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Letteratura scientifica selezionata sul tema "Small Cell Lung Cancer"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 31 gennaio 2023

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Articoli di riviste sul tema "Small Cell Lung Cancer"

Greschuchna, D. "Surgical Treatment of Small Cell Lung Cancer". Journal of the Japanese Association for Chest Surgery 3, n. 2 (1989): 169. http://dx.doi.org/10.2995/jacsurg1987.3.2_169.

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_, _. "Small Cell Lung Cancer". Journal of the National Comprehensive Cancer Network 6, n. 3 (marzo 2008): 294. http://dx.doi.org/10.6004/jnccn.2008.0025.

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Small cell lung cancer (SCLC) accounts for 15% of lung cancers. Nearly all cases of SCLC are attributable to cigarette smoking, and the remaining cases are presumably caused by environmental or genetic factors. Compared with non-small cell lung cancer, SCLC generally has a more rapid doubling time, a higher growth fraction, and earlier development of widespread metastases. SCLC is highly sensitive to initial chemotherapy and radiotherapy, but most patients eventually die from recurrent disease. These guidelines detail the management of SCLC from initial diagnosis and staging through treatment, and include information on supportive and palliative care. Important updates to the 2008 version include refined categories for performance status and the addition of topotecan as an option for patients who experience relapse. For the most recent version of the guidelines, please visit NCCN.org

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Hellriegel, H. "ADVANCED NON-SMALL-CELL LUNG CANCER. THE SIGNIFICANCE OF PERSONALIZED THERAPY". Siberian Medical Review, n. 6 (2017): 6–12. http://dx.doi.org/10.20333/2500136-2017-6-12.

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Klaus-Peter, K. "ADVANCED NON-SMALL-CELL LUNG CANCER. THE SIGNIFICANCE OF PERSONALIZED THERAPY". Siberian Medical Review, n. 6 (2017): 6–12. http://dx.doi.org/10.20333/2500136-2017-6-6-12.

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Kalemkerian, Gregory P., Wallace Akerley, Paul Bogner, Hossein Borghaei, Laura Chow, Robert J. Downey, Leena Gandhi et al. "Small Cell Lung Cancer". Journal of the National Comprehensive Cancer Network 9, n. 10 (ottobre 2011): 1086–113. http://dx.doi.org/10.6004/jnccn.2011.0092.

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Kalemkerian, Gregory P., Wallace Akerley, Paul Bogner, Hossein Borghaei, Laura QM Chow, Robert J. Downey, Leena Gandhi et al. "Small Cell Lung Cancer". Journal of the National Comprehensive Cancer Network 11, n. 1 (gennaio 2013): 78–98. http://dx.doi.org/10.6004/jnccn.2013.0011.

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Byrne, Bernadette. "Small cell lung cancer". Nursing Standard 8, n. 9 (23 novembre 1993): 23–28. http://dx.doi.org/10.7748/ns.8.9.23.s42.

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Hinson, J. A., e M. C. Perry. "Small cell lung cancer". CA: A Cancer Journal for Clinicians 43, n. 4 (1 luglio 1993): 216–25. http://dx.doi.org/10.3322/canjclin.43.4.216.

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Bakhmutsky, Nicolay G., Vladimir A. Porkhanov, Vadim N. Bodnya e Rostislav P. Schiryayev. "Small-cell lung cancer". Medical Herald of the South of Russia 8, n. 4 (1 gennaio 2017): 6–13. http://dx.doi.org/10.21886/2219-8075-2017-8-4-6-13.

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Sher, Taimur, Grace K. Dy e Alex A. Adjei. "Small Cell Lung Cancer". Mayo Clinic Proceedings 83, n. 3 (marzo 2008): 355–67. http://dx.doi.org/10.4065/83.3.355.

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Tesi sul tema "Small Cell Lung Cancer"

Sarvi, Sana. "Small cell lung cancer and cancer stem cell-like cells". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9542.

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Small cell lung cancer (SCLC) is a highly aggressive malignancy with extreme mortality and morbidity. Although initially chemo- and radio-sensitive, almost inevitable recurrence and resistance occurs. SCLC patients often present with metastases, making surgery not feasible. Current therapies, rationally designed on underlying pathogenesis, produce in vitro results, however, these have failed to translate into satisfactory clinical outcomes. Recently, research into cancer stem cells (CSCs) has gained momentum and form an attractive target for novel therapies. Based on this concept, CSCs are the cause of neoplastic tissue development that are inherently resistant to chemotherapy, explaining why conventional therapies can shrink the tumour but are unable to eliminate the tumour completely, leading to eventual recurrence. Here I demonstrate that SCLC H345 and H69 cell lines contain a subset of cells expressing CD133, a known CSC marker. CD133+ SCLC sub-population maintained their stem cell-like phenotype over a prolonged period of culture, differentiated in appropriate conditions and expressed the embryonic stem cell marker Oct-4 indicating their stem-like phenotype. Additionally, these cells displayed augmented clonogenic efficacy, were chemoresistant and tumorigenic in vivo, distinct from the CD133- cells. Thus, the SCLC CD133 expressing cells fulfil most criteria of CSClike definition. The molecular mechanisms associated with CD133+ SCLC chemoresistance and growth is unknown. Up-regulated Akt activity, a known promoter of resistance with survival advantage, was observed in CD133+ SCLC cells. Likewise, these cells demonstrated elevated expression of Bcl-2, an anti-apoptotic protein compared to their negative counterpart explaining CD133+ cell chemoresistance phenotype. Additionally, CD133+ cells revealed greater expression of neuropeptide receptors, gastrin releasing peptide (GRP) and V1A receptors compared to the CD133- cells. Addition of exogenous GRP and arginine vasopressin (AVP) to CD133+ SCLC cells promoted their clonogenic growth in semi-solid medium, illustrating for the first time neuropeptide dependent growth of these cells. A novel peptide (peptide-1) was designed based on the known structure of the substance P analogues that have shown benefit in animal models and in early clinical trials. This compound inhibited the growth of SCLC cells in in vitro with improved potency and stability compared to previous analogues and reduced tumorigenicity in vivo. Interestingly, peptide-1 was more effective in CD133+ cells due to increased expression of neuropeptide receptors on these cells. In conclusion, my results show that SCLC cells retain a sub-population of cells that demonstrate CSC-like phenotype. Preferential activation of Akt and Bcl-2 survival pathways and enhanced expression of neuropeptide receptors contribute to CD133+ SCLC chemoresistance and growth. Therefore, it can be proposed that CD133+ cells are the possible cause of SCLC development, treatment resistance and disease recurrence. Despite being chemoresistant, CD133+ cells demonstrated sensitivity to peptide-1. The identification of such new analogue that demonstrates efficacy towards resistant CD133+ SCLC cells is a very exciting step forward in the identification of a potential new therapy for resistant disease.

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Kapeleris, Joanna C. "Circulating tumour cells in non-small cell lung cancer". Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/228607/1/Joanna_Kapeleris_Thesis.pdf.

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Circulating tumour cells (CTCs) have the potential to transform the management of patients with non-small cell lung cancer (NSCLC). The applications of CTCs can identify clinically actionable targets to predict treatment response and to better understand metastasis. CTCs isolated using microfluidics can be used as prognostic indicators of NSCLC as well as characterizing for markers of immunotherapy (PD-L1), molecular targets (ALK, EGFR). Short term cultures were successfully expanded in 9/70 NSCLC patients and cultured for up to 3 months. Optimization of this novel CTC culture model provides opportunity to identify new therapeutics for NSCLC patients in a precision medicine approach.

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Wang, Wei. "Modulation of immune cell responses by small cell lung cancer cells". Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/modulation-of-immune-cell-responses-by-small-cell-lung-cancer-cells(7bdc85c2-acd8-4f13-9d2b-e2ce07d1567b).html.

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Small Cell Lung Cancer (SCLC) accounts for 15-20% of all lung cancers and kills at least one person every 2 hours in the UK. There is no effective treatment and overall 2-year survival is less than 5%. Patients with SCLC have poorly understood local and systemic immune defects. Previous studies have shown several important defects in cell-mediated immune responses in patients with SCLC. A better understanding of interactions between SCLC tumour cells and immune cells may lead to the development of novel therapeutic approaches. There is increasing recognition that immunological biomarkers may add to traditional histological analyses and can be exploited in the management of multiple epithelial malignancies. There are currently no such markers used in the management of SCLC. In my PhD project, I have shown that cell lines from different SCLC patients have differential immunosuppressive capabilities. These properties are mediated by the secretion of differing levels of soluble molecules that can suppress the mixed leukocyte reaction (MLR) and CD4+ T cell proliferation, induce IL-10 secretion and differentiation of functional CD4+CD25+CD127+FoxP3+Helios- regulatory T cells (Tregs) from naïve CD4+ T cells. IL-15 is secreted by SCLC cells in culture in proportion to their immunosuppressive capability. Its in vivo relevance is supported by its presence in tumour biopsy samples. The suppressive effect on CD4+ T cell proliferation and the induction of Treg cell population was not affected by blocking IL-10 or TGF-β signalling but was partially reversed by blocking IL-15 activity. Therefore, IL-15 is one, though not the only, soluble molecule produced by SCLC cells to mediate immune suppression by inducing increased population of Treg cells. This may represent a mechanism by which SCLC cells can suppress the immune response. In addition, SCLC cells supressed TNF-α release from monocytes in response to LPS stimulation, down-regulated expression of CD16 and CD86 and upregulated expression of CD163 and CD206 on monocyte-derived macrophages (MDMs) upon activation. This M2-like phenotype poralization was associated with decreased TNF-α and IL-6 production and increased IL-10 secretion. These effects were abrogated by blocking the signalling of bombesin-like peptides (BLPs) that are neuropeptides produced by SCLC cells using a GRP receptor (GRP-R) antagonist. Therefore, the polarization of macrophages to an M2-like phenotype by SCLC cell-derived BLPs may represent another mechanism by which SCLC tumours suppress the immune response. Finally, SCLC tumour biopsies were shown to be infiltrated with various mononuclear immune cells and Treg cells. CD45 and FoxP3 were used as paninflammatory cell and Treg cell markers respectively. An elevated CD45+ infiltrate was predictive of prolonged survival in SCLC independent of age, sex, stage or treatment strategy. An elevated FoxP3+/CD45+ ratio was predictive of a significantly worse prognosis. This study identifies potential mechanisms by which SCLC tumour cells may downregulate local and systemic immune response, and also identifies an independent prognostic marker to predict patient survival in SCLC. Further, IL- 15 and BLPs are potential novel therapeutic targets in SCLC.

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Oosterhout, Anselmus Gerardus Maria van. "Small cell lung cancer and brain metastasis". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=6643.

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Seute, Tatjana. "Neurologic complications in small cell lung cancer". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=9520.

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Macaulay, Valentine. "Growth regulation in small cell lung cancer". Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47547.

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Sikkink, Stephen K. "Genetic pathology of non-small cell lung cancer". Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250405.

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Brena, Romulo Martin. "Aberrant DNA methylation in human non-small cell lung cancer". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172083621.

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Wong, Wing-sze, e 黃詠詩. "Fusion genes in non-small cell lung cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43781378.

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Ng, Sheng Rong. "CRISPR-mediated interrogation of small cell lung cancer". Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117782.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged student-submitted from PDF version of thesis. Vita.
Includes bibliographical references.
Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine lung carcinoma that remains among the most lethal of solid tumor malignancies. Despite decades of research, treatment outcomes for SCLC remain very poor, highlighting the need for novel approaches to target the disease. Recent genomic sequencing studies have identified multiple recurrently altered genes in human SCLC tumors, many of which remain to be functionally validated. Genetically engineered mouse models (GEMMs) of SCLC have been developed that recapitulate many key features of human SCLC. These models have been used extensively to investigate various aspects of SCLC biology, including tumor initiation, progression and metastasis. The development of the CRISPR-Cas9 system has greatly facilitated genome editing in mammalian cells, leading to its widespread adoption for various applications in cancer biology. We have utilized this system in two complementary ways to investigate the molecular mechanisms involved in SCLC initiation, progression and maintenance. Firstly, we have adapted the CRISPR-Cas9 system for use in GEMMs of SCLC, to enable rapid modeling and functional validation of candidate tumor suppressor genes in vivo. Using this system, we have demonstrated that p107, a member of the retinoblastoma family that is mutated in a significant fraction of human SCLC tumors, is a functional tumor suppressor in SCLC. Notably, loss of p107 in SCLC tumors resulted in significant phenotypic differences compared with loss of its close relative, p130. We also demonstrated that CRISPR-induced mutations can be used to infer lineage relationships between primary and metastatic tumors in the same animal. Secondly, we have performed a CRISPR-based genetic screen, utilizing a custom sgRNA library targeting the druggable genome, to identify novel SCLC-specific genetic vulnerabilities. We found that SCLC cells displayed enhanced sensitivity towards disruption of several key metabolic pathways, including the de novo pyrimidine biosynthesis pathway. Pharmacological inhibition of Dhodh, a key enzyme in this pathway, reduced the viability of SCLC cells in vitro and strongly suppressed SCLC tumor growth in vivo, validating this pathway as a promising therapeutic target in SCLC. Taken together, the work presented here demonstrates the utility of the CRISPR-Cas9 system for performing functional interrogation of SCLC.
by Sheng Rong Ng.
Ph. D.

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Più fonti

Libri sul tema "Small Cell Lung Cancer"

Seeber, Siegfried, a cura di. Small Cell Lung Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82372-5.

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Ramaswamy, Govindan, a cura di. Locally advanced non-small-cell lung cancer. Manhasset, NY: CMP United Business Media, 2004.

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Carr, David T. Selected abstracts on small cell lung cancer. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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1935-, Skarin Arthur T., e Alexander Eben, a cura di. Multimodality treatment of lung cancer. New York: M. Dekker, 2000.

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Recent advances in locally advanced non-small-cell lung cancer. Manhasset, N.Y: CMPMedica, 2006.

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IASLC Workshop on Small Cell Lung Cancer (3rd 1989 Helsingør, Denmark). Management of small cell lung cancer: Third IASLC Workshop on Small Cell Lung Cancer, Elsinore, Denmark, 18-22 June, 1989. A cura di Hansen Heine Høi, Kristjansen Paul E. G e International Association for the Study of Lung Cancer. Amsterdam: Elsevier, 1989.

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M, Marangolo, e Fiorentini G, a cura di. Small cell lung cancer: Proceedings of the International Conference on Small Cell Lung Cancer, 27-28 March 1987, Ravenna, Italy. Oxford: Pergamon Press, 1988.

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International Workshop on Small Cell Lung Cancer Antigens (2nd 1990 Royal Society of Medicine). Small cell lung cancer antigens: Proceedings of the Second International Workshop on Small Cell Lung Cancer Antigens held at the Royal Society of Medicine, 25-27 April 1990. [Basingstoke, Hampshire: published for Cancer Research Campaign by Macmillan, 1991.

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Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Ettinger, David S. The role of chemotherapy in non-small cell lung cancer. Syracuse, NY: Bristol Laboratories Oncology Products, Bristol-Myers Oncology Division, 1986.

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Capitoli di libri sul tema "Small Cell Lung Cancer"

Ravenel, James G. "Small Cell Carcinoma". In Lung Cancer Imaging, 79–88. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-60761-620-7_7.

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Munden, Reginald F., e Jeremy J. Erasmus. "Thoracic Imaging Techniques for Non-Small Cell and Small Cell Lung Cancer". In Lung Cancer, 35–56. New York, NY: Springer New York, 2003. http://dx.doi.org/10.1007/0-387-22652-4_3.

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Hansen, Heine H. "Small Cell Lung Cancer Treatment". In Lung Cancer, 44–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-76031-0_20.

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Hanrahan, Emer O., e Bonnie Glisson. "Small Cell Carcinoma of the Lung". In Lung Cancer, 395–434. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-524-8_16.

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Hann, Christine L. "Small Cell Lung Cancer: Biology Advances". In Lung Cancer, 197–211. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74028-3_9.

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Gomez, Daniel, Zhongxing Liao, Pierre Saintigny e Ritsuko U. Komaki. "Combinations of Radiation Therapy and Chemotherapy for Non-Small Cell and Small-Cell Lung Carcinoma". In Lung Cancer, 353–78. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118468791.ch23.

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Gadgeel, Shirish. "Small Cell Lung Cancer". In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_6764-2.

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Gadgeel, Shirish. "Small Cell Lung Cancer". In Encyclopedia of Cancer, 4261–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_6764.

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Gadgeel, Shirish. "Small Cell Lung Cancer". In Encyclopedia of Cancer, 3444–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6764.

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Wahl, Michael, e Adam Garsa. "Small Cell Lung Cancer". In Handbook of Evidence-Based Radiation Oncology, 285–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_14.

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Atti di convegni sul tema "Small Cell Lung Cancer"

Patel, Sagar S., Ramesh Natarajan e Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.

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Benammar, Sarra, Fatima Mraiche, Jensa Mariam Joseph e Katerina Gorachinova. "Glucose and Transferrin Liganded PLGA Nanoparticles Internalization in Non-Small Lung Cancer Cells". In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0227.

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Introduction: Recently, after a decade of confusing results, several studies pointed out that overexpression of GLUT1 (glucose transporter 1) is a biomarker of worse prognosis in NSCLC. Nonetheless, the presence of transferrin (Tf receptor), which is overexpressed in most cancer tissues and most lung cancers as well, in NSCLC is also an indicator of very poor prognosis. Therefore, these ligands can be used for active targeting of lung cancer cells and improved efficacy of internalization of cancer therapy using nanomedicines. Objectives: Having the background, the main goal of the project was the assessment of the influence of the glucose and transferrin ligands on the efficacy of internalization of the designed (i) glucose decorated PLGA (poly lactic-coglycolic acid) nanoparticles (Glu-PLGA NPs) and (ii) transferrin decorated PLGA nanoparticles (Tf-PLGA NPs) in comparison to (iii) non-liganded PLGA NPs using a A549 lung cancer cells. Methods: Glu-PLGA NPs, Tf-PLGA NPs and PLGA NP - fluorescently labelled), were designed using a sonication assisted nanoprecipitation method. Further, physicochemical properties characterization (particle size analysis, zeta potential, FTIR analysis, DSC analysis), cytotoxicity evaluation using MTT test, and cell internalization studies of DTAF labelled NPs using fluorimetry in A549 NSCLC cell line were performed. Results: The results pointed to a significantly improved internalization rate of the liganded compared to PLGA NPs. Glu-PLGA NPs showed higher internalization rate compared to Tf-PLGA and PLGA NPs, in the serum-supplemented and serumfree medium even at normal levels of glucose in the cell growth medium. Conclusion: The developed nanocarriers offer unique advantages of enhanced targetability, improved cell internalization and decreased toxicity, which makes them promising solution for current therapeutic limitations.

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Hider, Nabilah Hanani, Anis Salwa Binti Mohd Khairuddin e Effariza Binti Hanafi. "VGG Classification Model for Lung Cancer Diagnosis". In International Technical Postgraduate Conference 2022. AIJR Publisher, 2022. http://dx.doi.org/10.21467/proceedings.141.9.

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Lung cancer is one of the most common cancers worldwide that leads to small survival rate. It is important to detect the presence of these harmful cells in human body at early stages to prevent it from worsening. The primary goal of this study is to propose an efficient lung cancer image classification model using deep learning method. The cancer image classification framework is proposed by using transfer learning with Convolutional Neural Network (CNN) to classify three categories of 5,100 cancer images namely lung adenocarcinoma, lung squamous cell carcinoma and benign lung tissues obtained from the dataset. Several experiments have been performed to improve the VGG19 model performance by varying the optimizers including RMSprop, Adam and SGD. The performance of all experiments conducted were analyzed based on the training and validation curves, classification reports and the confusion metrics.

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Jabbour, E., P. Sidhom e R. El-Bizri. "Small Cell Lung Cancer, Does It Cavitate". In 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.a7012.

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Xing, Fuyong, e Lin Yang. "Robust cell segmentation for non-small cell lung cancer". In 2013 IEEE 10th International Symposium on Biomedical Imaging (ISBI 2013). IEEE, 2013. http://dx.doi.org/10.1109/isbi.2013.6556493.

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Hamedi, Z., S. Kamboj, S. Kumar, R. A. Jiwani e N. Sharma. "Transformation of Non-Small Cell Lung Cancer (NSCLC) to Small Cell Lung Cancer (SCLC), Mechanism of Treatment Resistance?" In 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.a4871.

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Doerr, F., S. Stange, A. Gassa, J. Seo, M. Heldwein, T. Wahlers e K. Hekmat. "It Is Worth Operating Small Cell Lung Cancer?" In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678934.

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Dias, Margarida, Raquel Marçoa, Rita Linhas, Sérgio Campainha, Sara Conde e Ana Barroso. "Non-small cell lung cancer in never-smokers". In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2796.

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Neffati, O., L. Fekih, H. Kammoun, A. Ayari, I. Mejri, H. Smadhi, I. Akrout et al. "Prognostic factors in non-small cell lung cancer". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4294.

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Fu, Pin-Kuei. "Octogenarians With Operable Non-Small Cell Lung Cancer". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4407.

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Rapporti di organizzazioni sul tema "Small Cell Lung Cancer"

Freire, Mariana, Diana Martins, Maria Filomena Botelho e Fernando Mendes. Biomarkers of resistance mechanisms in innovative lung cancer treatments - A systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, settembre 2022. http://dx.doi.org/10.37766/inplasy2022.9.0011.

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Review question / Objective: This systematic review aims to provide an overview of the immunotherapy resistance mechanisms and identify potential biomarkers associated with immunotherapy response in NSCLC, as well as examine new treatment options to overcome this hurdle. Condition being studied: Lung Cancer (LC) remains one of the leading cancers worldwide. In 2020, were globally estimated 2 206 771 new cases and 1 796 144 deaths, representing the uttermost frequent cause of cancer death. LC is classified histologically into small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC), being the last one the most common, representing 80 to 85% of all LC. The three predominantly subtypes of NSCLC are lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large cell carcinoma (LCLC). NSCLC is usually diagnosed in advanced-staged disease due to ambiguous and delayed severe symptoms.

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Watson, Mark A. Genomic Characterization of Brain Metastasis in Non-Small Cell Lung Cancer Patients. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2014. http://dx.doi.org/10.21236/ada606182.

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Sage, Julien. Development of Antidepressants as Novel Agents To Treat Small Cell Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, agosto 2014. http://dx.doi.org/10.21236/ada613784.

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Rudin, Charles M. Genetic and Epigenetic Determinants of Lung Cancer Subtype: Adenocarcinoma to Small Cell Conversion. Fort Belvoir, VA: Defense Technical Information Center, agosto 2015. http://dx.doi.org/10.21236/ada623599.

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Kang, Jing, Jun Zhang, Zongsheng Tian, Ye Xu, Jiangbi Li e Mingxina Li. The efficacy and safety of immune-checkpoint inhibitor plus chemotherapy versus chemotherapy for non-small cell lung cancer: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maggio 2022. http://dx.doi.org/10.37766/inplasy2022.5.0156.

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Review question / Objective: Population: histologically confirmed advanced NSCLC patients; Intervention: received immune-checkpoint inhibitor plus chemotherapy; Comparison:received chemotherapy; Outcome: reported OS, PFS, ORR and TRAEs; Study design: RCT. Condition being studied: Lung cancer is the primary cause of cancer-related deaths, with an estimated 2.20 million new cases and 1.79 million deaths every year, and 85% of all primary lung cancers are non-small cell lung cancer. Eligibility criteria: Studies were considered eligible if they met the following criteria: (1) being an randomized controlled trial published in English, (2) histologically confirmed advanced NSCLC patients, (3) reported OS, PFS, ORR and TRAEs, (4) the intervention group received immune-checkpoint inhibitor plus chemotherapy, while the control group received chemotherapy, (5) When numerous papers reporting the same trial were found, the most current or most complete publications were chosen. The following were the exclusion criteria: (1) duplicate articles, (2) reviews, meta-analyses, case reports, editorials and letters, (3) molecular biology or animal research, (4) retrospective or prospective observational cohort studies.

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Nelkin, Barry D. Role of CDK5 as a Tumor Suppressor Gene in Non-Small Cell Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, agosto 2014. http://dx.doi.org/10.21236/ada610950.

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Yu, Guocan, Qingshan Cai, Xudong Xu, Yanqin Shen e Kan Xu. Anlotinib-containing regimen for advanced small-cell lung cancer: A protocol of meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, gennaio 2021. http://dx.doi.org/10.37766/inplasy2021.1.0034.

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Li, Yong, Fang Yang e Ya-Yong Huang. Sublobar resection versus ablation for stage I non-small-cell lung cancer: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, gennaio 2021. http://dx.doi.org/10.37766/inplasy2021.1.0075.

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Chen, Zhong-Ke, e Yuan-Shun Xu. I-125 seeds with chemotherapy for progressive non-small-cell lung cancer after first-line treatment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, ottobre 2021. http://dx.doi.org/10.37766/inplasy2021.10.0120.

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