Bibliografías temáticas / Pulmonary adenocarcinoma

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Literatura académica sobre el tema "Pulmonary adenocarcinoma"

Autor: Grafiati

Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "Pulmonary adenocarcinoma"

Faccin, Mayane, Filipe Cestari, Mônica Matos, João Pedro Cavasin, Anna Zimmermann, Flávio Carvalho, Geane Pagliosa y Aline Viott. "Pulmonary adenocarcinoma in mare". Brazilian Journal of Veterinary Pathology 11, n.º 3 (29 de noviembre de 2018): 108–12. http://dx.doi.org/10.24070/bjvp.1983-0246.v11i3p108-112.

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Carey, F. A. "Pulmonary adenocarcinoma". Current Diagnostic Pathology 7, n.º 3 (septiembre de 2001): 187–93. http://dx.doi.org/10.1054/cdip.2001.0070.

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Zhao, Wei, Tong-bing Chen y Hui Wang. "Ikaros is heterogeneously expressed in lung adenocarcinoma and is involved in its progression". Journal of International Medical Research 48, n.º 8 (agosto de 2020): 030006052094586. http://dx.doi.org/10.1177/0300060520945860.

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Objective The aim of the present study was to assess the expression of the Ikaros transcription factor (IKZF1) in lung adenocarcinoma and investigate whether expression levels of Ikaros are correlated with lung adenocarcinoma progression. Methods We conducted a retrospective study of 325 cases of resected stage I pulmonary adenocarcinoma, in which histological subtyping was performed according to the 2015 World Health Organization classification. We performed immunohistochemical examinations to assess expression of Ikaros in pulmonary adenocarcinomas and evaluated the correlation between Ikaros expression and cancer progression. Results Immunohistochemical staining was heterogeneous, with the majority of well-differentiated and moderately differentiated lung adenocarcinomas being weakly positive and the majority of the poorly differentiated lung adenocarcinomas exhibiting strong positive staining. Higher expression of Ikaros was associated with tumor recurrence or metastasis. Conclusions Ikaros is heterogeneously expressed in different subtypes of lung adenocarcinoma; higher expression of Ikaros was found to be associated with cancer progression.

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Aulakh, Kanwaijit S., Cary D. Chisholm, Daniel A. Smith y V. O. Speights. "TTF-1 and Napsin A Do Not Differentiate Metastatic Lung Adenocarcinomas From Primary Esophageal Adenocarcinomas: Proposal of a Novel Staining Panel". Archives of Pathology & Laboratory Medicine 137, n.º 8 (1 de agosto de 2013): 1094–98. http://dx.doi.org/10.5858/arpa.2012-0305-oa.

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Context.—When adenocarcinomas arise within the esophagus, particularly when located away from the gastroesophageal junction, it may be important in some patients to differentiate between a primary esophageal adenocarcinoma and metastasis from another site. Lung adenocarcinoma is one tumor that has been reported to frequently metastasize to the esophagus. Objectives.—To create a panel of immunohistochemical markers that can reliably distinguish between an esophageal and pulmonary primary; within the gastrointestinal pathology literature, including published articles and textbooks, common lung immunohistochemical markers, such as TTF-1, are assumed to be negative in esophageal adenocarcinoma, yet, to our knowledge, no study has yet investigated the veracity of that presumption. Design.—In this study, 24 cases each of pulmonary and esophageal adenocarcinomas were stained with TTF-1, napsin A, CDX2, 34βE12, N-cadherin, and IMP3 in an attempt to define an optimal panel for differentiation. Esophageal adenocarcinomas occurring at the gastroesophageal junction were excluded in this study because a gastric primary tumor cannot be excluded in those cases. Results.—Surprisingly, TTF-1 and napsin A were positive in similar proportions of tumors from both sites. Those markers that differentiated statistically between esophageal and pulmonary adenocarcinoma were IMP3, CDX2, and N-cadherin. Conclusions.—When differentiating the origin of a tumor as either esophageal or pulmonary, an immunohistochemical panel consisting of IMP3, CDX2, and N-cadherin is superior to either TTF-1 or napsin A.

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Usacheva, A. Yu, N. K. Silanteva, A. P. Petrosian, V. S. Usachev, A. V. Sidorin y S. A. Ivanov. "Pulmonary Mucinous Adenocarcinoma". Journal of radiology and nuclear medicine 102, n.º 1 (10 de marzo de 2021): 42–46. http://dx.doi.org/10.20862/0042-4676-2021-102-1-42-46.

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Mucinous adenocarcinoma is a rare malignant tumor of the lung, which is accompanied by extremely scarce and nonspecific symptoms. This leads to an increase in the timing of its recognition, especially in young women. Given the poor prognosis of the pathlogy, the problem of its early diagnosis with histological and immuno-histochemical studies is extremely urgent. The presented clinical case demonstrates the possibilities of computed tomography with intravenous contrast enhancement in a young woman for the diagnosis of mucinous lung adenocarcinoma.

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Gong, Jiali, Ying Fan y Hongyang Lu. "Pulmonary enteric adenocarcinoma". Translational Oncology 14, n.º 8 (agosto de 2021): 101123. http://dx.doi.org/10.1016/j.tranon.2021.101123.

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Ayub, Adil, Omar Nunez Lopez, Adam Booth y Ikenna Okereke. "Pulmonary hepatoid adenocarcinoma". Journal of Thoracic and Cardiovascular Surgery 158, n.º 4 (octubre de 2019): e139-e140. http://dx.doi.org/10.1016/j.jtcvs.2019.06.023.

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Handa, Yoshinori, Yuichiro Kai, Takuhiro Ikeda, Hidenori Mukaida, Hiromi Egawa y Mayumi Kaneko. "Pulmonary enteric adenocarcinoma". General Thoracic and Cardiovascular Surgery 64, n.º 12 (3 de julio de 2015): 749–51. http://dx.doi.org/10.1007/s11748-015-0569-0.

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Moran, Cesar A. "Pulmonary Adenocarcinoma: The Expanding Spectrum of Histologic Variants". Archives of Pathology & Laboratory Medicine 130, n.º 7 (1 de julio de 2006): 958–62. http://dx.doi.org/10.5858/2006-130-958-pateso.

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Abstract Pulmonary adenocarcinoma is one of the most common types of lung cancer. Traditionally, adenocarcinomas have been divided based on their degree of resemblance to their parent tissues into 3 histopathologic types: well, moderately, and poorly differentiated. In the majority of cases, this schema is sufficient to categorize these lung tumors. However, there is a considerable group of tumors in which the histology is not that of the classic gland-forming neoplasm. Thus, although the terminology of adenocarcinoma is applied in such cases, the histopathologic features are different from those of the more conventional variants. The current review addresses these unusual variants and the importance of recognizing and properly categorizing them to avoid unnecessary additional workup or possible misdiagnosis.

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Yang, Kun, Huifeng Jiang y Qiuyao Li. "Primary pulmonary hepatoid adenocarcinoma". Medicine 98, n.º 14 (abril de 2019): e15053. http://dx.doi.org/10.1097/md.0000000000015053.

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Tesis sobre el tema "Pulmonary adenocarcinoma"

Brocksmith, Debra. "Identification and analysis of differentially expressed genes in human pulmonary adenocarcinoma". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29447.

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Increasing evidence indicates a shift is occurring in the distribution of lung cancer subtypes, with relative and absolute increases in the number of adenocarcinomas. The exact reason for this remains unclear. Molecular and cytogenetic studies have identified several genetic changes occurring in the development of pulmonary adenocarcinoma but many more remain unknown. Until recently, identification of unknown genes relied heavily on the use of linkage-based studies, which are both laborious and time-consuming. Recently, a new technique has been developed to investigate gene expression with greater accuracy and experimental ease: differential display reverse transcription polymerase chain reaction (DDRT-PCR).;In this study DDRT-PCR has been applied to search for novel, differentially expressed genes in human pulmonary adenocarcinoma, using both human normal and adenocarcinoma cell lines and matched surgical tissues. Human cell lines were used in preliminary experiments to adapt and establish the experimental techniques. Results from these studies produced three differentially expressed bands, one of which was a true positive. This cDNA tag was found to show 100% sequence homology to human fibronectin mRNA. Fibronectin is known to show different patterns of expression in various tumours. Similar studies were set up using human surgical specimens collected from two major thoracic units. Results from one matched human tissue sample identified eight differentially expressed bands. Again only one of these demonstrated true differential expression with a northern blot.;Expression of the tissue-positive band, called H8, was diminished in pulmonary adenocarcinoma RNA samples and may represent a novel tumour suppressor gene. The sequence data that has been obtained from the H8 cDNA tag appears to correspond to the 3' untranslated region. Northern blotting studies revealed high levels of H8 in normal lung tissue matched to other types of lung tumour, normal liver, stomach and colon, with lower expression in the corresponding tumour samples.

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Salvatori, Daniela. "Studies on the pathogenesis and epidemiology of ovine pulmonary adenocarcinoma (OPA)". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29348.

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OPA is caused by a retrovirus known as jaagsiekte sheep retrovirus 9JSRV). A unique feature of OPA is the absence of a specific humoral immune response to JRSV, despite the highly productive infection in the lungs and the disseminated lymphoid infection. JRSV cannot be cultivated on cell culture. The aim of this work is to develop tools for the diagnosis and control of the disease. The first part of the thesis has been dedicated to the production of recombinant proteins to use for immunization trials, immunological assays and immunohistochemistry techniques. Knowing the peculiar relationship between the virus and the immune system the starting point is to prove the hypothesis that immunization with JSRV can overcome tolerance and stimulate protective immune responses. Another key point in the aim of finding a vaccine for the control of OPA was to develop and animal model for the evaluation of potential vaccine preparations. The neonatal lambs’ model has been very useful to unravelling the role of JSRV and some of its pathogenesis, but because of the age of the lambs, it, clearly, is not suitable for assessment of potential vaccines. In the present study different age groups of lambs (1 month, 3 months, 6 months) have been inoculated intratracheally with the same dos of infectious lung fluid. The disease was recognised in all groups by clinical observations, gross pathology and histopathology. During the experiment viraemia was successfully detected using a novel PCR technique. Inducing OPA in older lambs and developing a method for detecting viraemia due to JSRV infection mean to move forward a system for the diagnosis and control of the disease.

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Aldujaily, Esraa Abdulaal. "An investigation of tumour-associated macrophages and statin therapy in human pulmonary adenocarcinoma". Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/43086.

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Introduction: Pulmonary adenocarcinoma represents a major area of unmet clinical need in cancer treatment. Recent advances in immunotherapy which target the PD-L1 immune checkpoint promise great improvements in outcomes for some patients. The immune system offers several other possible targets. Tumour associated macrophages (TAMs) are a common feature of lung tumour stroma. Epidemiological data have indicated a possible role of statins in reducing cancer mortality via their anti-inflammatory effects, but the mechanisms underpinning this are not clear. The possible roles of pro-tumour versus anti-tumour macrophages were investigated in lung adenocarcinomas, and the possibility of influencing this axis with statin drugs. Methods: Immunohistochemical evaluation was used with phenotyping of TAMs using multiplex immunohistochemistry in tissue microarray sections of about 300 lung adenocarcinomas with matched clinicopathological data. Quantitative digital pathology, using Hamamatsu scanner images and Visiopharm software to count and phenotype TAMs in TMA sections. Results: It has been found that the pro-tumourigenic (CD68+CD163+) TAM numbers are elevated in invasive versus in situ tumour regions. Interestingly, statin users have significantly lower protumourigenic macrophage numbers than non-statin users, significantly in areas of in situ tumour growth in comparison to invasive lesions. Tumours in statin users were also of significantly lower histological grade, showing a higher percentage of in situ components than non-statin users. Conclusion: Automated image analysis methods efficiently count and classify macrophages in tumour tissue. Statin therapy is related to macrophage class, specifically within in situ lesions. These data support a model whereby statins target protumourigenic TAMs in early disease, highlighting their potential as cancer-preventive agents.

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Summers, Christina. "Immune responses during jaagsiekte sheep retrovirus infection and development of ovine pulmonary adenocarcinoma". Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/30805.

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Jaagsiekte sheep retrovirus (JSRV) is the aetiological agent of sheep pulmonary adenomatosis (SPA), a contagious bronchioloalveolar carcinoma, which imposes a serious economic burden on the sheep farming industry. This study evaluated the immunological responses during experimentally induced JSRV infection and tumorigenesis in conventionally housed and specific pathogen free (SPF) neonatal lambs, and in adult field cases in the terminal stages of SPA. This study identified, for the first time, changes in cellular function in the peripheral blood of JSRV-infected animals by measuring the in vitro lymphoproliferative response to various mitogens. The presence of JSRV did not affect the level of response to phytohaemagglutin (PHA) and pokeweed mitogen (PWM) stimulation, but a reduced response to concanavalin A (ConA) was demonstrated in the JSRV-infected animals. The reduced response to ConA was detected prior to the diagnosis of clinical symptoms and was also evident in the terminal stages of SPA. The presence of JSRV also affected the mitogenicity of the mannose-specific, monocotyledonous Narcissus pseudonarcissus lectin (NPA). The level of proliferation was comparable between JSRV-infected and control lambs, but post-stimulation phenotyping revealed an altered phenotypic profile, with elevated numbers of T and B lymphocytes from JSRV-infected animals. Furthermore, the addition of exogenous mannnose completely inhibited NPA mitogenicity in control but not in JSRV infected lambs. It has been established that NPA possesses insecticidal properties, which could potentially increase pest resistance in transgenic crops. During this study we revealed that NPA mitogenicity is age-dependent in sheep, with no lymphoproliferative response detected in adult animals. This research was extended to include human subjects, and we have shown that NPA is slightly mitogenic for adult lymphocytes but that mitogenicity is increased more than sevenfold for lymphocytes purified from umbilical cord blood. These findings indicate possible physiological implications as a result of introducing foreign lectins into human and animal food sources.

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Agrawal, Deepti [Verfasser], Philipp J. [Akademischer Betreuer] Jost, Radu Roland [Gutachter] Rad y Marc [Gutachter] Schmidt-Supprian. "RIPK3 suppresses Kras-driven pulmonary adenoma and adenocarcinoma formation / Deepti Agrawal ; Gutachter: Radu Roland Rad, Marc Schmidt-Supprian ; Betreuer: Philipp J. Jost". München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1211725278/34.

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França, Fernanda Stapenhorst. "Reprogramação metabólica e possíveis alvos terapêuticos em adenocarcinoma pulmonar". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/151298.

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O câncer de pulmão é a neoplasia maligna mais insidiosa da oncologia, sendo responsável pelo maior número de mortes relacionadas ao câncer no mundo. Oitenta e cinco por cento dos casos de câncer de pulmão são de não-pequenas células (CPNPC), onde sua maioria é adenocarcinoma. Apesar dos progressos nas pesquisas em câncer, o prognóstico de pacientes em estágios avançados permanece ruim, portanto faz-se necessária o desenvolvimento de novas abordagens terapêuticas. Nesse trabalho, focamos no metabolismo energético tumoral, o qual apresenta alto consumo de glicose e liberação de lactato mesmo na presença de oxigênio, o chamado Efeito Warburg. Outras vias metabólicas também encontram-se alteradas, processo conhecido como reprogramação metabólica. Dessa forma, o objetivo desse trabalho é buscar possíveis marcadores tumorais e alvos terapêuticos envolvidos no metabolismo energético, através de uma abordagem que começa na bioinformática, de forma a prospectar candidatos a partir de uma vasta gama de genes envolvidos com o metabolismo. Foram selecionados os genes IDH1, LDHA e PYGB a partir de uma análise de enriquecimento gênico, os quais foram submetidos a análises de sobrevida em bancos de dados de microarranjo. Em seguida, o nível de expressão das proteínas IDH1 e LDHA foi avaliado por imunohistoquímica em uma coorte clínica, onde pudemos observar um aumento na expressão de IDH1 em tumores em relação a tecidos pulmonares sadios. Ainda, em modelo celular, observamos que ambas as proteínas estavam aumentadas em células tumorais de adenocarcinoma pulmonar em relação a células sadias de pulmão. Ao combinar o inibidor de LDHA, oxamato, com cisplatina na linhagem de adenocarcinoma pulmonar A549, foi observado uma interação de sinergismo e, na linhagem pulmonar sadia NHBE, foi observado um antagonismo, de forma que essa abordagem se mostra promissora na terapêutica. Já ao combinar o inibidor de IDH1, oxalomalato, com cisplatina na linhagem A549, foi observado um antagonismo. Assim, esse estudo demonstrou um possível papel de biomarcador para adenocarcinoma pulmonar para a enzima IDH1 e um possível papel terapêutico para a enzima LDHA.

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Balbinotti, Helier. "Investigação dos possíveis papéis de vesículas extracelulares e suas proteínas na transferência intercelular de resistência à cisplatin em adenocarcinoma de pulmão humano". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2018. http://hdl.handle.net/10183/187265.

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Muitos pacientes com câncer de pulmão possuem tumores em estágio avançado, sendo que a principal droga utilizada para o seu tratamento é a cisplatina (CDDP). O uso da CDDP é limitado, pois tumores podem adquirir resistência a sua ação. Vesículas extracelulares (VEs) apresentam funções na transferência de quimiorresistência entre células tumorais, sendo que proteínas participam desse efeito. O estudo do perfil proteico de VEs de células tumorais sensíveis e resistentes a drogas permite compreender melhor os mecanismos dessa transferência. Portanto, este trabalho focou na investigação dos possíveis papéis de VEs e suas proteínas na transferência intercelular de resistência entre células humanas de adenocarcinoma de pulmão sensíveis e resistentes à CDDP. Sublinhagem celular com resistência (RA-A549) foi estabelecida, expondo a linhagem A549 a concentrações de CDDP. Após, foram realizados cocultivos transwell entre as células RA-A549 com células A549 para verificar a internalização celular de VEs e para avaliar a transferência de resistência entre as linhagens. No ensaio de transferência, células A549 foram cocultivadas com células A549 ou RA-A549 na presença ou não de CDDP por 72 h e, após, marcadas com FDA. As VEs foram isoladas do sobrenadante de cultivo pelo método de centrifugação diferencial e ultracentrifugação e analisadas por diferentes técnicas. As proteínas de VEs isoladas de RA-A549 e A549 foram analisadas por LC-MS/MS. A sublinhagem RA-A549 apresentou valor de IC50 superior ao da linhagem A549 (cerca de 4,5 vezes). Células A549 cocultivadas com RA-A549 foram capazes de internalizar as VEs de RA-A549 e apresentaram uma menor sensibilidade a CDDP (p < 0,001), sugerindo transferência intercelular de quimiorresistência. As VEs isoladas apresentaram diâmetro variável (10-420 nm), com predominância de ~100 nm, sendo que a sua presença foi ainda confirmada por detecção da proteína CD63. Foram identificadas 225 proteínas diferentes nas VEs das células A549 e RA-A549, entre essas, marcadores clássicos de VEs, como CD9, CD8, Alix, anexinas, Rab GTPases e HSPs. Foram identificadas proteínas nas VEs potencialmente envolvidas na transferência de resistência a CDDP e associadas com a proliferação e adesão celular, o bloqueio de fluxo da droga, invasão e migração celular, evasão de apoptose, atenuação do sistema imune e da coagulação, angiogênese, regulação do ciclo celular, o reparo de DNA, modulação do metabolismo energético, o efluxo ou a neutralização da droga, degradação proteica, reorganização da estrutura e formato das células tumorais.
Many patients with lung cancer have tumors in advanced stage and the main drug used for their treatment is cisplatin (CDDP). The CDDP use is limited, because tumors may become resistant to their action. Extracellular vesicles (EVs) have functions in chemoresistance transfer between tumor cells and proteins participate in this effect. The study of VEs protein profile from drug–sensitive and –resistant tumor cells allows a better understanding of the mechanisms of this transfer. Therefore, this work focused on the investigation of the possible roles of EVs and their proteins in the resistance intercellular transfer between CDDP–resistant and –sensitive lung adenocarcinoma human cells. Cell subline with resistance (RA-A549) was established, exposing the A549 line to CDDP concentrations. After, transwell co-cultures were performed between RA-A549 cells with A549 cells to verify EVs cell uptake and to assess the resistance transfer between the lines. In the transfer assay, A549 cells were co-cultivated with the A549 cells or RA-A549 with CDDP or not by 72 h and thereafter labeled with FDA. The EVs were isolated from culture supernatant by the differential centrifugation and ultracentrifugation method and analyzed by different techniques. The isolated EVs protein from RA-A549 and A549 were analyzed by LC-MS/MS. The RA-A549 subline showed IC50 value greater than of A549 line (about 4.5 fold). A549 cells co-cultivated with RA-A549 were able to RA-A549 EVs uptake and showed a lower sensitivity to CDDP (p < 0,001), suggesting chemoresistance intercellular transfer. The isolated EVs showed a variable diameter (10-420 nm) with a predominance of ~100 nm, and their presence was further confirmed by detection of CD63 protein. Two hundred and twenty-five different proteins were identified in the A549 and RA-A549 cell EVs, among these EVs classic protein markers, such as CD9, CD8, Alix, annexins, Rab GTPases e HSPs. Proteins were identified in the EVs potentially involved in the CDDP-resistance transfer and associated with cell proliferation and adhesion, drug flow blockage, cell invasion and migration, apoptosis evasion, attenuation of immune system and coagulation, angiogenesis, cell cycle regulation, DNA repair, modulation of energy metabolism, efflux or neutralization of the drug, protein degradation, reorganization of the tumor cell structure and shape.

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Dutra, Cristine de Souza. "Análise proteômica de proteínas sintetizadas em resposta acisplatina em células de adenocarcinoma de pulmão humano resistentes e sensíveis a droga". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2018. http://hdl.handle.net/10183/180571.

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O câncer de pulmão está entre os mais frequentes na população mundial e é o responsável pelo maior número de mortes relacionadas ao câncer. Como o câncer de pulmão é identificado em estágios avançados de desenvolvimento, o principal tratamento é baseado em quimioterapia utilizando moléculas derivadas de platina, principalmente a cisplatina (CDDP). A CDDP é capaz de formar ligações cruzadas no DNA resultando em morte celular, porém muitos pacientes apresentam tumores que são resistentes ao tratamento com CDDP. Esta resistência é uma das principais barreiras para o sucesso do tratamento do câncer de pulmão através de quimioterapia. Para entendermos melhor os mecanismos envolvidas na resistência a CDDP em células de câncer de pulmão, foram utilizadas células sensíveis (A549) e resistentes a CDDP (A549/CDDP) para a identificação de proteínas recém-sintetizadas em resposta ao tratamento com a droga através da técnica BONCAT. Através desta técnica foi possível a identificação de 173 e 136 proteínas reguladas por CDDP nas células A549 e A549/CDDP, respectivamente As proteínas identificadas estão relacionadas a diversos mecanismos moleculares distintos que potencialmente estão envolvidos na resposta a CDDP, como por exemplo splicing alternativo, resposta a estresse oxidativo, manutenção do telômero, regulação da apoptose e reorganização do citoesqueleto. Os resultados mostram que as células A549/CDDP são menos suscetíveis ao dano no DNA causado por CDDP do que as células sensíveis, A549. Além disso, as células A549/CDDP são capazes de aumentar a expressão de proteínas capazes de combater as espécies reativas de oxigênio geradas devido a presença de CDDP. Além disto, CDDP é capaz de induzir diferentes vias apoptóticas em células com diferentes sensibilidades à droga. Nas células A549, CDDP induz a ativação da via extrínseca enquanto que nas A549/CDDP ela é capaz de induzir a ativação da via intrínseca de apoptose. Portanto, nosso estudo foi capaz de fornecer evidencias de proteínas e vias que são diferencialmente expressas e ativadas após o tratamento com CDDP.
Lung cancer is among the most frequent cancer in the world population and it is the leading cause of cancer-related deaths. Since lung cancer is identified in advanced stages of development, the main treatment is based in chemotherapy using platinum containing compounds, mainly cisplatin (CDDP). CDDP is able to crosslink with DNA leading to cell death, however many patients show tumor that are resistance to CDDP. This resistance is one of the main barriers for the success of lung cancer treatment by chemotherapy. To understand the mechanisms involved in CDDP resistance in lung cancer, we used CDDPsensitive (A549) and –resistant (A549/CDDP) cells to identify the newly synthesized proteins in response to drug exposure by BONCAT technique. It was possible the identification of 173 and 136 proteins regulated by CDDP in A549 and A549/CDDP cells, respectively. The identified proteins were related to several distinct molecular mechanisms potentially involved in CDDP response, including alternative splicing, response to oxidative stress, telomere maintenance, apoptosis regulation and cystoskeleton reorganization. Our results showed that A549/CDDP cells are less susceptible to DNA damage caused by CDDP than A549 cells. A549/CDDP also are able to increase the expression of proteins that combat the reactive oxygen species generated due to CDDP presence. In addition, CDDP induces different apoptotic pathways in drug-sensitive and resistant cell. In the A549 cells, CDDP induces the activation of the extrinsic pathway, while in A549/CDDP cells CDDP induces the intrinsic apoptotic pathway. So, our study was able to provide evidence of proteins and pathways that are differentially express and activated after CDDP treatment.

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Rocha, José Aurillo. "Perfil epidemiológico e molecular em pacientes com câncer de pulmão e adenocarcinoma no Ceará". reponame:Repositório Institucional da UFC, 2015. http://www.repositorio.ufc.br/handle/riufc/15374.

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ROCHA, José Aurillo. Perfil epidemiológico e molecular em pacientes com câncer de pulmão e adenocarcinoma no Ceará. 2015. 105 f. Tese (Doutorado em Farmacologia) – Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, 2015.
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Introduction: Cancer is a leading global health problems and one of the most important causes of morbidity and mortality in public health. According to the World Health Organization (WHO) is the second leading cause of death worldwide, second only to the diseases cardiovasculares.Temos national high incidence of patients with advanced lung cancer. There unpredictability of epidemiological profiles and therapeutic responses. Molecular biology has been important in the characterization of tumor differentiation and prognosis of the disease. New treatments are directed by pharmacogenomic characteristics. Little is known about the prevalence of these genes in Cearáand Latin America as well as on clinical characteristics and outcomes related. Objective: To identify the characteristics and distribution of the epidemiological profile of patients with advanced lung cancer, treated at the oncology clinic at the Messejana Hospital - Dr. Carlos Alberto Studart. Material and Methods: An observational, prospective and analytical study with inclusion of 135 patients with advanced lung cancer, between 08/2012 to 12/2014; being analyzed for the distribution of origin by frequency, sex, race, education, clinical complaints, smoking and molecular profile. Results: There was a predominance in the success of patients from small towns of Ceará(69%); female patients (51.1%), low education (first degree or less -19%), farmers (22.4%), Pardos (47.4%) and smokers. (79%) The histological subtype was adenocarcinoma predominantly (32.5%). Dyspnea was the main complaint clinica.O predominant initial treatment occurred in hospital stay (75.5%). Conclusion: In this group of patients identified a profile of epidemiological characteristics. Created a hospital cancer registry. There proportionality results with the literature.
Introdução: O câncer éum dos principais problemas mundiais de saúde e uma das causas mais importantes de morbidade e mortalidade em saúde pública. Segundo a Organização Mundial de Saúde (OMS) éa segunda causa de morte no mundo;perdendo apenas para as doenças cardiovasculares.Temos alta incidência nacional de pacientes com câncer de pulmão avançado. Há imprevisibilidade de perfis epidemiológicos e respostas terapêuticas. A biologia molecular tem sido importante na caracterização sobre a diferenciação tumoral e prognóstico da doença.Novos tratamentos são direcionados por características farmacogenômicas. Pouco se sabe sobre a prevalência desses genes no Cearáe na América Latina, bem como sobre características clínicas e desfechos relacionados. Objetivo: Identificar as características e distribuição do perfil epidemiológico dos pacientes portadores de neoplasia de pulmão avançado, atendidos no ambulatório de oncologia do Hospital de Messejana - Dr. Carlos Alberto Studart. Material e Métodos: Estudo observacional, prospectivo e analítico com inclusão de 135 pacientes portadores de neoplasia de pulmão avançado, entre 08/2012 a 12/2014; sendo analisados quanto a distribuição de frequência por procedência, sexo, raça, escolaridade, queixas clinicas, tabagismo e perfil molecular. Resultados: Houve predominância na procedência de pacientes oriundos de cidades do interior do Ceará (69%); pacientes do sexo feminino (51,1%), baixa escolaridade (1o grau ou menos -19%), agricultores (22,4%), Pardos (47,4%) e tabagistas.(79%)O subtipo histológico adenocarcinoma foi predominante (32,5%). Dispnéia foi a principal queixa clinica. O atendimento inicial predominante se deu no período de internamento (75,5%). Conclusão: Neste grupo de pacientes identificou-se um perfil de características epidemiológicas próprias. Criou-se um registro de câncer do hospital.Há proporcionalidade de resultados com a literatura.

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Spilimbergo, Fernanda Brum. "Carcinoma bronquioloalveolar (CBA) : aspectos diagnósticos e terapêuticos em uma série de 72 casos estudados entre 1965 e 2006". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/60751.

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O carcinoma bronquioloalveolar (CBA), definido originalmente como um subtipo de adenocarcinoma com origem em zonas pulmonares periféricas, citologicamente bem diferenciado, com crescimento ao longo dos septos alveolares íntegros e propagação canalicular, teve seu conceito restringido, a partir de 2004: “Carcinoma bronquioloalveolar puro” para os tumores com padrão de crescimento lepídico ao longo dos septos alveolares, sem evidências de invasão do estroma, vascular, linfática ou pleural, preservando a arquitetura pulmonar, e “Adenocarcinoma tipo misto com componente bronquioloalveolar”, no caso de haver alguma evidência de invasão. No presente trabalho foram estudados 72 pacientes com adenocarcinoma de pulmão, internados no período entre 1965 e 2006 em um Serviço especializado em doenças pulmonares, cuja análise do conjunto laudo anatomopatológico, manifestações clínicas e achados radiográficos levaram à conclusão diagnóstica de carcinoma bronquioloalveolar (CBA). O estudo dividiu-se em dois períodos: 1965- 2001com 51 casos, e 2002-2006 com 21 casos. A série completa, constituída de 72 pacientes com CBA, representou 4,0% dos casos de adenocarcinoma e cerca de 1,0 % de todos os casos de câncer de pulmão atendidos no Serviço em 42 anos. Dos 72 pacientes com o diagnóstico de CBA, a maioria (95,8%) era da raça branca, e 45 (62,5%) do sexo masculino. A média de idade foi de 68,6 anos para o sexo masculino e 64,7 anos para o feminino. Do total de pacientes, 65,0% eram tabagistas. Os sintomas clínicos mais freqüentes foram tosse, dispnéia, perda de peso e broncorréia. Hipocratismo digital esteve presente em 20,8% dos pacientes e febre em 13,9%. O padrão acinar-lobular foi observado ao radiograma de tórax em 61,1% dos casos, nódulo-massa em 29,2% e intersticial em 16,7%; as lesões pulmonares foram unilaterais em 72,2% dos casos, unilobares em 30,6%; adenopatias mediastinais foram observadas em 9,7% dos pacientes, e derrame pleural ocorreu em um caso (1,4%). Em 50,0% dos casos o material para diagnóstico foi obtido por toracotomia; em 18,1% por endoscopia (biópsia/lavado), em 13,9% por punção pulmonar transcutânea, e em 20,8% inicialmente por citologia de escarro. Em todos os casos, todavia, o diagnóstico de CBA acabou sendo corroborado por exame histopatológico – na maioria das vezes em material obtido por toracotomia e, em 2 casos, à necropsia. A conduta terapêutica adotada foi cirurgia de ressecção pulmonar em 39 (54,2%) pacientes (19 lobectomias, 3 segmentectomias, 14 reseccções parciais maiores, e 3 pneumonectomias); 18 pacientes (25,0%) receberam quimioterapia e 4 (5,6%) radioterapia, isoladamente ou associadas a procedimento cirúrgico (4,0%); e 15 pacientes (20,8%) tiveram somente tratamento paliativo.
The Bronchioloalveolar carcinoma (BAC), at first defined as a sub type of adenocarcinoma originating in peripheral pulmonary zones, cytologically well differentiated, growing along the alveolar septa, and propagating via bronchial tree, had since 2004 its concept restricted: Pure bronchioloalveolar carcinoma for tumors growing along the alveolar septa without stroma, vessel, lymphatic or pleural invasion, preserving the pulmonary architecture, and Mixed type of adenocarcinoma with bronchioloalveolar component when invasion is present. In this work there were studied 72 patients with adenocacrcinoma of the lung, who were admitted between 1965 and 2006 in a Service of Chest Diseases, whose the histopathologic, clinical manifestations and radiographic findings concluded by the diagnostic of bronchioloalveolar carcinoma (BAC). The study was divided in two parts: a 1965-2001 one with 51 cases, and another from 2001 to 2006 with 21 cases. The whole series of 72 patients represented 4.0 per cent of the adenocarcinoma and 1.0 per cent of the lung cancer cases verified in 42 years. Of 72 patients with BAC, 45 (62.5%) were male, most (95.8%) white. The mean age was 68.6 years for males and 64.7 years for females, and 65.5% were smokers. The most frequent clinical symptoms were cough, dyspnea, weight loss and bronchorrea. Digital clubbing was present in 20.8% of the patients and fever in 13.9% . At the X-ray, 61.1 % of the cases presented as an acinar-lobular pattern, in 29.2% as a nodule-mass and in 16.7% as an interstitial aspect. Unilateral lesions were observed in 72.2% of the cases, in one pulmonary lobe in 30.6%; in 9.7% there were mediastinal lymphadenopathies, and in one case (1.4%) a pleural effusion was identified. Diagnostic material was obtained in 50% of cases by toracotomy, in 18.1% by endoscopy, in 13.9% by punch lung biopsy, and in 20.8% by sputum cytology. In all cases, however, the BAC diagnosis was confirmed by histopathologic criteria – mostly at thoracotomy ,and in two cases at necropsy. The therapeutic conduction in these 72 cases of BAC was pulmonary resection in 39 (54.2%) patients (lobectomy 19, segmentectomy 3, major partial resection 14, pneumonectomy 3); chemotherapy in 18 (25.0%) and radiotherapy in 4 (5.5%), alone or combined with a surgical procedure (4.0%); and 15 patients (20.8%) received only symptomatic medication.

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Libros sobre el tema "Pulmonary adenocarcinoma"

Pulmonary Adenocarcinoma: Approaches to Treatment. Elsevier, 2019. http://dx.doi.org/10.1016/c2017-0-00337-3.

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Horn, Leora. Pulmonary Adenocarcinoma: Approaches to Treatment. Elsevier - Health Sciences Division, 2018.

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Horn, Leora. Pulmonary Adenocarcinoma: Approaches to Treatment. Elsevier - Health Sciences Division, 2018.

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Frank, Kelly. Fibrosis and Pulmonary Adenocarcinoma: Everything You Need to Know about Cystic Fibrosis and Pulmonary Adenocarcinoma. Independently Published, 2020.

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Capítulos de libros sobre el tema "Pulmonary adenocarcinoma"

Kini, Sudha R. "Pulmonary Adenocarcinoma". En Color Atlas of Pulmonary Cytopathology, 91–102. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/978-0-387-21641-6_7.

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Blackmon, Shanda, Armin Ernst, Philip T. Cagle, Timothy C. Allen y Armando E. Fraire. "Adenocarcinoma". En Atlas of Neoplastic Pulmonary Disease, 145–49. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89839-1_33.

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Ghosh, Subha. "Adenocarcinoma". En Handbook of Imaging in Pulmonary Disease, 3–7. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68165-4_1.

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De Las Heras, M., L. González y J. M. Sharp. "Pathology of Ovine Pulmonary Adenocarcinoma". En Current Topics in Microbiology and Immunology, 25–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55638-8_2.

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Kycko, Anna y Michal Reichert. "Proteins overexpressed in ovine pulmonary adenocarcinoma". En Farm animal proteomics, 98–101. Wageningen: Wageningen Academic Publishers, 2012. http://dx.doi.org/10.3920/978-90-8686-751-6_23.

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Cobb, Jared y Chen Zhang. "Solid Pulmonary Adenocarcinoma Versus Large-Cell Undifferentiated Carcinoma". En Practical Lung Pathology, 39–43. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-14402-8_7.

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Liu, Dongyou. "Pulmonary Adenocarcinoma, Squamous Cell Carcinoma, and Adenosquamous Carcinoma". En Tumors and Cancers, 79–84. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/b22275-15.

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Rambaldi, Pier Francesco. "Pulmonary Solitary Nodule in Patient with Prostatic Adenocarcinoma in Follow-Up". En Whole-Body FDG PET Imaging in Oncology, 301–3. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5295-6_69.

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Rambaldi, Pier Francesco. "Pulmonary Adenocarcinoma with Pleural Metastases: Restaging After Radiotherapy and Pleural Talcage". En Whole-Body FDG PET Imaging in Oncology, 313–17. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5295-6_72.

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York, D. F. y G. Querat. "A History of Ovine Pulmonary Adenocarcinoma (Jaagsiekte) and Experiments Leading to the Deduction of the JSRV Nucleotide Sequence". En Current Topics in Microbiology and Immunology, 1–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55638-8_1.

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Actas de conferencias sobre el tema "Pulmonary adenocarcinoma"

Kang, V. y K. Jordan. "Idiopathic Pulmonary Fibrosis Concealing Lung Adenocarcinoma". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6347.

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Kan, F., M. Ueoka, A. Abdul-Ghani y S. J. Evans. "Anomalies in Sweating Due to Pulmonary Adenocarcinoma". En American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4850.

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Siriphand, C. y A. Benchakroun. "The Morphologic Mimicry of Pulmonary Hepatoid Adenocarcinoma". En American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3377.

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Wang, H., H. Li y N. Xu. "A Case-Control Study of Primary Pulmonary Mucinous Adenocarcinoma and Non-Mucinous Lung Adenocarcinoma". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2464.

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Xie, M. y X. Li. "Two Cases of Pulmonary Enteric Adenocarcinoma in One Family". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5715.

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Alsharif, M., K. Islam, M. Abdou y T. Vo. "Eosinophilia in Pulmonary Adenocarcinoma; An Extremely Rare Paraneoplastic Manifestation". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6927.

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Sirikonda, N. y A. Ali. "Sarcoid Like Reaction Confounding the Diagnosis of Pulmonary Adenocarcinoma". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2312.

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Gabitan, M. C. y M. A. G. Donguines. "VA-ECMO Assisted Tumor Resection of Pulmonary Adenocarcinoma : A Case Report". En American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3348.

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Yi, E., C. Lopez y N. Seetharamu. "Hypertrophic Osteoarthropathy Treatment with Octreotide for Patient with Unresectable Pulmonary Adenocarcinoma". En American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3369.

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Sharma, P., S. Deitz, C. V. Teba, P. Linden y J. Wasman. "A Rare Case of Synchronous Primary Pulmonary Malt Lymphoma and Lung Adenocarcinoma". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5866.

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