Relevant bibliographies by topics / Lung Neuroendocrine tumor

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Lung Neuroendocrine tumor'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Lung Neuroendocrine tumor.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Lung Neuroendocrine tumor"

1

Tamási, Lilla, and Veronika Müller. "Symptoms and diagnostics of lung neuroendocrine tumors." Orvosi Hetilap 152, no. 10 (March 2011): 366–70. http://dx.doi.org/10.1556/oh.2011.29041.

Full text
Abstract:
Pulmonary neuroendocrine tumors comprise 20% of all lung cancers. They are separated into 4 subgroups: typical carcinoid tumor, atypical carcinoid tumor, large-cell neuroendocrine carcinoma, and small-cell lung carcinoma. The major symptoms present in 60% of patients are cough, hemoptysis, and obstructive pneumonia. They may also exhibit hormonally related symptoms e.g. carcinoid syndrome. Small cell lung cancer is the most common subgroup, with rapid progression, aggressive metastatic potential and the worst prognosis. Large cell neuroendocrine carcinoma is rare but also has a poor prognosis. Typical carcinoid may be accompanied with hormone related symptoms and has the best prognosis; atypical one on the contrary may cause lymph node and distant metastases in half of the cases. Elevated plasma levels of chromogranin-A are present in majority of pulmonary neuroendocrine tumors and act as tumor marker. The mainstay of treatment is radical surgery if possible. In locally advanced or metastatic disease combination chemotherapy and somatostatin-analogues may have beneficial effect. This review focuses on the general features, and current diagnostic options of pulmonary neuroendocrine tumors. Orv. Hetil., 2011, 152, 366–370.
APA, Harvard, Vancouver, ISO, and other styles
2

Miura, Kentaro, Kimihiro Shimizu, Shogo Ide, Shuji Mishima, Shunichiro Matsuoka, Tetsu Takeda, Takashi Eguchi, Kazutoshi Hamanaka, and Takeshi Uehara. "A Novel Strategy for the Diagnosis of Pulmonary High-Grade Neuroendocrine Tumor." Diagnostics 11, no. 11 (October 20, 2021): 1945. http://dx.doi.org/10.3390/diagnostics11111945.

Full text
Abstract:
Correctly diagnosing a histologic type of lung cancer is important for selecting the appropriate treatment because the aggressiveness, chemotherapy regimen, surgical approach, and prognosis vary significantly among histologic types. Pulmonary NETs, which are characterized by neuroendocrine morphologies, represent approximately 20% of all lung cancers. In particular, high-grade neuroendocrine tumors (small cell lung cancer and large cell neuroendocrine tumor) are highly proliferative cancers that have a poorer prognosis than other non-small cell lung cancers. The combination of hematoxylin and eosin staining, Ki-67, and immunostaining of classic neuroendocrine markers, such as chromogranin A, CD56, and synaptophysin, are normally used to diagnose high-grade neuroendocrine tumors; however, they are frequently heterogeneous. This article reviews the diagnostic methods of lung cancer diagnosis focused on immunostaining. In particular, we describe the usefulness of immunostaining by Stathmin-1, which is a cytosolic phosphoprotein and a key regulator of cell division due to its microtubule depolymerization in a phosphorylation-dependent manner, for the diagnosis of high-grade neuroendocrine tumors.
APA, Harvard, Vancouver, ISO, and other styles
3

Kasajima, Atsuko, Yuichi Ishikawa, Ayaka Iwata, Katja Steiger, Naomi Oka, Hirotaka Ishida, Akira Sakurada, et al. "Inflammation and PD-L1 expression in pulmonary neuroendocrine tumors." Endocrine-Related Cancer 25, no. 3 (March 2018): 339–50. http://dx.doi.org/10.1530/erc-17-0427.

Full text
Abstract:
In the light of novel cancer immune therapies, the status of antitumor inflammatory response and its regulation has gained much attention in patients with lung cancer. Ample datasets exist for non-small-cell lung cancer, but those for pulmonary neuroendocrine tumors are scarce and controversial. Here, tumor-associated inflammation, CD8+ cell infiltration and PD-L1 status were evaluated in a cohort of 57 resected carcinoids and 185 resected neuroendocrine carcinomas of the lung (58 large cell carcinomas and 127 small cell carcinomas). Data were correlated with clinicopathological factors and survival. Moderate or high tumor-associated inflammation was detected in 4 carcinoids (7%) and in 37 neuroendocrine carcinomas (20%). PD-L1 immunoreactivity was seen in immune cells of 73 (39%) neuroendocrine carcinomas, while tumor cells were labeled in 21 (11%) cases. Inflammatory cells and tumor cells in carcinoids lacked any PD-L1 expression. In neuroendocrine carcinomas, PD-L1 positivity in immune cells, but not in tumor cells, was associated with intratumoral CD8+ cell infiltration (P < 0.001), as well as with the severity of tumor-associated inflammation (P < 0.001). In neuroendocrine carcinomas, tumor-associated inflammation and PD-L1 positivity in immune cells correlated with prolonged survival and the latter factor was also an independent prognosticator (P < 0.01, hazard ratio 0.4 for overall survival,P < 0.001 hazard ratio 0.4 for disease-free survival). Taken together, in neuroendocrine tumors, antitumor inflammatory response and PD-L1 expression are largely restricted to neuroendocrine carcinomas, and in this tumor entity, PD-L1 expression in inflammatory cells is positively correlated to patient survival.
APA, Harvard, Vancouver, ISO, and other styles
4

Mouna, Bourhafour, Chekrine Tarik, Bouchbika Zineb, Benchakroun Nadia, Jouhadi Hassan, Tawfiq Nezha, Benider Abdellatif, and Sahraoui Souha. "NON SURGICAL TREATMENT OF CARCINOID LUNGS TUMORS." International Journal of Advanced Research 9, no. 12 (December 31, 2021): 647–51. http://dx.doi.org/10.21474/ijar01/13954.

Full text
Abstract:
Typical carcinoid lungs tumors are neuroendocrine bronchopulmonary tumors with a low-grade malignancy, and an atypical carcinoid is an intermediate form of these tumors. Their systemic treatment is greatly influenced by therapeutic evidence derived from the more frequent gastroenteropancreatic neuroendocrine neoplasms. Currently, systemic therapies for lung carcinoids, aiming at controlling tumor growth include long acting somatostatin analogues (SSAs), peptide receptor radionuclide therapy, chemotherapy and molecular-targeted therapy.
APA, Harvard, Vancouver, ISO, and other styles
5

Chytaieva, Halyna, Bohdana Shkurupii, and Liubov Zakhartseva. "Correlation between expression of immunohistochemical markers and morphology in lung neuroendocrine neoplasms." Ukrainian Scientific Medical Youth Journal 128, no. 1 (March 27, 2022): 6–18. http://dx.doi.org/10.32345/usmyj.1(128).2022.6-18.

Full text
Abstract:
lung neuroendocrine neoplasms embrace rather heterogeneous and rare malignancies which are usually characterized by nonspecific, “blurred” clinical signs thus complicating correct diagnosis or seriously delays it. Pulmonary neuroendocrine neoplasms accurate diagnostics and classification need to be improved. Histological examination should be supplemented by immunohistochemical tests to verify the neuroendocrine component, assess proliferative index of tumor cells, and confirm its bronchopulmonary origin. Immunohistochemistry is especially important in case of small or crushed biopsies, which account more than 50% of all specimens in lungs neuroendocrine neoplasms. Modern classification of lung neuroendocrine neoplasms and their grading are based on morphological criteria. Immunohistochemical markers expression is quite variable in different histological subtypes of bronchopulmonary neuroendocrine neoplasms, often data are descriptive, and correlation with morphology is studied insufficiently. The aim of this study was to define any significant correlation between different immunohistochemical markers expression, necrosis, proliferative index (Ki-67 ratio), and tumor grade in broncho-pulmonary neuroendocrine neoplasms. Histological blocks of lung neuroendocrine neoplasms from 113 unique patients (36 resections and 77 biopsies (54.5% of biopsies appeared to be small or crushed) were used in this study. The sample comprised 91 male and 22 female patients; the mean age was 59.2, CI 95% (56.9–61.4) years (from 19 to 77 years). Histological examination (including neuroendocrine morphology, necrosis, and grade) was provided in all cases. Also, immunohistochemistry, using Chr A, Syn, CD56, TTF-1, CK7, and Ki-67 before chemotherapy was performed. All morphological and immunohistochemical data were assessed by two different independent pathologists without the access to patient’s clinical data. All the observations were classified based on 2021 WHO Thoracic Tumors Classification. The sample was censored. We used nonparametric statistics (Spearman’s rank correlation) for this study. In was found that Chr A expression strongly (p<0.05) correlated with immunohistochemical markers of primary lung malignancies (TTF-1 and CK7) that are mainly expressed in highly and moderately differentiated neuroendocrine neoplasms. Also, positive expression for TTF-1 and CK7 correlated with each other (p<0.01). There was a strong negative correlation (p<0.05) between Chr A staining and necrosis presence and it’s severity; between Chr A expression and tumor cells proliferation (Ki-67 ratio) (p<0.01); and between Chr A labeling and tumor grade (p<0.01). The correlation of immunohistochemical markers expression with necrosis, Ki-67 ratio and tumor grade was significant only for Chr A. All other tested options, for other markers were not statistically significant. It was defined that decrease or loss of Chr A expression reliably indicates tumors progression. Chr A expression can be used as an additional tool for grading of lung neuroendocrine neoplasms.
APA, Harvard, Vancouver, ISO, and other styles
6

Slodkowska, J., J. Zych, M. Szturmowicz, U. Demkow, E. Rowinska-Zakrzewska, and K. Roszkowski-Sliz. "Neuroendocrine Phenotype of Non-Small Cell Lung Carcinoma: Immunohistological Evaluation and Biochemical Study." International Journal of Biological Markers 20, no. 4 (October 2005): 217–26. http://dx.doi.org/10.1177/172460080502000404.

Full text
Abstract:
Aims and methods The prevalence and distribution of neuroendocrine differentiation in non-small cell lung cancer (NSCLC) was estimated by assays for synaptophysin (SYN), chromogranin A (CgA), Leu7 and neuron-specific enolase (NSE). Serum NSE and CgA were determined in parallel to find the values of these markers for distinguishing neuroendocrine differentiation in NSCLC. Fifty-eight resected NSCLC specimens and 34 sera of NSCLC patients entered the study. Neuroendocrine differentiation was graded according to the percentage of neuroendocrine tumor cells as NE0 – 0%, NE1–NE4 – 1%->76%. Serum NSE <12.5 ng/mL and serum CgA <46 U/L were taken as cutoff levels. Results 63.8% (37/58) of NSCLC were scored as NE1–NE4 according to the SYN, CgA and Leu7 levels; 34.5% as NE1; 29.3% as NE2–NE4. 56.8% of tumors were positive for SYN, 34.4% for CgA, 22.4% for Leu7, and 79.3% for NSE. A significant relationship was found between tumor SYN and tumor CgA expression, and between tumor SYN expression and tumor stage. Adenocarcinomas showed a significantly higher rate of neuroendocrine differentiation than squamous cell carcinomas. All normal serum CgA levels corresponded to a lack of CgA expression in the tumors. The increased serum NSE levels presented by 26% of NSCLC patients (mainly <16 ng/mL) did not correlate with tumor NSE expression. Conclusions The prevalence of neuroendocrine differentiation in NSCLC varies and depends on the immunohistochemical criteria used; this warrants standardization of the immunohistochemical criteria for neuroendocrine differentiation in NSCLC. NSE expression in the tumor and a mild increase in serum NSE are poor markers for distinguishing neuroendocrine differentiation in NSCLC.
APA, Harvard, Vancouver, ISO, and other styles
7

Travis, William D., Anthony A. Gal, Thomas V. Colby, David S. Klimstra, Roni Falk, and Michael N. Koss. "Reproducibility of neuroendocrine lung tumor classification." Human Pathology 29, no. 3 (March 1998): 272–79. http://dx.doi.org/10.1016/s0046-8177(98)90047-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Song, Jie, Mei Li, Maria Tretiakova, Ravi Salgia, Philip T. Cagle, and Aliya N. Husain. "Expression Patterns of PAX5, c-Met, and Paxillin in Neuroendocrine Tumors of the Lung." Archives of Pathology & Laboratory Medicine 134, no. 11 (November 1, 2010): 1702–5. http://dx.doi.org/10.5858/2009-0664-oar1.1.

Full text
Abstract:
Abstract Context.—c-Met is important in the pathogenesis, invasion, and spread of several forms of lung cancer, and multiple c-Met inhibitors are undergoing clinical trials. PAX5 has been shown to upregulate c-Met in small cell lung carcinoma (SCLC), and coinhibiting PAX5 and c-Met had a synergic effect in killing tumor cells. Paxillin is a downstream target of activated c-Met, and its activation leads to enhanced cell motility and tumor spread. The expression patterns of these functionally related proteins have not, to our knowledge, been systemically studied in neuroendocrine tumors of the lung. Objective.—To investigate the expression patterns of PAX5, paxillin, c-Met, and phosphorylated c-Met in 4 categories of pulmonary neuroendocrine tumors. Design.—Tissue microarrays of 38 typical carcinoids, 6 atypical carcinoids, 34 SCLCs, and 11 large cell neuroendocrine carcinomas were studied with immunohistochemistry. Results.—Most of the 4 tumor types expressed c-Met, phosphorylated c-Met, and paxillin. PAX5 was frequently expressed in atypical carcinoids, SCLCs, and large cell neuroendocrine carcinomas but tended to be negative in typical carcinoids. Coexpression of PAX5 with c-Met or phosphorylated c-Met was present in most of the atypical carcinoids, SCLCs, and large cell neuroendocrine carcinomas. Significant correlation between PAX5 and paxillin was detected in SCLCs and large cell neuroendocrine carcinomas but not in carcinoid tumors. Conclusions.—The frequent coexpression of PAX5 with c-Met or phosphorylated c-Met in intermediate-grade and high-grade neuroendocrine tumors supports the therapeutic strategy of coinhibiting these proteins. The discrepancy between high-grade and low-grade neuroendocrine tumors in PAX5/paxillin expression correlation may be due to the different underlying molecular genetics of these tumors.
APA, Harvard, Vancouver, ISO, and other styles
9

Kumar, Kishore, Rafeeq Ahmed, Chime Chukwunonso, Hassan Tariq, Masooma Niazi, Jasbir Makker, and Ariyo Ihimoyan. "Poorly Differentiated Small-Cell-Type Neuroendocrine Carcinoma of the Prostate: A Case Report and Literature Review." Case Reports in Oncology 11, no. 3 (October 31, 2018): 676–81. http://dx.doi.org/10.1159/000493255.

Full text
Abstract:
Neuroendocrine cells are widespread throughout the body and can give rise of neuroendocrine tumors due to abnormal growth of the chromaffin cells. Neuroendocrine tumors divide into many subtypes based on tumor grade (Ki-67 index and mitotic count) and differentiation. These tumors can be further divided into secretory and nonsecretory types based on the production of peptide hormone by tumor cells. Poorly differentiated small-cell-type neuroendocrine tumors are one of the subtypes of neuroendocrine tumors. These tumors are less common; however, they tend to be locally invasive and aggressive in behavior with poor overall median survival. Treatment of the nonsecretory small-cell type is modeled to small-cell lung cancer with a regimen consisting of platinum-based chemotherapy and etoposide with variable response. Here, we present a case of poorly differentiated small-cell neuroendocrine tumor originating from the prostate.
APA, Harvard, Vancouver, ISO, and other styles
10

Børglum, Tine, Jens F. Rehfeld, Lars B. Drivsholm, and Linda Hilsted. "Processing-Independent Quantitation of Chromogranin A in Plasma from Patients with Neuroendocrine Tumors and Small-Cell Lung Carcinomas." Clinical Chemistry 53, no. 3 (March 1, 2007): 438–46. http://dx.doi.org/10.1373/clinchem.2006.076158.

Full text
Abstract:
Abstract Background: Most neuroendocrine tumors express chromogranin A (CgA). The posttranslational processing of neuroendocrine proteins such as CgA is often specific for the individual tumor. To cope with this variability and improve tumor diagnosis, we developed a processing-independent analysis (PIA) method to measure the total CgA product. Methods: For PIA, samples underwent trypsin treatment followed by measurement of CgA by the “CgA(340→)” assay, in which the antiserum binds an epitope starting at amino acid 340 of CgA and including amino acid residues located in the C-terminal direction. The diagnostic accuracy of the CgA PIA and 3 sequence-specific assays for CgA were evaluated on plasma samples from patients with neuroendocrine tumors and small-cell lung carcinomas. Furthermore, we investigated whether the CgA plasma concentrations correlated with the tumor burden. Results: Size-exclusion chromatography of plasma showed that CgA immunoreactivity mainly consisted of high–molecular-weight forms, indicating that neuroendocrine tumors may secrete large amounts of poorly processed CgA. Accordingly, trypsination of plasma from 54 patients with neuroendocrine tumors or small-cell lung carcinomas increased the CgA(340→) immunoreactivity up to 500-fold. Both the CgA(340→) assay and the PIA measured significantly higher plasma concentrations in patients with very extensive disease than in patients with less widespread disease. The diagnostic sensitivity was 0.91 when using the CgA(340→) assay and 0.82 using the CgA PIA. Conclusion: The CgA(340→) assay and CgA PIA are both useful for diagnosis of neuroendocrine tumors and small-cell lung carcinomas and both assays correlate with tumor burden.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Lung Neuroendocrine tumor"

1

SARONNI, DAVIDE. "TYROSINE KINASE INHIBITORS IN NEUROENDOCRINE TUMORS: FROM IN VITRO TO ZEBRAFISH MODEL." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/917967.

Full text
Abstract:
(1) Background: Neuroendocrine neoplasms (NENs) are a group of tumors that arise from neuroendocrine cells throughout the body, with the lungs and gastrointestinal tract being the most common sites of origin. In patients with NENs and distant metastases, surgery is generally not curative. Although well-differentiated and low-grade NENs, classified as neuroendocrine tumors (NETs), are usually less aggressive than poorly-differentiated NENs, they can develop distant metastases in about 15% of cases. These patients require chronic medical management. However, the clinical efficacy of these treatments is limited by the low objective response rate, due to the occurrence of tumor resistance and the high biological heterogeneity of these neoplasms. (2) Research problem: We addressed this study on two rare NETs: lung neuroendocrine tumors (LNETs) and medullary thyroid carcinoma (MTC). LNETs represent about 2% of lung tumors, while MTCs are rare thyroid tumors caused by mutations in the RET proto-oncogene. Both NETs are well-differentiated neoplasms and are known to be highly vascularized. Therefore, they represent a potential target for tyrosine kinase inhibitors (TKIs) selective for receptors involved in angiogenesis. The aim of this project was to evaluate the antitumor activity of several new TKIs both in vitro, using LNETs (NCI-H727, UMC-11 and NCI-H835) and MTC (TT and MZ-CRC-1) cell lines, and in vivo, adopting a novel zebrafish xenograft model to study angiogenesis. In LNETs we tested: sulfatinib, a small molecule that inhibits the Vascular Endothelial Growth Factor Receptor (VEGFR) 1, 2, and 3, and the Fibroblast Growth Factor Receptor type 1 (FGFR1); cabozantinib, a multi-target inhibitor selective for VEGFR2, c-Met, Kit, Axl and Flt3; and axitinib, a multi-target TKI of VEGFR1, 2, 3 and Platelet-Derived Growth Factor Receptor-beta (PDGFRβ). In MTC we tested: sulfatinib; SPP86, a RET-specific inhibitor; and SU5402, an inhibitor of the FGFR1 and VEGFR2. (3) Methodology: In LNETs and MTC cells the effects of selected TKIs have been evaluated in vitro through: MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assays, for assessing cell viability; flow-cytometer analysis, for the evaluation of cell cycle and apoptosis; and wound-healing assay, to study cell migration. In vivo we took advantage of the transgenic zebrafish line of Tg(fli1a:EGFP)y1. Through the xenotransplantation of NET cells in the subperidermal space near the subintestinal vein, we assessed the effects of TKIs on tumor-induced angiogenesis and cancer dissemination. (4) Key Results: In LNET cell lines we observed a dose-dependent decrease in cell viability after incubation with all TKIs. This effect seems to be related to the perturbation of the cell cycle and induction in apoptosis. In NCI-H727 wound healing assay showed a significant reduction in cell migration only after incubation with cabozantinib. In the zebrafish model, we found a significant reduction of the tumor-induced angiogenesis in implanted LNET cell lines after treatment with all TKIs. Cabozantinib and axitinib were more potent than sulfatinib in inhibition of angiogenesis, while cabozantinib was the most efficient in reducing cell migration from the transplantation site to the tail. In MTC cell lines, sulfatinib, SU5402 and SPP86 showed a decrease in cell viability, confirmed by the significant reduction in S phase cell population. Moreover, sulfatinib and SPP86 showed for both cell lines a significant induction of apoptosis. Sulfatinib and SPP86 inhibited the migration of TT and MZCRC-1 cells, evaluated through the wound healing assay, while SU5402 was able to inhibit migration only in TT cells. In vivo we observed a significant reduction of TT cells-induced angiogenesis in zebrafish embryos after treatment with sulfatinib and SPP86. (5) Conclusions: Despite sulfatinib resulted the most potent compound in terms of inhibition of LNET cell proliferation, cabozantinib showed in vivo the most effective impact in reducing tumor-induced angiogenesis. Cabozantinib was the only TKI able to inhibit in vivo the dissemination of implanted LNET cells. According to these data, cabozantinib could represent a potential candidate in the therapy of patients with highly vascularized LNET. In MTC cell lines, SPP86 and sulfatinib displayed a similar antitumor activity both in vitro and in vivo, suggesting a good efficacy of specific RET inhibitors (SPP86) with potentially less adverse effects than multitarget TKIs (sulfatinib). In addition, this study showed that the zebrafish model for NETs represents an innovative tool for drug screening with several advantages compared with rodent models: rapidity of procedure, animal immune suppression is not required, lower number of tumor cells for implant and the optical transparency provides a real-time monitoring of cell-stromal interactions and cancer progression in living animals.
APA, Harvard, Vancouver, ISO, and other styles
2

Bari, Muhammad Furqan. "Biomarkers for the classification of high grade neuroendocrine lung cancers." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/56420/.

Full text
Abstract:
In the management of lung cancer the most important step beyond establishing the presence a malignant tumour is identifying whether the tumour is small cell lung cancer (SCLC) or one of the variants of non-small cell carcinoma (NSCLC), which includes adenocarcinoma (AD), squamous (SCC), large cell carcinoma (LCC), large cell neuroendocrine carcinoma (LCNEC), typical carcinoids (TC) and atypical carcinoids (AT). SCLC is a high grade neuroendocrine tumour which usually presents as central mass. These tumours are not usually amenable to curative surgical resection and are treated primarily by chemotherapy resulting in a treatment dichotomy of SCLC and NSCLC. The diagnosis of the tumour subtypes is routinely established on cytology or histology samples and in case of AD, LCC and SCC, which are not neuroendocrine tumours, the diagnosis is aided by neuroendocrine markers. However for TC, AT and LCNEC which are neuroendocrine tumours, the diagnosis is based on morphological features alone, which in some cases overlap and result in difficulty in diagnosis. This inter-observer variability is common among the neuroendocrine lung tumours and is highest between SCLC and LCNEC followed by TC and AC. Currently no marker or ancillary stain are clinically in practice which can aid in classification of these neuroendocrine tumours. In an attempt to address this issue, this project evaluated the use of bioinformatics to analyze publicly available high through-put transcriptomic data to identify markers which would aid in the distinction of SCLC from LCNEC. However, the markers identified were found to have low specificity and sensitivity, leading to the conduction of a de novo gene expression study utilizing laser micro-dissection of pure tumour samples of SCLC and LCNEC. This experiment yielded a different set of top ranked discriminator genes of which validation at the protein level by immunocytochemistry supported CDX2, CD99 and CD44 as LCNEC specific markers and BAI3 as a SCLC specific marker.
APA, Harvard, Vancouver, ISO, and other styles
3

Cui, Tao. "Novel Circulating and Tissue Biomarkers for Small Intestine Neuroendocrine Tumors and Lung Carcinoids." Doctoral thesis, Uppsala universitet, Onkologisk endokrinologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-205570.

Full text
Abstract:
Small intestine neuroendocrine tumors (SI-NETs) and lung carcinoids (LCs) are relatively indolent tumors, which originate from neuroendocrine (NE) cells of the diffuse NE system. Metastases can spread before diagnosis. Thus, potential cures become unavailable, which entitles new biomarker development. Indeed, we aimed at developing Ma2 autoantibodies and olfactory receptor 51E1 (OR51E1) as potential novel biomarkers and exploring other candidate protein markers in patients’ serum. First, we established a sensitive, specific and reliable anti-Ma2 indirect ELISA to distinguish SI-NET patients from healthy controls. We detected longer progression-free and recurrence-free survivals in patients expressing low anti-Ma2 titers. Moreover, a high anti-Ma2 titer was more sensitive than chromogranin A for the risk of recurrence after radical operation of SI-NET patients. We then investigated OR51E1 expression in SI-NETs and LCs. OR51E1 mRNA expression, analyzed by quantitative real-time PCR, was high in microdissected SI-NET cells, in LC cell lines and in frozen LC specimens. Immunohistochemistry (IHC) showed abundant OR51E1 protein expression in SI-NETs. OR51E1 co-expressed with vesicular-monoamine-transporter-1 in the majority of normal and neoplastic enterochromaffin cells. Furthermore, the study on LCs revealed that OR51E1, somatostatin receptor (SSTR) 2, SSTR3, and SSTR5 are expressed in 85%, 71%, 25% and 39% of typical carcinoids (TCs), whereas in 86%, 79%, 43% and 36% of atypical carcinoids (ACs). Based on the proposed IHC scoring system, in the LC cases, where all SSTR subtypes were absent, membrane OR51E1 expression was detected in 10 out of 17 TCs and 1 out of 2 ACs. Moreover, higher OR51E1 scores were detected in 5 out of 6 OctreoScan-negative LC lesions. In addition, the last presented study used a novel suspension bead array, which targeted 124 unique proteins, by using Human Protein Atlas antibodies, to profile biotinylated serum samples from SI-NET patients and healthy controls. We showed 9 proteins, IGFBP2, IGF1, SHKBP1, ETS1, IL1α, STX2, MAML3, EGR3 and XIAP as significant contributors to tumor classification. In conclusion, we proposed Ma2 autoantibodies as a sensitive circulating marker for SI-NET recurrence; OR51E1 as a candidate therapeutic target for SI-NETs; whereas as a novel diagnostic marker for LCs and 9 serum proteins as novel potential SI-NET markers.
小肠神经内分泌肿瘤(SI-NET)和肺类癌(LC)是起源于不同神经内分泌细胞的生长缓慢的肿瘤。肿瘤往往于诊断前已经转移。这导致目前缺乏有效的治疗方法，同时也使得对于新的生物标记物的研发变得有意义。因此，我们在本论文中分别研究了Ma2自身抗体(抗Ma2)，以及潜在的新型生物标记物嗅觉受体51E1(OR51E1)。我们还探讨了患者血清中的其他候选蛋白标记物。 首先，我们建立了一个灵敏特异而可靠的抗Ma2间接酶联免疫吸附试验，用以区分SI-NET患者组和健康对照组。在表达低滴度抗Ma2的患者中，我们检测到了较长的病情无恶化存活率以及肿瘤无复发存活率。此外，高滴度抗Ma2比嗜铬粒蛋白A更为灵敏地检测到了SI-NET患者根治手术后复发的风险。     接下来，我们研究了SI-NET和LC患者肿瘤中的OR51E1受体蛋白的表达。我们用实时定量PCR技术检测到了OR51E1信使核糖核酸在显微切除的SI-NET肿瘤细胞中，以及在LC细胞系和冷冻LC标本中的高度表达。免疫组化结果显示出OR51E1蛋白在SI-NET肿瘤组织中的高度表达。OR51E1与囊泡单胺转运蛋白1在大多数正常和肿瘤的肠嗜铬细胞中可共表达。 另外，我们针对LC患者的研究显示，OR51E1受体蛋白以及促生长素抑制素受体(SSTR)2，SSTR3和SSTR5分别在85％，71％，25％和39％的典型性肺类癌(TC)，以及86％，79％，43％和36的非典型性肺类癌(AC)中表达。基于我们我提出的免疫组化结果得分系统，在无SSTR表达的LC中，OR51E1蛋白在17个TC中的10个以及2个AC中的1个中呈细胞膜表达。而且，在6个OctreoScan显象呈阴性的LC中，有5个OR51E1免疫组化得分很高。     此外，在本论文最后的一项研究中，我们采用了一种新型的悬浮磁珠阵列技术，通过使用来自于人类蛋白质图谱项目的针对124种独特蛋白质的抗体，对SI-NET患者和健康对照组的用生物素标记过的血清样本进行了分析。结果显示，通过利用9种蛋白，即IGFBP2，IGF1，SHKBP1，ETS1，STX2，IL1α，MAML3，EGR3和XIAP，我们可以显著的对肿瘤进行分类。     综上所述，我们提出Ma2自身抗体可作为一个体液中灵敏的生物标记物用以暗示SI-NET肿瘤的复发; OR51E1受体蛋白可作为一个在SI-NET治疗中所能用及的候选生物靶分子，并在LC中作为一种新型的潜在生物标记物。此外，我们在SI-NET患者血清中检测到了9种新的候选标记物蛋白。
APA, Harvard, Vancouver, ISO, and other styles
4

Rêgo, Juliana Florinda de Mendonça. "Análise e comparação da expressão imunoistoquímica de marcadores moleculares (ERCC1, Bcl-2, Lin28a e Ki67) potencialmente preditores de resposta à quimioterapia em carcinomas neuroendócrinos extra-pulmonares e carcinoma de pequenas células de pulmão." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-06022017-155301/.

Full text
Abstract:
INTRODUÇÃO: O carcinoma de pulmão de pequenas células (CPPC) e o carcinoma neuroendócrino (CNE) extra-pulmonar apresentam características histopatológicas e tratamentos similares, porém os desfechos encontrados nos dois grupos podem ser diferentes. Avaliamos a expressão de alguns biomarcadores e a associação destes com taxa de resposta (TR) à quimioterapia baseada em platina e sobrevida global (SG) nos dois grupos. METODOS: Realizamos estudo retrospectivo de pacientes com CPPC e CNE extra-pulmonares tratados com quimioterapia baseada em platina. Todas as amostras tumorais foram revisadas pelo mesmo patologista (R.S.S.M.) e analisadas quanto a expressão imunoistoquímica de Ki-67, ERCC1, Bcl-2 e Lin28a, a qual foi determinada através do H-escore (calculado multiplicando o produto da intensidade da coloração - 0 a 3 - com a porcentagem de células positivas - 0 a 100 -, podendo variar de 0 a 300 - positivo quando >= 200). Os biomarcadores foram analisados tanto como variáveis contínuas quanto categóricas e a TR foi determinada por RECIST 1.1. A associação entre a expressão de cada biomarcador e a TR foi avaliada através do teste de qui-quadrado ou teste exato de Fisher para variáveis categóricas e regressão logística simples para variáveis contínuas. Sobrevida global foi estimada por Kaplan-Meier e as curvas foram comparadas por log-rank. O modelo de regressão de cox foi utilizado para avaliar associação entre SG e a expressão de biomarcadores como variável contínua. RESULTADOS: Entre Julho de 2006 e Julho de 2014, 142 pacientes foram identificados: N=82 (57,7%) com CPPC e N=60 (42,3%) com CNE extra-pulmonar. As características clínicas eram semelhantes em ambos os grupos. Mediana de ki67 foi de 60% (7-100) no CPPC e de 50% (20-95%) no segundo grupo (p=0,858). Com uma mediana de 5 ciclos por paciente (N=123 elegíveis para análise de TR), a TR foi de 86,8% no CPPC, enquanto nos com CNE extra-pulmonar, foi de 44,6% (p < 0.001). A mediana de SG (N=132 elegíveis para análise da SG) foi similar entre os grupos (10,3 meses em CPPC e 11,1 meses em CNE extra-pulmonar; p=0,069). Não houve diferença no padrão de expressão do ERCC1 (p=0,277) e do Lin28a (p=0,051) entre os grupos. Bcl2 foi expresso em 38 pacientes (46,3%) com CPPC e em 17 pacientes (28,3%) com CNE extra-pulmonar (p=0,030). Apenas no grupo com CNE extra-pulmonar, a alta expressão do Bcl2 foi associada com pior prognóstico (8,0 meses vs 14,7 meses; p=0,025). A expressão dos demais marcadores em CNE extra-pulmonar e dos quatro em CPPC não apresentou influência sobre a SG, não havendo também associação entre estes e a taxa de resposta à quimioterapia. Dentre os pacientes com CNE extra-pulmonar, não houve diferença na SG ou na TR entre os pacientes com carcinoma bem diferenciado (N=13;) e com carcinoma pouco diferenciado (N=47). CONCLUSÃO: Apesar do CPPC e do CNE extra-pulmonar serem tratados de forma semelhante, nesta coorte a taxa de resposta entre os grupos foi significativamente diferente. Quando comparado com CPPC, os pacientes com CNE extra-pulmonar apresentam uma menor responsividade à quimioterapia baseada em platina, mas com tendência a maior SG. Dentre os CNE extra-pulmonares, a alta expressão de Bcl-2 foi associada a pior prognóstico. Os demais biomarcadores não apresentaram papel preditor de resposta ou prognóstico
INTRODUCTION: Small cell lung cancer (SCLC) and high-grade extrapulmonary neuroendocrine carcinomas (EPNEC) share similar histopathological features and treatment, but outcomes may differ. We evaluated the expression of biomarkers and their association with response rate (RR) to platin-based chemotherapy and overall survival (OS) in these entities. METHODS: We conducted a retrospective analysis of patients with advanced EPNEC and SCLC treated with platinum-based chemotherapy. A single pathologist (R.S.S.M.) revised all samples. Paraffin-embedded tumor samples were tested for Ki-67, ERCC1, Bcl-2 and Lin28a expression by immunohistochemistry (IHC). Final IHC score (H-score) was calculated multiplying the intensity of staining by grading (0-300, with >= 200 considered positive). Biomarkers were analyzed as both categorical and continuous variables. RR was determined by RECIST 1.1. Associations between each biomarkers expression and RR were assessed using Chi-square or Fisher\'s exact test for categorical variables and univariate logistic regression for continuous variables. OS was estimated by the Kaplan-Meier method and curves were compared by log-rank. Cox regression analysis was used to evaluate any association between biomarkers expression (continuous variables) and OS. RESULTS: From July 2006 to July 2014, 142 patients were identified: N=82 (57,7%) with SCLC and N=60 (42,3%) with EPNEC. Baseline clinical characteristics were similar. Median Ki67 was 60% (7-100) among SCLC patients and 50% (20-95%) in EPNEC (p=0,858). With a median of 5 cycles per patient in both groups (N=123 evaluable patients), the RR was significantly higher in the SCLC group (86,8% vs 44.6%; p < 0.001). Median OS (N=132 evaluable patients) was similar between the groups (10.3 months in SCLC and 11.1 months in EPNEC; p=0,069). In the EPNEC group, there wasn\'t any difference in OS or RR between the patients with welldifferentiated (N=13) and poorly differentiated carcinoma (N=47). ERCC1 (p=0.277) and Lin28a (p=0.051) were similarly expressed between the groups. Bcl2 was expressed in 38 SCLC patients (46.3%) and in 17 EPNEC patients (28.3%; p=0.030). Only in the EPNEC group, Bcl2 high expression was associated with worse survival (8.0 months vs 14.7 months; p = 0.025). RR to chemotherapy was not influenced by the expression of the ERCC1, Lin28a, Bcl-2, Ki-67 in either EPNEC or SCLC groups. CONCLUSION: Even though SCLC and EPNEC are treated similarly, in this cohort, the rate response differed significantly. When compared with SCLC, patients with EPNEC apparently had tumors less responsive to platin-based chemotherapy, but tended to live longer. In EPNEC treated with platin, high expression of Bcl2 was associated with poor prognosis. We could not identify additional predictive or prognostic biomarkers
APA, Harvard, Vancouver, ISO, and other styles
5

Ferguson, Mary L. "Angiogenesis in human lung tumours." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:865de25c-1ac3-4a30-85fa-a9fc677bfcc2.

Full text
Abstract:
Angiogenesis, the growth of new blood vessels, is vital to tumour growth. Prevailing dogma has been that tumours cannot grow without angiogenesis. Based on this premise, anti-angiogenic drugs are used clinically. However, the principle of angiogenesis as an absolute requirement for tumour growth has been challenged with reports that many tumours are entirely or partially non-angiogenic. This study describes and quantifies characteristics of non-angiogenic non-small cell lung tumours, demonstrates non-angiogenic growth in small-cell/neuroendocrine lung tumours and investigates the underlying pathogenetic processes by comparison with angiogenic lung tumours. Hypoxia is an important stimulus for angiogenesis. Differences in response to hypoxia may determine whether a tumour produces new vessels. In order to test this, levels of. necrosis, often considered a surrogate marker of hypoxic stress, were quantified but no difference in quantity of necrosis was found Moreover, immunohistochemical investigation of hypoxia and angiogenesis factors provided no unambiguous explanation for the differences in angiogenesis. Significant differences were seen, however, in fibrosis and inflammation, which were both greater in angiogenic tumours. Differences were greater for lymphocytes rather than cells of the ‘innate’ immune system. This provided an alternative hypothesis: angiogenesis occurs during wound healing and in the growth of granulation tissue, so it is possible that tumour angiogenesis is a response to factors produced by immune cells rather than the tumour itself. A tumour’s angiogenic status may, therefore, be determined by the response it provokes from the immune system. Further work to test this theory would compare levels of immunogenic factors such as Tumour Necrosis Factor and tumour cell surface antigens such as the HLA class I molecules. The study concludes with an investigation into the molecular basis of non-angiogenic growth using the technique of comparative genomic hybridisation (CGH) which allows amplifications and deletions of areas of DNA to be calculated. High-resolution array CGH was evaluated against conventional CGH, and the results compared with previous RNA studies from our laboratory. These revealed a set of genes with consistent changes in both RNA and DNA, several of which form part of known angiogenic and inflammatory pathways.
APA, Harvard, Vancouver, ISO, and other styles
6

Figueiredo, João Daniel Amaral. "Tumores Carcinóides do Pulmão - Abordagem Terapêutica." Master's thesis, 2018. http://hdl.handle.net/10316/82783.

Full text
Abstract:
Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina
Os tumores neuroendócrinos do pulmão representam aproximadamente 25% dos tumores pulmonares primários, podendo ser classificados em baixo (carcinóides típicos), intermédio (carcinóides atípicos) e alto grau (carcinoma neuroendócrino de grandes células e carcinoma de pequenas células do pulmão). Apesar dos tumores carcinóides típicos e atípicos apenas contemplarem 1-5% das neoplasias pulmonares, a sua incidência tem vindo a aumentar significativamente nas últimas décadas, captando a atenção da comunidade médica e científica. A clínica destes tumores é muitas vezes indolente ou inespecífica, tornando o diagnóstico desafiante e obrigando a uma abordagem multidisciplinar. A opção cirúrgica é reconhecida como o tratamento de escolha na doença loco-regional, sendo a única que possibilita a cura; contudo, na doença avançada não se encontra estabelecido nenhum tratamento padronizado, existindo atualmente várias opções terapêuticas em investigação. Esta revisão pretende sistematizar o conhecimento atual sobre os tumores carcinóides, principalmente no que diz respeito à abordagem terapêutica na doença sistémica. .
Neuroendocrine tumours of the lung represent approximately 25% of all primary lung tumours and can be classified as low (typical carcinoids), intermediate (atypical carcinoids), or high grade (large cell neuroendocrine carcinoma or small cell lung carcinoma).Although typical and atypical carcinoid tumours account for only 1-5% of lung neoplasms, their incidence has increased significantly in recent decades, drawing attention to medical and scientific community. The clinical features of these tumours are often indolent or non-specific, making the diagnosis challenging and requiring a multidisciplinary approach. The surgical option is recognized as the treatment of choice in loco-regional disease being the only curative possibility; however, in advanced disease, no standardized treatment has been established and there are currently several therapeutic options under investigation. This review intends to summarize current knowledge about carcinoid tumours, especially regarding the therapeutic approach of systemic disease. .
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Lung Neuroendocrine tumor"

1

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Filosso, Pier Luigi. Clinical Management of Neuroendocrine Tumors of the Lung, an Issue of Thoracic Surgery Clinics. Elsevier - Health Sciences Division, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Filosso, Pier Luigi. Clinical Management of Neuroendocrine Tumors of the Lung, an Issue of Thoracic Surgery Clinics. Elsevier - Health Sciences Division, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Lung Neuroendocrine tumor"

1

Yoon, Esther C., and Guoping Cai. "Atypical Carcinoid Tumor Versus Large-Cell Neuroendocrine Carcinoma." In Practical Lung Pathology, 75–81. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-14402-8_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Filosso, Pier Luigi, Elisa Carla Fontana, and Matteo Roffinella. "Primary Neuroendocrine Tumors of the Lung." In Neuroendocrine Tumors, 209–22. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62241-1_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Dacic, Sanja. "Neuroendocrine Lung Tumors." In Molecular Pathology Library, 271–75. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1707-2_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Granberg, Dan. "Neuroendocrine Tumors of the Lung." In Neuroendocrine Tumours, 143–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45215-8_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Weissferdt, Annikka. "Neuroendocrine Tumors of the Lung." In Diagnostic Thoracic Pathology, 401–34. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36438-0_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Khalil, Farah. "Neuroendocrine Tumors of the Lung." In Neuroendocrine Tumors: Review of Pathology, Molecular and Therapeutic Advances, 153–78. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3426-3_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Fraire, Armando E., Ulrike M. Gruber-Mösenbacher, and Helmut H. Popper. "Endocrine Tumors of the Lung and Upper Airways." In Surgical Pathology of Endocrine and Neuroendocrine Tumors, 131–42. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-396-1_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Liu, Dongyou. "Large Cell Carcinoma and Large Cell Neuroendocrine Carcinoma of the Lung." In Tumors and Cancers, 65–70. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/b22275-13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Senderovitz, Thomas, Birgit G. Skov, and Fred R. Hirsch. "Neuroendocrine characteristics in malignant lung tumors: Implications for diagnosis, treatment, and prognosis." In Cancer Treatment and Research, 143–54. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2630-8_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

"Neuroendocrine Tumors of the Lung." In Tumors and Tumor-Like Conditions of the Lung and Pleura, 137–64. Elsevier, 2010. http://dx.doi.org/10.1016/b978-1-4160-3624-1.00005-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Lung Neuroendocrine tumor"

1

Masood, S., N. Habib, R. Alalawi, N. Sher, and Z. Saeed. "Focal Bronchiectasis Due to a Lung Neuroendocrine Tumor." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7509.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ireland, Abbie S., Alexi M. Micinski, David W. Kastner, Bingqian Guo, Sarah J. Wait, Kyle B. Spainhower, Christopher C. Conley, et al. "Abstract PO-120: MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate." In Abstracts: AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-po-120.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Gabasa, Marta, Rafael Ikemori, Marselina Arshakyan, Evette Radisky, Noemí Reguard, Derek Radisky, and Jordi Alcaraz. "Abstract 5099: Large-cell neuroendocrine carcinoma cells of the lung induce a tumor-promoting senescent phenotype in fibroblasts through MMP1 overexpression and TGFβ1." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5099.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

George, Julie. "Abstract IA28: The genomic landscape of SCLC and other neuroendocrine lung tumors." In Abstracts: Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; January 8-11, 2018; San Diego, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.aacriaslc18-ia28.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

George, Julie, Lynnette Fernandez-Cuesta, Vonn Walter, Neil Hayes, and Roman Thomas. "Abstract 122: Comparative analysis of small cell lung cancer and other pulmonary neuroendocrine tumors." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-122.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Jahchan, Nadine S., Joel T. Dudley, Pawel K. Mazur, Natasha Flores, Dian Yang, Alec Palmerton, Anne-Flore Zmoos, et al. "Abstract 4610: A drug repositioning approach identifies tricyclic antidepressants as inhibitors of small cell lung cancer and other neuroendocrine tumors." 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.am2014-4610.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Fernandez-Cuesta, Lynnette, Martin Peifer, Xin Lu, Danila Seidel, Thomas Zander, Frauke Leenders, Luka Ozretić, et al. "Abstract 1531: Cross-entity mutation analysis of lung neuroendocrine tumors sheds light into their molecular origin and identifies new therapeutic targets." 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.am2014-1531.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Hassan, Wafaa, Atef Darwish, and Abeer Darwish. "Abstract B22: Is there a role of estrogen and progesterone receptors in differentiating primary neuroendocrinal lung tumors from metastatic adenocarcinoma?" In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-b22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Nawaz, Nava K., Fan Lin, Azadeh Stark, and Conrad Schuerch. "Abstract 829: A panel of three biomarkers for differentiating high from low grade neuroendocrine tumors of the lung: Findings from a Pilot Project." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-829.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Lung Neuroendocrine tumor' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography