Готові списки джерел за темами / Lung carcinomas

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Добірка наукової літератури з теми "Lung carcinomas"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Lung carcinomas"

1

Sica, Gabriel, Patrick L. Wagner, Nassar Altorki, Jeffrey Port, Paul C. Lee, Madeline F. Vazquez, and Anjali Saqi. "Immunohistochemical Expression of Estrogen and Progesterone Receptors in Primary Pulmonary Neuroendocrine Tumors." Archives of Pathology & Laboratory Medicine 132, no. 12 (December 1, 2008): 1889–95. http://dx.doi.org/10.5858/132.12.1889.

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Анотація:
Abstract Context.—Lung and breast carcinomas are among the most prevalent cancers. Advances in cancer therapies can provide survival benefit and be potentially curative, even in metastatic disease. Due to the high prevalence of these carcinomas, it is not unusual to encounter lung nodule(s) in a patient with breast carcinoma, and distinguishing between primary and metastatic disease is critical for management/treatment. Occasionally neuroendocrine differentiation is present in breast carcinoma, making its distinction from pulmonary/nonpulmonary neuroendocrine tumors in the lung difficult. Objective.—To assess estrogen and progesterone receptor expression in the entire spectrum of pulmonary neuroendocrine tumors. Design.—Seventy-one neuroendocrine neoplasms including typical carcinoids (42), atypical carcinoids (7), small cell carcinomas (14), large cell neuroendocrine carcinomas (2), and combined small cell carcinomas (6) were evaluated for estrogen and progesterone receptors. Mammary and non–small cell lung carcinomas were also stained for comparison. Results.—The entire spectrum of neuroendocrine neoplasms demonstrated focal to diffuse estrogen (typical carcinoid, 23; atypical carcinoid, 6; small cell carcinoma, 8; large cell neuroendocrine carcinoma, 2; combined small cell carcinoma, 4) and progesterone (typical carcinoid, 11; atypical carcinoid, 2; small cell carcinoma, 7; large cell neuroendocrine carcinoma, 0; combined small cell carcinoma, 2) expression. There was no correlation between sex and estrogen/progesterone status. Estrogen and progesterone staining were also noted in endothelial cells. Relative to neuroendocrine carcinomas, mammary carcinomas expressed estrogen and progesterone more frequently. Non–small cell carcinomas had greater and similar immunoreactivity for estrogen and progesterone, respectively. Conclusions.—Although estrogen and progesterone receptor staining is frequently associated with breast and gynecologic primaries, it can also be observed in “nontarget” organs. Therefore, presence of estrogen and/or progesterone expression in neuroendocrine tumors involving the lung should not exclude a primary pulmonary neoplasm.
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2

Shilo, Konstantin, Tatiana Dracheva, Haresh Mani, Junya Fukuoka, Isabell A. Sesterhenn, Wei-Sing Chu, Joanna H. Shih, Jin Jen, William D. Travis та Teri J. Franks. "α-Methylacyl CoA Racemase in Pulmonary Adenocarcinoma, Squamous Cell Carcinoma, and Neuroendocrine Tumors: Expression and Survival Analysis". Archives of Pathology & Laboratory Medicine 131, № 10 (1 жовтня 2007): 1555–60. http://dx.doi.org/10.5858/2007-131-1555-mcripa.

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Abstract Context.—α-Methylacyl CoA racemase (AMACR) is an oxidative enzyme involved in isomeric transformation of fatty acids entering the beta-oxidation pathway. AMACR serves as a useful marker in establishing a diagnosis of prostatic malignancy; however, limited information is available in regard to its presence in pulmonary neoplasms. Objective.—To investigate AMACR expression within a spectrum of lung carcinomas and its correlation with patients' survival. Design.—Four hundred seventy-seven pulmonary carcinomas, including 150 squamous cell carcinomas, 150 adenocarcinomas, 46 typical carcinoids, 31 atypical carcinoids, 28 large cell neuroendocrine carcinomas, and 72 small cell carcinomas, were studied immunohistochemically using tissue microarray–based samples. Results.—Overall, pulmonary tumors were positive for AMACR in a significant percentage (47%) of cases. Among tumor types, 22% of squamous cell carcinoma, 56% of adenocarcinoma, 72% of typical carcinoid, 52% of atypical carcinoid, 70% of large cell neuroendocrine carcinoma, and 51% of small cell lung carcinoma were positive for AMACR. Furthermore, the Kaplan-Meier analysis revealed that the patients with AMACR-positive small cell carcinoma had better survival (19% vs 5% after 5 years, P = .04) than patients with AMACR-negative tumors. Such survival advantage was seen for patients with stage I–II (P = .01) but not stage III–IV small cell carcinomas (P = .58). Conclusions.—These results indicate that, similar to prostate cancer, the overexpression of AMACR frequently occurs in pulmonary carcinomas. Additionally, its positive correlation with outcome of stage I–II small cell lung carcinoma warrants further investigation of the AMACR role in the prognosis of this tumor.
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3

Turner, Bradley M., Philip T. Cagle, Irma M. Sainz, Junya Fukuoka, Steven S. Shen, and Jaishree Jagirdar. "Napsin A, a New Marker for Lung Adenocarcinoma, Is Complementary and More Sensitive and Specific Than Thyroid Transcription Factor 1 in the Differential Diagnosis of Primary Pulmonary Carcinoma: Evaluation of 1674 Cases by Tissue Microarray." Archives of Pathology & Laboratory Medicine 136, no. 2 (February 1, 2012): 163–71. http://dx.doi.org/10.5858/arpa.2011-0320-oa.

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Context.—Differentiation of non–small cell carcinoma into histologic types is important because of new, successful therapies that target lung adenocarcinoma (ACA). TTF-1 is a favored marker for lung ACA but has limited sensitivity and specificity. Napsin A (Nap-A) is a functional aspartic proteinase that may be an alternative marker for primary lung ACA. Objectives.—To compare Nap-A versus TTF-1 in the typing of primary lung carcinoma and the differentiation of primary lung ACA from carcinomas of other sites. Design.—Immunohistochemistry for Nap-A and TTF-1 was performed on tissue microarrays of 1674 cases of carcinoma: 303 primary lung ACAs (18.1%), 200 primary squamous cell lung carcinomas (11.9%), 52 primary small cell carcinomas of the lung (3.1%), and carcinomas of the kidney (n = 320; 19.1%), thyroid (n = 96; 5.7%), biliary (n = 89; 5.3%), bladder (n = 47; 2.8%), breast (n = 93; 5.6%), colon (n = 95; 5.7%), liver (n = 96; 5.7%), ovaries (n = 45; 2.7%), pancreas (n = 48; 2.9%), prostate (n = 49; 2.9%), stomach (n = 93; 5.6%), and uterus (n = 48; 2.9%). Cases were evaluated against a negative control as negative, weak positive, and strong positive. Results.—Nap-A was more sensitive than TTF-1 for primary lung ACA (87% versus 64%; P < .001). Nap-A was more specific than TTF-1 for primary lung ACA versus all tumors, excluding kidney, independent of tumor type (P < .001). Conclusions.—Nap-A is superior to TTF-1 in distinguishing primary lung ACA from other carcinomas (except kidney), particularly primary lung small cell carcinoma, and primary thyroid carcinoma. A combination of Nap-A and TTF-1 is useful in the distinction of primary lung ACA (Nap-A+, TTF-1+) from primary lung squamous cell carcinoma (Nap-A−, TTF-1−) and primary lung small cell carcinoma (Nap-A−, TTF-1+).
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4

Grygoruk, O. G., D. A. Tsoi, L. M. Bazulina, and I. V. Vihlyanov. "Small‑cell lung carcinoma. Cytological diagnosis." Malignant tumours 12, no. 1 (April 8, 2022): 36–43. http://dx.doi.org/10.18027/2224-5057-2022-12-1-36-43.

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Анотація:
The purpose of this article is to evaluate the possibilities of cytology for lung neuroendocrine tumors (small‑cell lung carcinoma and carcinoids) diagnostics. Cytology specimens obtained by bronchoscopy (n = 112), biopsy of metastatic lymph nodes (n = 27) or from pleural effusion (n = 8) were collected within over 1 year from 147 patients and studied. Small-cell lung carcinoma was diagnosed in 143 patients, representing 23,9 % of all lung carcinomas. The proportion of carcinoid tumors was 2,7 % of all neuroendocrine tumors. Typical carcinoid was observed in three cases, and atypical carcinoid — in one case. Cytologic features most significant for cytological diagnosis of small‑cell lung carcinoma and carcinoids were identified (n = 11). Discriminant analysis demonstrated that the proportion of accurate cytological diagnosis of small‑cell lung carcinoma and carcinoids was 96,69 %. Cytology is a reliable method for neuroendocrine tumor diagnosis. Immunocytochemistry with neuroendocrine markers along with light microscopy should be used to differentiate small‑cell lung carcinoma metastases from other tumors and non‑malignant pathology in pleural effusion specimens.
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5

Dacic, Sanja. "Molecular Diagnostics of Lung Carcinomas." Archives of Pathology & Laboratory Medicine 135, no. 5 (May 1, 2011): 622–29. http://dx.doi.org/10.5858/2010-0625-rair.1.

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Анотація:
Abstract Context.—The development of targeted therapies in the treatment of lung carcinoma is a rapidly growing area that requires a precise histologic classification of lung carcinomas and the implementation into clinical practice of testing for predictive biomarkers of therapy response. Molecular testing has added another layer of complexity in the routine workup of rather limited diagnostic tumor tissue. Objective.—To review the most important lung carcinoma biomarkers predictive of response and to discuss proposed routine molecular testing in clinical practice. Data Sources.—PubMed (US National Library of Medicine)–available review articles, peer-reviewed original articles, and experience of the author. Conclusions.—Histologic profile, clinical characteristics, and mutational profile of lung carcinoma have all been reported as predictive factors of response to epidermal growth factor receptor–tyrosine kinase inhibitors (EGFR-TKIs) and other targeted therapies. Recently published results of large clinical trials indicate that mutational profiling, particularly identification of activating epidermal growth factor receptor (EGFR) mutations, is the best predictor for EGFR-TKI response. Despite all these observations, molecular profiling of lung carcinomas has not been standardized or validated in clinical practice. Rapid development of targeted therapies will probably require molecular testing for a panel of mutations to identify molecular subtypes of non–small cell lung carcinomas that will benefit from new therapeutic approaches in personalized patient care.
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6

Capelli, Marco, Giulia Bertino, Patrizia Morbini, Chiara Villa, Stefano Zorzi, and Marco Benazzo. "Neuroendocrine Carcinomas of the Upper Airways: A Small Case Series with Histopathological Considerations." Tumori Journal 93, no. 5 (September 2007): 499–503. http://dx.doi.org/10.1177/030089160709300517.

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Анотація:
Neuroendocrine carcinomas are rare tumors. In the head and neck region they are most common in the larynx, where they represent 0.5-1% of epithelial cancers. Diagnosis requires the recognition of the typical neuroendocrine architecture and morphology and the immunohistochemical confirmation of neuroendocrine differentiation. In the 1991 WHO classification laryngeal neuroendocrine carcinomas have been divided into carcinoids, atypical carcinoids, small cell carcinomas and paragangliomas. Atypical carcinoids in the head and neck region usually show an aggressive behavior analogous to poorly differentiated carcinomas, and are resistant to chemo- and radiotherapy. For this reason, it was recently proposed to change their designation to “moderately differentiated neuroendocrine carcinomas”. We present the clinical and histopathological features of 2 moderately differentiated neuroendocrine carcinomas of the larynx, one large cell poorly differentiated neuroendocrine carcinoma of the oropharynx, and one small cell carcinoma of the minor salivary glands of the tongue. The patient with small cell carcinoma was free from disease 26 months after radical surgery, while the other patients showed liver, lung and bone metastases 18, 26 and 24 months after the diagnosis despite radical surgery or concomitant intra-arterial chemotherapy and radiotherapy.
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7

Gupta, Amit, Ashutosh Tandon, Abhay Kumar, Sunil Kumar, and Usha Rani Singh. "Large Cell Neuroendocrine Carcinoma of Lung metastasizing to Jejunum – A rare presentation with review of Literature." Asian Journal of Medical Sciences 4, no. 2 (May 13, 2013): 47–50. http://dx.doi.org/10.3126/ajms.v4i2.5370.

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Анотація:
Large cell neuroendocrine carcinoma of lung is not one of the commoner varieties of neoplasia found in the lungs. There are around 100 cases in literature which suggest the metastasis of various kinds of lung carcinomas to gastro intestinal tract (GIT). Metastasis of large cell neuroendocrine carcinoma to small bowel is rare. This is a rare case in which the primary neuroendocrine carcinoma of lung presented with metastasis and perforation of small bowel.DOI: http://dx.doi.org/10.3126/ajms.v4i2.5370Asian Journal of Medical Sciences 4(2013) 47-50
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8

Altree-Tacha, David, Jillian Tyrrell, and Faqian Li. "mASH1 is Highly Specific for Neuroendocrine Carcinomas: An Immunohistochemical Evaluation on Normal and Various Neoplastic Tissues." Archives of Pathology & Laboratory Medicine 141, no. 2 (September 15, 2016): 288–92. http://dx.doi.org/10.5858/arpa.2015-0489-oa.

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Анотація:
Context.—High-grade neuroendocrine carcinomas and carcinoids can arise in different sites such as lung, gastrointestinal tract, prostate, and skin. Classic neuroendocrine markers such as CD56, synaptophysin, and chromogranin cannot distinguish carcinoids from high-grade neuroendocrine carcinomas. Recently, mouse monoclonal mASH1 has been shown to help discriminate carcinoids from high-grade neuroendocrine carcinomas in various neoplastic sites. To date, there have been no comprehensive immunohistochemistry studies with mASH1 on nonneuroendocrine neoplasms. Objective.—To evaluate the specificity and sensitivity of mASH1 in various normal and neoplastic tissues, including lung cancers. Design.—Formalin-fixed, paraffin-embedded tissue microarrays consisting of normal tissues and various neoplastic tissues were immunohistochemically evaluated with mASH1. Results.—In normal tissues (n = 30), mASH1 (nuclear staining) was sparsely expressed in the molecular cell layer, white matter, and granular cell layer of cerebellum; C cells in thyroid; and epithelial cells in thymus. In lung cancers, mASH1 stained 1.1% (1 of 93) of adenocarcinomas, 0.9% (1 of 111) of squamous cell carcinomas, 0% (0 of 30) of large cell carcinomas, 66.7% (6 of 9) of large cell neuroendocrine carcinomas, and 82.5% (94 of 114) of small cell carcinomas. In various other neoplastic tissues (n = 1114), mASH1 was expressed in thyroid medullary carcinomas, thymic carcinomas, and brain cancers; mASH1 was also expressed in a very low percentage of breast carcinomas, ovarian cancers, and pancreatic neuroendocrine tumors. All typical carcinoids of various sites were negative (0 of 11), however, in lung atypical carcinoids, mASH1 was expressed in 42.9% (9 of 21). Conclusions.—Although not organ specific, mASH1 is highly specific for high-grade neuroendocrine carcinomas versus carcinoids and other nonneuroendocrine neoplasms.
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9

Henderson, Douglas W. "Lung Carcinomas." Pathology 20, no. 2 (1988): 205. http://dx.doi.org/10.1016/s0031-3025(16)36644-2.

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10

Travis, William D. "Sarcomatoid Neoplasms of the Lung and Pleura." Archives of Pathology & Laboratory Medicine 134, no. 11 (November 1, 2010): 1645–58. http://dx.doi.org/10.5858/2010-0086-rar.1.

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Анотація:
Abstract Sarcomatoid neoplasms of the lung and pleura are rare tumors that present a complex differential diagnosis, making them challenging for surgical pathologists. In the lung, the main tumors are the sarcomatoid carcinomas, including pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma. They are characterized by histologic heterogeneity; molecular data support their origin from a pluripotent stem cell that undergoes neoplastic transformation with divergent epithelial and sarcomatous differentiation. Diagnosis is difficult in small biopsy specimens and typically requires a resection specimen. Despite the presence of sarcomatoid features, these tumors are classified as lung carcinomas. Pulmonary blastomas must be distinguished from pleuropulmonary blastomas, which are a unique type of thoracic sarcoma typically occurring in young children. In the pleura, the main tumors to consider are the sarcomatoid and desmoplastic types of malignant mesothelioma, solitary fibrous tumor, and desmoid tumor. While light microscopy is sufficient to diagnose most of these tumors, immunohistochemistry can be useful in selected settings. In particular, it can aid to confirm epithelial differentiation in spindle cell carcinomas and the presence of rhabdomyosarcoma in sarcomatoid carcinomas, mesotheliomas, or pleuropulmonary blastomas. For sarcomatoid and desmoplastic mesothelioma, keratin is the most useful stain because it can highlight invasive growth and mesothelial markers are positive in only the minority of cases. Clinical and radiologic correlation is needed to separate some pleomorphic carcinomas with pleural involvement from sarcomatoid malignant mesothelioma, since these poorly differentiated tumors may not express the usual immunohistochemical markers for carcinoma or mesothelioma.
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Більше джерел

Дисертації з теми "Lung carcinomas"

1

Xinarianos, George. "Genetic alterations in non-small cell lung carcinomas." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343688.

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2

Kim, Young. "The Effects of Tarsh Overexpression on Lung Carcinomas." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/498.

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Анотація:
Lung cancer arises from epithelial cells that line the air passages of the lungs. It is the second most common malignancy in the United States; trends suggest that over 228,000 new patients will be diagnosed with lung cancer in 2013. Due to the fact that lung cancer is highly aggressive, it has proven difficult to control. The 5-year survival rate has been shown to be only 15.9%, despite the advances made in terms of diagnosis and treatment. Therefore, we are faced with the problem of finding more effective methods that allow for an earlier diagnosis and the improved treatment of lung cancer. This study attempts to address these issues by investigating Tarsh, a novel molecule that is involved in the regulation of cellular senescence. Previous studies have shown that Tarsh is expressed in normal lung cells, but is significantly downregulated in lung tumors. These studies also determined that Tarsh is likely dependent upon the expression of p53, a tumor suppressor gene. The current study investigated these results, in addition to the biological effects of ectopically increasing Tarsh and/or knocking down p53 expression in two lung cancer cell lines: A549 and H1299 cell lines. It was determined that increasing the expression of Tarsh decreased the rate of proliferation in both cell lines. Additionally, it was shown that the knockdown of p53 increased proliferation in A549 cells. In regards to the migration rate of these cell lines, the overexpression of Tarsh decreased migration in A549 cells, but had no effect on H1299 cells. However, the role of p53 in migration is still unclear. The results of this study suggest that the knockdown of p53 decreases cell migration in A549 cells. This contradicts the fact that H1299 cells do not express p53, yet was found to have the highest migration rate. It is evident that a further investigation is needed to make more concrete conclusions. Nevertheless, the suppressive features of Tarsh on cell proliferation, and possibly migration, make it a promising target of research for lung cancer therapy.
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3

Merikallio, H. (Heta). "Claudins and epitheliomesenchymal transition in lung carcinomas and chronic obstructive pulmonary disease." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526202471.

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Анотація:
Abstract Lung cancers and chronic obstructive pulmonary disease (COPD) are the most common smoking-related lung diseases and both have high mortality rate. Tight junctions (TJ) are apical junctions between epithelial cells that regulate the permeability of epithelium and form the tight junction along with occludin. Dysfunction of the TJ and dysregulation of TJ proteins leads to a loss of cell-cell adhesion and a loss of cohesion as well as epitheliomesenchymal transition. These increase invasion of lung carcinomas and possibly predispose to the exacerbations in COPD. Therefore, the aim of this thesis was to study expression and regulation of claudins in different lung carcinomas and COPD. Carcinomas expressed claudins 1, 2, 3, 4, 5 and 7 in different variations. Claudin 5 expression was weak in all carcinoma types. Strong claudin 1, 4 and 7 expression was associated with better survival in squamous cell carcinoma and adenocarcinoma. Claudin 3 expression was associated with COPD in large airways. Claudins 3 and 4 was found to be stronger in small airways of smokers and COPD patients than in non-smokers. Transcription factor snail had prognostic value in lung carcinomas. Negative snail expression was associated with longer life expectancy in lung carcinoma patients. Negative snail expression was associated with up-regulated claudin 5 and 7 expression, while strong expression was associated with low claudin 1 and 3 expression. Transcription factors slug and twist were inversely associated with claudins 3 and 4 in small and large airways. Slug expression was higher in non-smokers than in COPD patients and smokers. Transcription factor knockdown increased claudin expression in normal bronchial cell line. Except for claudin 2 and 7, which were decreased. Adenocarcinoma-like cell line was not affected by snail knockdown and in squamous cell carcinoma-like cell line claudin 3, 4 and 7 expression was increased. Transcription factor snail knockdown inhibited invasion of cell lines. Twist knockdown increased transepithelial resistance in normal bronchial cell line indicating higher barrier function in cell layer
Tiivistelmä Keuhkosyöpä ja keuhkoahtaumatauti ovat yleisiä tupakoinnin aiheuttamia keuhkosairauksia, joissa on korkea kuolleisuus. Tupakointi aiheuttaa muutoksia keuhkojen epiteelisoluissa ja solujen välisissä liitoksissa. Tiivisliitokset solujen välillä säätelevät epiteelin rakennetta ja läpäisevyyttä. Klaudiinit ovat proteiineja, jotka muodostavat tiivisliitoksen yhdessä okkludiinin kanssa. Tiivisliitos proteiinien toimintahäiriöt voivat johtaa solujen välisten liitosten katoamiseen ja epiteelin hajoamiseen sekä epiteelisolujen muuntumiseen mesenkymaalisten solujan kaltaisiksi. Nämä seikat lisäävät invaasiota keuhkosyövissä ja saattavat altistaa pahenemisvaiheisiin keuhkoahtaumataudissa. Väitöskirjassa tutkittiin klaudiinien ilmentymistä ja säätelyä keuhkosyövässä ja keuhkoahtaumataudissa. Klaudiinien1, 2, 3, 4, 5 ja 7 esiintyminen keuhkosyövän histologisissa alatyypeissä vaihteli. Klaudiinien 1, 4 ja 7 voimakas ilmentyminen voitiin yhdistää pidempään elinikään potilailla, joilla oli levyepiteeli- tai adenokarsinooma. Klaudiini 3:n ilmentyminen liittyi keuhkoahtaumatautiin suurissa hengitysteissä. Klaudiinien 3 ja 4 voimakas ilmeneminen pienissä ilmateissä oli yleisempää keuhkoahtaumatautipotilailla ja tupakoitsijoilla kuin tupakoimattomilla henkilöillä. Transkriptiotekijä snailin puuttuminen keuhkosyövässä liittyi potilaiden pidempään elinaikaan. Klaudiinien 5 ja 7 ilmeneminen oli voimakkaampaa, kun snailin määrä oli vähäinen. Klaudiinien 1 ja 3 ilmeneminen väheni snail:in ollessa voimakas keuhkosyövässä. Traskriptiotekijöiden (slug ja twist) ilmeneminen liittyi käänteisesti klaudiinien ilmentymiseen pienissä ja suurissa ilmateissä. Slugin ilmeneminen oli voimakkaampaa tupakoimattomilla henkilöillä kuin tupakoivilla tai keuhkoahtaumatautia sairastavilla. Transkriptiotekijöiden snail, slug ja twist toiminnan estäminen lisäsi klaudiinien määrää normaaleissa keuhkon epiteelisoluissa. Poikkeuksen muodostivat klaudiinit 2 ja 7, joiden määrä väheni kun snail:in toiminta oli estetty. Adenokarsinooma-soluissa snailin estolla ei ollut vaikutusta, ja levyepiteelisyövän soluissa klaudiinien 3, 4 ja 7 määrä kasvoi. Snail myös vähensi solujen invaasiota. Transkriptiotekijä twistin toiminnan esto normaaleissa keuhkoepiteelisoluissa nosti solumaton läpi kulkevan sähkön resistenssiä, mikä on osoitus tiiviistä solujen välisistä liitoksista
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4

Vieira, Thibault. "Caractérisation des carcinomes sarcomatoïdes primitifs pulmonaires." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066552/document.

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Анотація:
Les carcinomes sarcomatoïdes sont un sous type rare de cancer bronchique non à petites cellules (CBNPC). Leur pronostic semble plus défavorable que celui des autres sous-types de CBNPC. Notre équipe travaille sur le démembrement moléculaire de ces tumeurs. Dans ce travail, nous démontrons que les carcinomes sarcomatoïdes sont chimiorésistants aux sels de platine à partir d'étude in vivo et in vitro (cultures primaires) comparativement aux autres sous-types de CBNPC. Nous démontrons que tumeurs partagent les caractéristiques phénotypiques des CBNPC tant d'un point de vue immunohistochimique que moléculaire, confortant la classification OMS. Il est possible que ces tumeurs dérivent de cellules souches de CBNPC ou utilisent un processus de transition épithélio-mésenchymateuses. Les spécificités de cette transition restent à déterminer. De plus, ces tumeurs présentent de très nombreuses altérations moléculaires permettant d'envisager de nouvelles pistes de traitements ciblés notamment les anti-MET. Enfin, nous montrons l'implication du système immunitaire avec une infiltration importante de lymphocytes T CD8+, de macrophages CD163+ et une forte expression de PD-L1 ce qui ouvre de nouvelles perspectives de recherche et de traitements innovants
Sarcomatoid carcinomas are a rare subtype of non-small cell lung cancer (NSCLC). Prognostic seems less favourable than other subtypes of NSCLC. Our team works to determine molecular characteristics of these tumors. In this work, we demonstrated that sarcomatoid carcinomas are chemoresistant to platinum based regimen in vitro and in vivo (primary cell lines) compared to other NSCLC. We demonstrated that this tumors share immunohistchemical, moleculary similarities with NSCLC validating the WHO classification. It is possible that these tumors came from cancer stem cell or underwent an epithelial-mesenchymal transition. Specificities of this transition remained undefined. Moreover these tumors presented a lot of molecular alterations allowing to investigate targeted therapies such as MET inhibitors. At last, we shows the implication of the immune system, the strong infiltration of TCD8+ lymphcoytes CD163+ macrophages and the expression of PD-L1, allowing to hope new perspective of research, innovative treatment
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5

Blat, Irene Catherine. "Functional miRNA regulation of metastatic genes promotes tumor cell dissemination in non-small cell and small cell lung carcinomas." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/80982.

Повний текст джерела
Анотація:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2013.
Cataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Tumor progression, from initiation to advanced metastatic disease, requires the orchestration of a diverse group of cell-intrinsic and extrinsic factors. This multifactorial disease is promoted by an accumulation of genetic and epigenetic changes that confer selective advantage to cells and enable unrestrained proliferation, survival, motility, and self-renewal. While much emphasis over the last 35 years has been dedicated to understanding the regulators of tumor initiation, the number of cancer-related deaths worldwide continues to rise, of which the majority are attributed to metastasis. The lengthy progression to metastasis requires invasion out of the primary tumor site and into the bloodstream, survival in and exit from circulation, and colonization and expansion in a foreign environment. Developmental pathways such as the Transforming Growth Factor [beta] (TGF[beta]) signaling network are frequently dysregulated during metastatic progression due to the similarities between early embryogenesis and tumor progression. Furthermore, the TGF[beta] pathway highlights how cell-intrinsic and extrinsic signals help coordinate the complex interactions required between tumor cells, as well as those of the tumor microenvironment to achieve metastasis. Facilitating alterations to pathways such as TGF[beta] and many others are modulators of gene expression that can target multiple nodes of the signaling cascade instead of requiring genetic alterations to single genes. Moreover, in the last decade, emphasis on the role of noncoding RNAs in post-transcriptional modifications has revealed their important contribution in the regulation of developmental programs across metazoan species. More recently, the role of alterations in expression of small noncoding RNAs, microRNAs (miRNAs) has emerged as a significant contributor to disease states, including each stage of tumor progression from initiation to metastatic colonization. miRNAs hold great promise not only as biomarkers but also as potential therapeutics. For these reasons, we have characterized the role of two important examples of miRNA families - the miRNA-200 family and the miRNA-1 7~92 cluster - that regulate early stages of tumor initiation in addition to later steps of cell migration, invasion, survival, and colonization. Examination of their contribution to tumor progression in relevant in vitro and in vivo cellular contexts using genetic tools reveals they are functional contributors to tumor cell dissemination. Furthermore, modulation of their expression in the appropriate tumor microenvironments elucidates a network of targets underlying the molecular mechanisms of metastasis.
by Irene Catherine Blat.
Ph.D.
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6

Gonterman, Ryan M. "Parathyroid hormone-related protein gene expression and function relationship with oncogenic pathways in the skin and squamous cell carcinomas of the lung /." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3324517.

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Thesis (Ph.D.)--Indiana University, Dept. of Medical Sciences, 2008.
Title from PDF t.p. (viewed on May 13, 2009). Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4693. Adviser: John G. Foley.
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7

Zschaeck, Sebastian, Monique Simon, Steffen Löck, Esther G. C. Troost, Kristin Stützer, Patrick Wohlfahrt, Steffen Appold, et al. "PRONTOX – proton therapy to reduce acute normal tissue toxicity in locally advanced non-small-cell lung carcinomas (NSCLC): study protocol for a randomised controlled trial." BioMed Central, 2016. https://tud.qucosa.de/id/qucosa%3A30184.

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Background Primary radiochemotherapy with photons is the standard treatment for locally advanced-stage non-small cell lung cancer (NSCLC) patients. Acute radiation-induced side effects such as oesophagitis and radiation pneumonitis limit patients’ quality of life, and the latter can be potentially life-threatening. Due to its distinct physical characteristics, proton therapy enables better sparing of normal tissues, which is supposed to translate into a reduction of radiation-induced side effects. Methods/design This is a single-centre, prospective, randomised controlled, phase II clinical trial to compare photon to proton radiotherapy up to 66 Gy (RBE) with concomitant standard chemotherapy in patients with locally advanced-stage NSCLC. Patients will be allocated in a 1:1 ratio to photon or proton therapy, and treatment will be delivered slightly accelerated with six fractions of 2 Gy (RBE) per week. Discussion The overall aim of the study is to show a decrease of early and intermediate radiation-induced toxicity using proton therapy. For the primary endpoint of the study we postulate a decrease of radiation-induced side effects (oesophagitis and pneumonitis grade II or higher) from 39 to 12%. Secondary endpoints are locoregional and distant failure, overall survival and late side effects. Trial registration Registered at ClinicalTrials.gov with Identifier NCT02731001 on 1 April 2016.
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8

Zschaeck, Sebastian, Monique Simon, Steffen Löck, Esther G. C. Troost, Kristin Stützer, Patrick Wohlfahrt, Steffen Appold, et al. "PRONTOX – proton therapy to reduce acute normal tissue toxicity in locally advanced non-small-cell lung carcinomas (NSCLC): study protocol for a randomised controlled trial." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-219714.

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Background Primary radiochemotherapy with photons is the standard treatment for locally advanced-stage non-small cell lung cancer (NSCLC) patients. Acute radiation-induced side effects such as oesophagitis and radiation pneumonitis limit patients’ quality of life, and the latter can be potentially life-threatening. Due to its distinct physical characteristics, proton therapy enables better sparing of normal tissues, which is supposed to translate into a reduction of radiation-induced side effects. Methods/design This is a single-centre, prospective, randomised controlled, phase II clinical trial to compare photon to proton radiotherapy up to 66 Gy (RBE) with concomitant standard chemotherapy in patients with locally advanced-stage NSCLC. Patients will be allocated in a 1:1 ratio to photon or proton therapy, and treatment will be delivered slightly accelerated with six fractions of 2 Gy (RBE) per week. Discussion The overall aim of the study is to show a decrease of early and intermediate radiation-induced toxicity using proton therapy. For the primary endpoint of the study we postulate a decrease of radiation-induced side effects (oesophagitis and pneumonitis grade II or higher) from 39 to 12%. Secondary endpoints are locoregional and distant failure, overall survival and late side effects. Trial registration Registered at ClinicalTrials.gov with Identifier NCT02731001 on 1 April 2016.
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9

Rangel, Maristela Peres. "Relevância dos proteoglicanos como biomarcadores prognósticos e preditivos em carcinomas não-pequenas células e seu impacto na carcinogênese pulmonar." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01032017-140343/.

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Introdução. Os glicosaminoglicanos e os proteoglicanos são moléculas abundantes na matriz extracelular. Vários estudos têm demonstrado que uma produção ou degradação aberrante dessas moléculas tem influência no comportamento do câncer de mama, cólon e pâncreas. Outras proteínas como o solCD44 e a cofilina-1 também tem demonstrado influência direta na progressão dos tumores. Desta forma, a análise da expressão destas moléculas em tecidos e fluidos corporais tem despertado grande interesse como rastreador de indivíduos de alto risco e marcador diagnóstico e/ou prognóstico da doença. Objetivos. Conhecer o impacto do ácido hialurônico e dos proteoglicanos (biglicam, glipicam, perlecam, sindecam e versicam) na carcinogênese bem como seu impacto na sobrevida dos pacientes; verificar se a concentração de solCD44 e cofilina-1 presente no escarro de pacientes com câncer de pulmão permite rastreá-los entre pacientes com doença pulmonar obstrutiva crônica e voluntários saudáveis. Resultados. Uma associação significativa direta foi encontrada entre os tumores com alto percentual de expressão de AH e de microvasos no estroma tumoral. As concentrações de heparam e condroitim sulfato nas amostras tumorais foram mais elevadas quando comparadas às amostras não tumorais. Com exceção do sindecam, todos os outros proteoglicanos apresentaram uma expressão gênica significativamente menor nos tecidos tumorais e biglicam e versicam apresentaram associações com as características clinico patológicas. A expressão proteica de biglicam, perlecam e versicam foi significativamente maior no tecido normal do que nas áreas de estroma tumoral e de células tumorais. Pela análise de regressão de COX controlada para idade, tipo histológico e expressão gênica de biglicam, sindecam e glipicam obtiveram alta taxa de sobrevida os pacientes do sexo feminino com elevada expressão gênica de perlecam e menor risco de óbito em estadio T1, ausência de metástases nodais e expressão gênica de versicam. A Maristela Peres Rangel Tese de doutorado - USP concentração de cofilina demonstrou-se mais elevada no escarro de pacientes com câncer de pulmão quando comparado ao escarro de pacientes de alto risco e de voluntários saudáveis. A concentração de solCD44 também demonstrou-se mais elevada no escarro de pacientes com câncer de pulmão quando comparado ao escarro de pacientes de alto risco e de voluntários saudáveis. Através da curva ROC, a cofilina-1 presente no escarro foi capaz de distinguir os pacientes de alto risco dos pacientes com câncer de pulmão com área abaixo da curva de 0.69 e com um ponto de corte de 802.5 pg/mL a curva apresentou 60% de sensibilidade e 54% de especificidade. O solCD44 presente no escarro também foi capaz de distinguir os pacientes de alto risco dos pacientes com câncer de pulmão através da curva ROC com área abaixo da curva de 0.67 e com um ponto de corte de 65.8 pg/mL a curva apresentou 50% de sensibilidade e 84% de especificidade. Conclusão. A expressão do ácido hialurônico demonstrou ter correlação no processo de crescimento tumoral através da angiogênese. A análise biomolecular apontou a diminuição dos proteoglicanos no tecido tumoral e, portanto, estes podem ser potenciais biomarcadores prognósticos de câncer de pulmão. As análises feitas em escarro demonstraram que a elevada expressão proteica de solCD44 e da cofilina-1 no escarro nos pacientes com câncer de pulmão mostram-se como promissores alvos de detecção do CP
Introduction. The relationship between the extracellular matrix (ECM) components and cancer cells have an important role on cancer development and progression. Between the most important molecules present on the ECM are the glycosaminoglycans and their respective proteoglycans. Studies have reported that they have different behaviours when in the presence of malignant tissues and influence the development of breast, pancreas and colon cancers. Likewise, proteins as solCD44 and cofilin-1 also have shown direct influence in tumor progression. Regarding that, there is growing interest among scientists in analyzing the expression of these molecules in body fluids as a screening tool of high risk patients and as a diagnostic and prognostic lung cancer biomarker. Objectives. The aims of this study were to recognize the impact of hyaluronan and the proteoglycans (biglycan, glypican, perlecan, syndecan e versican) on lung cancer carcinogenesis as well as its impact on patient\'s survival; verify if the solCD44 e cofilina-1 concentrations in the sputum of lung cancer patients could distinguish them from patients with COPD and healthy volunteers. Results. A direct association was found between tumors expressing high amounts of hyaluronan and CD34 in tumoral stroma. Heparan and chondroitin sulphate concentrations were higher in tumor specimens when compared to normal lung tissue. All proteoglycans, in exception of syndecan, showed a lower expression in tumoral tissue and biglycan and versican showed association with the clinical pathological features. Protein expression of biglycan, perlecan and versican was higher in the normal tissue when compared to stroma and tumoral cells. COX regression controlled by age, histological types and gene expression of biglycan, syndecan e glypican demonstrated that female patients had higher survival rates with high gene expression of perlecan and the patients with T1 stage, lack of linfonode Maristela Peres Rangel Tese de doutorado - USP metastasis and gene expression of versican had lower risk of death. Cofilin-1 concentration was higher in the sputum of lung cancer patients when compared to a high risk group and healthy volunteers. Also, the solCD44 concentration was higher in the sputum of lung cancer patients when compared to a high risk group and healthy volunteers. ROC cruve analysis demonstrated that sputum cofilin-1 was capable to distinguish high risk patients from lung cancer patients with na area under the curve of 0.69 and with a cut off at 802.5 pg/mL the curve presented 60% de sensitivity and 54% specificity. Sputum solCD44 was also capable to distinguish high risk patients from lung cancer patients with na area under the curve of 0.67 and with a cut off at 65.8 pg/mL the curve presented 50% de sensitivity and 84% specificity. Conclusions. Hyaluronan expression showed a correlation with tumoral growth through angiogenesis processes. The biomolecular analysis demonstrated that matrix proteoglycans are potencial lung cancer prognostic biomarkers. Sputum analyses showed that solCD44 and cofilin-1 are potencial molecules in lung cancer detection
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Rangel, Maristela Peres. "Relevância clínica da concentração do ácido hialurônico no escarro e em espécimes tumorais de pacientes portadores de carcinomas de pulmão." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-25102012-162649/.

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Introdução. O ácido hialurônico é um glicosaminoglicano não sulfatado presente na matriz extracelular. Vários estudos têm demonstrado que uma produção ou degradação aberrante dessa molécula tem influência no comportamento do câncer de mama, próstata, bexiga e pulmão. Desta forma, a dosagem do ácido hialurônico em tecidos e fluidos corporais como sangue, urina e escarro tem despertado grande interesse como rastreador de indivíduos de alto risco e marcador diagnóstico e/ou prognóstico da doença estabelecida. Objetivos. Verificar se há diferenças nos níveis de ácido hialurônico entre espécimes tumorais e não tumorais de câncer de pulmão, bem como seu impacto na sobrevida dos pacientes; verificar se diferenças encontradas nos tecidos estão também presentes no escarro; verificar se a dosagem do ácido hialurônico no escarro permite rastrear pacientes com câncer de pulmão entre pacientes com doença pulmonar obstrutiva crônica e voluntários saudáveis. Resultados. Houve uma elevação significativa nos níveis de ácido hialurônico nos espécimes tumorais em relação aos espécimes não tumorais, mesmo quando histologicamente categorizados. Não houve associação entre as concentrações do ácido hialurônico com características clínicas dos pacientes, porém houve impacto na sobrevida dos pacientes: pacientes com tumores contendo ácido hialurônico > 364,36 g/g apresentaram menor sobrevida global que pacientes cujos tumores evidenciaram ácido hialurônico < 364,36 ug/g. Demonstramos que pacientes com câncer de pulmão apresentam elevações altamente significativas da produção de ácido hialurônico no escarro independente das características clínicas dos pacientes, porém dependente do tipo histológico. Valores de ácido hialurônico >11,13ng/mg no escarro tem sensibilidade de 87% para rastreamento de pacientes com câncer de pulmão e voluntários saudáveis. Nesse grupo valores > 31,44ng/mg tem especificidade de 100% e sensibilidade de 51%. Houve exclusão com sensibilidade de 33% e especificidade de 100% de pacientes com doença pulmonar obstrutiva crônica em relação aos pacientes com câncer de pulmão para valores > 48,36ng/mg. Conclusão. Diferentes níveis de ácido hialurônico forma observados nos tumores e tecidos normais com impacto na sobrevida dos pacientes, tornando a dosagem do ácido hialurônico como promissor marcador prognóstico no câncer de pulmão. Diferenças observadas nos tecidos foram também constatadas no escarro, despontando a dosagem do ácido hialurônico como promissora no rastreamento de indivíduos com risco para câncer de pulmão
Introduction. Hyaluronan is an extracellular matrix non-sulfated glycosaminoglycan. Some have reported that its abnormal production and degradation can influence the behaviour of different types of tumours like breast, prostate, bladder and lung cancer. Therefore, hyaluronan quantitative analysis in tissues and body fluids like blood, urine and sputum has shown promise on the high risk patients screening and as diagnostic/prognostic marker of some diseases. Objectives. Verify if there are differences in the levels of hyaluronan in tumoral and non-tumoral lung cancer specimens, as well as its impact on the patients survival; verify if sputum samples present the same differences; verify the role of hyaluronan quantitative analysis in the screening of lung cancer patients between patients with chronic obstructive pulmonary disease and healthy volunteers. Results. Lung cancer tumoral specimens showed higher levels of hyaluronan when compared to non-tumoral specimens even when the specimens were histologically categorized. There was no correlation between hyaluronan levels and the patients clinical features, however, an impact in the patients survival was observed: patients with tumoral hyaluronan levels > 364,36 g/g had a lower survival rate than patients with < 364,36 ug/g. We have shown that lung cancer patients show an elevated production of hyaluronan in the sputum. This characteristic was independent of the clinical features but dependent of the histologic type. The hyaluronan quantitative analysis for the screening of lung cancer patients between healthy volunteers showed a sensitivity of 87% for hyaluronan levels >11,13ng/mg in the sputum. In this group levels > 31,44ng/mg showed 100% specificity and 51% sensibility. On a second group (lung cancer patients vs chronic obstructive pulmonary disease patients) levels of sputum hyaluronan > 48,36ng/mg showed 100% specificity to exclude chronic obstructive pulmonary disease patients from lung cancer patients. The sensibility for this cut-off point was 33%. Conclusion. Hyaluronan quantitative analysis in the tissues is a promising lung cancer prognostic marker considering the differences between hyaluronan levels on tumoral and nontumoral tissues. Not only this, but, the differences observed in the tissues were observed in the sputum as well. Hence, the hyaluronan quantitative analysis is a promising strategy in the screening of high risk individuals that might develop lung cancer
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Книги з теми "Lung carcinomas"

1

M, McDowell Elizabeth, ed. Lung carcinomas. Edinburgh: Churchill Livingstone, 1987.

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1940-, Hayat M. A., ed. Lung and breast carcinomas. Amsterdam: Elsevier, Academic Press, 2008.

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3

Hastie, G. Michael. Ribonucleic acid isolation from small cell lung carcinomas. Sudbury, Ont: Laurentian University, 1992.

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4

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

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5

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

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6

G, Maldonado Jonathon, and Cervantes Mikayla K, eds. Small cell carcinomas: Causes, diagnosis and treatment. Hauppauge, N.Y: Nova Science, 2009.

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7

Maldonado, Jonathon G., and Mikayla K. Cervantes. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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8

Burton, Jean. A study of cellular proliferation rates in squamous cell carcinomas of the lung, with relation to p53 status. [S.l: The Author], 1994.

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9

Nael, Martini, ed. Surgical treatment of lung carcinoma. Philadelphia: Saunders, 1987.

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10

1931-, Martini Nael, ed. Surgical treatment of lung carcinoma. Philadelphia, PA: W.B. Saunders, 1987.

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Частини книг з теми "Lung carcinomas"

1

Pelosi, Giuseppe, Alessandra Fabbri, and Angelica Sonzogni. "Sarcomatoid Carcinomas, Lung." In Encyclopedia of Pathology, 395–98. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-69263-0_304.

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2

Corrin, B. "Small Cell Carcinomas Versus (Atypical) Carcinoids." In Clinical and Experimental Pathology of Lung Cancer, 47–52. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-5036-8_5.

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3

Kádár, András, and Tibor A. Rauch. "Epigenetic Reprogramming in Lung Carcinomas." In Patho-Epigenetics of Disease, 159–77. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3345-3_7.

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4

Beasley, Mary Beth. "Molecular Biopsy of Neuroendocrine Carcinomas Other Than Small Cell Carcinoma." In Molecular Pathology of Lung Cancer, 189–92. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3197-8_17.

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5

Borczuk, Alain C. "Molecular Pathology of Uncommon Carcinomas." In Molecular Pathology of Lung Cancer, 193–200. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3197-8_18.

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6

Borczuk, Alain C. "Molecular Pathology of Uncommon Carcinomas." In Precision Molecular Pathology of Lung Cancer, 183–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-62941-4_15.

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7

Beasley, Mary Beth. "Molecular Pathology of Small Cell Carcinomas." In Molecular Pathology of Lung Cancer, 185–88. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3197-8_16.

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8

Kini, Sudha R. "Classification of Lung Tumors: An Overview of Lung Carcinomas." In Color Atlas of Pulmonary Cytopathology, 78–81. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/978-0-387-21641-6_5.

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9

Ming Dong, Zhao, and Paul D. Simonson. "Primary Pulmonary Diffuse Large B-Cell Lymphoma Versus Poorly Differentiated Carcinomas." In Practical Lung Pathology, 207–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-14402-8_34.

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10

Mendelsohn, Geoffrey, Margaret Suarez, Medhat Omar Hassan, Suja Subramanyan, and John A. Maksem. "Histopathologic, Immunohistochemical, and Ultrastructural Studies of Lung Carcinomas." In Progress in Surgical Pathology, 127–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-662-12817-6_5.

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Тези доповідей конференцій з теми "Lung carcinomas"

1

Lemos, Nathalia Oliveira, Fábio Bagnoli, Maria Antonieta Longo Galvão Silva, José Francisco Rinaldi, and Vilmar Marques de Oliveira. "INVASIVE LOBULAR BREAST CANCER METASTATIC TO THE ORBIT: A CASE REPORT." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1048.

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Invasive lobular carcinoma represents 5%–15% of breast carcinomas, presenting in many cases as multicentric and bilateral tumors with low mammographic detection. The most common breast cancer metastases are the bones, lungs, brain, and liver. However, the disease can also spread to abdominal cavity, ovaries, and skin. The orbit is an infrequent site of tumor metastasis, ranging from 1% to 13% among all orbital tumors, and breast, lung, and prostate are among the most common primary sites. We report the case of a 73-year-old female patient who presented with a palpable mass in the left orbital rim, whose incisional biopsy revealed a pattern compatible with invasive breast carcinoma with lobular characteristics and E-cadherin overexpression, luminal molecular subtype B. She denied breast complaints and palpable nodules, but on clinical examination she showed a tumor in the inferolateral quadrant of the left breast measuring 6 cm and a left axilla with lymph node enlargement suspected of lymph node involvement. Mammography identified suspicious nodulation in this topography, confirmed by ultrasound. The diagnosis made through core biopsy was an invasive breast carcinoma with lobular characteristics, and the immunohistochemical profile showed luminal molecular subtype B. Systemic staging revealed involvement of the retroperitoneum, left ovarian annex, vertebral bodies, pelvis, right femur, and left iliac suspected for secondary involvement. The patient is currently undergoing adjuvant systemic treatment.
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2

Stravinskaite, Kristina, and Raimundas Sakalauskas. "Multiple Primary Carcinomas: Kidney Clear Cell Carcinoma, Rectum Adenocarcinoma, Recessus Piriformis Squamose Cell Carcinoma And Non Small Cell Lung Carcinoma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5876.

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Cuentas, Edwin Roger, Carmen Behrens, Jaime Rodriguez-Canales, Mei Jiang, Apar Pataer, Arelene Correa, Stephen Swisher, et al. "Abstract 2934: Neoadjuvant chemotherapy influence changes of the immune response in non-small cell lung carcinomas immune response in non-small cell lung carcinomas." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2934.

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Xiao, Zuoxiang, Qun Jiang, Jami Willette-Brown, Feng Zhu, Howard A. Young, Fanching Lin, Sandra Burkett та ін. "Abstract 2560: IKKα inactivation predisposes to spontaneous lung squamous cell carcinomas". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2560.

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5

Menoux, Inès, Delphine Antoni, Pierre Truntzer, Audrey Keller, Gilbert Massard, and Georges Noël. "Hypofractionated radiotherapy for stage I lung carcinomas: moderate hypofractionation optimizes outcome." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2212.

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6

Li, Aihua, Yongfu Gao, Yuekai Zhang, Hongyang Pan, Jackie K. Chan, Ximing J. Yang, and Taiying Chen. "Abstract 3416: IHC assessment of PBRM1 loss in colon and lung carcinomas." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3416.

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Song, Kai, Guangqiang Zheng, Luc Girard, Ignacio I. Wistuba, Jack A. Roth, Carmen Behrens, Milind B. Suraokar, John D. Minna, and Adi F. Gazdar. "Abstract 613: Copy number variations distinguish lung adenocarcinomas from squamous cell carcinomas." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-613.

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Becker-Santos, Daiana D., Emily A. Vucic, Stephen Lam, Wan L. Lam, and Victor D. Martinez. "Abstract A32: Genomic and epigenomic alterations in arsenic-related lung squamous cell carcinomas." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a32.

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Lal, Anita, Rebecca Panos, Mira Marjanovic, Michael Walker, Eloisa Fuentes, W. David Henner, Ljubomir Buturovic, and Meredith Halks-Miller. "Abstract 1724: A gene expression profile test to resolve squamous cell carcinomas of head & neck from squamous cell carcinomas of the lung." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1724.

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Kim, Youngwook, Peter S. Hammerman, Jaegil Kim, Gad Getz, Matthew Meyerson, and Keunchil Park. "Abstract 1526: Integrative and comparative genomic analysis of East-Asian lung squamous cell carcinomas." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1526.

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Звіти організацій з теми "Lung carcinomas"

1

Freire, Mariana, Diana Martins, Maria Filomena Botelho, and 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, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0011.

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Анотація:
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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2

Watabe, Kounosuke. Roles of microRNA-Mediated Drug Resistance in Tumor Stem Cells of Small Cell Lung Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada614451.

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3

Watabe, Kounosuke. Roles of MicroRNA-mediated Drug Resistance in Tumor Stem Cells of Small Cell Lung Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598410.

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4

Wu, Liang. Optimal treatment and clinical outcomes of intramedullary spinal cord metastasis from lung carcinoma: a systematic review. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0063.

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Valeri, C. R., John Dittmer, Toshio Ichikura, Hong Qu, and Linda E. Pivacek. Effects of Syngeneic Fresh and Liquid Preserved Red Blood Cells on Primary and Metastatic Growth of the Lewis Lung Carcinoma in Mice. Fort Belvoir, VA: Defense Technical Information Center, August 1993. http://dx.doi.org/10.21236/ada360153.

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6

Zamora, P. O., H. Bender, H. J. Biersack, and F. F. Jr Knapp. Interim report on intrathoracic radiotherapy of human small-cell lung carcinoma in nude mice with Re-188-RC-160, a radiolabeled somatostatin analogue. Office of Scientific and Technical Information (OSTI), July 1995. http://dx.doi.org/10.2172/87003.

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