Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 10 de 10
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Am J Cancer Res ; 4(2): 161-71, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24660105

RESUMO

Radiation-induced lung injury (RILI) is a significant dose limiting complication of thoracic radiation for lung, breast, and esophageal cancer. Strategies for increasing the therapeutic index of radiation involve the use of radiosensitizing agents. We investigated the potential of M867 to sensitize non-small cell lung cancer (NSCLC) to radiation in vivo, while assessing its protective effects in normal lung parenchyma. H460-Luc2 cells were implanted into the mediastinum of athymic nude mice, which were separated into four treatment groups: control, M867, radiation therapy (RT) or combination. H460-Luc2 cell cultures were treated in parallel. Tumor growth was followed using bioluminescence imaging. Immunohistochemistry staining was used to detect phospho-Smad2/3 and cleaved caspase-3 expression. Western blot was done for the detection of cleaved caspase-3 and phospho-Smad2/3. TUNEL assays were used to measure apoptosis. M867+RT group had significantly increased tumor growth inhibition relative to either treatment alone (p=0.02). M867+RT was associated with increased levels of apoptosis (p<0.01), but combination treatment was associated with a decrease in caspase-dependent apoptosis relative to RT alone (p<0.01). We found that this increase in apoptosis in the M867+RT group was due to caspase-independent cell death. Based on early biomarker analyses of phospho-Smad 2/3 and cleaved caspase-3, M867+RT had a radio-protective effect on normal lung parenchyma. M867 may increase the therapeutic ratio of RT by enhancing the radiosensitivity of NSCLC while mitigating RILI. Further research is warranted to examine the late effects of lung injury and to study differences in the mechanism of action of M867 on lung cancer and normal tissue.

2.
Int J Radiat Oncol Biol Phys ; 84(4): e525-31, 2012 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-22836051

RESUMO

PURPOSE: c-Met is overexpressed in some non-small cell lung cancer (NSCLC) cell lines and tissues. Cell lines with higher levels of c-Met expression and phosphorylation depend on this receptor for survival. We studied the effects of AMG-458 on 2 NSCLC cell lines. METHODS AND MATERIALS: 3-(4,5-Dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assays assessed the sensitivities of the cells to AMG-458. Clonogenic survival assays illustrated the radiosensitizing effects of AMG-458. Western blot for cleaved caspase 3 measured apoptosis. Immunoblotting for c-Met, phospho-Met (p-Met), Akt/p-Akt, and Erk/p-Erk was performed to observe downstream signaling. RESULTS: AMG-458 enhanced radiosensitivity in H441 but not in A549. H441 showed constitutive phosphorylation of c-Met. A549 expressed low levels of c-Met, which were phosphorylated only in the presence of exogenous hepatocyte growth factor. The combination of radiation therapy and AMG-458 treatment was found to synergistically increase apoptosis in the H441 cell line but not in A549. Radiation therapy, AMG-458, and combination treatment were found to reduce p-Akt and p-Erk levels in H441 but not in A549. H441 became less sensitive to AMG-458 after small interfering RNA knockdown of c-Met; there was no change in A549. After overexpression of c-Met, A549 became more sensitive, while H441 became less sensitive to AMG-458. CONCLUSIONS: AMG-458 was more effective in cells that expressed higher levels of c-Met/p-Met, suggesting that higher levels of c-Met and p-Met in NSCLC tissue may classify a subset of tumors that are more sensitive to molecular therapies against this receptor.


Assuntos
Aminopiridinas/farmacologia , Carcinoma Pulmonar de Células não Pequenas/radioterapia , Neoplasias Pulmonares/radioterapia , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores , Pirazóis/farmacologia , Tolerância a Radiação/efeitos dos fármacos , Radiossensibilizantes/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/efeitos da radiação , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral/efeitos dos fármacos , Linhagem Celular Tumoral/efeitos da radiação , Sobrevivência Celular , Ensaios de Seleção de Medicamentos Antitumorais/métodos , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Proteínas de Neoplasias/metabolismo , Fosforilação , Proteínas Proto-Oncogênicas c-met/metabolismo
3.
Med Oncol ; 29(5): 3258-64, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22729368

RESUMO

Aberrant activation and dysfunction of the EGFR/PI3K/Akt signaling pathways are commonly reported in breast cancer. Constitutive activation of the PI3K/Akt pathway by the lack of PTEN regulation is associated with resistance to novel targeted therapies including EGFR inhibitors. We aimed to study whether Ly294002, an inhibitor of PI3K, could enhance the cytotoxicity of AG1478, an inhibitor of EGFR, on breast cancer cells. We tested these agents in the MDA-MB-468 and MCF-7 breast cancer cell lines with different EGFR and PTEN profiles (MDA-MB-468: high expression of EGFR and PTEN mutation; MCF-7: low expression of EGFR and PTEN wild type). Simultaneous inhibition of EGFR and PI3K in MDA-MB-468 cells with combined Ly294002 and AG1478 treatment had a greater anti-proliferative effect and increased mitotic death than either treatment alone. In addition, more apoptosis and increased induction of cell arrest at G0/G1 phase were observed in MDA-MB-468 cells with the combined treatment. Phosphor-EGFR and its downstream signal transducer, phosphor-Akt, were fully attenuated only by simultaneous treatment with Ly294002 and AG1478. These data suggest that the inhibition of PI3K could enhance the cytotoxicity of EGFR inhibitors on breast cancer cells and tumors which overexpress EGFR and demonstrate mutated PTEN. This dual inhibition treatment protocol may have important therapeutic implication in the treatment of a subset of breast cancer patients with high expression of EGFR and deficient function of PTEN.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Apoptose/efeitos dos fármacos , Cromonas/administração & dosagem , Inibidores Enzimáticos/farmacologia , Morfolinas/administração & dosagem , Quinazolinas/administração & dosagem , Tirfostinas/administração & dosagem , Western Blotting , Neoplasias da Mama , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Sinergismo Farmacológico , Receptores ErbB/antagonistas & inibidores , Feminino , Citometria de Fluxo , Humanos , Inibidores de Fosfoinositídeo-3 Quinase
4.
Int J Gynecol Cancer ; 22(5): 718-24, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22552829

RESUMO

OBJECTIVE: Artemisinin has been shown to inhibit the growth of some human cancer cells. In this study, we investigated the radiosensitizing effects of artemisinin on cervical cancer cells and normal human fibroblast cells and also assessed some possible mechanisms for these effects. MATERIALS AND METHODS: Two cervical cancer cell lines, HeLa and SiHa cells, and GM0639 normal human fibroblast cell line were treated with various concentrations of artemisinin plus radiation; the cell viability was tested using both 3-(4,5-dimethylthiazolyl-2-y1)-2, 5-diphenyltetrazolium bromide and clonogenic assays. Radiation dose-modifying factors were measured by clonogenic survival assay. Annexin V/propidium iodide assay for the evaluation of apoptosis and cell cycle phase were determined by flow cytometry, and the expression of the cell cycle-associated proteins Wee 1 and cyclin B1 were analyzed by Western blot analysis. RESULTS: Artemisinin showed higher cytotoxicity in cervical cancer cell lines, especially in SiHa cells, than in the normal cell line. In both clonogenic assay and apoptosis, artemisinin sensitized the HeLa cancer cells to the cytotoxicity of radiation, yielding a dose-modifying factor of 1.24, but not SiHa cancer cells and GM normal cells. At a dose of 110 nmol/L, artemisinin did not change the distribution of cell cycle in 3 tested cell lines, but artemisinin abrogated the radiation-induced G2 blockade. Analyses of G2-checkpoint-related proteins, the activation of Wee 1 and depression of cyclin B1 expression induced by radiation, could be restored to the control level by artemisinin. CONCLUSIONS: Given the unique cytotoxic profile of artemisinin on cancer cells and normal cells, artemisinin may be a potentially promising radiosensitizer through the regulation of the expression of G2 checkpoint-related proteins like Wee 1 and cyclin B1, and improve therapeutic ratios for the combination of artemisinin and ionizing irradiation in the treatment of patients with cervical cancer.


Assuntos
Artemisininas/farmacologia , Fibroblastos/efeitos dos fármacos , Fase G2/efeitos dos fármacos , Fase G2/efeitos da radiação , Tolerância a Radiação/efeitos dos fármacos , Radiossensibilizantes/farmacologia , Neoplasias do Colo do Útero/tratamento farmacológico , Anti-Infecciosos/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/efeitos da radiação , Western Blotting , Proteínas de Ciclo Celular/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos da radiação , Células Cultivadas , Ensaio de Unidades Formadoras de Colônias , Feminino , Fibroblastos/citologia , Fibroblastos/efeitos da radiação , Humanos , Neoplasias do Colo do Útero/patologia , Neoplasias do Colo do Útero/radioterapia , Raios X
5.
Int J Radiat Oncol Biol Phys ; 83(4): e453-64, 2012 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-22520478

RESUMO

Therapeutic decisions in non-small cell lung cancer (NSCLC) have been mainly based on disease stage, performance status, and co-morbidities, and rarely on histological or molecular classification. Rather than applying broad treatments to unselected patients that may result in survival increase of only weeks to months, research efforts should be, and are being, focused on identifying predictive markers for molecularly targeted therapy and determining genomic signatures that predict survival and response to specific therapies. The availability of such targeted biologics requires their use to be matched to tumors of corresponding molecular vulnerability for maximum efficacy. Molecular markers such as epidermal growth factor receptor (EGFR), K-ras, vascular endothelial growth factor (VEGF), mammalian target of rapamycin (mTOR), and anaplastic lymphoma kinase (ALK) represent potential parameters guide treatment decisions. Ultimately, identifying patients who will respond to specific therapies will allow optimal efficacy with minimal toxicity, which will result in more judicious and effective application of expensive targeted therapy as the new paradigm of personalized medicine develops.


Assuntos
Biomarcadores Tumorais/antagonistas & inibidores , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Terapia de Alvo Molecular/métodos , Biomarcadores Tumorais/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Carcinoma Pulmonar de Células não Pequenas/radioterapia , Expressão Gênica , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/radioterapia , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas de Neoplasias/metabolismo , Pesquisa Translacional Biomédica
6.
Int J Radiat Oncol Biol Phys ; 83(3): e391-7, 2012 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-22414288

RESUMO

PURPOSE: Mutations in the epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/Akt signaling transduction pathway are common in cancer. This pathway is imperative to the radiosensitivity of cancer cells. We aimed to investigate the radiosensitizing effects of the simultaneous inhibition of EGFR and PI3K in breast cancer cells. METHODS AND MATERIALS: MCF-7 cell lines with low expression of EGFR and wild-type PTEN and MDA-MB-468 cell lines with high expression of EGFR and mutant PTEN were used. The radiosensitizing effects by the inhibition of EGFR with AG1478 and/or PI3K with Ly294002 were determined by colony formation assay, Western blot was used to investigate the effects on downstream signaling. Flow cytometry was used for apoptosis and cell cycle analysis. Mice-bearing xenografts of MDA-MB-468 breast cancer cells were also used to observe the radiosensitizing effect. RESULTS: Simultaneous inhibition of EGFR and PI3K greatly enhanced radiosensitizing effect in MDA-MB-468 in terms of apoptosis and mitotic death, either inhibition of EGFR or PI3K alone could enhance radiosensitivity with a dose-modifying factor (DMF(SF2)) of 1.311 and 1.437, radiosensitizing effect was further enhanced by simultaneous inhibition of EGFR and PI3K with a DMF(SF2) at 2.698. DNA flow cytometric analysis indicated that dual inhibition combined with irradiation significantly induced G0/G1 phase arrest in MDA-MB-468 cells. The expression of phosphor-Akt and phosphor-Erk1/2 (induced by irradiation and PI3K inhibitor) were fully attenuated by simultaneous treatment with both inhibitors in combination with irradiation. In addition, dual inhibition combined with irradiation induced dramatic tumor growth delay in MDA-MB-468 xenografts. CONCLUSIONS: Our study indicated that simultaneous inhibition of EGFR and PI3K could further sensitize the cancer cells to irradiation compared to the single inhibitor with irradiation in vitro and in vivo. The approach may have important therapeutic implication in the treatment of a subset of breast cancer patients with high expression of EGFR and deficient function of PTEN.


Assuntos
Neoplasias da Mama/radioterapia , Receptores ErbB/antagonistas & inibidores , Proteínas de Neoplasias/antagonistas & inibidores , Inibidores de Fosfoinositídeo-3 Quinase , Tolerância a Radiação , Animais , Apoptose , Neoplasias da Mama/metabolismo , Linhagem Celular Tumoral , Cromonas/farmacologia , Receptores ErbB/genética , Feminino , Fase G1/fisiologia , Fase G1/efeitos da radiação , Humanos , Camundongos , Camundongos Nus , Morfolinas/farmacologia , PTEN Fosfo-Hidrolase/genética , Fosfatidilinositol 3-Quinases/genética , Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-akt/metabolismo , Quinazolinas/farmacologia , Radiossensibilizantes/farmacologia , Distribuição Aleatória , Fase de Repouso do Ciclo Celular/fisiologia , Fase de Repouso do Ciclo Celular/efeitos da radiação , Tirfostinas/farmacologia
7.
Int J Radiat Oncol Biol Phys ; 82(3): e563-72, 2012 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-22197230

RESUMO

PURPOSE: The development of drug-resistant phenotypes has been a major obstacle to cisplatin use in non-small-cell lung cancer. We aimed to identify some of the molecular mechanisms that underlie cisplatin resistance using microarray expression analysis. METHODS AND MATERIALS: H460 cells were treated with cisplatin. The differences between cisplatin-resistant lung cancer cells and parental H460 cells were studied using Western blot, MTS, and clonogenic assays, in vivo tumor implantation, and microarray analysis. The cisplatin-R cells were treated with human recombinant insulin-like growth factor (IGF) binding protein-3 and siRNA targeting IGF-1 receptor. RESULTS: Cisplatin-R cells illustrated greater expression of the markers CD133 and aldehyde dehydrogenase, more rapid in vivo tumor growth, more resistance to cisplatin- and etoposide-induced apoptosis, and greater survival after treatment with cisplatin or radiation than the parental H460 cells. Also, cisplatin-R demonstrated decreased expression of insulin-like growth factor binding protein-3 and increased activation of IGF-1 receptor signaling compared with parental H460 cells in the presence of IGF-1. Human recombinant IGF binding protein-3 reversed cisplatin resistance in cisplatin-R cells and targeting of IGF-1 receptor using siRNA resulted in sensitization of cisplatin-R-cells to cisplatin and radiation. CONCLUSIONS: The IGF-1 signaling pathway contributes to cisplatin-R to cisplatin and radiation. Thus, this pathway represents a potential target for improved lung cancer response to treatment.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/terapia , Cisplatino/farmacologia , Resistencia a Medicamentos Antineoplásicos/fisiologia , Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/fisiologia , Fator de Crescimento Insulin-Like I/fisiologia , Neoplasias Pulmonares/terapia , Radiossensibilizantes/farmacologia , Antígeno AC133 , Aldeído Desidrogenase/metabolismo , Animais , Antígenos CD/metabolismo , Apoptose/efeitos dos fármacos , Biomarcadores Tumorais/metabolismo , Western Blotting , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Sobrevivência Celular/efeitos da radiação , Quimiorradioterapia/métodos , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Feminino , Glicoproteínas/metabolismo , Humanos , Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/farmacologia , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Camundongos , Camundongos Nus , Análise em Microsséries , Peptídeos/metabolismo , RNA Interferente Pequeno/farmacologia , Tolerância a Radiação/efeitos dos fármacos , Tolerância a Radiação/fisiologia , Tolerância a Radiação/efeitos da radiação , Receptor IGF Tipo 1/antagonistas & inibidores , Proteínas Recombinantes/farmacologia , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/efeitos da radiação , Ensaios Antitumorais Modelo de Xenoenxerto/métodos
8.
J Thorac Oncol ; 6(11): 1801-9, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21760551

RESUMO

INTRODUCTION: Defects in the apoptosis pathway limit the effectiveness of radiation in non-small cell lung cancer (NSCLC) therapy. BV6 is an antagonist of cIAP1 and XIAP, members of the inhibitors of apoptosis (IAP) family. We investigated the potential of BV6 to sensitize NSCLC cell lines to radiation. METHODS: HCC193 and H460 lung cancer cell lines were treated with BV6 to investigate the effects of drug administration on cell proliferation, apoptosis, inhibition of XIAP and cIAP1, and radiosensitivity. Subsequent immunoblotting and Hoechst staining were used to determine the role of apoptosis in radiosensitization. Finally, the pathway of apoptosis was characterized by Western blot analysis for cleaved caspase-8 and cleaved caspase-9 and enzyme-linked immunosorbent assays for TNF-α. RESULTS: HCC193 was found to be more sensitive than H460 to BV6-induced apoptosis in a concentration-dependent and time-dependent manner. BV6 significantly sensitized both cell lines to radiation (HCC193-DER = 1.38, p < 0.05 at 1 µM BV6; H460-DER = 1.42, p < 0.05 at 5 µM BV6), but a higher concentration of and longer incubation time with BV6 was necessary for H460 cells. The BV6-induced radiosensitization of HCC193 favored the extrinsic pathway of apoptosis, whereas that of H460 favored the intrinsic pathway. CONCLUSIONS: BV6, an IAP antagonist, significantly enhanced the radiosensitization of HCC193 and H460 cells in vitro. More research is warranted to test the mechanism of action of BV6 and to assess its potential in vivo and in the clinical setting.


Assuntos
Adenocarcinoma/patologia , Apoptose/efeitos dos fármacos , Carcinoma Pulmonar de Células não Pequenas/patologia , Radioisótopos de Césio , Proteínas Inibidoras de Apoptose/antagonistas & inibidores , Neoplasias Pulmonares/patologia , Radiossensibilizantes/farmacologia , Adenocarcinoma/tratamento farmacológico , Adenocarcinoma/radioterapia , Apoptose/efeitos da radiação , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/radioterapia , Quimiorradioterapia , Inibidores Enzimáticos/farmacologia , Ensaio de Imunoadsorção Enzimática , Humanos , Técnicas In Vitro , Proteínas Inibidoras de Apoptose/metabolismo , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/radioterapia , Células Tumorais Cultivadas , Fator de Necrose Tumoral alfa/metabolismo
9.
Mol Pain ; 7: 45, 2011 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-21645415

RESUMO

BACKGROUND: Electrical acupuncture (EA) has been utilized in acute pain management. However, the neuronal mechanisms that lead to the analgesic effect are still not well defined. The current study assessed the intensity [optimal EA (OI-EA) vs. minimal EA (MI-EA)] effect of non-noxious EA on supraspinal regions related to noxious heat pain (HP) stimulation utilizing an EA treatment protocol for acute pain and functional magnetic resonance imaging (fMRI) with correlation in behavioral changes. Subjects underwent five fMRI scanning paradigms: one with heat pain (HP), two with OI-EA and MI-EA, and two with OI-EA and HP, and MI-EA and HP. RESULTS: While HP resulted in activations (excitatory effect) in supraspinal areas known for pain processing and perception, EA paradigms primarily resulted in deactivations (suppressive effect) in most of these corresponding areas. In addition, OI-EA resulted in a more robust supraspinal sedative effect in comparison to MI-EA. As a result, OI-EA is more effective than MI-EA in suppressing the excitatory effect of HP in supraspinal areas related to both pain processing and perception. CONCLUSION: Intensities of EA plays an important role in modulating central pain perception.


Assuntos
Analgesia por Acupuntura/métodos , Mapeamento Encefálico , Eletroacupuntura/métodos , Imageamento por Ressonância Magnética , Percepção da Dor/fisiologia , Doença Aguda , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Encéfalo/fisiopatologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Medição da Dor , Limiar da Dor/fisiologia , Temperatura , Adulto Jovem
10.
Radiat Res ; 176(4): 486-93, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21663394

RESUMO

Lung cancer is the leading cause of cancer-related death in the United States despite recent advances in our understanding of this challenging disease. An animal model for high-throughput screening of therapeutic agents for advanced lung cancer could help promote the development of more successful treatment interventions. To develop our orthotopic lung cancer model, luciferase-expressing A549 cancer cells were injected into the mediastinum of athymic nude mice. To determine whether the model would allow easy monitoring of response to therapeutic interventions, tumors were treated with 30 mg/kg Paclitaxel or were irradiated with 5 fractions of 2 Gy, and tumor burden was monitored using bioluminescence imaging. Evidence of radiation-induced lung injury was assessed using immunohistochemical staining for phospho-Smad2/3 and cleaved caspase-3. We found that tumor implantation recapitulated advanced human lung cancer as evidenced by tumor establishment and proliferation within the mediastinum. The tumor responded to Paclitaxel or radiation as shown by decreased tumor bioluminescence and improved overall survival. Immunohistochemistry revealed increased phospho-Smad2/3 and cleaved caspase-3 in irradiated lungs, consistent with radiation-induced lung injury. This orthotopic lung cancer model may help provide a method to assess therapeutic interventions in a preclinical setting that recapitulates locally advanced lung cancer.


Assuntos
Modelos Animais de Doenças , Medições Luminescentes , Neoplasias Pulmonares/patologia , Animais , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/efeitos da radiação , Feminino , Humanos , Injeções , Luciferases/genética , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Pulmão/efeitos da radiação , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/radioterapia , Camundongos , Imagem Molecular , Estadiamento de Neoplasias , Paclitaxel/farmacologia , Paclitaxel/uso terapêutico , Lesões Experimentais por Radiação/metabolismo , Transfecção
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...