Carcinoma
, Non-
Small
-
Cell Lung
/ blood.
Carcinoma
, Squamous
Cell
/ blood.
Lung
Neoplasms / blood
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.
NCI CPTAC Assay Portal.
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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
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.
NCI CPTAC Assay Portal.
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.
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.
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.
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(PMID = 19003761.001).
[ISSN]
0867-7077
[Journal-full-title]
Pneumonologia i alergologia polska
[ISO-abbreviation]
Pneumonol Alergol Pol
[Language]
pol
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
0 / Acute-Phase Proteins; 0 / Biomarkers, Tumor; 0 / Haptoglobins; 0 / Orosomucoid; 0 / alpha-Macroglobulins; 9007-41-4 / C-Reactive Protein; EC 1.16.3.1 / Ceruloplasmin
85.
Hassan KA, Chen G, Kalemkerian GP, Wicha MS, Beer DG:
An embryonic stem cell-like signature identifies poorly differentiated lung adenocarcinoma but not squamous cell carcinoma.
Clin Cancer Res
; 2009 Oct 15;15(20):6386-90
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[Title]
An embryonic stem
cell
-like signature identifies poorly differentiated
lung adenocarcinoma
but not squamous
cell carcinoma
.
PURPOSE: An embryonic stem
cell
(ESC) profile correlates with poorly differentiated breast, bladder, and glioma cancers.
In this article, we assess the correlation between the ESC profile and clinical variables in
lung
cancer.
EXPERIMENTAL DESIGN: Microarray gene expression analysis was done using Affymetrix Human Genome U133A on 443 samples of human
lung adenocarcinoma
and 130 samples of squamous
cell carcinoma
(SCC).
RESULTS: Our analysis showed that an increased expression of the ESC gene set and a decreased expression of the Polycomb target gene set identified poorly differentiated
lung adenocarcinoma
.
In addition, this gene expression signature was associated with markers of poor prognosis and worse overall survival in
lung adenocarcinoma
.
However, there was no correlation between this ESC gene signature and any histologic or clinical variable assessed in
lung
SCC.
CONCLUSIONS: This work suggests that not all poorly differentiated non-
small cell lung
cancers exhibit a gene expression profile similar to that of ESC, and that other characteristics may play a more important role in the determination of differentiation and survival in SCC of the
lung
.
[MeSH-major]
Adenocarcinoma
/ genetics.
Carcinoma
, Squamous
Cell
/ genetics.
Lung
Neoplasms / genetics
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[Cites]
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[
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[Cites]
Mol Cell Biol. 2001 Jul;21(13):4330-6
[
11390661.001
]
(PMID = 19808871.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K08 CA158425; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / P30 CA046592-14; United States / NCI NIH HHS / CA / 5P30 CA46592
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS143924; NLM/ PMC2787085
86.
Kaira K, Oriuchi N, Shimizu K, Tominaga H, Yanagitani N, Sunaga N, Ishizuka T, Kanai Y, Mori M, Endo K:
18F-FMT uptake seen within primary cancer on PET helps predict outcome of non-small cell lung cancer.
J Nucl Med
; 2009 Nov;50(11):1770-6
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[Title]
18F-FMT uptake seen within primary cancer on PET helps predict outcome of non-
small cell lung
cancer.
We evaluated the prognostic significance of (18)F-FMT PET in patients with non-
small cell lung
cancer.
METHODS: Ninety-eight patients (80 men and 18 women; age range, 42-82 y; median age, 69 y) with stage I-IV non-
small cell lung
cancer were enrolled in this study.
They included 57 with
adenocarcinoma
, 31 with squamous
cell carcinoma
, 5 with large
cell carcinoma
, and 5 with other conditions.
According to histologic types, (18)F-FMT and (18)F-FDG uptake were a stronger prognostic predictor in
adenocarcinoma
than in nonadenocarcinomatous disease.
Patients with a high SUV(max) for (18)F-FMT showed significantly worse disease-free survival rates than those with a low SUV(max), and multivariate analysis confirmed that a high SUV(max) for (18)F-FMT was an independent and significant factor in predicting a poor prognosis in patients with
adenocarcinoma
(P = 0.0191).
CONCLUSION: Uptake of (18)F-FMT in primary tumors was an independent prognostic factor in patients with pulmonary
adenocarcinoma
.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ diagnosis.
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism. Fluorine Radioisotopes / chemistry.
Lung
Neoplasms / diagnosis.
Lung
Neoplasms / metabolism. alpha-Methyltyrosine / chemistry. alpha-Methyltyrosine / metabolism
[MeSH-minor]
Adenocarcinoma
/ diagnosis.
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ radionuclide imaging. Adult. Aged. Aged, 80 and over. Analysis of Variance. Female. Fluorodeoxyglucose F18 / metabolism. Humans. Male. Middle Aged. Positron-Emission Tomography. Prognosis. Survival Rate
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(PMID = 19837768.001).
[ISSN]
1535-5667
[Journal-full-title]
Journal of nuclear medicine : official publication, Society of Nuclear Medicine
[ISO-abbreviation]
J. Nucl. Med.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00464282
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Fluorine Radioisotopes; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 658-48-0 / alpha-Methyltyrosine
87.
Chen XL, Zhang WG, Chen XY, Sun ZM, Liu SH:
[Correlations of S100A4 protein expression to invasion and metastasis of non-small cell lung cancer].
Ai Zheng
; 2006 Sep;25(9):1134-7
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[Title]
[Correlations of S100A4 protein expression to invasion and metastasis of non-
small cell lung
cancer].
This study was to determine the expression of S100A4 in human non-
small cell lung
cancer (NSCLC), and to investigate its correlations to invasion and metastasis of NSCLC.
METHODS: The expression of S100A4 in 41 specimens of NSCLC and 6 specimens of normal
lung
tissues was detected by SP immunohistochemistry.
RESULTS: The positive rate of S100A4 was significantly higher in NSCLC than in normal
lung
tissues (70.7% vs. 16.7%, P<0.05), and was significantly higher in
adenocarcinoma
than in squamous
cell carcinoma
(90.0% vs. 52.4%, P<0.01).
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism.
Lung
Neoplasms / metabolism. S100 Proteins / metabolism
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Adult. Aged.
Carcinoma
, Squamous
Cell
/ metabolism.
Carcinoma
, Squamous
Cell
/ pathology. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging
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(PMID = 16965657.001).
[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 / S100 Proteins; 142662-27-9 / S100A4 protein, human
88.
Nyman J, Johansson KA, Hultén U:
Stereotactic hypofractionated radiotherapy for stage I non-small cell lung cancer--mature results for medically inoperable patients.
Lung Cancer
; 2006 Jan;51(1):97-103
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[Title]
Stereotactic hypofractionated radiotherapy for stage I non-
small cell lung
cancer--mature results for medically inoperable patients.
HISTOLOGY: 18 squamous
cell carcinoma
, 15
adenocarcinoma
, 3 NSCLC and histology was missing in nine patients.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ radiotherapy.
Lung
Neoplasms / radiotherapy
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(PMID = 16213059.001).
[ISSN]
0169-5002
[Journal-full-title]
Lung cancer (Amsterdam, Netherlands)
[ISO-abbreviation]
Lung Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Ireland
89.
Bircan A, Bircan S, Kapucuoglu N, Songur N, Ozturk O, Akkaya A:
Maspin, VEGF and p53 expression in small biopsies of primary advanced lung cancer and relationship with clinicopathologic parameters.
Pathol Oncol Res
; 2010 Dec;16(4):553-61
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[Title]
Maspin, VEGF and p53 expression in
small
biopsies of primary advanced
lung
cancer and relationship with clinicopathologic parameters.
We aimed to investigate maspin, p53 and VEGF expression in patients with squamous
cell carcinoma
(SCC),
adenocarcinoma
(AC)
and small cell lung carcinoma
(SCLC).
The rate was significantly higher in non-
small cell lung
cancer (NSCLC) and SCC than SCLC (p = 0.013, p = 0.021, respectively).
Larger scale studies are needed to reveal the exact role of maspin in
lung
cancer pathogenesis.
[MeSH-major]
Biomarkers, Tumor / biosynthesis.
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism.
Lung
Neoplasms / metabolism.
Lung
Neoplasms / pathology. Serpins / biosynthesis.
Small Cell Lung Carcinoma
/ metabolism. Tumor Suppressor Protein p53 / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Adult. Aged. Aged, 80 and over. Biopsy.
Carcinoma
, Squamous
Cell
/ metabolism.
Carcinoma
, Squamous
Cell
/ pathology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models
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J Biol Chem. 2000 Mar 3;275(9):6051-4
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10692390.001
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(PMID = 20349288.001).
[ISSN]
1532-2807
[Journal-full-title]
Pathology oncology research : POR
[ISO-abbreviation]
Pathol. Oncol. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
90.
Liu GZ, Wu YM, Yang JY:
[Significance of combined detection of plasma RASSF1A and p16 gene methylation in diagnosis of non-small cell lung cancers].
Zhonghua Zhong Liu Za Zhi
; 2007 Aug;29(8):613-4
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[Title]
[Significance
of combined
detection of plasma RASSF1A and p16 gene methylation in diagnosis of non-
small cell lung
cancers].
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ diagnosis. DNA Methylation. Genes, p16.
Lung
Neoplasms / diagnosis. Tumor Suppressor Proteins
[MeSH-minor]
Adenocarcinoma
/ diagnosis.
Adenocarcinoma
/ genetics.
Carcinoma
, Squamous
Cell
/ diagnosis.
Carcinoma
, Squamous
Cell
/ genetics. Cyclin-Dependent Kinase Inhibitor p16 / blood. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Humans
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(PMID = 18210883.001).
[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]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins
91.
Longo F, Giovanni M:
[Erlotinib in the treatment of NSCLC: current and novel prospects from the ASCO 2006].
Tumori
; 2006 Sep-Oct;92(5):suppl 13-22
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[MeSH-major]
Antineoplastic Agents / therapeutic use.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Lung
Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
[MeSH-minor]
Adenocarcinoma
/ drug therapy. Asian Continental Ancestry Group. Clinical Trials as Topic. Erlotinib Hydrochloride. Evidence-Based Medicine. Humans. Sex Factors. Smoking / adverse effects. Survival Analysis
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(PMID = 17168450.001).
[ISSN]
0300-8916
[Journal-full-title]
Tumori
[ISO-abbreviation]
Tumori
[Language]
ita
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride
[Number-of-references]
16
92.
Kwon JH, Kim JH, Lee JA, Shin HC, Kim HJ, Song HH, Jung JY, Kim HY, Choi DR, Kim HS, Park YI, Zang DY:
Phase II study with fractionated schedule of docetaxel and cisplatin in patients with advanced non-small cell lung cancer.
Cancer Chemother Pharmacol
; 2010 Oct;66(5):889-97
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[Title]
Phase II study with fractionated schedule of docetaxel and cisplatin in patients with advanced non-
small cell lung
cancer.
BACKGROUND: Docetaxel and cisplatin combination chemotherapy is established first-line chemotherapy for advanced non-
small cell lung
cancer (NSCLC).
Fifty seven percentage (20/35) of patients had
adenocarcinoma and
74.3% (26/35) had stage IV disease.
[MeSH-major]
Antineoplastic
Combined
Chemotherapy Protocols / therapeutic use.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Lung
Neoplasms / drug therapy
[MeSH-minor]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ pathology. Adult. Aged. Cisplatin / administration & dosage. Disease Progression. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Survival. Taxoids / administration & dosage. Time Factors. Treatment Outcome
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DOCETAXEL
.
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CIS-DIAMINEDICHLOROPLATINUM
.
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(PMID = 20091311.001).
[ISSN]
1432-0843
[Journal-full-title]
Cancer chemotherapy and pharmacology
[ISO-abbreviation]
Cancer Chemother. Pharmacol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study
[Publication-country]
Germany
[Chemical-registry-number]
0 / Taxoids; 15H5577CQD / docetaxel; Q20Q21Q62J / Cisplatin
93.
Meyer SE, Hasenstein JR, Baktula A, Velu CS, Xu Y, Wan H, Whitsett JA, Gilks CB, Grimes HL:
Kruppel-like factor 5 is not required for K-RasG12D lung tumorigenesis, but represses ABCG2 expression and is associated with better disease-specific survival.
Am J Pathol
; 2010 Sep;177(3):1503-13
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[Title]
Kruppel-like factor 5 is not required for K-RasG12D
lung
tumorigenesis, but represses ABCG2 expression and is associated with better disease-specific survival.
K-RAS mutations are found in approximately 30% of
lung
cancers.
The transcription factor Krüppel-like Factor 5 (KLF5) has been shown to mediate cellular transformation signaling events downstream of oncogenic RAS in other cancers, but a role for KLF5 in
lung
tumorigenesis has not been defined.
We show here that knockdown of KLF5 expression significantly decreased anchorage-independent growth, but did not affect proliferation of human
lung adenocarcinoma
cells.
Moreover, Klf5 is not required for
lung
tumor formation in an inducible oncogenic K-Ras(G12D) mouse model of
lung
tumorigenesis, and non-
small cell lung
cancer patients expressing high levels of KLF5 (21/258) have a significantly better disease-specific survival than those with intermediate to no KLF5 expression.
Further, KLF5 knockdown in K-RAS-mutant human
lung
cancer cells resulted in a fivefold increase in ATP-binding cassette, subfamily G (WHITE), member 2 (ABCG2), an anthracycline drug transporter, which lead to significantly increased resistance to doxorubicin treatment, a chemotherapeutic agent clinically used to treat
lung
cancer.
In summary, while KLF5 is not required for oncogenic mutant K-Ras-induced
lung
tumorigenesis, KLF5 regulation of ABCG2 expression may be important for chemotherapeutic resistance and patient survival.
[MeSH-major]
ATP-Binding Cassette Transporters / metabolism.
Carcinoma
, Non-
Small
-
Cell Lung
/ metabolism. Kruppel-Like Transcription Factors / metabolism.
Lung
Neoplasms / metabolism. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins / metabolism. ras Proteins / metabolism
[MeSH-minor]
ATP Binding Cassette Transporter, Sub-Family G, Member 2. Analysis of Variance. Animals. Blotting, Western.
Cell
Line, Tumor.
Cell
Proliferation.
Cell
Transformation, Neoplastic / genetics. Cells, Cultured. Chromatin Immunoprecipitation. Disease-Free Survival. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Mice. Proto-Oncogene Proteins p21(ras). Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis
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Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 20639455.001).
[ISSN]
1525-2191
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA112405; United States / NHLBI NIH HHS / HL / R01 HL079574; United States / NCI NIH HHS / CA / R01 CA112405; United States / NHLBI NIH HHS / HL / HL079574-06S1; United States / NHLBI NIH HHS / HL / R01 HL090156; United States / NCI NIH HHS / CA / CA105152; United States / NHLBI NIH HHS / HL / HL090156; United States / NCI NIH HHS / CA / R01 CA105152
[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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / KLF5 protein, human; 0 / KRAS protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 3.6.5.2 / ras Proteins
[Other-IDs]
NLM/ PMC2928981
94.
Tanai C, Yamamoto N, Ohe Y, Takahashi T, Kunitoh H, Murakami H, Yamamoto N, Nakamura Y, Nokihara H, Shukuya T, Baldwin JR, Koshiji M, Tamura T:
A phase I study of enzastaurin combined with pemetrexed in advanced non-small cell lung cancer.
J Thorac Oncol
; 2010 Jul;5(7):1068-74
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[Title]
A phase I study of enzastaurin
combined
with pemetrexed in advanced non-
small cell lung
cancer.
We conducted this phase I study to evaluate the safety, pharmacokinetics, and clinical activity of this combination in patients with previously treated advanced non-
small cell lung
cancer.
CONCLUSIONS: Both schedules of enzastaurin in combination with pemetrexed were well tolerated and clinically active in patients with advanced non-
small cell lung
cancer.
[MeSH-major]
Adenocarcinoma
/ drug therapy. Antineoplastic
Combined
Chemotherapy Protocols / therapeutic use.
Carcinoma
, Non-
Small
-
Cell Lung
/ drug therapy.
Lung
Neoplasms / drug therapy. Neoplasms, Squamous
Cell
/ drug therapy
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Hazardous Substances Data Bank.
PEMETREXED
.
Hazardous Substances Data Bank.
GUANINE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 20453691.001).
[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 I; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Glutamates; 0 / Indoles; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; UC96G28EQF / enzastaurin
95.
Daniele L, Cassoni P, Bacillo E, Cappia S, Righi L, Volante M, Tondat F, Inghirami G, Sapino A, Scagliotti GV, Papotti M, Novello S:
Epidermal growth factor receptor gene in primary tumor and metastatic sites from non-small cell lung cancer.
J Thorac Oncol
; 2009 Jun;4(6):684-8
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[Title]
Epidermal growth factor receptor gene in primary tumor and metastatic sites from non-
small cell lung
cancer.
INTRODUCTION: The majority of patients with non-
small cell lung
cancer (NSCLC) develop distant metastases.
[MeSH-major]
Adrenal Gland Neoplasms / genetics. Brain Neoplasms / genetics.
Carcinoma
, Non-
Small
-
Cell Lung
/ genetics.
Lung
Neoplasms / genetics. Receptor, Epidermal Growth Factor / genetics
[MeSH-minor]
Adenocarcinoma
/ genetics.
Adenocarcinoma
/ secondary. Aged. Aged, 80 and over.
Carcinoma
, Large
Cell
/ genetics.
Carcinoma
, Large
Cell
/ secondary.
Carcinoma
, Squamous
Cell
/ genetics.
Carcinoma
, Squamous
Cell
/ secondary. Chromosomes, Human, Pair 7 / genetics. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis.
Small Cell Lung Carcinoma
/ genetics.
Small Cell Lung Carcinoma
/ secondary. Survival Rate
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(PMID = 19404216.001).
[ISSN]
1556-1380
[Journal-full-title]
Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
[ISO-abbreviation]
J Thorac Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
96.
Oxnard GR, Fidias P, Muzikansky A, Sequist LV:
Non-small cell lung cancer in octogenarians: treatment practices and preferences.
J Thorac Oncol
; 2007 Nov;2(11):1029-35
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[Title]
Non-
small cell lung
cancer in octogenarians: treatment practices and preferences.
INTRODUCTION: Among patients with non-
small cell lung
cancer (NSCLC), patients aged 80 or older have inferior survival.
Although many patients choose aggressive therapies, a
small
but clinically significant portion chose not to receive the offered GRT.
[MeSH-major]
Carcinoma
, Non-
Small
-
Cell Lung
/ therapy.
Lung
Neoplasms / therapy
[MeSH-minor]
Adenocarcinoma
/ therapy. Age Distribution. Aged. Aged, 80 and over.
Carcinoma
, Squamous
Cell
/ therapy. Female. Humans. Male. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome
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