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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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(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

   

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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

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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

   

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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.

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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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[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]

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(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

   

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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

   

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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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(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

   

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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

   

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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

   

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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

   

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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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[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

   

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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

   

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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

   

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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

   

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

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

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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

   

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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

   

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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

   

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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

   

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

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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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[Cites] BMJ. 1995 Oct 7;311(7010):899-909 [7580546.001]

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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

   

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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

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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

   

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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

   

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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

   

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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

   

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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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(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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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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(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

   

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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

   

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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

   

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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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(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

   

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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

   

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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

   

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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

   

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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

   

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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