Gotowe bibliografie tematyczne / Lung alveolar cells

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Lung alveolar cells”

Autor: Grafiati
Data publikacji: 3 czerwca 2025
Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Lung alveolar cells"

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Zhang, Honglei, Yong Cui, Zhiyu Zhou, Yan Ding, and Hongguang Nie. "Alveolar Type 2 Epithelial Cells as Potential Therapeutics for Acute Lung Injury/Acute Respiratory Distress Syndrome." Current Pharmaceutical Design 25, no. 46 (2020): 4877–82. http://dx.doi.org/10.2174/1381612825666191204092456.

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: Acute lung injury/acute respiratory distress syndrome is a common clinical illness with high morbidity and mortality, which is still one of the medical problems urgently needed to be solved. Alveolar type 2 epithelial cells are an important component of lung epithelial cells and as a kind of stem cells, they can proliferate and differentiate into alveolar type 1 epithelial cells, thus contributing to lung epithelial repairment. In addition, they synthesize and secrete all components of the surfactant that regulates alveolar surface tension in the lungs. Moreover, alveolar type 2 epithelial c
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Wu, Huijuan, and Nan Tang. "Stem cells in pulmonary alveolar regeneration." Development 148, no. 2 (2021): dev193458. http://dx.doi.org/10.1242/dev.193458.

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ABSTRACTThe lungs are constantly exposed to the external environment and are therefore vulnerable to insults that can cause infection and injury. Maintaining the integrity and barrier function of the lung epithelium requires complex interactions of multiple cell lineages. Elucidating the cellular players and their regulation mechanisms provides fundamental information to deepen understanding about the responses and contributions of lung stem cells. This Review focuses on advances in our understanding of mammalian alveolar epithelial stem cell subpopulations and discusses insights about the reg
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Herrero, Raquel, Mishie Tanino, Lincoln S. Smith, et al. "The Fas/FasL pathway impairs the alveolar fluid clearance in mouse lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 5 (2013): L377—L388. http://dx.doi.org/10.1152/ajplung.00271.2012.

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Alveolar epithelial damage is a critical event that leads to protein-rich edema in acute lung injury (ALI), but the mechanisms leading to epithelial damage are not completely understood. Cell death by necrosis and apoptosis occurs in alveolar epithelial cells in the lungs of patients with ALI. Fas activation induces apoptosis of alveolar epithelial cells, but its role in the formation of lung edema is unclear. The main goal of this study was to determine whether activation of the Fas/Fas ligand pathway in the lungs could alter the function of the lung epithelium, and the mechanisms involved. T
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Rakhmonova, H.N, S.M Mukhitdinova, and F.Z Rakhmonov. "MORPHOLOGICAL STRUCTURE OF NEUROEPITHELIAL CELLS IN RABBIT LUNGS." Journal of Science-Innovative Research in Uzbekistan 2, no. 2 (2024): 153–56. https://doi.org/10.5281/zenodo.10645714.

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The morphofunctional features of NET in the developing respiratory lung have been studied. Lungs of 23 rabbits aged 1-30 days served as a material for the study. Paraffin sections were stained with hematoxylin and eosin, according to the Van-Gizon method, impregnated according to the Grimelius method. Histochemical detection of acetylcholinesterase (AChE) activity was carried out on frozen sections of unfixed lungs by the method of M. Karnovsky and L. Roots. The study allowed to establish that in the rabbit lung NET cells are detected in the respiratory secti
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Khalil, N., R. N. O'Connor, K. C. Flanders, W. Shing, and C. I. Whitman. "Regulation of type II alveolar epithelial cell proliferation by TGF-beta during bleomycin-induced lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 5 (1994): L498—L507. http://dx.doi.org/10.1152/ajplung.1994.267.5.l498.

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Three isoforms of transforming growth factor-beta (TGF-beta) are found in mammalian cells and are potent regulators of inflammation, connective tissue synthesis, cellular proliferation, and differentiation. To determine the distribution and regulation of TGF-beta isoforms during pulmonary injury, a rat model of bleomycin-induced lung inflammation and repair was used. Using immunohistochemistry, we demonstrate that TGF-beta 2 and TGF-beta 3 were localized to alveolar macrophages as well as epithelial and smooth muscle cells of both normal rat lungs and rat lungs obtained at all time intervals a
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Alder, Jonathan K., Christina E. Barkauskas, Nathachit Limjunyawong, et al. "Telomere dysfunction causes alveolar stem cell failure." Proceedings of the National Academy of Sciences 112, no. 16 (2015): 5099–104. http://dx.doi.org/10.1073/pnas.1504780112.

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Telomere syndromes have their most common manifestation in lung disease that is recognized as idiopathic pulmonary fibrosis and emphysema. In both conditions, there is loss of alveolar integrity, but the underlying mechanisms are not known. We tested the capacity of alveolar epithelial and stromal cells from mice with short telomeres to support alveolar organoid colony formation and found that type 2 alveolar epithelial cells (AEC2s), the stem cell-containing population, were limiting. When telomere dysfunction was induced in adult AEC2s by conditional deletion of the shelterin component telom
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Lindahl, P., L. Karlsson, M. Hellstrom, et al. "Alveogenesis failure in PDGF-A-deficient mice is coupled to lack of distal spreading of alveolar smooth muscle cell progenitors during lung development." Development 124, no. 20 (1997): 3943–53. http://dx.doi.org/10.1242/dev.124.20.3943.

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PDGF-A(−/−) mice lack lung alveolar smooth muscle cells (SMC), exhibit reduced deposition of elastin fibres in the lung parenchyma, and develop lung emphysema due to complete failure of alveogenesis. We have mapped the expression of PDGF-A, PDGF receptor-alpha, tropoelastin, smooth muscle alpha-actin and desmin in developing lungs from wild type and PDGF-A(−/−) mice of pre- and postnatal ages in order to get insight into the mechanisms of PDGF-A-induced alveolar SMC formation and elastin deposition. PDGF-A was expressed by developing lung epithelium. Clusters of PDGF-Ralpha-positive (PDGF-Ralp
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Wu, Ailing, and Hai Song. "Regulation of alveolar type 2 stem/progenitor cells in lung injury and regeneration." Acta Biochimica et Biophysica Sinica 52, no. 7 (2020): 716–22. http://dx.doi.org/10.1093/abbs/gmaa052.

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Abstract The renewal of lung epithelial cells is normally slow unless the lung is injured. The resident epithelial stem cells rapidly proliferate and differentiate to maintain lung structure and function when the lung is damaged. The alveolar epithelium is characterized by alveolar type 1 (AT1) and alveolar type 2 (AT2) cells. AT2 cells are the stem cells for alveoli, as they can both self-renew and generate AT1 cells. Abnormal proliferation and regulation of AT2 cells will lead to serious lung diseases including cancers. In this review, we focused on the alveolar stem/progenitor cells, the ke
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Wodopia, Ralf, Hyun Soo Ko, Javiera Billian, Rudolf Wiesner, Peter Bärtsch, and Heimo Mairbäurl. "Hypoxia decreases proteins involved in epithelial electrolyte transport in A549 cells and rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (2000): L1110—L1119. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1110.

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Fluid reabsorption from alveolar space is driven by active Na reabsorption via epithelial Na channels (ENaCs) and Na-K-ATPase. Both are inhibited by hypoxia. Here we tested whether hypoxia decreases Na transport by decreasing the number of copies of transporters in alveolar epithelial cells and in lungs of hypoxic rats. Membrane fractions were prepared from A549 cells exposed to hypoxia (3% O2) as well as from whole lung tissue and alveolar type II cells from rats exposed to hypoxia. Transport proteins were measured by Western blot analysis. In A549 cells, α1- and β1-Na-K-ATPase, Na/K/2Cl cotr
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Hastings, Randolph H., John T. Berg, Daphne Summers-Torres, Douglas W. Burton, and Leonard J. Deftos. "Parathyroid hormone-related protein reduces alveolar epithelial cell proliferation during lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 1 (2000): L194—L200. http://dx.doi.org/10.1152/ajplung.2000.279.1.l194.

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Parathyroid hormone-related protein (PTHrP) is a growth inhibitor for alveolar type II cells and could be a regulatory factor for alveolar epithelial cell proliferation after lung injury. We investigated lung PTHrP expression in rats exposed to 85% oxygen. Lung levels of PTHrP were significantly decreased between 4 and 8 days of hyperoxia, concurrent with increased expression of proliferating cell nuclear antigen and increased incorporation of 5-bromo-2′-deoxyuridine (BrdU) into DNA in lung corner cells. PTHrP receptor was present in both normal and hyperoxic lung. To test whether the fall in
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Rozprawy doktorskie na temat "Lung alveolar cells"

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Mattes, Charlott, and Ulrich H. Thome. "Rapid elevation of sodium transport through insulin is mediated by AKT in alveolar cells." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142643.

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Alveolar fluid clearance is driven by vectorial Na+ transport and promotes postnatal lung adaptation. The effect of insulin on alveolar epithelial Na+ transport was studied in isolated alveolar cells from 18–19-day gestational age rat fetuses. Equivalent short-circuit currents (ISC) were measured in Ussing chambers and different kinase inhibitors were used to determine the pathway of insulin stimulation. In Western Blot measurements the activation of mediators stimulated by insulin was analyzed. The ISC showed a fast dose-dependent increase by insulin, which could be attributed to an increased
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Sitaraman, Sneha. "Alveolar type 2 epithelial cells in lung development and disease." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1571062200291287.

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Bhandari, R. N. B. "Characterization of a cell adhesion receptor on rat lung alveolar type 2 cells." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/46962.

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Cherlet, Tracy C. "Tetrahydrocannabinol and lung surfactant metabolism in isolated fetal type II alveolar cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0025/MQ51693.pdf.

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Barth, Kathrin, Robert Bläsche та Michael Kasper. "T1α/Podoplanin Shows Raft-Associated Distribution in Mouse Lung Alveolar Epithelial E10 Cells". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-137577.

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Aims: T1α/(podoplanin) is abundantly expressed in the alveolar epithelial type I cells (ATI) of rodent and human lungs. Caveolin-1 is a classical primary structural protein of plasmalemal invaginations, so-called caveolae, which represent specialized lipid rafts, and which are particularly abundant in ATI cells. The biological functions of T1α in the alveolar epithelium are unknown. Here we report on the characteristics of raft domains in the microplicae/microvillar protrusions of ATI cells, which contain T1α. Methods: Detergent resistant membranes (DRMs) from cell lysates of the mouse epithel
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Barth, Kathrin, Robert Bläsche та Michael Kasper. "T1α/Podoplanin Shows Raft-Associated Distribution in Mouse Lung Alveolar Epithelial E10 Cells". Karger, 2010. https://tud.qucosa.de/id/qucosa%3A27742.

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Aims: T1α/(podoplanin) is abundantly expressed in the alveolar epithelial type I cells (ATI) of rodent and human lungs. Caveolin-1 is a classical primary structural protein of plasmalemal invaginations, so-called caveolae, which represent specialized lipid rafts, and which are particularly abundant in ATI cells. The biological functions of T1α in the alveolar epithelium are unknown. Here we report on the characteristics of raft domains in the microplicae/microvillar protrusions of ATI cells, which contain T1α. Methods: Detergent resistant membranes (DRMs) from cell lysates of the mouse epithel
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Naranjo, Santiago(Santiago Jose). "An organoid platform to study alveolar stem cells in lung generation and cancer." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/129032.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2020<br>Cataloged from student-submitted PDF of thesis. Vita.<br>Includes bibliographical references.<br>Lung adenocarcinoma (LADC) remains the most common and lethal cancer type worldwide. Although recent breakthroughs using a new class of immune-modulatory therapeutics have improved patient survival in the clinic, the majority still invariably succumb to this disease, highlighting the importance of improving treatment strategies. A wide variety of models have been developed to study LADC. Cell line- and transplant-
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Medina-Tato, David A. "Role of phosphoinositide 3-kinase in TNFα signalling in A549 lung alveolar cells". Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441522.

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Hasegawa, Kouichi. "Fraction of MHCII and EpCAM expression characterizes distal lung epithelial cells for alveolar type 2 cell isolation." Kyoto University, 2018. http://hdl.handle.net/2433/232118.

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Wong, Yin-ling. "The effects of respiratory syncytial virus on alveolar epithelial cells toll-like receptors expressions and T cell apoptosis." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4218230X.

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Książki na temat "Lung alveolar cells"

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Sebastio, Gianfranco, Manuel Schiff, and Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progr
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Części książek na temat "Lung alveolar cells"

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Panos, Ralph J. "Cytokines and Alveolar Type II Cells." In Cytokines of the Lung. CRC Press, 2022. http://dx.doi.org/10.1201/9781003066927-17.

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Li, Jiao, and Nan Tang. "Alveolar stem cells in lung development and regrowth." In Lung Stem Cells in Development, Health and Disease. European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10009520.

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Liu, Yuru. "Type II Cells as Progenitors in Alveolar Repair." In Lung Stem Cells in the Epithelium and Vasculature. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16232-4_2.

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Toth, Andrea, Barbara Zhao, and William J. Zacharias. "Alveolar epithelial stem cells in homeostasis and repair." In Lung Stem Cells in Development, Health and Disease. European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10009420.

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Cunningham, A. C., J. A. Kirby, I. W. Colquhoun, and J. H. Dark. "Lung transplantation: pulmonary cell lysis mediated by alveolar mononuclear cells." In Transplant International Official Journal of the European Society for Organ Transplantation. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77423-2_90.

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Huang, Jessie, and Darrell N. Kotton. "Induced pluripotent stem cells for generating lung alveolar epithelial cells and modelling respiratory disease." In Lung Stem Cells in Development, Health and Disease. European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10010220.

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Oeztuerk-Winder, Feride, and Juan-Jose Ventura. "Isolation, Culture, and Potentiality Assessment of Lung Alveolar Stem Cells." In Methods in Molecular Biology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-980-8_3.

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Hiemstra, Pieter S., Xinhui Wu, P. Padmini S. J. Khedoe, and Reinoud Gosens. "The role of altered stem cell function in airway and alveolar repair and remodelling in COPD." In Lung Stem Cells in Development, Health and Disease. European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10010620.

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Donaldson, Kenneth, Joan Slight, and Robert E. Bolton. "Proteases and Oxidants in Injury to Alveolar Epithelial Cells Caused by Lung-Derived Neutrophils In Vitro." In Cells, Membranes, and Disease, Including Renal. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1283-3_39.

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Trefz, G., G. Klitsche, V. Schulz, and W. Ebert. "Effect of Nicotine on the Elastinolytic Activity of Human Lung Tumor Cells and Human Alveolar Macrophages." In Effects of Nicotine on Biological Systems. Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7457-1_21.

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Streszczenia konferencji na temat "Lung alveolar cells"

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Merrikh, A. A., and J. L. Lage. "Time-Dependent Diffusion in the Alveolar Region of the Lungs: Effect of Moving Red Blood Cells." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-39530.

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Results from a preliminary numerical simulation of alveolar gas diffusion with moving capillary red blood cells (RBCs) are presented. The alveolar region is modeled with four basic constituents, namely the alveolus (or gas region), the tissue (a region lumping the alveolar and capillary membranes, and the interstitial fluid), the blood plasma (a liquid region) and the RBCs. A single, straight capillary with equally spaced RBCs moving together with the blood plasma is considered in this preliminary study. The numerical simulation attempts also to mimic the time-varying gas concentration in the
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Ribeiro Baptista, B., M. Zysman, C. Thibault De Menonville, et al. "Targeting p16INK4a in alveolar type 2 cells to induce endogenous lung alveolar regeneration." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.66.

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Higuita-Castro, Natalia, Cosmin Mihai, Derek J. Hansford, and Samir N. Ghadiali. "In-Vitro Model of the Microscale Alveolar Environment." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53648.

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The present work describes the development of a novel micro-nanoscale system that more closely resembles the alveolar-capillary barrier in the lung by recapitulating different parameters of the cellular microenvironment, including fibrous geometry, fiber stiffness, chemistry, and cell-cell interactions. The system consists of a three-dimensional multilayered structure. Two microchannel chambers that resemble alveolar/airway space and the capillary lumen, interfaced with a porous mesh of polymeric nanofibers that act as the basal substrate for seeding lung epithelial and endothelial cell. The t
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Steinacher, Linda, Bruno Gjeta, Marisa Pimentel Mendes, et al. "Alveolar organoids with innate and adaptive immune cells." In ERS Lung Science Conference 2025 abstracts. European Respiratory Society, 2025. https://doi.org/10.1183/23120541.lsc-2025.op3.

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Llamazares Prada, M., U. Schwartz, D. Pease, et al. "Epigenetic deregulation in AT2 cells impairs alveolar regeneration in COPD." In ERS Lung Science Conference 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/23120541.lsc-2024.328.

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Gaver, Donald P., Melissa A. Krueger, and Samir N. Ghadiali. "The Influence of Surfactant Physicochemical Properties on Pulmonary Interfacial Flow Analogues." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0218.

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Abstract Many of the lung’s mechanical properties are influenced by pulmonary surfactant physicochemical characteristics. Pulmonary surfactant is a complex lipid-protein mixture formed in the type II alveolar cells and secreted into the alveolar subphase [1]. These substances reduce the surface tension at the air-liquid interface of the lining fluid that coats the interior of the lung. At sufficiently high concentrations, pulmonary surfactant reduces the surface tension to near zero and. in the process, stabilizes the alveoli and small airways [2–4].
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Tsarik, A. A., M. A. Kokhnyuk, P. V. Alkhovik, and M. Yu Yurkevich. "METHODOLOGICAL APPROACHES FOR ALVEOLAR EPITHELIAL CELL PRIMARY CULTURES OBTAINING." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-135-138.

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Evaluation of various proteolytic enzymes efficiency for disaggregation of lung tissue is carried out and an optimized method for alveolar epithelial cells isolation is presented. This method includes mechanical disaggregation of tissue followed by processing of explanations with 0.25% trypsin solution in combination with filtration of the cell suspension through pores with a diameter of 100 gm and 50 gm. The obtained cell cultures were characterized by high viability (more than 91%) and morphological heterogeneity. Along with actively dividing rounded cells, differentiated alveolar epithelial
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Lazko, Alexey, Larisa Udochkina, and Nina Losovskaya. "Histochemical changes of the lung tissue in experimental chronic alcoholic intoxication." In Innovations in Medical Science and Education. Dela Press Publishing House, 2022. http://dx.doi.org/10.56199/dpcsms.nrjc3772.

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Among organ systems in the human body affected by alcohol abuse, the lungs are particularly vulnerable to infections and injury. Chronic alcoholism causesalterations in host defence of the upper and lower airways, disruption of alveolar epithelial barrier integrity, alcohol-induced ciliary lesions and alveolar macrophages dysfunction. Currently with a spread of SARS-COV 2 infections which instantly destroys the lung tissue, the alcohol-induced lung damage issues acquire vital importance, as they might further increase severity of lesions of lung tissue in the infected alcohol abusers.Recent in
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Murphy, Cormac, Anja Schweikert, Amy Duffy, Xi Jing Teoh, Mari Ozaki, and Killian Hurley. "3D-Bioprinting of induced pluripotent stem cell-derived alveolar epithelial type 2 cells (iAT2) spheroids." In ERS Lung Science Conference 2025 abstracts. European Respiratory Society, 2025. https://doi.org/10.1183/23120541.lsc-2025.tp116.

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Liang, C., G. Huang, X. Liu, et al. "Single Cell RNA-seq Reveals Zinc Metabolism Defect of Alveolar Type II Cells with Aging in IPF." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.8.

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Raporty organizacyjne na temat "Lung alveolar cells"

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Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.

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Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmo
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Incidence of Lung Cancer Types. National Center for Chronic Disease Prevention and Health Promotion (U.S.). Division of Cancer Prevention and Control., 2024. https://doi.org/10.15620/cdc/174572.

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More lung cancers, including small cell carcinomas, adenocarcinomas, and squamous cell carcinomas, are being found at an early stage when they are more treatable. Screening can help find lung cancers of all types before they start spreading. Lung cancer begins in the airways of the lungs. These include the bronchi (the tubes leading to the lungs), the bronchioles (tiny branches of air tubes in the lungs), and the alveoli (the tiny air sacs at the end of the bronchioles). Types of lung cancer are named after the cells found in the cancer. Doctors use special tests to determine what type of cell
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